Dụng Cụ Chỉnh Hình Và Chân Tay Giả Trong Phục Hồi Chức Năng (Ấn Bản Thứ 3)

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Section II  Orthoses in Rehabilitation
Component
Dimension
Examination Strategies
Neuromotor status
Muscle tone
(compliance vs stiffness)
Resistance to passive movement at various speeds
Palpation
tone scales (e.g., modified Ashworth),
descriptive category (hypertonic/spastic, rigid, hypotonic,
fluctuating, flaccid)
Tonal response to deep tendon
reflex testing
Amplitude of response (absent/0, diminished /+1,
normal/+2, brisk/3, clonus/+4, sustained clonus +5)
Pattern of response (distal-proximal)
Symmetry of response (right-left)
Tonal response to change in position
Appearance or influence of abnormal developmental reflexes
(e.g., ATNR, positive supportive reaction)
Antigravity stiffness/postural tone
Assessing stiffness to support trunk or body segment in
various antigravity positions
Involuntary movement
Observation at rest and during movement;
descriptive category (e.g., chorea, athetosis, tremor, tics)
Muscle performance
Strength
Speed/power
Accuracy
Timing
Fluidity
Muscle endurance
Observation of antigravity movement
Manual muscle testing, dynamometer
Isokinetic testing
Description: hypokinetic, functional, hyperkinetic
Motor control
Postural control
Static balance tests (e.g., timed single limb stance)
Anticipatory balance tests (e.g., reach distances, ability to
change direction)
Reactionary balance test: perturbation
Recruitment/adaptation of contractions
Ability to move between concentric, eccentric, and holding
contractions during functional activity
Ability to initiate, sustain, and terminate contraction and
movement
Ability to isolate limb segments as needed
for effective task performance
Observation of motor performance during functional tasks or
challenges
Influence of abnormal synergy or abnormal developmental
reflexes
Ability to adapt movement strategies to
task demands
Observation of ability to generate appropriate force and type
of contract at appropriate times
Ability to adapt movement strategies in
different environment
Observation of movement in low light, different floor
surfaces, inclines, stairs, closed versus open (distracting,
demanding) environments
Relationship of agonist/antagonist
Ability to alter muscle activity of agonist/antagonist on
demand (within the limb, across limb and limb girdle,
within trunk) during functional activities
Dexterity, coordination, agility
Observation of performance during functional activity
Special tests
Developmental scales and profiles
Functional movement ability








Activities of daily living (ADL)
Observation of movement during task
Self-report of individual or caregiver
Various ADL scales
Ability to don/doff orthosis
Transitional movements and transfers
To/from floor
Sit to stand
Bathroom transfers
Car transfers
Observation during performance
Movement strategy
Assistance required
Level of difficulty
Task analysis to identify where in movement difficulty occurs
and contributors to difficulty
TABLE 10-7  Components of a Physical Therapy Examination and Evaluation in Preparation for Serial Casting,
or Prescription/Fitting of Appropriate Splint or Orthoses—cont'd

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
293
Component
Dimension
Examination Strategies
Mobility and locomotion
Observational gait analysis, with and without orthosis
Gait speed, other kinematic measures
Use of assistive devices
Level of assistance required
Gait lab kinetic measures (moments, torques, and muscle
activity via video, force plate, and EMG analysis)
UE function and use of hands
Observation during various fine and gross UE motor tasks
Cardiovascular endurance
Heart rate, blood pressure, oxygen saturation during activity
Ratings of perceived exertion during tasks
6-Minute walk test
Fatigue scales
Environmental assessment (home, work,
school, leisure)
Environmental safety checklists
Interview with individual and caregivers about characteristics
of environments in which individual must function
Integumentary integrity
Skin condition
Inspection for neuropathic, dysvascular, or traumatic wounds
Document callus and scarring
Document pressure sensitive areas
Document protective sensation, insensate weight-bearing
areas
Sensory organization and
processing
Sensory integrity
Adequacy of vision (acuity, peripheral vision, tracking,
visual field loss)
Screening for exteroception, proprioception ability
Document insensate areas, especially of hands/feet
Document paresthesia and dysesthesia
Perceptual function
Visual spatial perception
Awareness of position in space
Awareness of body parts
Observation of movement during functional tasks
Developmental tests, measures
Special perceptual tests, measures
Sensory integration
Habituation to stimulus
Ability to sort through conflicting sensory
information
Observation of movement during functional tasks
of increasing demand
Cognitive function
Communication
Adequacy of hearing and auditory processing
Ability to understand language
Ability to use language
Oral-motor function (dysarthria)
Impact of position on voice
Ability to learn and remember
Reports of teachers, neuropsychological testing
Ability to problem solve
Observation when presented with challenge
Results of neuropsychological testing
Motivation
Observation
Self-report of individual and caregivers
Distractiblility/focus
Observation
Self-report of individual, caregiver, teachers
Results of neuropsychological testing
Ability to manage frustration, uncertainty
Observation
Self-report of individual, caregiver, teachers
Psychosocial factors



Family and caregiver
Availability and capacity with respect to use of orthosis
School or work-related activities
Typical activities and roles: demands and barriers
encountered
Leisure or play activities
Typical activities and roles: demands and barriers
encountered
ACL, anterior collateral ligament of the knee; ATNR, asymmetrical tonic neck reflex; EMG, electromyographic; PCL, posterior collateral
ligament of the knee; ROM, range of motion; UE, upper extremity.
TABLE 10-7  Components of a Physical Therapy Examination and Evaluation in Preparation for Serial Casting,
or Prescription/Fitting of Appropriate Splint or Orthoses—cont'd

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Section II  Orthoses in Rehabilitation
5. protect a limb following orthopedic surgery performed
to correct deformity or instability;
6. enhance alignment following pharmacological inter­
vention with botulinum toxin; and
7. provide alternative methods for mobility.
The risk for developing secondary musculoskeletal impair­
ments is high in the presence of hypertonicity.108,197–200 Passive
stretching programs alone are generally ineffective as a man­
agement strategy for reducing risk for contracture develop­
ment.201,202 Prolonged positioning for several hours a day is
a critical adjunct to stretching.203–206 Adaptive equipment can
be used to provide structural alignment for prolonged peri­
ods of time to maintain extensibility of muscles, decrease
the effect of muscle imbalance across joints, and provide
postural support. An adaptive seating system, for example,
would provide upright postural support for sitting; main­
tain spinal alignment and pelvic positioning; support optimal
hip, knee, and ankle positions; and promote the best posi­
tion for upper extremity function.207–210 Positioning devices
for supported standing are often used to maintain exten­
sibility of muscles, promote bone mineral density through
weight bearing, and promote musculoskeletal development
such as acetabular depth in a developing child with hyper­
tonicity (Figure  10-7).211–213 Other examples of positioning
devices include prone, supine and sidelyer systems, bathing
and toileting seating systems, and a variety of mobility alter­
natives such as gait trainers.214–217 Although there are many
options for adaptive equipment designed to assist function
and caregiving for persons with neurological and neuromus­
cular dysfunction, knowledge about options and limitations
in funding limit access for many who might otherwise benefit
from such devices.218–221
Serial corrective casts have long been used as a primary
intervention for individuals with significant hypertonus to
provide a prolonged elongation of soft tissue over a long time
period. They increase the length of a contracted muscle and
its supportive tissues and reset the threshold for response to
stretch reflex.155–160 Some splints or dynamic orthoses are used
primarily at night to provide 8 or more hours of stretch on
a regular basis; others can be worn during daily activities to
provide a longer period of stretch (Figure 10-8).222–226 More
recently, serial casting and dynamic splinting have been used
in conjunction with pharmacological interventions for man­
agement of spasticity in both children and adults with severe
hypertonicity (Figure 10-9).227,228 Although the pharmacolog­
ical agent may reduce the degree of spasticity in hypertonic
muscles, concomitant shortening of the muscles and tendons
must be addressed while the neurological influence is altered,
as should concomitant deficits in other dimensions of muscle
performance and motor control.229–231 A young child with spas­
tic diplegic CP, for example, may receive botulinum injections
to the gastrocnemius and soleus muscles to reduce severity of
spasticity as an alternative to early orthopedic surgery.232,233
Selecting the Appropriate Orthosis
Rehabilitation professionals play an active role in deciding
what type of orthosis would be most appropriate for an indi­
vidual with neuromuscular impairment. A number of fac­
tors contribute to the decision-making process; the collective
wisdom of physical and occupational therapists, orthotists,
physicians, family, and the patient who might benefit from
orthotic intervention is necessary for appropriate and effec­
tive casting or orthotic intervention.192,234,235
The primary goal of orthotic prescription is to select the
device and components that will best improve function, given
the individual's pathology and prognosis, desired activities,
and participation needs, both in the immediate situation and
over time. To do this, the cast, splint, or orthosis might provide
external support, control or limit ROM, optimally position
a limb for function, reduce risk of secondary musculoskel­
etal complications, or provide a base for adaptive equipment
that would make function more efficient. What evidence is
available to support clinical decision making with respect to
orthotic prescription? Although many professionals rely on
expertise gained by working with persons with neuromotor
impairment over years of clinical practice, a growing number
of articles on orthotic design for particular patient popula­
tions in the rehabilitation and orthotic research literature are
available to guide decision making, not only for individuals
with hypertonicity but also for those with spinal cord injury,
myelomeningocele, and muscular dystrophy.195,234–241
FIGURE 10-7  Example of adaptive equipment (stander) available to
assist appropriate alignment and function in the presence of impair­
ment of muscle tone, muscle performance, postural control, or dif­
ficulty with movement and coordination. (Used with permission of
)

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
295
If the primary goal of orthotic intervention is to improve
safety and functionality during ambulation, it is imperative
to identify where in the gait cycle abnormal tone or muscle
performance is impaired (refer to Chapter 5 for more infor­
mation on critical events in each subphase of gait, as well
as detailed information about strategies to examine gait).
Systematic consideration of a series of questions can help
identify where within the gait cycle (considering both stance
and swing phases) problems occur.242–244
Rehabilitation professions must recognize that no orthosis
will normalize gait for persons with neurologically based gait
difficulties. Whenever an external device is placed on a limb, it is
likely to solve one problem while at the same time ­creating other
constraints on limb function. The therapist, orthotist, and patient
collectively problem solve during the orthotic prescription phase
to prioritize the difficulties the individual is having during gait
and then select the design and components that will allow the
person to be most functional while walking, with the least addi­
tional constraint on other mobility and functional tasks.
The rehabilitation team at Rancho Los Amigos National
Rehabilitation Center has developed an algorithm that is
particularly useful in guiding clinical decision making and
sorting through possible orthotic options for adults with neu­
romotor impairment (ROADMAP: Recommendations for
Orthotic Assessment, Decision Making, and Prescription).192
When considering orthotic interventions for persons having
FIGURE 10-9  Example of a custom-molded orthosis, worn in the immediate postoperative period and later during sleep, designed to enhance
range of motion following botulinum toxin type A injection. The goal was to reduce hypertonicity and delay corrective orthopedic surgery for
a child with spastic cerebral palsy. (Courtesy Ultraflex Systems Inc., Downingtown, Pa.)
FIGURE 10-8  Examples of a serial cast (A) used to provide sustained stretch to the Achilles tendon and foot in a child with spastic cerebral
palsy, and of dynamic orthoses used to provide prolonged stretch to tissues contributing to joint contracture at the knee (B) and elbow (C).
Both serial casts and dynamic orthoses can be used for persons with both musculoskeletal and neuromuscular pathologies that have resulted
in joint contracture, and may be used as an adjunct to surgical and pharmacological interventions for persons with hypertonicity. (B and C
Courtesy Ortho Innovations, Rochester, Minn.)

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Section II  Orthoses in Rehabilitation
­difficulty with ambulation, this team suggests asking the fol­
lowing questions:
1. Is there adequate ROM in the lower extremities to appro­
priately align or position limb segments in each subphase
of gait?
2. Does the individual have the motivation and cognitive
resources necessary to work toward meeting the goal of
ambulation?
3. Does the individual have enough endurance (cardio­
vascular and cardiopulmonary resources) to be able to
functionally ambulate? If endurance is not currently suf­
ficient, might it be improved by a concurrent conditioning
program?
4. Does the individual have adequate upper extremity,
trunk, and lower extremity strength; power; motor con­
trol; and postural control for ambulation (with an appro­
priate assistive device, if necessary)? If these dimensions
of movement are not currently sufficient, might they be
improved with concurrent rehabilitation intervention?
5. Is there sufficient awareness of lower limb position (pro­
prioception, kinesthesia) for controlled forward progres­
sion in gait? If not, might alternative sensory strategies be
learned or used to substitute for limb position sense?
If the answers to most of these questions are “yes,” the indi­
vidual is considered to be a candidate for orthotic interven­
tion. The next determinant is knee control and strength: If the
individual has antigravity knee extension with the ability to
respond to some resistance (MMT [Manual Muscle Testing]
grade of 3+ strength), even if there is impaired propriocep­
tion in the involved limb, then an ankle-foot orthosis may be
appropriate. If there is impairment of strength or of proprio­
ception (or both), then the team is more likely to recommend
a knee-ankle-foot orthosis. Box 10-1 is an example of a deci­
sion tree used to guide the selection of components.
IS A KNEE-ANKLE-FOOT ORTHOSIS (KAFO)
INDICATED?
• Is there at least antigravity with some resistance (MMT
3+/5 strength) in quadriceps bilaterally?
• Is proprioception intact bilaterally?
If yes: continue with the assessment for AFO
If no: KAFO may improve gait, continue assessment process
WHICH KAFO COMPONENTS ARE THE MOST
APPROPRIATE?
• Is there at least antigravity with some resistance (MMT
3+/5 strength) in one lower extremity?
• Is proprioception intact in at least one lower extremity?
If no: consider trial of bilateral KAFOs or a reciprocal
gait orthosis
If yes: unilateral KAFO may be indicated—continue assess­
ment to determine if knee locking mechanism necessary
CAN THE KNEE BE FULLY EXTENDED, WITHOUT
PAIN, DURING STANCE?
If no: consider KAFO with knee lock
If yes: consider KAFO with variable knee mechanism
and continue assessment
IS THERE AT EFFECTIVE ACTIVE CONTROL OF
KNEE EXTENSION DURING STANCE?
If no: consider stance control knee mechanism
If yes: consider free motion knee mechanism
Continue with ankle-foot orthosis (AFO) decision tree
to determine appropriate ankle control strategy
IS AN AFO INDICATED?
• Is there impairment of ankle strength?
• Is there impairment of proprioception?
• Is there hypertonicity of plantar flexors?
• Is there a combination of all of the above?
If no: may not require lower extremity orthosis
If yes: lower extremity orthosis may improve gait—continue
assessment process
WHICH AFO DESIGN AND COMPONENTS ARE
THE BEST OPTION?
• Does impaired strength hamper foot position in stance
or swing?
• Does impaired proprioception hamper foot placement in
stance or swing?
• Does hypertonicity/spasticity hamper foot position in
stance or swing?
If no: consider adjustable articulating ankle joint (allows
full dorsiflexion [DF] and plantar flexion [PF])
If yes: consider limiting or blocking ankle motion, ­continue
assessment process
IS THERE MORE THAN MINIMAL IMPAIRMENT OF
STATIC AND DYNAMIC POSTURAL CONTROL IN
STANDING?
• Is there significant spasticity?
• Is proprioception significantly impaired?
If no: consider adjustable articulating ankle joint that
blocks PF beyond neutral ankle position and continue
assessment
If yes: consider solid-ankle AFO or adjustable articulat­
ing ankle that is fully locked (consider rocker bottom shoe)
• Is there also plantar flexion strength ≤ MMT 4 in standing?
• Is there also excessive knee flexion and dorsiflexion dur­
ing stance?
• Is there also excessive plantar flexion with knee hyperex­
tension during stance?
If no: consider adjustable articulating ankle joint with PF
stop, and continue assessment
If yes: consider adjustable articulating ankle joint with PF
stop and limited DF excursion, and continue assessment
• Is there also dorsiflexion strength ≤ 4 in standing?
If no: consider adjustable articulating ankle with PF stop,
limited DF excursion in stance, no DF assist necessary
If yes: consider adjustable articulating ankle with PF stop,
limited DF excursion, and DF assist for effective swing phase
BOX 10-1  Decision Tree for Orthotic Options

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
297
Especially important is that the individual who will use the
orthosis and caregivers, as appropriate, are actively involved
in the decision-making process. To make an informed deci­
sion, the person needing an orthosis must understand both
the benefits and constraints associated with the orthotic
designs and components being considered. He or she must
be able to consider the range of orthotic options, as well as
medical/surgical intervention and additional rehabilitation
interventions that might affect his or her ability to walk. The
entire team must consider what the individual who will be
wearing the orthosis wants to accomplish, as well as the pref­
erences he or she might have in terms of ease of donning/
doffing, wearing schedule, and cosmesis of the device being
recommended. Beginning with a trial orthosis, perhaps a pre­
fabricated or multiadjustable version, is helpful before finaliz­
ing the orthotic prescription, especially if it is unclear whether
ambulation will eventually be possible. Certainly, most indi­
viduals with neuromuscular conditions that compromise
their ability to walk benefit from a chance to experience what
ambulation with an orthosis requires, given their individual
constellation of impairments. Some may decide that using
orthoses and an appropriate assistive device for functional
ambulation throughout the day meets their mobility needs.
Others may opt, because of the energy cost of walking with
knee-ankle-foot orthoses or hip-knee-ankle-foot orthoses, to
use a wheelchair for primary mobility and reserve the use of
orthoses to exercise bouts aimed at building cardiovascular
endurance. Finally, some may decide that orthotic interven­
tion will not meet their needs and pursue other avenues to
address mobility and endurance issues.
SUMMARY
This chapter reviews the functions and roles of structures and
systems in both the central and peripheral nervous systems,
the impairments that are likely to occur when particular struc­
tures or systems are damaged by injury or disease process,
abnormalities of tone and motor control that influence an indi­
vidual's ability to ambulate and affect the likelihood of devel­
oping secondary musculoskeletal impairments, and some of
the pharmacological and surgical options that are available to
manage hypertonicity and correct deformity that may develop
over time. Strategies to determine where in the gait cycle an
individual with various neuromotor impairments is likely to
have difficulty are explored, as are the orthotic options that
might best address the limitations that the individual faces.
This chapter provides a strong foundation for physical therapy
examination and evaluation. Next, the reader should consider
physical therapy interventions that will focus on wearing,
using, and caring for the prescribed orthosis, including (1)
strategies to enhance motor learning when a new ambulatory
aid (orthosis and/or assistive device) is introduced, (2) prac­
tice using the device under various environmental conditions
(surfaces, obstacles, people moving within the environment),
and (3) the ability to use the orthosis and ambulatory assistive
device during functional activities beyond walking at comfort­
able gait speed.
CASE EXAMPLE 1
A Young Child with Spastic Diplegic Cerebral Palsy
T. H. is a 4-year-old child who was born prematurely at
32 weeks of gestation and diagnosed with spastic diplegic
CP at 10 months of age. She is being evaluated for potential
botulinum A injection as a strategy to manage significant
extensor hypertonicity that is increasingly limiting her
ability to ambulate as she grows. At present she uses bilat­
eral articulating ankle-foot orthoses with a plantar flexion
stop and a posterior rolling walker for locomotion at her
preschool program; she prefers creeping in quadruped for
mobility at home. Her articulating orthoses allow her to
move into some dorsiflexion as she transitions to and from
the floor during play. She has difficulty pushing to stand
from half-kneel secondary to poor force production of hip
and knee extensors. Muscle endurance is impaired, con­
tributing to a crouch gait position, especially as she tires
after a full day of activity. She falls frequently when she
tries to run. She has been monitored in a CP clinic at the
regional children's hospital; the team is concerned that she
is developing rotational deformity of the lower extremities,
as well as plantar flexion contracture and forefoot defor­
mity due to her longstanding hypertonicity.
Questions to Consider
• In which subphases of the gait cycle is function or safety
compromised when T. H. ambulates without her orthoses?
• In what way does T. H.'s hypertonicity contribute to her
difficulty with floor mobility and ambulation?
• In what ways does T. H.'s inadequate muscle perfor­
mance contribute to her difficulty with floor mobility
and ambulation? What are the most likely dimensions
of muscle performance that are impaired, given her
diagnosis of spastic diplegia?
• In what ways does T. H.'s impaired postural control con­
tribute to her difficulty with locomotion/ambulation?
What are the most likely dimensions of her impairment in
postural control, given her diagnosis of spastic diplegia?
• Are there primary or secondary musculoskeletal impair­
ments that are influencing her function and safety during
ambulation? How do her age and future growth influ­
ence her risk for developing secondary impairments?
• Given her constellation of impairments, what compen­
satory strategies is T. H. likely to use to accomplish the
task of locomotion?
• Which of T. H.'s anticipated or observed impairments
are remediable? Which will require accommodation?
• What orthotic options (design, components) are avail­
able to address T. H.'s impairment of locomotion and
related functional limitations? What are the pros and
cons of each?
• What alternative or concurrent medical (surgical/phar­
macological) interventions might assist improvement
in safety and function for T. H.?
Continued

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Section II  Orthoses in Rehabilitation
• What additional rehabilitation interventions might
assist improvement in function and safety for T. H.?
• How do you anticipate T. H.'s orthotic needs might
change as she develops and grows?
• What outcome measures can be used to assess efficacy
of orthotic, therapeutic, pharmacological, or surgical
intervention for T. H.?
CASE EXAMPLE 2
A Child with Spastic Quadriplegic Cerebral Palsy
J. T. is an 11-year-old boy with significant spastic quad­
riplegic CP who is in the midst of a preadolescent growth
spurt. He currently uses a custom seating system in a power
wheelchair for self-directed mobility at school and in the
community. Recently he has nearly fallen out of his chair
when negotiating around sharp corners. At home he divides
his time between his chair and rolling/crawling on the floor.
J. T.'s mom reports that it is becoming increasingly difficult
to assist him in transfers into the family's sport utility vehi­
cle and help him with self-care activities because of upper
extremity flexor tightness, increasing hip and knee flexion
contractures, and plantar flexion tightness.
In addition, when supine, J. T.'s resting position is
becoming more obviously “windswept”, with excessive
right hip external rotation and excessive left hip inter­
nal rotation, causing a pelvic obliquity. He attends physi­
cal therapy at school several times each week to help him
with functional abilities in the classroom and around cam­
pus, with additional outpatient visits focusing on improv­
ing postural control and muscle performance. Both of his
therapists are becoming concerned about his increasing
limitation in ROM, as well as the risk for increasing rota­
tional deformity and hip dysfunction as he grows. His out­
patient therapist accompanies J. T. and his mother to the
CP orthotics clinic at the regional children's medical center
to explore the possibility of functional bracing or dynamic
orthoses, or both, to manage the musculoskeletal compli­
cations that are developing because of his spasticity. They
also have questions about surgical and pharmacological
intervention.
Questions to Consider
• In what way does J. T.'s hypertonicity contribute to his
difficulty with mobility/locomotion and other func­
tional activities?
• In what ways does J. T.'s impaired muscle performance
contribute to his difficulty with functional activities?
• In what ways does J. T.'s impaired postural control con­
tribute to his difficulty with locomotion/ambulation?
What are the most likely dimensions of his impairment
in postural control, given his diagnosis of spastic quad­
riplegic cerebral palsy?
• Are any primary or secondary musculoskeletal impair­
ments influencing J. T.'s function and safety during
mobility and transfer tasks?
• Given his constellation of impairments, what compen­
satory strategies is J. T. likely to use to accomplish his
functional tasks at school and at home?
• Which of J. T.'s anticipated or observed impairments
are remediable? Which will require accommodation?
• What orthotic options (design, components) are avail­
able to address J. T.'s impairments and functional limi­
tations? What are the pros and cons of each?
• Given the pelvic obliquity, what secondary musculoskel­
etal complications need to be monitored as he grows?
How might these concerns be addressed by seating?
• What alternative or concurrent medical (surgical/phar­
macological) interventions might assist improvement
in safety and function for J. T.?
• What additional rehabilitation interventions might
assist improvement in function and safety for J. T.?
• How do you anticipate J. T.'s orthotic needs might
change as he develops and grows?
• What outcome measures can be used to assess efficacy
of orthotic, therapeutic, pharmacological, or surgical
intervention for J. T.?
CASE EXAMPLE 3
A Young Adult with Acquired Brain Injury and
Decerebrate Pattern Hypertonicity
P. G. is a 17-year-old girl who sustained significant closed-
head injury in a motor vehicle accident 3 weeks ago. She
was admitted to the brain injury unit at the regional reha­
bilitation hospital earlier this week. Now functioning at
a Rancho Los Amigos Cognitive Level 5 (confused and
inappropriate), P. G. exhibits significant decorticate pos­
turing whenever she attempts to move volitionally (right
greater than left). She has marked limitations in passive
ROM at the elbow and wrist, as well as equinovarus at the
ankle, both of which are limiting her ability to stand and
effectively propel her wheelchair. While sitting, she falls
when she tries to throw a ball to her therapist. Her gait
is characterized by large range ballistic extensor thrust
throughout stance, which impedes forward progression.
She is most focused and responsive to intervention when
involved in ambulation-oriented activities. Currently,
her hypertonicity is being managed with oral baclofen
(Lioresal). However, her therapists are concerned that
contracture formation continues. During rehabilitation
rounds, the physiatrist, neurologists, and therapists agree
that a trial of serial casting should be added to her regi­
men to enhance her rehabilitation.
Questions to Consider
• In which subphases of the gait cycle is function or safety
compromised when G. P. attempts to ambulate?
• In what way does G. P.'s hypertonicity contribute to her
difficulty with locomotion/ambulation?

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
299
• In what ways does G. P.'s impaired muscle performance
contribute to her difficulty with locomotion/ambu­
lation? What are the most likely dimensions of her
impairment in muscle performance, given her diagno­
sis of acquired brain injury?
• In what ways does G. P.'s impaired postural control con­
tribute to her difficulty with locomotion/ambulation?
What are the most likely dimensions of her impairment
in motor control, given her diagnosis of acquired brain
injury?
• Are any primary or secondary musculoskeletal impair­
ments influencing her function and safety during
ambulation? What do you think is likely to develop as
she recovers from her head injury?
• Given her constellation of impairments, what compen­
satory strategies is G. P. likely to use to accomplish the
task of locomotion?
• Which of G. P.'s anticipated or observed impairments
are remediable? Which will require accommodation?
• What orthotic options (design, components) are avail­
able to address G. P.'s impairment of locomotion and
related functional limitations? What are the pros and
cons of each?
• What alternative or concurrent medical (surgical/phar­
macological) interventions might assist improvement
in safety and function for G. P.?
• What additional rehabilitation interventions might
assist improvement in function and safety for G. P.?
• How do you anticipate G. P.'s orthotic needs might
change as she recovers over the next year?
• What outcome measures can be used to assess efficacy
of orthotic, therapeutic, pharmacological, or surgical
intervention for G. P.?
CASE EXAMPLE 4
Two Individuals with Recent Stroke
You work in the short-term rehabilitation unit associated
with the regional tertiary care hospital in your area. This
week two gentlemen recovering from stroke/brain attack sus­
tained 3 days ago were admitted to the unit for a short stay
in preparation for discharge home. Both indicate that their
primary goals at this time are to be able to walk functional
distances within their homes, manage stairs to enter/leave the
house, and get to bedrooms on the second floor. You antici­
pate that they will receive intensive rehabilitation services for
5 to 8 days, with home care for follow-up after discharge.
M. O., 73 years old with a history of hypertension,
mild chronic obstructive pulmonary disease, and an
­uncomplicated myocardial infarction 2 years ago, has been
diagnosed with a lacunar infarct within the left posterior
limb of internal capsule. On passive motion, he has been
given modified Ashworth scores of 3 in his right upper
extremity and 2 in his right lower extremity. When asked
to bend his knee (when supine), he demonstrates difficulty
initiating flexion, and when he finally begins to move, his
ankle, knee, and hip move in a mass-flexion pattern; he
is unable to isolate limb segments. When asked to slowly
lower his leg to the bed, he “shoots” into a full lower extrem­
ity synergy pattern. He rises from sitting to standing with
verbal and tactile cueing, somewhat asymmetrically, relying
on his left extremities. Once upright, he can shift his center
of mass to the midline, holding an effective upright posture,
but feels unsteady when shifted beyond midline to the right.
With encouragement and facilitation, he can shift weight
toward his right in preparation for swing-limb advance­
ment of the left lower extremity, and he is pleased to have
taken a few steps, however short, in the parallel bars. Before
his infarct, he was an avid golfer and enjoyed bowling. He is
fearful that he will never be able to resume these activities.
E. B., 64, is a recently retired car mechanic with an 8-year
history of diabetes mellitus previously controlled by diet
and oral medications but requiring insulin since his stroke.
MRI indicates probable occlusion in the right posteroinfe­
rior branch of the middle cerebral artery, with ischemia and
resultant inflammation in the parietal lobe. Because E. B.
has been afraid of hospitals for most of his life, he resisted
seeking medical care as his symptoms began, arriving at the
emergency department 12 hours after onset of hemiplegia.
He currently displays a heavy, hypotonic, somewhat edem­
atous left upper extremity. He is unusually unconcerned
about the fact that he has had a stroke and tells you that he
should be able to function “well enough” when he returns
home to his familiar environment. On examination, he dem­
onstrates homonymous hemianopsia, especially of the lower
left visual field, and impaired kinesthetic awareness of his
left extremities. You observe that he appears to be unaware
when his lower upper extremity slips off the tray table of his
wheelchair and his fingers become entangled in the spokes
of the wheel as he propels forward using his right leg. When
assisted to standing in the parallel bars, he does not seem to
be accurately aware of his upright position, requiring moder­
ate assistance to keep from falling to the left. When asked to
try to walk forward a few paces, he repeatedly advances his
right lower extremity, even when prompted to consider the
position and activity of his lower left extremity.
Questions to Consider
• In what ways are the stroke-related impairments
observed in these two gentlemen similar or different?
How can you explain these differences?
• In what subphases of the gait cycle is function or safety
compromised when each of these gentleman attempts
to ambulate?
• In what way does each gentleman's abnormal tone con­
tribute to his difficulty with locomotion/ambulation?
• In what ways does each gentleman's impaired muscle per­
formance contribute to his difficulty with locomotion/
Continued

300
Section II  Orthoses in Rehabilitation
ambulation? What are the most likely dimensions of each
man's impairment in muscle performance, given his etiol­
ogy and location of stroke?
• In what ways does each gentleman's impaired postural
control contribute to his difficulty with locomotion/
ambulation? What are the most likely dimensions of
each man's impairment in postural control, given the
etiology and location of his stroke?
• Are any primary or secondary musculoskeletal impair­
ments influencing each man's function and safety
during ambulation? How does each man's age and
concomitant medical conditions influence his risk for
developing secondary impairments?
• Given each gentleman's constellation of impairments,
what compensatory strategies is each likely to use to
accomplish the task of locomotion?
• Which of each gentleman's anticipated or observed
impairments are remediable? Which will require
accommodation?
• What orthotic options are available to address each gen­
tleman's impairment of locomotion and related func­
tional limitations? What are the pros and cons of each?
• What alternative or concurrent medical (surgical/
pharmacological) interventions might help improve in
safety and function for each individual?
• What additional rehabilitation interventions might help
improve in function and safety for M. O. and E. B.?
• How do you anticipate each gentleman's orthotic needs
might change as he recovers from CNS damage?
• What outcome measures can be used to assess the effi­
cacy of orthotic, therapeutic, pharmacological, or sur­
gical intervention for each gentleman?
CASE EXAMPLE 5
A Young Adult with Incomplete Spinal Cord Injury
Z. C. is a 23-year-old man who sustained an incomplete
C7 spinal cord injury 3 weeks ago when he lost control
and crash-landed during a failed acrobatic stunt during a
half-pipe snowboard competition at a local ski resort. After
being stabilized on site, he was quickly airlifted to a regional
spinal cord injury/trauma center. Methylprednisolone was
administered within 1.5 hours of injury, and his cervical
fractures were repaired by fusion (C5 through T1) the day
after injury; he now wears a Miami J cervical orthosis. He
was admitted to your rehabilitation center 5 days ago. He
demonstrates no activity of triceps brachii bilaterally but
reports dysesthesia in the C7 and C8 dermatomes and can
point his index finger on the left. He is aware of lower limb
position in space and can activate toe flexors and extensors,
plantar flexors, knee extensors, and hip flexors and abduc­
tors at 2 +/5 levels of strength. Deep tendon reflex at the
Achilles heel is brisk bilaterally, while more proximal lower
extremity reflexes are diminished. He demonstrates positive
Babinski reflex bilaterally. Biceps and wrist extensor deep
tendon reflexes, initially diminished, are now more consis­
tently rated 2+; the triceps reflex, initially diminished, is now
quite brisk. He requires moderate assistance of 1 to come to
sitting from supine but can hold a static posture in sitting,
demonstrating a limited sway envelope when attempting to
shift his weight anteriorly, posteriorly, and mediolaterally.
He requires moderate assistance of 1 to rise from seated in
his wheelchair to standing position in the parallel bars. He is
determined to “walk” out of the facility on discharge, antici­
pated after 3 more weeks of rehabilitation.
Questions to Consider
• Given Z. C.'s history and present point in recovery
from spinal cord injury, what is the anticipated progno­
sis concerning his functional performance and ability
to ambulate?
• In what subphases of the gait cycle is function or safety
likely to be compromised when Z. C. attempts to ambulate?
• In what way does Z. C.'s abnormal tone contribute to
his difficulty with locomotion/ambulation? What strat­
egies would be useful in documenting/assessing the
severity and type of his abnormal tone?
• In what ways does Z. C.'s impaired muscle perfor­
mance contribute to his difficulty with locomotion/
ambulation? What are the most likely dimensions of his
impairment in muscle performance, given his etiology
and level of injury?
• In what ways does Z. C.'s impaired postural control con­
tribute to his difficulty with locomotion/ambulation?
What are the most likely dimensions of Z. C.'s impairment
in postural control, given his etiology and level of injury?
• Are any primary or secondary musculoskeletal impair­
ments likely to influence Z. C.'s function and safety
during ambulation? How do Z. C.'s age and concomi­
tant medical conditions influence his risk for develop­
ing secondary impairments?
• Given Z. C.'s constellation of impairments, what com­
pensatory strategies is he likely to use to accomplish the
task of locomotion?
• Which of Z. C.'s anticipated or observed impairments
are remediable? Which will require accommodation?
• What orthotic options (design, components) are avail­
able to address Z. C.'s difficulty with locomotion and
related functional limitations? What are the pros and
cons of each?
• What alternative or concurrent medical (surgical/phar­
macological) interventions might assist improvement
in safety and function?
• What additional rehabilitation interventions might
assist improvement in function and safety for Z. C.?
• How do you anticipate Z. C.'s orthotic needs might
change as he recovers from his spinal cord injury?
• What outcome measures can be used to assess the
­efficacy of orthotic, therapeutic, pharmacological, or
surgical intervention for Z. C.?

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
301
REFERENCES

1 Who are physical therapists? Guide to Physical Therapist Practice.
Alexandria, Va: American Physical Therapy Association.
Available at:
2. Dean E. Physical therapy in the 21st century (part II): evi­
dence-based practice within the context of evidence-informed
practice. Physiother Theory Pract. 2009;25(5/6):354–368.
3. Sullivan KJ, Hershberg J, Howard R, et  al. Neurologic dif­
ferential diagnosis for physical therapy. J Neurol Phys Ther.
2004;28(4):162–168.
4. Lewis SL. An approach to neurological symptoms. In: Weiner
WJ, Goetz CG, Shin RK, Lewis SL, eds. Neurology for the
Non Neurologist. 6th ed. Philadelphia: Lippincott Williams &
Wilkins; 2010:20–42.
5. Weiner WJ, Lang KE. Behavioral Neurology of Movement
Disorders. Philadelphia: Lippincott Williams & Wilkins;
2005.
6. Biller J, Grueer G, Brazis PW. DeMyer's The Neurological
Examination: A Programmed Text. 6th ed. New York: McGraw
Hill; 2010.
7. Azar NJ, Arain AM. Focus on Clinical Neurophysiology.
Philadelphia: Lippincott Williams & Wilkins; 2009.
8. Osborn AG, Salzman KL, Barkovich AJ, eds. Diagnostic Imaging:
Brain. 2nd ed. Philadelphia: Lippincott Williams & Wilkins;
2009.
9. American Physical Therapy Association. What are tests and
measures? Guide to Physical Therapist Practice. Alexandria, VA:
American Physical Therapy Association. Available at: http://
guidetoptpractice.apta.org.
10. Lazarro RT, Roller M, Umphred DA. Differential diagnosis phase
2: examination and intervention of functional movement activi­
ties and system/subsystem impairment. In: Umphred DA, ed.
Neurological Rehabilitation. 5th ed. St. Louis: Mosby; 2007:163–186.
11. Strax TE, Luciano L, Dunn AM, et al. Aging and developmental
disability. Phys Med Rehabil Clin N Am. 2010;21(2):419–427.
12. Klingbeil H, Baer HR, Wilson PE. Aging with a disability. Arch
Phys Med Rehabil 2004;85(7 suppl 3):S68–S75 S85–S86.
13. Shumway-Cook A, Woollacott MH. Physiology of motor con­
trol. In: Shumway-Cook A, Woollacott MH, eds. Motor Control:
Translating Research into Clinical Practice. 4th ed. Philadelphia:
Wolters Kluwer/Lippincott Williams & Wilkins; 2012:45–82.
14. Rehme AK, Fink GR, von Cramon DY, et al. The role of the
contralesional motor cortex for motor recovery in the early
days after stroke assessed with longitudinal FMRI. Cereb
Cortex. 2011;21(4):756–768.
15. Cramer SC, Riley JD. Neuroplasticity and brain repair after
stroke. Curr Opin Neurol. 2008;21(1):76–82.
16. Shumway-Cook A, Woollacott MH. Physiological basis of
motor learning and recovery of function. In: Shumway-Cook
A, Woollacott MH, eds. Motor Control: Translating Research
into Clinical Practice. 4th ed. Philadelphia: Wolters Kluwer/
Lippincott Williams & Wilkins; 2012:83–103.
17. Alarcon F, Zijlmans JC, Duenas G, et al. Post-stroke movement
disorders: report of 56 patients. J Neurol Neurosurg Psychiatry.
2004;75(11):1568–1574.
18. Ryerson SD. Hemiplegia. In: Umphred DA, ed. Neurological
Rehabilitation. 5th ed. St. Louis: Mosby; 2007:857–901.
19. Bear MF, Connors BW, Paradiso MA. Brain control of
movement. In: Bear MF, Connors BW, Paradiso MA, eds.
Neuroscience: Exploring the Brain. 3rd ed. Philadelphia:
Lippincott Williams & Wilkins; 2006:451–478.
20. Gravenhorst RM, Walter CB. Cognitive mechanisms of visuo­
motor transformation in movement imitation: Examining pre­
dictions based on models of apraxia and motor control. Brain
Cogn. 2009;71(2):118–128.
21. Galbreath AD, Goldstein LB. Dysnomia, ataxia, choreoathe­
tosis, sensory impairment, and gait imbalance after lentiform
nucleus stroke. J Stroke Cerebrovasc Dis. 2009;18(6):494–496.
22. Grandas F. Hemiballismus. Handbook Clin Neurol. 2011;
100:249–260.
23. Pahwa R, Lyons KE. Handbook of Parkinson's Disease. 4th ed.
New York: Informa Healthcare; 2007.
24. Haber SN, Calzavara R. The cortico-basal ganglia inte­
grative network: the role of the thalamus. Brain Res Bull.
2009;78(2/3):69–74.
25. Garcia-Rill E, Homma Y, Skinner RD. Arousal mechanisms
related to posture and locomotion: 1. Descending modulation.
Prog Brain Res. 2004;143:281–290.
26. Kiernan JA. Motor systems. In: Kiernan JA, ed. Barr's The
Human Nervous System. 8th ed. Philadelphia: Lippincott
Williams & Wilkins; 2005:374–390.
27. Shinoda Y, Sugiuchi Y, Izawa Y, et al. Long descending motor
tract axons and their control of neck and axial muscles. Prog
Brain Res. 2006;151:527–563.
28. Melnick ME. Clients with cerebellar dysfunction. In: Umphred
DA, ed. Neurological Rehabilitation. 5th ed. St. Louis: Mosby;
2007:834–856.
29. Stoodley CJ, Schmahmann JD. Evidence for topographic orga­
nization in the cerebellum of motor control versus cognitive
and affective processing. Cortex. 2010;46(7):831–844.
30. Bear MR, Connors BW, Paradiso MA. The somatic sensory
system. In: Bear MF, Connors BW, et  al., eds. Neuroscience:
Exploring the Brain. 3rd ed. Philadelphia: Lippincott Williams
& Wilkins; 2006:387–422.
31. Marini E, Schoen JH. A reappraisal of the ascending systems
in man, with emphasis on the medial lemniscus. In: Advances
in Anatomy, Embryology and Cell Biology. New York: Springer
Verlag; 2005.
32. Kiernan JA. Functional localization in the cerebral cor­
tex. In: Kiernan JA, ed. Barr's The Human Nervous System,
An Anatomical Viewpoint. 9th ed. Philadelphia: Lippincott
Williams & Wilkins; 2008:227–244.
33. Zucker-Levin A. Sensory and perceptual issues related to
motor control. In: Montgomery PC, Connolly BH, eds. Clinical
Applications for Motor Control. Thorofare, NJ: Slack Inc;
2003:207–243.
34. Zoltan B. Vision, Perceptions and Cognition: A Manual for the
Evaluation and Treatment of the Adult with Acquired Brain
Injury. 4th ed. Thorofare, NJ: Slack Inc; 2007.
35. Kiernan JA. The visual system. In: Kiernan JA, ed. Barr's The
Human Nervous System, an Anatomical Viewpoint. 9th ed.
Philadelphia: Lippincott Williams & Wilkins; 2005:303–318.
36. Chaikin LE. Disorders of vision and visual perceptual dysfunc­
tion. In: Umphred DA, ed. Neurological Rehabilitation. 5th ed.
St. Louis: Mosby; 2007:973–1004.
37. Schwartz SH. Visual Perception: A Clinical Orientation. New
York: McGraw Hill; 2010.
38. Isableu B, Ohlmann T, Cremieux J, et  al. Individual differ­
ences in the ability to identify, select and use appropriate
frames of reference for perceptuo-motor control. Neuroscience.
2010;169(3):1199–1215.
39. Medendorp WP. Spatial constancy mechanisms in motor con­
trol. Philos Trans R Soc Lond B Biol Sci. 2011;366(1564):476–491.

302
Section II  Orthoses in Rehabilitation
40. Scheiman M. Understanding and Managing Vision Deficits:
A  Guide for Occupational Therapists. 3rd ed. Thorofare, NJ:
Slack Inc; 2011.
41. Anderson A, Jacobs R, Anerson P, eds. Executive Functions and
the Frontal Lobe: A Lifespan Perspective. New York: Taylor &
Francis; 2010.
42. Miller BL, Cummings JL, eds. The Human Frontal Lobe: Functions
and Disorders. 2nd ed. New York: Guilford Press; 2007.
43. Sliver JM, McAllister TW, Yudofsky SC, eds. Textbook of
Traumatic Brain Injury. 2nd ed. Washington, DC: American
Psychiatric Publishing; 2011.
44. Winkler PA. Traumatic brain injury. In: Umphred DA, ed.
Neurological Rehabilitation. 5th ed. St. Louis: Mosby; 2007:
532–566.
45. Rudy JW. The Neurobiology of Learning and Memory.
Sunderland, MA: Sinaur; 2008.
46. Umphred DA. The limbic system: influence over motor control
and learning. In: Umphred DA, ed. Neurological Rehabilitation.
5th ed. St. Louis: Mosby; 2007:71–118.
47. Cunningham WA, Van Bavel JJ, Johnsen IR. Affective flexibil­
ity: evaluative processing goals shape amygdala activity. Psychol
Sci. 2008;19(2):152–160.
48. Reeve JM. Understanding Motivation and Emotion. 5th ed.
Hoboken, NJ: John Wiley & Sons; 2009.
49. Light KE. Issues of cognition for motor control. In: Montgomery
PC, Connolly BH, eds. Clinical Applications for Motor Control.
Thorofare, NJ: Slack Inc; 2003:245–268.
50. Kiernan JA. Reticular formation. In: Kiernan JA, ed. Barr's
The Human Nervous System: An Anatomical Viewpoint. 9th ed.
Philadelphia: Lippincott Williams & Wilkins; 2009:141–156.
51. Lin JS, Anaclet S, Sergeeva O, et  al. The waking brain: an
update. Cell Mol Life Sci. 2011;68(15):2499–2512.
52. Fernández-Gil MA, Palacios-Bote R, Leo-Barahona M, et al.
Anatomy of the brainstem: a gaze into the stem of life. Semin
Ultrasound CT MR. 2010;31(3):196–219.
53. Laureys S, Tononi G. The Neurology of Consciousness: Cognitive
Neuroscience and Neuropathology. London: Academic Press; 2009.
54. Liebmann O, Simon B. Evaluating the patient with altered level
of consciousness. Emerg Med. 2006;38(2):35–36, 39–42.
55. Poster JB, Saper CB, Schiff ND, et al. Plum and Posner's Diagnosis
of Stupor and Coma. 4th ed. Oxford: New York; 2007.
56. Janig W. Integrative Action of the Autonomic Nervous System:
Neurobiology of Homeostasis. New York: Cambridge University
Press; 2008.
57. Hall JE. Behavioral and motivational mechanisms of the brain:
the limbic system and the hypothalamus. In: Guyton and
Hall Textbook of Medical Physiology. 12th ed. Philadelphia:
Saunders; 2011: 711–720.
58. Bear MF, Connors BW, Paradiso MA. Chemical control of the
brain and behavior. In: Bear MF, Connors BW, Paradiso MA,
eds. Neuroscience: Exploring the Brain. 3rd ed. Philadelphia:
Lippincott Williams & Wilkins; 2006:481–508.
59. Gescheider GA, Wright JH, Verrillo RT. Information Processing
Channels in the Tactile Sensory System. New York: Psychology
Press/Taylor & Francis Group; 2009.
60. Newton RA. Neural systems underlying motor control. In:
Montgomery PT, Connelly BH, eds. Clinical Applications for
Motor Control. Thorofare, NJ: Slack Inc; 2003:53–77.
61. Schmidt RA, Lee TD. Central contributions to motor control.
In: Schmidt RA, Lee TD, eds. Motor Control and Learning: A
Behavioral Emphasis. 3rd ed. Champaign, IL: Human Kinetics;
2005:131–169.
62. Bear MF, Connors BW, Paradiso MA. Spinal control of
movement. In: Bear MF, Connors BW, Paradiso MA, eds.
Neuroscience: Exploring the Brain. 3rd ed. Philadelphia:
Lippincott Williams & Wilkins; 2006:423–478.
63. Keynes RD, Aidley DJ, Huang CL. Nerve and Muscle. 4th ed.
Cambridge, UK: Cambridge University Press; 2011.
64. Hughes R. Peripheral nerve diseases: the bare essentials.
Practical Neurol. 2008;8(6):396–405.
65. Cohen JA, Mowchun J, Grudem J. Peripheral Nerve and Muscle
Diseases (What Do I Do Now?). New York: Oxford University
Press; 2009.
66. Shumway-Cook A, Woollacott MH. A conceptual framework
for clinical practice. In: Shumway-Cook A, Woollacott MH,
eds. Motor Control: Translating Research into Clinical Practice.
4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams &
Wilkins; 2011:141–158.
67. Gurfinkel V, Cacciatore TW, Cordo P, et  al. Postural mus­
cle tone in the body axis of healthy humans. J Neurophysiol.
2006;96(5):2678–2687.
68. Fort P, Bassetti CL, Luppi PH. Alternating vigilance states: new
insights regarding neuronal networks and mechanisms. Eur J
Neurosci. 2009;29(9):1741–1753.
69. Takakusaki K. Forebrain control of locomotor behaviors. Brain
Res Rev. 2008;57(1):192–198.
70. Gardiner PF. Advanced Neuromuscular Exercise Physiology.
Champaign, Ill: Human Kinetics; 2011.
71. Paterson DH, Jones GR, Rice CL. Ageing and physical activ­
ity: evidence to develop exercise recommendations for older
adults. Appl Physiol Nutr Metab. 2007;32(2E):S69–S108.
72. Marcus RL, Westlen-Boyer K, LaStayo P. Impaired muscle per­
formance. In: Giccione AA, Avers D, Wong RA, eds. Geriatric
Physical Therapy. 3rd ed. St. Louis: Mosby; 2012:263–271.
73. Hurley BF, Hanson ED, Sheaff AK. Strength training as a coun­
termeasure to aging muscle and chronic disease. Sports Med.
2011;41(4):289–306.
74. Hvid L, Aagaard P, Justesen L, et al. Effects of aging on mus­
cle mechanical function and muscle fiber morphology during
short-term immobilization and subsequent retraining. J Appl
Physiol. 2010;109(6):1628–1634.
75. Nielsen JB, Crone C, Hultborn H. The spinal pathophysiology
of spasticity—from a basic science point of view. Acta Physiol
(Oxf). 2007;189(2):171–180.
76. Ryu JS, Lee JW, Lee SI, et al. Factors predictive of spasticity and
their effects on motor recovery and functional outcomes in
stroke patients. Top Stroke Rehabil. 2010;17(5):380–388.
77. Wu YN, Ren Y, Goldsmith A, et al. Characterization of spastic­
ity in cerebral palsy: dependence of catch angle on velocity. Dev
Med Child Neurol. 2010;52(6):563–569.
78. Hsieh JT, Wolfe DL, Connolly S. Spasticity after spinal cord
injury: an evidence-based review of current interventions. Top
Spinal Cord Injury Rehabil. 2007;13(1):81–97.
79. Sosnoff JJ, Shin S, Motl RW. Multiple sclerosis and pos­
tural control: the role of spasticity. Arch Phys Med Rehabil.
2010;91(1):93–99.
80. Brashear A, Elovic E, eds. Spasticity: Diagnosis and Management.
New York: Demos Medical; 2011.
81. Sheean G, McGuire JR. Spastic hypertonia and movement dis­
orders: pathophysiology, clinical presentation, and quantifica­
tion. PMR. 2009;1(9):827–833.
82. Dietz V, Sinkjaer T. Spastic movement disorder: impaired
reflex function and altered muscle mechanics. Lancet Neurol.
2007;6(8):725–733.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
303
83. Mueller MJ, Kaluf KS. Tissue adaptation to physical stress: a pro­
posed “physical stress theory” to guide physical therapist prac­
tice, education and research. Phys Ther. 2002;82(4):383–403.
84. Guiliani CA. Spasticity and motor control. In: Montgomery
PC, Connolly BH, eds. Clinical Applications for Motor Control.
Thorofare, NJ: Slack Inc; 2003:309–332.
85. Borges CA, Castao KC, Souto PA, et al. Effect of resisted exer­
cise on muscular strength, spasticity and functionality in
chronic hemiparetic subjects: a systematic review. J Appl Res.
2009;9(4):147–158.
86. Patten C, Lexell J, Brown HE. Weakness and strength training
in persons with poststroke hemiplegia: rationale, method, and
efficacy. J Rehabil Res Dev. 2004;41(3A):293–312.
87. Pak S, Patten C. Strengthening to promote functional recov­
ery poststroke: an evidence-based review. Top Stroke Rehabil.
2008;15(3):177–199.
88. Ahlskog JE. Parkinson's Disease: Treatment Guide for Physicians.
New York: Oxford University Press; 2009.
89. Ransmayr G. Physical, occupational, speech and swallowing
therapies and physical exercise in Parkinson's disease. J Neural
Transm. 2011;118(5):773–781.
90. Hypes B. Heads Up on Hypotonia: Understanding Complexities
of Hypotonia and Strategies for Treatment. Brooklyn, NY:
Therapeutic Services Inc; 2008.
91. Harris S. Congenital hypotonia: clinical and developmental
assessment. Dev Med Child Neurol. 2008;50(12):889–892.
92. Stephens BE, Liu J, Lester B. Neurobehavioral assess­
ment predicts motor outcome in preterm infants. J Pediatr.
2010;156(3):366–371.
93. Deon LL, Gaebler-Spira D. Assessment and treatment of move­
ment disorders in children with cerebral palsy. Orthop Clin
North Am. 2010;41(4):507–517.
94. Rigoldi C, Galli M, Mainardi L, et al. Postural control in chil­
dren, teenagers and adults with Down syndrome. Res Dev
Disabil. 2011;32(1):170–175.
95. Goldstein S, Reynolds CR. Handbook of Neurodevelopmental
and Genetic Disorders in Children. 2nd ed. New York: Guilford
Press; 2011.
96. Ming X, Brimacombe M, Wagner GC. Prevalence of motor
impairment in autism spectrum disorders. Brain Dev.
2007;29(9):565–570.
97. Martin K, Inman J, Kirschner A, et  al. Characteristics of
hypotonia in children: a consensus opinion of pediat­
ric occupational and physical therapists. Pediatr Phys Ther.
2005;17(4):275–282.
98. Fitzgerald D, Stokes M. Muscle imbalance in neurological con­
ditions. In: Stokes M, ed. Physical Management in Neurological
Rehabilitation. 2nd ed. Edinburgh: Mosby; 2004:501–516.
99. Wissel J, Schelosky LE, Scott J, et  al. Early development of
spasticity following stroke: a prospective, observational trial.
J Neurol. 2010;257(7):1067–1072.
100. Sheerin F. Spinal cord injury: acute care management. Emerg
Nurse. 2005;12(10):26–34.
101. Young PA, Yound PH, Tolbert DL. Lower motor neurons;
flaccid paralysis. Clinical Neuroscience. 2nd ed. Philadelphia:
Wolters Kluwer/Lippincott Williams & Wilkins; 2008 47–64.
102. Salmons S, Ashley Z, Sutherland H, et al. Functional electrical
stimulation of denervated muscles: basic issues. Artif Organs.
2005;29(3):199–202.
103. Krosschell KJ, Pesavento MJ. Congenital spinal cord injury. In:
Umphred DA, ed. Neurological Rehabilitation. 5th ed. St. Louis:
Mosby; 2007:567–604.
104. Atrice MB, Morrison SA, McDowell SL, et al. Traumatic spinal
cord injury. In: Umphred DA, ed. Neurological Rehabilitation.
5th ed. St. Louis: Mosby; 2007:605–657.
105. Parry GJ, Steinberg MD. Guillain-Barré Syndrome: From
Diagnosis to Recovery. St. Paul, MN: American Academy of
Neurology Press; 2007.
106. Osterbauer PJ. Botulinum neurotoxin. In: Dobbs MR, ed.
Clinical Neurotoxicology: Syndromes, Substances, Environments.
Philadelphia: Saunders; 2009:421–426.
107. Singer HS, Jankovic J, Mink JW, Gilberts DL, eds. Chorea,
athetosis and ballism. In Movement Disorders in Childhood.
Philadelphia: Saunders; 2010:76–95.
108. Wright MJ, Wallman L. Cerebral palsy. In: Campbell SK,
Vander Linden DW, Palisano RJ, eds. Physical Therapy for
Children. 4th ed. St. Louis: Saunders; 2012:577–626.
109. Jensen MP, Molton IR. Aging With a Disability. Philadelphia:
Saunders; 2010.
110. Shumway-Cook A, Woollacott MH. Normal postural con­
trol. In: Shumway-Cook A, Woollacott MH, eds. Motor
Control: Translating Research into Clinical Practice. 4th ed.
Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins;
2012:161–194.
111. Allison L, Fuller K. Balance and vestibular disorders. In:
Umphred DA, ed. Neurological Rehabilitation. 5th ed. St. Louis:
Mosby; 2007:732–774.
112. Takakusaki K, Okumura T. Neurobiological basis of controlling
posture and locomotion. Adv Robot. 2008;22(15):1629–1663.
113. Seeger MA. Balance deficits: examination, evaluation and
intervention. In: Montgomery PC, Connolly BH, eds. Clinical
Applications for Motor Control. Thorofare, NJ: Slack Inc;
2003:271–308.
114. Pagnacco G, Oggero E, Carrick FR. Repeatability of posturo­
graphic measures of the MCTSIB static balance tests a prelimi­
nary investigation. Biomed Sci Instrum. 2008;44(1):41–46.
115. Santos MJ, Knekar N, Aruin AS. The role of anticipatory pos­
tural adjustments in compensatory control of posture: 1.
Electromyographic analysis. J Electromyogr Kinesiol. 2010;
20(3):388–397.
116. Santos MJ, Kanekar N, Aruin AS. The role of anticipa­
tory postural adjustments in compensatory control of pos­
ture: 2. Biomechanical analysis. J Electromyogr Kinesiol.
2010;20(3):398–405.
117. Duncan PW, Studenski S, Chandler J, et al. Functional reach:
a new clinical measure of balance. J Gerontol. 1990;45(6):
M192–M197.
118. Newton RA. Validity of the multi-directional reach test: a prac­
tical measure for limits of stability in older adults. J Gerontol.
2001;56A(4):M248–M252.
119. Bartlett D, Birmingham T. Validity and reliability of a pediatric
reach test. Pediatr Phys Ther. 2003;15(2):84–92.
120. Washington K, Shumway-Cook A, Price R, et  al. Muscle
responses to seated perturbations for typically developing
infants and those at risk for motor delays. Dev Med Child
Neurol. 2004;46(10):681–688.
121. Sang IL, Woollacott M. Association between sensorimotor
function and functional and reactive balance control in the
elderly. Age Ageing. 2005;34(4):358–363.
122. Mackey DC, Robinovitch SN. Postural steadiness during quiet
stance does not associate with ability to recover balance in older
women. Clin Biomech (Bristol, Avon). 2005;20(8):776–783.
123. Shumway-Cook A, Woollacott MH. Abnormal postural
control. In: Shumway-Cook A, Woollacott MH, eds. Motor

304
Section II  Orthoses in Rehabilitation
Control: Translating Research into Clinical Practice. 4th ed.
Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins;
2012:246–270.
124. Sosnoff JJ, Shin S, Motl RW. Multiple sclerosis and pos­
tural control: the role of spasticity. Arch Phys Med Rehabil.
2010;91(1):93–99.
125. Westcott SL, Burtner P. Postural control in children: implications
for pediatric practice. Phys Occup Ther Pediatr. 2004;24(1/2):5–55.
126. Shumway-Cook A, Woollacott MH. Normal reach, grasp and
manipulation. In: Shumway-Cook A, Woollacott MH, eds.
Motor Control: Translating Research into Clinical Practice.
4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams &
Wilkins; 2012:477–501.
127. Shumway-Cook A, Woollacott MH. Reach, grasp and manip­
ulation: changes across the lifespan. In: Shumway-Cook A,
Woollacott MH, eds. Motor Control: Translating Research
into Clinical Practice. 4th ed. Philadelphia: Wolters Kluwer/
Lippincott Williams & Wilkins; 2012:502–528.
128. Stout JL. Gait: development and analysis. In: Campbell SK,
Vander Linden DW, Palisano RJ, eds. Physical Therapy for
Children. 4th ed. St. Louis: Mosby; 2012.
129. Corrigan R, McBurney H. Community ambulation: environ­
mental impacts and assessment inadequacies. Disabil Rehabil.
2008;30(19):1411–1419.
130. Shumway-Cook A, Woollacott MH. Abnormal mobility.
In: Shumway-Cook A, Woollacott MH, eds. Motor Control:
Translating Research into Clinical Practice. 4th ed. Philadelphia:
Wolters Kluwer/Lippincott Williams & Wilkins; 2012:381–415.
131. Schmidt RA, Lee TL. Coordination. In: Schmidt RA, Lee TL,
eds. Motor Control and Learning: A Behavioral Emphasis. 4th
ed. Champaign, IL: Human Kinetics; 2005:243–270.
132. Schmitz TJ. Examination of coordination. In: O'Sullivan SB,
Schmitz TJ, eds. Physical Rehabilitation. 5th ed. Philadelphia:
FA Davis; 2007:193–225.
133. Shumway-Cook A, Woollacott MH. A lifespan perspective of
mobility. In: Shumway-Cook A, Woollacott MH, eds. Motor
Control: Translating Research into Clinical Practice. 4th ed.
Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins;
2012:348–380.
134. Richards CL, Malouin F, Dumas F. Patterns of locomotor
recovery after stroke. In: Stein J, Harvey RL, Macko RF, eds.
Stroke Recovery and Rehabilitation. New York: Demos Medical;
2009:245–268.
135. Smits DW, Gorter JW, Ketelaar M, et al. Relationship between
gross motor capacity and daily-life mobility in children with
cerebral palsy. Dev Med Child Neurol. 2010;52(3):60–66.
136. Shumway-Cook A, Woollacott MH. Abnormal reach grasp
and manipulation. In: Shumway-Cook A, Woollacott MH,
eds. Motor Control: Translating Research into Clinical Practice.
4th ed. Philadelphia: Wolters Kluwer/Lippincott Williams &
Wilkins; 2012:529–551.
137. Winstein CJ, Wolf SL. Task-oriented training to promote upper
extremity recovery. In: Stein J, Harvey RL, Macko RF, et al., eds.
Stroke Recovery and Rehabilitation. New York: Demos Medical;
2009:267–290.
138. Zackowski KM, Dromerick AW, Sahrman SA, et al. How do
strength, sensation, spasticity, and joint individuation relate
to the reaching deficits of people with chronic hemiparesis?
Brain. 2004;127(5):1035–1046.
139. Lynn AK, Turner M, Chambers HG. Surgical management of
spasticity in persons with cerebral palsy. Phys Med Rehabil.
2009;1(9):834–838.
140. Miller EL, Murray L, Richards L, et al. Comprehensive over­
view of nursing and interdisciplinary rehabilitation care of the
stroke patient: a scientific statement from the American Heart
Association. Stroke. 2010;41(10):2402–2448.
141. Stevenson VL, Playford ED. Rehabilitation and MS. Int MS J.
2007;14(3):85–92.
142. Verza R, Carvalho ML, Battaglia MA, et  al. An interdisci­
plinary approach to evaluating the need for assistive tech­
nology reduces equipment abandonment. Mult Scler.
2006;12(1):88–93.
143. Simon O, Yelnik AP. Managing spasticity with drugs. Eur J Phys
Rehabil Med. 2010;46(3):401–410.
144. Elbasiouny SM, Moroz D, Bakr MM, et al. Management of spas­
ticity after spinal cord injury: current techniques and future
directions. Neurorehabil Neural Repair. 2010;24(1):23–33.
145. Caty GD, Detrembleur C, Bleyenheuft C, et  al. Effect of
simultaneous botulinum toxin injections into several mus­
cles on impairment, activity, participation, and quality of life
among stroke patients presenting with a stiff knee gait. Stroke.
2008;39(10):2803–2808.
146. Damiano DL, Alter KE, Chambers H. New clinical and
research trends in lower extremity management for ambula­
tory children with cerebral palsy. Phys Med Rehabil Clin N Am.
2009;20(3):469–491.
147. Love SC, Novak I, Kentish M, et al. Botulinum toxin assess­
ment, intervention and after-care for lower limb spasticity in
children with cerebral palsy: international consensus state­
ment. Eur J Neurol. 2010;17(suppl 2):9–37.
148. Johnson J, Jarrett L, Porter B, et al. Strategies and challenges
in managing spasticity. In: Halper J, ed. Advanced Concepts
in Multiple Sclerosis Nursing Care. 2nd ed. New York: Demos
Medical Publishing; 2007:145–174.
149. Francisco GE, McGuire JR, Stein J, et al. Physiology and man­
agement of spasticity after stroke. In: Stein J, Harvey R, Macko
E, et  al., eds. Stroke Recovery & Rehabilitation. New York:
Demos Medical Publishing; 2009:413–436.
150. Ryan M. Drug therapies for the treatment of multiple sclerosis.
J Infus Nurs. 2009;32(3):137–144.
151. Derwenskus J. Current disease-modifying treatment of multi­
ple sclerosis. Mt Sinai J Med. 2011;78(2):161–175.
152. Ciccone CD. Antiepileptic drugs. In: Ciccone CD, ed.
Pharmacology in Rehabilitation. 4th ed. Philadelphia: FA Davis;
2007:105–117.
153. Papavasiliou AS. Management of motor problems in cerebral
palsy: a critical update for the clinician. Eur J Paediatr Neurol.
2009;13(5):387–396.
154. Burke-Doe A, Runion HI, Smith TJ. Impact of drug therapy
on patients receiving neurological rehabilitation. In: Umphred
DA, ed. Neurological Rehabilitation. 5th ed. St. Louis: Mosby;
2007:1119–1137.
155. Bollens B, Deltombe T, Detrembleur C, et al. Effects of selec­
tive tibial nerve neurotomy as a treatment for adults present­
ing with spastic equinovarus foot: a systematic review. J Rehabil
Med. 2011;43(4):277–282.
156. Palacio A, Milliez PY, Le Jean T, et al. Direct neurectomy of
the motor branches of the tibial nerve in hemiplegic adults: an
assessment with a mean follow-up period of 11 years. Ann Phys
Rehabil Med. 2010;53(6/7):417–433.
157. Maarrawi J, Mertens P, Luaute J, et  al. Long-term func­
tional results of selective peripheral neurotomy for the treat­
ment of spastic upper limb: prospective study in 31 patients.
J Neurosurg. 2006;104(2):215–225.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
305
158. Sindou MP, Simon F, Mertens P, et al. Selective peripheral neu­
rotomy (SPN) for spasticity in childhood. Child Nerv Syst.
2007;23(9):957–970.
159. Fitoussi F, Ilharreborde B, Presedo A, et al. Shoulder exter­
nal rotator selective neurotomy in cerebral palsy: anatomi­
cal study and preliminary clinical results. J Pediatr Orthop.
2010;19(1):71–76.
160. van Schie PE, Schothorst M, Dallmeijer AJ, et al. Short- and
long-term effects of selective dorsal rhizotomy on gross
motor function in ambulatory children with spastic diplegia.
J Neurosurg Pediatr. 2011;7(5):557–562.
161. Tedroff K, Lowing K, Jacobson DN, et  al. Does loss of
spasticity matter? A 10-year follow-up after selective dor­
sal rhizotomy in cerebral palsy. Dev Med Child Neurol.
2011;53(8):724–729.
162. Langerak NG, Hillier SL, Verkoeijen PP, et  al. Level of
activity and participation in adults with spastic diplegia
17-26 years after selective dorsal rhizotomy. J Rehabil Med.
2011;43(4):330–337.
163. Dvorak EM, Ketchum NC, McGuire JR. The underutiliza­
tion of intrathecal baclofen in poststroke spasticity. Top Stroke
Rehabil. 2011;18(3):195–202.
164. Keenan E. Spasticity management, part 3: surgery and the use
of intrathecal baclofen. Br J Neurosci Nurs. 2010;6(1):12–18.
165. Ward A, Hayden S, Dexter M, et  al. Continuous intrathe­
cal baclofen for children with spasticity and/or dystonia: goal
attainment and complications associated with treatment.
J Pediatr Child Health. 2009;45(12):720–726.
166. Rutz E, Baker R, Tirosh O, et  al. Tibialis anterior tendon
shortening in combination with Achilles tendon length­
ening in spastic equinus in cerebral palsy. Gait Posture.
2011;33(2):152–157.
167. de Morais Filho MC, Kawamura CM, Kanaji PR, et  al. The
relation of triceps surae surgical lengthening and crouch
gait in patients with cerebral palsy. J Pediatr Orthop B
2010;19(3):226–230.
168. Bernthal NM, Gamradt SC, Kay RM, et al. Static and dynamic
gait parameters before and after multilevel soft tissue surgery
in ambulating children with cerebral palsy. J Pediatr Orthop.
2010;30(2):174–179.
169. Paul SM, Siegel KL, Malley J, et al. Evaluating interventions
to improve gait in cerebral palsy: a meta-analysis of spa­
tiotemporal measures. Dev Med Child Neurol. 2007;49(7):
542–549.
170. Yun AG, Severino R, Reinker K. Varus derotational osteotomy
for spastic hip instability: the roles of femoral shortening and
obturator neurectomy. Am J Orthop. 2005;34(2):81–85.
171. Westwell M, Öunpuu S, DeLuca P. Effects of orthopedic inter­
vention in adolescents and young adults with cerebral palsy.
Gait Posture. 2009;30(2):201–206.
172. Amichai T, Harries N, Dvir Z, et al. The effects of femoral dero­
tation osteotomy in children with cerebral palsy: an evaluation
using energy cost and functional mobility. J Pediatr Orthop.
2009;29(1):68–72.
173. Novacheck TF, Stout JL, Gage JR, et al. Distal femoral exten­
sion osteotomy and patellar tendon advancement to treat per­
sistent crouch gait in cerebral palsy. J Bone Joint Surg. 2009;91A
(suppl 2):271–286.
174. Imrie MN, Yaszay B. Management of spinal deformity in cere­
bral palsy. Orthop Clin North Am. 2010;41(4):531–547.
175. Auerbach JD, Spiegel DA, Zgonis MH, et al. The correction of
pelvic obliquity in patients with cerebral palsy and neuromus­
cular scoliosis: is there a benefit of anterior release prior to pos­
terior spinal arthrodesis? Spine. 2009;34(21):E766–E774.
176. Keeler KA, Lenke LG, Good CR, et al. Spinal fusion for spas­
tic neuromuscular scoliosis: is anterior releasing necessary
when intraoperative halo-femoral traction is used? Spine.
2010;35(10):E427–E433.
177. Thomason P, Baker R, Dodd K, et al. Single-event multilevel
surgery in children with spastic diplegia: a pilot randomized
controlled trial. J Bone Joint Surg Am. 2011;93(5):451–456.
178. Akerstedt A, Risto O, Odman P, et al. Evaluation of single event
multilevel surgery and rehabilitation in children and youth
with cerebral palsy—a 2-year follow-up study. Disabil Rehabil.
2010;32(7):530–539.
179. Seniorou M, Thompson N, Harrington M, et al. Recovery of
muscle strength following multi-level orthopaedic surgery in
diplegic cerebral palsy. Gait Posture. 2007;26(4):475–481.
180. Kondratek M, McCollum H, Garland A. Long-term physical
therapy management following a single-event multiple level
surgery. Pediatr Phys Ther. 2010;22(4):427–438.
181. Capjon H, Bjork IT. Rehabilitation after multilevel sur­
gery in ambulant spastic children with cerebral palsy: chil­
dren and parent experiences. Dev Neurorehabil. 2010;13(3):
182–191.
182. Miller F. Spinal deformity secondary to impaired neurologic
control. J Bone Joint Surg Am. 2007;80(suppl 1):143–147.
183. Fowler EG, Kolobe TH, Damiano DL, et al. Promotion of phys­
ical fitness and prevention of secondary conditions for children
with cerebral palsy: section on pediatrics research summit pro­
ceedings. Phys Ther. 2007;87(11):1495–1510.
184. Tosi LL, Maher N, Moore DW, et al. Adults with cerebral palsy:
a workshop to define the challenges of treating and preventing
secondary musculoskeletal and neuromuscular complications
in this rapidly growing population. Dev Med Child Neurol.
2009;51(suppl 4):2–11.
185. Novacheck TF, Gage JR. Orthopedic management of spasticity
in cerebral palsy. Child Nerv Syst. 2007;23(9):L1015–L1031.
186. Rodda JM, Graham HK, Nattrass GR, et  al. Correction of
severe crouch gait in patients with spastic diplegia with
use of multilevel orthopaedic surgery. J Bone Joint Surg Am.
2006;88(12):2653–2664.
187. Novacheck TF, Stout JL, Gage JR, et al. Distal femoral extension
osteotomy and patellar tendon advancement to treat persistent
crouch gait in cerebral palsy. J Bone Joint Surg Am. 2009;19
(suppl 2):271–286.
188. de Vries G, Roy K, Chester V. Using three-dimensional gait
data for foot/ankle orthopaedic surgery. Open Orthop J.
2009;3:89–95.
189. Westcott SL, Goulet C. Neuromuscular system: structures,
functions, diagnoses, and evaluation. In: Effgen SK, ed. Meeting
the Physical Therapy Needs of Children. Philadelphia: FA Davis;
2005:185–244.
190. Lazaro RT, Roller M, Umphred DA. Differential diagnosis phase 2:
examination and evaluation of functional movement activities and
system/subsystem impairments. In: Umphred DA, ed. Neurological
Rehabilitation. 5th ed. St. Louis: Mosby; 2007:163–186.
191. American Physical Therapy Association. Basics of Patient/
Client Management: The Five Elements of Patient/Client
Management. Guide to Physical Therapist Practice. Alexandria
VA: American Physical Therapy Association. Available at:

192. Eberly V, Kubota K, Weiss W. To brace or not to brace: mak­
ing evidenced based decisions with our clients with neurological

306
Section II  Orthoses in Rehabilitation
impairments. Session handouts, American Physical Therapy
Association Combined Sections Meeting, San Diego, February 2
2006.
193. Racette W. Orthotics: evaluation, prognosis, and intervention.
In: Umphred DA, ed. Neurological Rehabilitation. 5th ed. St.
Louis: Mosby; 2007:1086–1118.
194. Effgen SK, McEwen IR. Review of selected physical therapy
interventions for school age children with disabilities. Phys
Ther Rev. 2008;13(5):297–312.
195. Morris C, Bowers R, Ross K, et al. Orthotic management of
cerebral palsy: recommendations from a consensus conference.
NeuroRehabilitation. 2001;28(1):37–46.
196. American Physical Therapy Association. What Are Interventions?
Guide to Physical Therapist Practice. Alexandria, VA: American
Physical Therapy Association. Available at:
tice.apta.org.
197. Lowes LP, Sveda M, Gajdosik CG, et al. Musculoskeletal devel­
opment and adaptation. In: Campbell SK, Vander Linden DW,
Palisano RJ, eds. Physical Therapy for Children. 4th ed. St. Louis:
Saunders; 2012:175–204.
198. Malhotra S, Pandyan AD, Rosewilliam S, et al. Spasticity and
contractures at the wrist after stroke: time course of develop­
ment and their association with functional recovery of the
upper limb. Clin Rehabil. 2011;25(2):184–191.
199. Sullivan KJ, Mulroy S, Kautz SA, et al. Walking recovery and
rehabilitation after stroke. In: Stein J, Harvey RL, Macko RF,
et  al., eds. Stroke Recovery and Rehabilitation. New York:
Demos Medical; 2009:323–342.
200. Pohl M, Mehrholz J, Rockstroh G, et  al. Contractures and
involuntary muscle overactivity in severe brain injury. Brain
Inj. 2007;21(4):421–432.
201. Katalinic OM, Harvey LA, Herbert RD. Effectiveness of stretch
for the treatment and prevention of contractures in people
with neurological conditions: a systematic review. Phys Ther.
2011;91(1):11–24.
202. Swanton R, Kinnear B. There is robust evidence that stretch
interventions do not prevent or reverse joint contractures
in people with neurological conditions. Aust Occup Ther J.
2011;58(2):134–135.
203. Lannin NA, Novak I, Cusick A. A systematic review of
upper extremity casting for children and adults with
central nervous system motor disorders. Clin Rehabil.
2007;21(11):963–976.
204. Harvey LA, Glinsky JA, Katalinic OM, et al. Contracture manage­
ment for people with spinal cord injuries. NeuroRehabilitation.
2011;28(1):17–20.
205. Gao F, Ren Y, Roth EJ, et al. Effects of repeated ankle stretching on
calf muscle–tendon and ankle biomechanical properties in stroke
survivors. Clin Biomech (Bristol, Avon). 2011;26(5):516–522.
206. Bonutti PM, McGrath MS, Ulrich SD, et  al. Static pro­
gressive stretch for the treatment of knee stiffness. Knee.
2008;15(4):272–276.
207. Redstone F. The importance of postural control for feeding.
Pediatr Nurs. 2004;30(2):97–100.
208. McDonald R, Surtees R, Wirz S. The International Classification
of Functioning, Disability and Health provides a model for
adaptive seating interventions for children with cerebral palsy.
Br J Occup Ther. 2004;67(7):293–302.
209. Hahn ME, Sihemkins SL, Gardner JK, et al. A dynamic seat­
ing system for children with cerebral palsy. J Musculoskel Res.
2009;12(1):21–30.
210. Stavness C. The effect of positioning for children with cerebral
palsy on upper-extremity function: a review of the evidence.
Phys Occup Ther Pediatr. 2006;26(3):39–53.
211. Gudjonsdottir B, Mercer VS. Effects of a dynamic versus static prone
stander on bone mineral density and behavior in four children with
severe cerebral palsy. Pediatr Phys Ther. 2002;14(1):38–46.
212. Dalén Y, Sääf M, Ringertz H, et al. Effects of standing on bone
density and hip dislocation in children with severe cerebral
palsy. Adv Physiother. 2010;12(4):187–193.
213. Farrell E, Naber E, Geigle P. Description of a multifaceted
rehabilitation program including overground gait training for
a child with cerebral palsy: a case report. Physiother Theory
Pract. 2010;26(1):56–61.
214. Peredo DE, Davis BE, Norvell DC, et al. Medical equipment
use in children with disabilities: a descriptive survey. J Pediatr
Rehabil Med. 2010;3(4):259–267.
215. Hong CW. Assessment for and provision of positioning equip­
ment for children with motor impairments. Int Ther Rehabil.
2005;12(3):126–131.
216. Jones MA, Gray S. Assistive technology: positioning and
mobility. In: Effgen SK, ed. Meeting the Physical Therapy Needs
of Children. Philadelphia: FA Davis; 2005:455–474.
217. Thorton H, Kilbride C. Physical management of abnormal
tone and movement. In: Stokes M, ed. Physical Management
in Neurological Rehabilitation. 2nd ed. Edinburgh: Mosby;
2004:431–450.
218. Beatty PW, Hagglund KJ, Neri MT, et  al. Access to health
care services among people with chronic or disabling con­
ditions: patterns and predictors. Arch Phys Med Rehabil.
2003;84(10):1417–1425.
219. Bingham SC, Beatty PW. Rates of access to assistive equipment
and medical rehabilitation services among people with disabili­
ties. Disabil Rehabil. 2003;25(9):487–490.
220. Gulley SP, Rasch EK, Chan L. The complex web of health: relation­
ships among chronic conditions, disability, and health services.
Public Health Rep. 2011;126(4):495–507.
221. O'Neil ME, Costigan TE, Gracely EJ, et al. Parents’ perspectives
on access to rehabilitation services for their children with spe­
cial healthcare needs. Pediatr Phys Ther. 2009;21(3):254–260.
222. Westberry DE, Davids JR, Jacobs JM, et  al. Effectiveness of
serial stretch casting for resistant or recurrent knee flexion
contractures following hamstring lengthening in children with
cerebral palsy. J Pediatr Orthop. 2006;26(1):109–114.
223. Jain S, Mathur M, Joshi JR, et  al. Effect of serial casting in
spastic cerebral palsy. Indian J Pediatr. 2008;75(10):997–1002.
224. McNee AE, Will E, Lin JP. The effect of serial casting on gait in
children with cerebral palsy: preliminary results from a cross­
over trial. Gait Posture. 2007;25(3):463–468.
225. Romeiser L. Rehabilitation techniques to maximize spasticity
management. Top Stroke Rehabil. 2011;18(3):203–211.
226. Marshall S, Teasell R, Bayona N. Motor impairment rehabilita­
tion post acquired brain injury. Brain Inj. 2007;21(2):133–160.
227. Yaşar E, Tok F, Safaz I, et al. The efficacy of serial casting after botu­
linum toxin type A injection in improving equinovarus deformity
in patients with chronic stroke. Brain Inj. 2010;24(5):736–739.
228. Park ES, Rha DW, Yoo JK, et al. Short-term effects of combined
serial casting and botulinum toxin injection for spastic equi­
nus in ambulatory children with cerebral palsy. Yonsei Med J.
2010;51(4):579–584.
229. Haslekorn JK, Loomis S. Multiple sclerosis and spasticity. Phys
Med Rehabil Clin N Am. 2005;16(2):467–481.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
307
230. Morris SL, Dodd KJ, Morris ME. Outcomes of progressive
resistance strength training following stroke; a systematic
review. Clin Rehabil. 2004;18(1):27–39.
231. Foran JR, Steinman S, Barash I, et al. Structural and mechani­
cal alterations in spastic skeletal muscle. Dev Med Child Neurol.
2005;47(10):713–717.
232. Hagglund G, Anderson S, Duppe H, et al. Prevention of severe
­contractures might replace multilevel surgery in cerebral
palsy: results of a population-based health care programme
and new techniques to reduce spasticity. J Pediatr Orthop.
2005;14(4):269–273.
233. Molenaers G, Desloovere K, Fabry G, et al. The effects of quan­
titative gait assessment and botulinum toxin A on musculo­
skeletal surgery in children with cerebral palsy. J Bone Joint
Surg. 2006;88A(1):161–170.
234. Fatone S. Orthotic management in stroke. In: Stein J, Harvey
R, Macko R, et al., eds. Stroke Recovery & Rehabilitation. New
York: Demos Medical Publishing; 2009:515–530.
235. Lannin NA, Ada L. Neurorehabilitation splinting: theory and
principles of clinical use. NeuroRehabilitation. 2011;28(1):21–88.
236. Webster JB, Miknevich MA, Stevens P, et al. Lower extremity
orthotic management in neurologic rehabilitation. Crit Rev
Phys Rehabil Med. 2009;21(1):1–23.
237. Knutson J, Audu M, Triolo R. Interventions for mobility and
manipulation after spinal cord injury: a review of orthotic
and neuroprosthetic options. Top Spinal Cord Injury Rehabil.
2006;11(4):61–81.
238. Kawashima N, Taguchi D, Nakazawa K, et al. Effect of lesion
level on the orthotic gait performance in individuals with com­
plete paraplegia. Spinal Cord. 2006;44(8):487–494.
239. Malas BS. What variables influence the ability of an AFO to
improve function and when are they indicated? Clin Orthop
Relat Res. 2011;469(5):1308–1314.
240. Shipley JS, Shipley RW. Orthotic considerations for pediatric
pathologies. J Nurse Life Care Planning. 2010;10(1):213–217.
241. Stevens PM. Lower limb orthotic management of Duchenne
muscular dystrophy: a literature review. J Prosthet Orthot.
2006;18(4):111–119.
242. Perry J, Burnfield J. Gait Analysis: Normal and Pathological
Function. 2nd ed. Thorofare, NJ: Slack Inc; 2010.
243. Gage JR, Schwartz MH, Koop SE, et al. The Identification and
Treatment of Gait Problems in Cerebral Palsy. 2nd ed. London:
MacKeith Press; 2009.
244. Observational Gait Analysis. Downey, CA: Pathokinesiology
Service & Physical Therapy Department, Rancho Los Amigos
Medical Center; 2001.

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11
Orthoses for Knee Dysfunction
Anthony E. “Toby” Kinney and Ellen Wetherbee
Knee braces have been used as a common intervention in
the protection and stabilization of the knee joint to decrease
a person's pain and improve their functional and recre­
ational activities (Figure 11-1). It has become commonplace
for anyone to walk into a pharmacy or drug store and pur­
chase a knee brace such as a neoprene sleeve (Figure 11-2).
However, their effectiveness in providing ligamentous stabil­
ity and optimal patellofemoral tracking has been debated.1,2
In 1984, the American Academy of Orthopaedic Surgeons
developed a classification system that grouped knee orthot­
ics by their intended function: prophylactic, rehabilitative, and
functional knee braces.3 Currently, patellofemoral braces and
unloader knee braces are additional classification ­categories.4,5
It could be debated that unloader braces are merely functional
osteoarthritis (OA) braces. Prophylactic knee orthoses are
designed to reduce the risk of knee injury for those individu­
als who are engaged in “high-risk” activities, especially those
individuals who have a history of previous knee dysfunc­
tion. Rehabilitative knee orthoses are used to protect a knee
that has been injured or surgically repaired until adequate
tissue healing has occurred. Functional knee orthoses (FKOs)
attempt to provide biomechanical stability when ligaments
are unable to do so during daily activities. Patellofemoral knee
braces are intended to optimize tracking of the patella and
decrease anterior knee pain. Unloader knee braces are meant
to decrease compressive forces across the tibiofemoral joint
and decrease arthritic knee pain. This functional classifica­
tion system continues to be helpful for health care providers
who work with patients who have knee dysfunction.
It is imperative during the clinical decision making process
that clinicians use a patient-centered approach while at the
same time incorporating the best available scientific research
and their own clinical expertise. Patient goals, function, pref­
erences, and impairments should be factors in deciding the
type of knee orthosis to use. For instance, a patient who has
anterior cruciate ligament (ACL) deficiency will use a differ­
ent brace than a patient with medial compartment knee OA.
In all circumstances, it is important to understand the anat­
omy and biomechanics of the knee joint and subsequent knee
dysfunction when providing a knee orthosis to a patient.
In order for a clinician to select the appropriate knee
orthosis for the patient, the clinician needs a mastery of
normal knee structure and function. This chapter reviews
the anatomy and biomechanical stability of the knee and
patellofemoral joints and the physiological and accessory
motions of the tibiofemoral and patellofemoral joints.
The implications of knee pathology on knee biomechan­
ics are discussed, and the design and functional goals of
prefabricated and custom-made knee orthoses are exam­
ined. Indications for knee orthoses in the management of
common knee injuries and dysfunction are also discussed.
Finally, the chapter concludes with discussion about strat­
egies for clinical decision making in choosing an appro­
priate functional orthosis for active patients and athletes
with ligamentous instability of the knee.
ANATOMY OF THE KNEE
The articulations at the tibiofemoral joint and the patellofem­
oral joint form the knee complex. An understanding of the
anatomy and biomechanics of each respective joint is critical in
11
LEARNING OBJECTIVES
On completion of this chapter, the reader will be able to:
1. Describe the normal anatomical structure and biome­
chanical function (kinematic and kinetic) of the human
tibiofemoral and patellofemoral joints.
2. Appreciate the anatomical structures of the knee that pro­
vide intraarticular stability.
3. Explain the most common mechanism of injury to the
knee while understanding the biomechanical implications
of pathological changes to the knee and lower extremity
mechanics.
4. Describe the various classification systems used to describe
knee orthoses.
5. Compare and contrast the purposes, indications, and limi­
tations of rehabilitative, functional, and prophylactic knee
orthoses.
6. Identify the force vectors used to control knee motion
used in various designs of knee orthoses.
7. Become familiar with current research evidence that will
drive clinical decision making in determining rationale for
brace intervention.
8. Use evidence of efficacy of various knee orthoses to
select the most appropriate device for a given injury to
the knee
9. Provide clinical rationale for utilizing bracing as an inter­
vention for impairments at the knee.

Chapter 11  Orthoses for Knee Dysfunction
309
knowing the potential stresses and implications of knee pathol­
ogy that can occur at the knee complex.
The Tibiofemoral Joint
The knee joint is a hinge-like articulation between the medial
and lateral condyles of the femur and the medial and lateral
tibial plateau (Figure 11-3). Because of the shape and asym­
metry of the condyles, the instantaneous axis of knee ­flexion/
extension motion changes through the arc of motion. As the
knee moves from extension to flexion, the instant cen­
ter moves posteriorly.6 In open chain movements (non–
weight-bearing activities), the tibia rotates around the
femoral condyles. In  closed chain movements (weight-­
bearing activities), an anatomical locking mechanism is pres­
ent in the final degrees of extension as the longer medial
femoral condyle rotates medially on the articular surfaces
of the tibia. Consequently, if the instant center of path­
way changes, it will alter the optimal joint mechanics
and therefore result in abnormal knee stressors. The align­
ment between an adducted femur and relatively upright tibia
­creates a vulnerability to valgus stress in many weight-­bearing
activities. The capsule that encases the knee joint is reinforced
by the ­collagen-rich medial and lateral retinaculum. The
medial and lateral menisci rest on the tibial plateau. They
are fibrocartilaginous, nearly ring-shaped disks that are
flexibly attached around the edges of the tibial plateau (see
Figure 11-3). These menisci increase the concavity of the
tibial articular surface, enhancing congruency of articula­
tion with the femoral condyles to facilitate normal gliding
and distribute weight-bearing forces within the knee during
gait and other loading activities.7 The menisci also play an
important role in nutrition and lubrication of the articular
surfaces of the knee joint.
Stability to the tibiofemoral joint is provided by sets of liga­
ments. The medial (tibial) collateral ligament and the lateral
(fibular) collateral ligament are extrinsic ligaments. The collat­
eral ligaments counter valgus and varus forces that act on the
knee. In addition, two intrinsic ligaments of the ­tibiofemoral
joint, the anterior cruciate and posterior cruciate ligaments
check translatory forces that displace the tibia on the femur.
FIGURE 11-1  An example of a basketball player using a knee ortho­
sis during activity. (Reprinted with permission, Hanger Orthopedic
Group, Inc., Jacksonville Beach FL)
A
B
FIGURE 11-2  Examples of neoprene sleeves used for knee pain and
protection. A, #402 Knee Support, Open Patella from McDavid. B,
PRO Orthopedic #100 Deluxe Knee Support Sleeve. (A, Reprinted
with permission from McDavid Inc., Woodridge, IL; B, Reprinted
with permission, PRO Orthopedic Devices Inc., Tucson, AZ.)

310
Section II  Orthoses in Rehabilitation
The location of attachments makes each of these ligaments
most effective at particular places in the knee's normal arc of
motion.7 Additionally, contraction of the quadriceps and knee
flexor muscle groups produce compressive forces that help sta­
bilize the knee. Muscles of the hip and lower leg also make
contributions to the mechanics of the femur and tibia, respec­
tively, which impact the movements of the knee complex.
Medial Collateral Ligament
The medial (tibial) collateral ligament (MCL) is a strong, flat
membranous band that overlays the middle portion of the
medial joint capsule (Figure 11-4). It is most effective in coun­
teracting valgus stressors when the knee is slightly flexed to fully
extended. Approximately 8 to 10 cm in length, it originates at
the medial epicondyle of the femur and attaches to the medial
surface of the tibial plateau. The MCL can be subdivided into a
set of oblique posterior fibers and anterior parallel fibers.
A bundle of meniscotibial fibers, also known as the poste­
rior oblique ligament, runs deep to the MCL, from the femur
to the midperipheral margin of the medial meniscus and
toward the tibia. These fibers connect the medial meniscus
to the tibia and help form the semimembranosus corner of
the medial knee. Additionally, the medial patellar retinacular
fibers play a reinforcing role.8
Lateral Collateral Ligament and Iliotibial Band
The lateral (fibular) collateral ligament (LCL) resists varus
stressors and lateral rotation of the tibia and is most effective
when the knee is slightly flexed. The LCL runs from the lateral
femoral condyle (the back part of the outer tuberosity of the
femur) to the proximal lateral aspect of the fibular head (see
Figure 11-4). The tendon of the popliteus muscle and the exter­
nal articular vessels and nerves pass beneath this ligament.
Another lateral structure that acts on the knee complex is the
iliotibial band (ITB). The ITB is positioned slightly anterior to
the LCL and is taut in all ranges of knee motion. Although the
position of the ITB allows it to stabilize against varus forces, as
does the LCL, the ITB also appears to assist the ACL, preventing
posterior displacement of the tibia when the knee is extended.9
Anterior Cruciate Ligament
The ACL runs at an oblique angle between the articular sur­
faces of the knee joint and prevents forward shift and excessive
medial rotation of the tibia as the knee moves toward exten­
sion (Figure 11-5). The ACL attaches to the tibia in a fossa just
anterior and lateral to the anterior tibial spine and to the femur
in a fossa on the posteromedial surface of the lateral femoral
condyle. The ACL's tibial attachment is somewhat wider and
stronger than its femoral attachment. Some authors divide the
fasciculi that make up the broad, somewhat flat ACL into two
or three distinct bundles. The ligament's anteromedial band,
with fibers running from the anteromedial tibia to the proxi­
mal femoral attachment, is most taut in flexion and relatively
lax in extension. The posterolateral bulk (PLB), which begins
at the posterolateral tibial attachment, is most taut in exten­
sion and relatively lax in flexion. An intermediate bundle of
transitional fibers between the anteromedial band and PLB
tends to tighten when the knee moves through the midranges
of motion. This arrangement of fibers ensures tension in the
ACL throughout the entire range of knee motion. The ACL is
most vulnerable to injury when the femur rotates internally on
the tibia when the knee is flexed and the foot is fixed on the
ground during weight-bearing activities.10
Posterior Cruciate Ligament
The posterior cruciate ligament (PCL) restrains posterior dis­
placement of the tibia in its articulation with the femur, espe­
cially as the knee moves toward full extension.7 The PCL is
shorter and less oblique in orientation than the ACL; it is the
strongest and most resistant ligament of the knee. PCL fibers
Medial
collateral
ligament
Iliopatellar
band
Iliotibial
band
Biceps
femoris
Lateral
collateral
ligament
FIGURE 11-4  A, A medial view of the right knee showing struc­
tures that provide medial support to the right knee. B, A lateral
view of the right knee illustrating structures that give lateral sup­
port to the knee. (Reprinted with permission from Levangie, PK,
Norkin CC. The knee complex. In Joint Structure and Function: A
Comprehensive Analysis, 3rd ed. Philadelphia: FA DAVIS; 2001.)
A
B
C
D
E
F
G
FIGURE 11-3  In this view of the surface of the tibia, we can identify
the medial collateral ligament (A), the C-shaped medial meniscus on
the large medial tibial plateau (B), the posterior cruciate ligament with
the accessory anterior and posterior meniscofemoral ligaments (C),
the tendon of the popliteus muscle (D), the circular lateral meniscus
on the smaller lateral tibial plateau (E), the anterior cruciate ligament
as it twists toward the inside of the lateral femoral condyle (F), and
the transverse ligament (G). (From Greenfield BH. Rehabilitation of
the Knee: A Problem Solving Approach. Philadelphia: FA Davis; 1993.)

Chapter 11  Orthoses for Knee Dysfunction
311
run from a slight depression between articular ­surfaces on
the posterior tibia to the posterolateral surface of the medial
femoral condyle (see Figures 11-3 and 11-5). Like the ACL,
the PCL can be divided into anterior and posterior segments.
The larger anterior medial band is most taut between 80 and
90 degrees of flexion and is relatively lax in extension. The
smaller PLB travels somewhat obliquely across the joint,
becoming taut as the knee moves into extension. The PCL
plays a role in the locking mechanism of the knee, as tension
in the ligament produces lateral (external) rotation of the
tibia on the femur in the final degrees of knee extension. The
PCL may also assist the collateral ligaments when varus or
valgus stressors are applied to the knee.7
Coursing along with fibers from the MCL is the menis­
cofemoral ligament, which stretches between the posterior
horn of the lateral meniscus and the lateral surface of the
medial femoral condyle. The meniscofemoral ligament has
sometimes been described as a third cruciate ligament.11 The
anterior meniscofemoral band (ligament of Humphry) runs
along the medial anterior surface of the PCL and may be up
to one-third its diameter. The posterior meniscofemoral band
(ligament of Wrisberg) lies posterior to the PCL and may be
as much as one-half its diameter. The meniscofemoral liga­
ments pull the lateral meniscus forward during flexion of the
weight-bearing knee to maintain as much articular congru­
ency as possible with the lateral femoral condyle.
Posterolateral Corner of the Knee
The lateral meniscus is somewhat more mobile than the
medial meniscus because of the anatomy of the ­posterolateral
corner of the knee. The arcuate complex and posterolateral
corner run from the styloid process of the fibula, joining
the posterior oblique ligament on the posterior aspect of the
femur and tibia. The arcuate ligament is firmly attached to
the underlying popliteus muscle and tendon. The tendon of
the popliteus muscle separates the deep joint capsule from the
rim of the lateral meniscus.
Patellofemoral Joint
The patella, a sesamoid bone embedded in the tendon of
the quadriceps femoris, is an integral part of the extensor
mechanism of the knee. The patella functions as an anatomi­
cal pulley, increasing the knee extension moment created by
contraction of the quadriceps femoris by as much as 50%.
It also guides the forces generated by the quadriceps ­femoris
to the patellar ligament, protects deeper knee joint anatomy,
protects the quadriceps tendon from frictional forces, and
increases the compressive forces to which the extensor mech­
anisms can be subjected.12–15
Although the anterior surface of the patella is convex,
the posterior surface has three distinct anatomical areas: a
lateral, medial, and odd facet. The lateral and medial facets
are separated by a vertical ridge. The odd facet articulates
with the medial condyle at the end range of knee extension
(Figure 11-6). The posterior patellar surface is covered with
hyaline articular cartilage, except for the distal apex, which is
roughened for the attachment of the patellar tendon. Pressure
between the patella and trochlear groove of the femur
increases substantially as the knee flexes. During knee flexion,
the patella moves in a complex but consistent three-­
dimensional pattern of flexion/extension rotation, medial/
lateral rotation, medial/lateral tilt (also described as ­wavering),
and a medial/lateral shift relative to the femur.13,15 These
motions occur biomechanically in the X, Y, and Z planes.
The stability of the patella is derived from the patello­
femoral joint's static structural characteristics and dynamic
(muscular) control. Static stability is a product of the anat­
omy of the patella, the depth of the intercondylar groove, and
the prominent and longer lateral condyle of the femur. The
sulcus angle, formed by the sloping edges of the condyles, is
A
B
Anterior
cruciate
Lateral
collateral
ligament
Transverse
ligament of
meniscus
Posterior
cruciate
Medial
collateral
ligament
Lateral
collateral
ligament
Anterior
cruciate
Medial
collateral
ligament
Posterior
cruciate
Intercondylar
notch
FIGURE  11-5  A, Anterior view of the tibiofemoral joint in 90
degrees of knee flexion showing the menisci and the ligamentous
structures that stabilize the knee. B, Posterior view of the knee in
extension. (Reprinted with permission from Antich TJ. Orthoses
for the knee; the tibiofemoral joint. In Nawoczenski DA, Epler ME
[eds], Orthotics in Functional Rehabilitation of the Lower Limb.
Philadelphia: Saunders, 1997. p. 59.)

312
Section II  Orthoses in Rehabilitation
normally between 114 and 120 degrees; however, it can vary
significantly from person to person.16 Wiberg17 divides the
patellofemoral joint into six types based on the size and shape
of facets (Table 11-1). The depth of the patellar trochlea and
the facet pattern are important in patellar stability.
Dynamic stability of the patellofemoral joint is derived pri­
marily from activity of the quadriceps femoris as well as from
the tensile properties of the patellar ligament (Figure 11-7).
The four components of the quadriceps muscle act together
to pull the patella obliquely upward along the shaft of the
femur, whereas the patellar ligament anchors it almost
straight downward along the anatomical axis of the lower leg.
The tibial tubercle is typically located at least 6 degrees lateral
to the mechanical axis of the femur.
Because the structure of the patellofemoral articulation and
the muscular/ligamentous forces that act on the patella are
complex, patellar dynamics involve much more than simple
cephalocaudal repositioning as the knee is flexed or extended.
Van Kampen and Huiskes15 describe the three-dimensional
motions of the patella as flexion rotation, medial rotation,
wavering tilt, and lateral shift. All of these patellar movements
(except flexion) are influenced by the rotation of the tibia and
the dynamic stabilization of the muscles that act on the patella.
BIOMECHANICS OF KNEE MOTION
Although it is beyond the scope of this book chapter to com­
prehensively cover the biomechanics of knee motion, it is
important to have a basic foundation of knee biomechanics
to understand the use of knee orthoses as an intervention
for knee pathology. Evaluating and managing injuries of the
knee requires an in-depth understanding of the biomechani­
cal characteristics of the knee joint. The kinematics of the knee
describe its motion in terms of the type and location and the
magnitude and direction of the motion.18 The kinetics of the
knee describe the forces that act on the knee, causing move­
ment.18 Kinetic forces are classified as either external forces
that work on the body (e.g., gravity) or as internal, body-
generated forces (e.g., friction, tensile strength of soft tissue
structures, muscle contraction).
Motion in the tibiofemoral joint can be best understood
by separating the motion into its physiological and acces­
sory components. Physiological motion can be controlled
­consciously, most often through voluntary contraction of mus­
cle. Osteokinematic (bone movement) and arthrokinematic
Lateral
Medial
Patella
Femur
Superior
Vertical
ridge
Lateral
Odd
facet
Medial
Inferior
A
B
FIGURE 11-6  A, The normal position of the patella in the intercon­
dylar groove of the distal femur. B, Underside of the patella with its
three facets and vertical ridge. (Reprinted with permission from Belyea
BC. Orthoses for the knee: The patellofemoral joint. In Nawoczenski
DA, Epler ME [eds], Orthotics in Functional Rehabilitation of the Lower
Limb. Philadelphia: Saunders, 1997. pp. 32-33.)
TABLE 11-1  Classification of Patellar Types, Listed from
Most to Least Stable17
Patellar Type
Description
I
Equal medial and lateral facets, both slightly
concave
II
Small medial facet, both facets slightly concave
II/III
Small, flat medial facet
III
Small, slightly convex medial facet
IV
Very small, steeply sloped medial facet, with
medial ridge
V (Jagerhut)
No medial facet, no central ridge
Quadriceps tendon
Patellar tendon
Medial retinaculum
and vastus medialis
Lateral retinaculum,
vastus lateralis, and
iliotibial tract
FIGURE 11-7  A schematic diagram of structures that act on the
patella. (Reprinted with permission from Neumann DA. Kinesiology
of the Musculoskeletal System: Foundations for Rehabilitation, 2nd ed.
St. Louis: Mosby Elsevier, 2010.)

Chapter 11  Orthoses for Knee Dysfunction
313
(joint surface motion) are examples of physiological motion.
Accessory motion occurs without conscious control and can­
not be reproduced voluntarily. Joint play, which is ­elicited by
passive movement during ­examination of a joint, is an exam­
ple of an accessory motion. The magnitude and type of acces­
sory motion possible are determined by the characteristics of
a particular articulation and the properties of the tissues that
surround it. The arthrokinematics of the tibiofemoral joint
will vary depending upon whether the lower-extremity is in
a weight-bearing or loaded position. For example, with tibial-
femoral extension the tibia moves anteriorly relative to the
femur and with femoral on tibia extension the femoral con­
dyles slide from anterior to posterior, while rolling anteriorly.8
One of the important accessory component motions of the
tibiofemoral joint is its screw home or locking mechanism.
In the final degrees of knee extension, the tibia continues to
rotate around the large articular surface of the medial fem­
oral condyle. This motion cannot be prevented or changed
by volitional effort; it is entirely the result of the configura­
tion of the articular surfaces. When the knee is flexed to or
beyond 90 degrees, however, conscious activation of muscles
can produce physiological (osteokinematic) external (lateral)
or internal (medial) rotation of the tibia on the femur.
Three osteokinematic motions are possible at the
­tibiofemoral joint. Knee flexion/extension occurs in the ­sagittal
plane around an axis in the frontal plane (x-axis). Internal/
external rotation of the tibia on the femur (or vice versa) occurs
in the transverse plane around a longitudinal axis (y-axis).
Abduction and adduction occur in the frontal plane around
a horizontal axis (z axis). The arthrokinematic movements
of the tibiofemoral joint are rolling, gliding, and sliding
(Figure 11-8). It is important to note that the roll-glide ratio is
not constant during tibiofemoral joint motion: Approximately
1:2 in early flexion, the roll-glide ratio becomes almost 1:4 in
late flexion.19 Rolling and gliding occur primarily on the poste­
rior portion of the femoral condyles. In the first 15 to 20 degrees
of flexion, a true rolling motion of the femoral condyles occurs
in concert with the tibial plateau. As the magnitude of flexion
increases, the femur begins to glide posteriorly on the tibia.
Gliding becomes more significant as flexion increases.11
From a kinematic standpoint, the ACLs and PCLs operate
as a true gear mechanism controlling the roll-glide motion of
the tibiofemoral joint. With rupture of either or both of the
cruciate ligaments, the gear mechanism becomes ineffec­
tive, and the arthrokinematic motion is altered. In an ACL-
deficient knee, the femur is able to roll beyond the posterior
half of the tibial plateau, increasing the likelihood of damage
or tear of the posterior horn of the medial or lateral meniscus.
Because the knee has characteristics of a hinge joint and an
arthrodial joint, two types of motion (translatory and rotatory)
can occur in each plane of motion (sagittal, frontal/coronal,
transverse). For this reason, knee motion is described as having
six degrees of freedom. The three translatory motions of the
knee include anteroposterior translation of 5 to 10 mm, medio­
lateral translation of 1 to 2 mm, and compression-­distraction
motion of 2 to 5 mm. The three rotatory motions occur in
­flexion/extension, varus/valgus, and internal (medial)/­external
(lateral) rotation.7,19 Hinge design of an orthosis will be
­discussed further in this chapter to help control these motions.
Single, dual, or multiple hinged orthoses that do not conform
with the A/P translation (or roll back) and the rotation of the
joint, will exert adverse mechanical effects.20
Orthoses for the Knee
As discussed previously, there are a few different categories
of orthoses for the knee. A sample of the many types of knee
orthoses that are commercially available to health profession­
als is listed in Table 11-2. The clinician should be aware that the
Femur
Tibia
fixed
Motion of the femoral
condyles during flexion
Motion of the femoral
condyles during extension
Posterior
rolling
Anterior
sliding
Anterior
rolling
Posterior
sliding
A
B
FIGURE 11-8  Diagram of femoral motion on a fixed tibia. A, As the knee flexes, the femoral con­
dyles roll posteriorly (curved arrow) while gliding/sliding forward (straight arrow). B, As the knee
extends, the condyles roll forward (curved arrow) while gliding posteriorly (straight arrow). (From
Hartigan E, Lewek M, Snyder-Mackler L. The knee. In Levangie PK, Norkin CC [eds], Joint Structure
and Function: A Comprehensive Analysis, 5th ed. Philadelphia: Davis, 2011. p. 355.)

314
Section II  Orthoses in Rehabilitation
TABLE 11-2  A Few Examples of Knee Orthoses by Manufacturer and Category
Manufacturer
Rehabilitative
Knee Orthoses
Functional
ACL/PCL
Functional
Osteoarthritis
Prophylactic
Patellofemoral
Bauerfeind USA
Kennesaw, Ga.
(800) 423-3405

Softech Genu
Secutech Genu
Softtech OA
Genutrain P3
Bledsoe by Medical
Technology
Grand Prairie, Texas
(888) 253-3763

Extender Plus
Leverlock
Revolution 3
Ultimate Dynamic
U2CI
Kneecage
Forcelite
Thruster RLF
Aligner ESE
20.50 Patella-
femoral
Brace International
Atlanta, Ga.
(800) 545-1161

FLUK Infrapatellar
Strap
Cropper Medical,
Inc./Bio Skin
Ashland, Ore.
(800) 541-2455

Gladiator Sport
Standard Knee Skin
Q Lok
Patella Stabilizer
Q Baby
dj Orthopedics, Inc.
Vista, Calif.
(800) 336-6569

IROM
Telescoping
IROM Bilateral
with Shells
Defiance III
Armor
Legend
4titude
OA Defiance
OA Full Force
OA Assist
Protective-Knee
Guard
Playmaker
TruPull Wraparound
H-Buttress
Generation II USA,
Inc./Ossur
Bothell, Wash.
(800) 462-7252

Generation II 3DX
Matrix
Extreme Select
GII Trainers
Unloader Select
Unloader Adj
Unloader Spirit
Unloader Bi-Com
Patellar Stabilizer
PS1
Innovation Sports, Inc.
Irvine, Calif.
(800) 222-4284

Sentry
Knee MD
Quicklock
Option
CTi Edge
C180
XCI
Aspire
CTI2
CTI2OA
Powerflex
Donut Stabilizer
Lateral J Stabiliz
McDavid Sports/Medical
Products
Woodridge, Ill.
(800) 237-8254

428R McDavid
Level 3 Knee
Brace with
Polycentric Hinges
419R McDavid
Level 2 Knee
Support
Pro Orthopedic
Devices, Inc
Tuscon, Ariz.
(800) 523-5611

PRO 190
Hinged Stabilizing
Knee Brace

















PRO 105
Spiral Knee
Support
Sleeve
Patellar Strap
PRO 135
Townsend Design
Bakersfield, Calif.
(800) 700-2722

ROM-SS
EZ-Pads

Premier Series
Rebel Series
Sports Series
RelieverOne








ACL, Anterior cruciate ligament; PCL, posterior cruciate ligament.

Chapter 11  Orthoses for Knee Dysfunction
315
brace names tend to change. Some are designed to immobilize
the knee after surgical repair of damaged or ­ruptured ­ligaments
or menisci during the acute phases of healing, whereas other
knee orthoses are used to improve biomechanical efficiency
at the knee joint and/or prevent injury. Rehabilitative orthoses
are designed to protect the knee and allow progressive increase
in active range of motion during rehabilitation. FKOs pro­
vide additional protection as rehabilitation is completed and
a patient returns to normal activities. Prophylactic knee ortho­
ses, attempt to prevent injury (or at least lessen the extent of
injury) in athletes who are at risk of injury during competition.
A patellofemoral knee bracing allows for improved tracking of
the patella during knee motions, whereas unloader knee braces
dissipate increased varus and valgus forces across the tibiofemo­
ral joint. The complexity of the knee joint (with its polycentric
axis of rotation for flexion/extension, asymmetry of the lateral
and medial compartments, and the arrangement of its muscular
and ligamentous attachments) creates a challenge when trying
to design a knee orthosis that is able to support, protect, and sta­
bilize the knee in a multiplanar fashion with the same efficiency
as its own physiological motion.
Rehabilitation Knee Orthoses
Orthoses used in the postoperative and early rehabilitation of
patients who have had surgical repair of damaged cartilage, lig­
aments, or bone are designed to control knee motion carefully
to minimize excessive loading on healing tissues (Figures 11-9
and 11-10).3 Although many rehabilitation knee orthoses are
on the market, an effective orthosis has several important char­
acteristics. The orthosis must be adjustable to accommodate
changes in limb girth due to edema or atrophy. It must remain
in the desired position on the limb during functional activities
in stance and in sitting. It must be comfortable, easy to don
and doff, durable, and economical. Most physicians require
an adjustable knee unit so that active range of motion can be
increased incrementally as the tissue heals and the patient's
condition improves. The ability to move in carefully controlled
ranges of motion is thought to improve ligamentous strength
and to minimize the risk of scar formation in the intracondylar
notch that is associated with flexion contracture.19
Functional Knee Orthoses
Use of knee orthoses as functional braces parallels the devel­
opment of the discipline of sports medicine since the early
1970s.21 In the years before 1970, orthoses that were designed
for patients with neuromuscular dysfunction were adapted to
meet the needs of injured athletes with a functionally unsta­
ble knee. Typically, the adapted orthosis was cumbersome and
significantly impaired the quality of the athlete's performance.
To assist professional athletes in quickly and safely return­
ing to competition, the sports medicine community explored
alternative orthotic interventions to manage an unstable knee.
The development of FKOs as alternatives to surgery (which
often sidelined athletes for considerable periods of time) was
especially welcomed.22
One of the first FKOs, the Lenox Hill Derotation knee brace,
was developed by Nicholas and Castiglia of Lenox Hill Hospital
in the early 1970s to protect the chronically unstable knees of
football quarterback Joe Namath.23 The Lenox Hill orthosis
was the primary design that was commercially available until
the late 1970s. The original orthosis had medial and lateral
uprights, a single-axis knee joint with a medial fulcrum pad,
a broad elastic thigh and calf cuff/strap to hold the orthosis in
place, and a set of derotation straps to control movement of
the tibia on the femur. The intent was to control mediolateral
instability, rotational instability, and multiple ligament impair­
ment.24 Subsequent versions of the Lenox Hill orthosis are avail­
able in standard, lightweight, and ultra-lightweight versions,
with a dial-lock option to adjust available range of motion and
with protective undersleeves and oversleeves (Figure 11-11).
The original design has evolved considerably: More than
three dozen functional braces are manufactured in today's
sports medicine market (see Table 11-2 for examples). Most are
based on a lightweight rigid suprastructure made from carbon
composite or titanium alloy. Many use adjustable elasticized
or Velcro strapping to apply a four-point stabilizing force and
hold the orthosis in position on the limb. Some have polycen­
tric knee units; others allow variable flexion control or assisted
extension. The basic design and components of most commer­
cially available FKOs are shown in Figure 11-12.
A
C
D
B
2
3
1
FIGURE  11-9  The components of most commercially avail­
able rehabilitation knee orthoses include open cell foam interface
that encase the calf and thigh (A) and nonelastic adjustable Velcro
strap for closures (B); lightweight metal, composite, or plastic side­
bars (C); and single-axis or polycentric hinge that can be locked or
adjusted to allow or restrict motion (D) within the therapeutically
desired range of motion. The force systems of these orthoses apply
a pair of anteriorly directed forces at the proximal posterior thigh
(1) and distal posterior calf (3), against a posteriorly directed force
(2) applied over or on either side of the patella. Varus and valgus
stressors are resisted by the sidebars. (Reprinted with permission
from Trautman P. Lower limb orthoses. In Redford JB, Basmajian
JV, Trautman P [eds], Orthotics: Clinical Practice and Rehabilitation
Technology. New York: Churchill Livingstone, 1995. pp. 195:230)

316
Section II  Orthoses in Rehabilitation
According to a survey of orthopedic surgeons per­
formed by Decoster and Vailas,25 87% of surgeons brace
their patients who have had ACL reconstruction. In addi­
tion, DeCoster and Vailas found that typically the surgeons
are more likely to prescribe “off the shelf” braces for patients
with ACL deficiency compared to those patients with ACL
reconstruction.25
Unfortunately, systematic critical evaluation of the effi­
cacy of FKOs has not kept pace with the development of new
designs; there is a paucity of clinical and laboratory research
defining the indications for, roles of, or outcomes of use for
these functional braces.22
Functional Knee Orthoses and Performance
Current available literature can be characterized by two
major approaches to comparing braced and unbraced per­
formances: (1) maximal effort tests, wherein subjects per­
formed at maximal intensity and the criterion measure was
an overall performance measure such as distance hopped
or the time to run a specified distance; (2) matched effort
tests, wherein subjects perform at submaximal intensity and
the criterion measures tend to be specific variables such as
muscle activation patterns determined via electromyogra­
phy (EMG) or ground reaction forces determined via force
plate.26 Nemeth and colleagues27 studied six expert downhill
skiers who had sustained ACL injuries. Surface electrodes
were used with an eight-channel telemetric EMG system to
collect recordings from the vastus medialis, biceps femo­
ris, semimembranosus, semitendinosus, and gastrocnemius
medialis muscles from both legs. Without a brace, the EMG
activity level of all muscles increased ­during knee flexion.
With a brace, the EMG activity increased in midphase dur­
ing the upward push for the weight transfer and the peak
activity occurred closer to knee flexion in midphase. The
authors suggest the brace caused an increase in afferent input
from proprioceptors, resulting in an adaptation of motor
control patterns secondarily modifying EMG activity and
timing.27 Research has also shown that the use of functional
knee bracing seems to protect the ACL from sagittal plane
shearing in non–weight-bearing and weight-bearing, and
internal torques in non–weight-bearing. However, the study
also found that the braced knee did not have any decrease in
strain in external torques or valgus-varus stressors in weight-
bearing and non–weight-bearing when compared with the
unbraced knee.28
Additionally, Sterett and colleagues29 found that fol­
lowing ACL reconstruction, those skiers who did not
use a functional brace during skiing had a higher rate of
reinjury.
A number of researchers have investigated the impact of
functional braces on performance and endurance in nonin­
jured and previously injured athletes. Stephens30 found little
impact on speed of running in noninjured collegiate basketball
players during straight line running tasks (end line to foul line,
full court) when comparing performance in two functional
braces with nonbraced speed. Although these results are posi­
tive, the in-brace time and types of activity used for the study
were significantly ­different than those of an active, full length
basketball game.
Highgenboten and colleagues31 found a 3% to 6% increase
in metabolic cost during steady-state treadmill running
when functional braces were worn. Subjects also had higher
­ratings of perceived exertion when exercising with the brace.
These effects were attributed to the weight of the brace. In
addition, research by Wojtys and colleagues32 showed that
most braces appear to slow hamstring muscle reaction times
at voluntary levels. The evidence from these maximal effort
and matched effort performance tests suggest no advantage
to use of FKOs.
Most functional knee braces weigh close to 1 pound.
Despite the use of lightweight materials that are resilient to var­
ious forces, it is possible that long in-brace times can lead to
fatigue or to injuries to other areas of the body that compen­
sate for the added weight of the orthosis. This may explain the
increase in injuries of the foot and ankle reported by Grace and
colleagues33 in athletes who wore braces. Styf and colleagues34
studied changes in intramuscular pressures within the anterior
compartment of the leg at rest, during exercise, and after exer­
cise, comparing three orthoses. Intramuscular pressures at rest
and muscle relaxation pressure during ­exercise were higher
when subjects wore each of the orthoses. To evaluate whether
distal strapping was responsible for this increase in pressure,
distal straps were removed and subjects retested; intramuscular
A
B
FIGURE 11-10  A, Townsend full shell padded knee brace typically
used following knee surgery. B, The premium sized knee immobi­
lizer from Ossür 2. (A, Reprinted with permission from Townsend
Design, Bakersfield, CA. B, Reprinted with permission from Ossür
Americas, Foothills Ranch, CA.)

Chapter 11  Orthoses for Knee Dysfunction
317
pressure and muscle relaxation pressure returned to levels that
were similar to nonbraced levels. This study demonstrates the
subtle yet potentially important impact of orthoses on muscle
function that may contribute to injury; external compression
elevates the intramuscular pressure beneath the thigh and leg
straps. Local muscle blood flow is impaired by the increased
intramuscular pressure, which leads to decreased oxygen ten­
sion and impaired muscle ­function.35 This could possibly
be the reason for ­premature leg muscle fatigue that has been
reported in other experimental studies on individuals using
knee braces.34,36,37
In their randomized, multicenter trial, McDevitt and col­
leagues38 compared patients who wore an off-the-shelf knee
brace daily for 6 months and for high-level activities there­
after with a group who did not wear any brace after 3 weeks
postoperatively. The authors found that there were no signifi­
cant differences between groups in multiple outcome mea­
sures, which included knee range of motion, knee stability,
and function.38
Prophylactic Knee Orthoses
In the 1990s, considerable debate took place concern­
ing the potential benefits or effectiveness of orthoses that
were designed to prevent knee injuries or to minimize the
­severity of injury for athletes involved in high-risk injury
activities.33,39–41 The objective of wearing a prophylactic
knee orthosis (PKO) is to provide protection to the soft
tissue restraints of the knee. Most commonly, these braces
have been worn by athletes who are exposed to lateral
impacts.
Lateral impacts can result in MCL and cruciate ligament inju­
ries.42 Prophylactic orthoses are designed to protect the integ­
rity of medial knee structures. Most prophylactic designs have
a hinged lateral frame, held in place by a set of thigh and calf
cuffs or straps. The hinge may be single axis, dual axis, or poly­
centric; many designs have also incorporated a hyperextension
stop for further protection of the athlete's knee against forceful
hyperextension injury (Figure 11-13). Some designs use a plastic
shell with medial and lateral uprights and polycentric hinges.43
A
B
FIGURE 11-11  Comparison of the original (A) and current (B) Lenox Hill Hill Rerotation Orthosis. (From Nawoczenski DA, Epler ME
[eds], Orthotics in Functional Rehabilitation of the Lower Limb. Philadelphia: Saunders, 1997.)

318
Section II  Orthoses in Rehabilitation
Recommendations for the Patient with a Prophylactic
Knee Orthosis
PKOs are available off-the-shelf or can be custom molded
for the individual athlete. Clinical practice and research have
not yet resolved the debate about the efficacy of prophylactic
orthoses. Questions remain about the relationship between
the biomechanical characteristics of the orthoses and the ana­
tomical knee, the response of the orthosis to valgus loading,
the impact of the orthosis on the continuum of locomotion
(walking to running), and the ability of the orthosis to pre­
vent injuries during activity as intended by its design.
Biomechanical Performance of Prophylactic
Knee Orthoses
Many of the studies that have investigated the biomechanical
performance of prophylactic braces have used either cadaver
knees or mechanical surrogate models of the knee. Most have
concluded that protection of the MCL has been inconsistent
and only borderline at best.40,44–48 Many health care providers
are concerned about how the orthosis might preload the MCL
before normal physiologic loading.44,46,47 Our understanding
of the interaction between the orthosis and the tissues of the
knee is based on the properties of human tissue and of brace
materials under static and dynamic loading conditions.
Manufacturers report high resistance of the braces to later­
ally directed impact loading; however, the research design and
methodology on which these claims are based can be debated.
3
1
2
4
B
A
E
F
C
D
FIGURE  11-12  Components of most contemporary functional
knee orthoses include the calf section/cuff with its closure (A);
medial or lateral condylar pads, or both (B); medial and lateral
uprights (C); the thigh section/cuff with its closure (D); an adjust­
able knee hinge (E); and the thigh strap (F). The stabilizing forces
that are typically applied by the orthosis include (1) a posterior force
over the anterior proximal thigh (1), an anterior force on the distal
posterior femur (2), a posterior force at the proximal anterior tibia
(3), and an anterior force at the midshaft of the posterior tibia (4).
(Reprinted with permission from Trautman P. Lower limb ortho­
ses. In Redford JB, Basmajian JV, Trautman P [eds], Orthotics:
Clinical Practice and Rehabilitation Technology. New York: Churchill
Livingstone, 1995. p. 31.)
A
B
FIGURE 11-13  Examples of a prophylactic knee orthosis, designed to reduce risk of knee injury
for athletes during practice and competition situations. A, BioSkin's Gladiator Sport used for knee
ligament protection. B, Pro Level Mueller Hinge 2100 for protection of the MCL. (A, Reprinted with
­permission from Cropper Medical, Inc/Bioskin, Ashland, OR; B, Reprinted with permission from
Mueller Sports Medicine, Inc., Prairie du Sac, WI.)

Chapter 11  Orthoses for Knee Dysfunction
319
In some cases, the braces are actually less rigid and resistant to
derangement during loading than is the anatomic knee itself.
The ability of a knee orthosis prepositioned in flexion to pro­
tect against major ligament damage is uncertain.41 Joint line
clearance during brace deformation is an additional concern.
Theoretically, the prophylactic brace is designed to transmit
valgus loads on the knee over the greatest possible area to dissi­
pate the forces away from susceptible ligaments effectively.41,46,47
The orthotic hinge forms a bridge over the joint line; its sites of
attachment are best placed as far as possible on the proximal
femur and distal tibia. Clearance between the hinge and the
joint themselves must be adequate. Contact between the hinge
and the joint creates a three-point bending system centered at
the joint, inadvertently preloading the MCL.46,47
Evidence of Efficacy of Prophylactic Knee Orthoses
There have been many studies directed at determining the
effectiveness of PKOs in preventing knee ligament injuries in
football players.33,49–52 In 1987, Teitz and colleagues52 reported
on data collected in 1984 and 1985 regarding football players
from Division I NCAA schools. Players who wore PKOs had
more injuries to the knee than players who did not wear these
braces. This study, however, did not control for players’ his­
tory of prior knee injury.52 In 1986, Hewson and colleagues49
reported findings on University of Arizona football players
from a study that spanned 8 years. The injury records of four
academic years in which players wore PKOs were compared
with the preceding 4 years in which players did not use PKOs.
It was mandatory for the players who were at the greatest risk
for injury, that is, linebackers, defensive linemen, and tight
ends to wear PKOs in the years when brace wear was being
monitored in this study. The results of this research indicated
that, when comparing groups of braced players to unbraced
players, there were no reductions in the number, rate, or type
of knee injuries that players sustained.49
A 3-year study of NCAA Division I college football play­
ers in the Big Ten Conference by Albright and colleagues53
revealed slightly different results. These researchers iden­
tified some trends that players who wore PKOs experi­
enced lower rates of MCL injuries when compared with
their unbraced peers. These trends were evident only when
influential factors such as playing position, skill level of the
player, and session (game or practice) in which the injury
was sustained were considered in the analysis. Starting
players and those who were substitutes in line positions,
linebackers, and tight end positions had lower injury rates
in practices and games. Backs, receivers, and kickers exhib­
ited trends indicating higher injury rates in games when
using a PKO.53
The implications that the benefits of PKO use may be
related to player position is also suggested in a study by Sitler
and colleagues.51 Participants in this study included young
men in an eight-man intramural tackle football program at
West Point between 1986 and 1987. Variables such as the ath­
letic shoe, playing surface, knee injury history, type of brace,
and injury assessment and documentation were all con­
trolled. Subjects wearing PKOs while on defense had signifi­
cantly fewer knee injuries than their nonbraced counterparts.
There were no significant differences for these parameters
noted when players were on offense.51
CASE EXAMPLE 1
High School Football Player
C. K., a 16-year-old high school quarterback, and his
father come into your outpatient physical therapy clinic
for a consultation regarding the potential benefits of
wearing a knee brace during football games and practices.
C. K. is a highly recruited quarterback on his high school
football team. He has no history of injury that prevents
him from playing or practicing football. He and his Dad
are aware that football players are susceptible to knee liga­
ment injuries due to the nature of the game. C. K.'s father
is concerned that his son's ability to play college football
would be compromised if he injured his knee. He wants to
know whether wearing a prophylactic knee brace (PKO)
would reduce the likelihood that C. K. would sustain a
severe knee injury.
Questions to Consider
• Given C. K.'s history and current presentation, what
additional tests and measures would provide helpful
information to use in your evaluation process?
• What is your movement dysfunction-related diagnosis
for C. K.?
• What is the rehabilitation prognosis for C.K.? What are
his goals for intervention? What are your rehabilitation
goals? How long to do you think it will take to achieve
any goals that you and C. K. agree upon?
• What is the current evidence in the clinical research liter­
ature about the efficacy of PKO to reduce incidence and
severity of knee injury in college football players?
• What impact does wearing a PKO have on athletic per­
formance? What are the risks associated with wearing a
PKO during athletic competition?
• Based on C. K.'s goals and expectations, your under­
standing of the risk for injury for football players, and
evidence available in the clinical research literature, what
recommendations would you make for intervention at
this point in time? Is the evidence convincing enough
that you would recommend that this high school athlete
should begin to wear a PKO?
• What PKO designs might be most appropriate for this
college-bound football player?
• How will you assess whether C. K.'s goals have been met?
• What type of follow-up would you recommend for C. K.?

320
Section II  Orthoses in Rehabilitation
Researchers and athletic trainers have concerns about the
risk of injury to other areas of the limb when these orthoses
are worn during competition. In a two-season prospective
study of potentially protective benefits of prophylactic brac­
ing in a sample of 580 high school football players, Grace
and colleagues33 found a dramatic increase in the number of
injuries of the ankle and foot among athletes who wore the
braces. In contrast, Sitler and colleagues51 found no signif­
icant difference in the frequency of ankle injuries between
a knee brace group and a control group of military cadets.
Additionally, the severity of MCL and ACL knee injury was
not reduced with the use of unilateral-biaxial prophylactic
knee braces.51
It is difficult to make an unequivocal statement regard­
ing the need for high school and college athletes to wear a
PKO. The research examining this issue is confusing because
data collection cannot take into account yearly variations in
coaching techniques or completely control the data collection
methods employed by all of the schools participating in the
studies. Furthermore, there is no standardization in injury
diagnosis between these studies. This makes it difficult to
compare results of the studies to each other.42 Many of the
studies have methodological problems and limited sample
size, making interpretation of their findings challenging.54–58
Despite the inconsistency of research methods and findings,
however, France and Paulos42 conclude that there is sufficient
evidence to indicate that bracing can be beneficial in reduc­
ing the number of MCL injuries sustained from direct lateral
blows to the knee, especially when the knee is near full exten­
sion. They recommend that a PKO be carefully fit, so that
the hinge maintains its position at the lateral joint line dur­
ing activity, that the brace provides enough clearance from
the joint line during impact, and that the materials used in
the brace construction are sufficient to control the amount of
impact delivered to the knee.42 The literature does not provide
enough information about the protection that these braces
offer to the other soft tissue structures of the knee.
A study of high school football players by Deppen and
Landfried59 found no significant reduction in knee injuries in
those football players wearing prophylactic knee braces com­
pared with unbraced football players.
An additional concern regarding the use of prophylactic
knee bracing is whether it diminishes athletic performance.
Greene and colleagues60 found that in football players
prophylactic knee bracing did not significantly reduce
40-yard dash speed or agility during four-cone drills.60
Sforzo and ­colleagues61 found that the use of prophylac­
tic bracing in ­college football players did not decrease
performance, whereas, in female lacrosse players, prophy­
lactic bracing negatively impacted athletic performance. In
healthy college aged subjects, Borsa and colleagues62 found
that during the use of prophylactic bracing, subjects had
decreased peak torque and torque acceleration energy dur­
ing isokinetic testing, as well as slower sprint speed time.62
Liggett and colleagues63 found that gait pattern was not
significantly altered when a prophylactic knee brace was
used during running in healthy males and females.63 In
“Technical Report: Knee Brace Use in the Young Athlete,”
the American Academy of Pediatrics stated that there was
“insufficient evidence to recommend prophylactic knee
bracing in the young athlete.”64
In a descriptive epidemiological study, Sanders and
­colleagues65 found that incidence of ligamentous knee injury
decreased with prophylactic knee bracing in off-road motor­
cyclists compared with motorcyclists who did not wear a brace.
If prophylactic braces are intended to prevent or reduce
the severity of injury, clinicians and brace manufacturers
must work to be responsible for critical evaluation of these
devices to define better define their appropriate use and out­
comes. Clinicians must hold vendors accountable for their
products, requesting well-designed and clearly reported
quantitative studies to support the narrative accounts in mar­
keting brochures about design criteria. Lastly, the clinician
should have a discussion with the patient that focuses on the
patient’s goals and how using a brace may help the patient
achieve those goals.
INFORMED CLINICAL DECISION MAKING
Because of the large number of FKOs currently marketed, it
is very challenging and often frustrating for clinicians and
surgeons to evaluate the information published in ­marketing
literature when research support is not always available. As
a clinician it may be challenging to remain well informed
because orthotic designs are constantly being modified and
improved. Making a sound decision about which design can
best meet the stability and activity needs of a given individual
can be a daunting task and must not be based on which sales
representative most recently shared information or which
orthosis is currently the most popular choice. Clinicians
should keep apprised of all bracing that is commercially avail­
able. Although patients may seek a functional orthosis to pro­
tect their knee or to improve their performance, many do not
have the knowledge or resources to understand the specifics
and idiosyncrasies of each brace. To make the best informed
decision, the clinician must consider the patient's specific
injury and pattern of instability, the present and anticipated
strength and bulk of their muscles around the injured knee,
and the activities and likely mechanism of being reinjured
in the patient's preferred activities. Decisions about orthotic
options must be deliberately made, with discussion involv­
ing the patient, physical therapist or athletic trainer, orthotist,
brace manufacturer, and physician. Quick decisions about an
FKO, made without carefully evaluating the match between
the patient's needs and the orthotic design, lead to frustration
and dissatisfaction for all involved.
In evaluating information presented about knee orthoses
published in the literature, health professionals must look
closely at research design and methodology and evaluate the
clinical relevance of the conclusions drawn from study results.
Important questions to ask include the following:
1. What type of brace is being studied?
2. What patient demographic is being used to evaluate the
efficacy of a knee orthosis?

Chapter 11  Orthoses for Knee Dysfunction
321
3. Does the study evaluate the orthosis under static condi­
tions or during dynamic use?
4. Does the study used cadaveric models or physiologically
active joints in the evaluation of orthotic performance?
5. Did the study test reconstructed ACL knees in the use of
knee orthosis?
6. What outcome measures were used to determine positive
outcomes?
Many of the most frequently cited studies evaluate brace
performance under static conditions, specifically the abil­
ity of particular orthoses to prevent anterior excursion of
the tibia on the femur as measured by standard clinical tests
for ligamentous instability (e.g., Lachman's, pivot shift, or
Losee's tests). Some studies have used electronic and mechan­
ical instrumentation to evaluate orthotic performance more
precisely under static and controlled dynamic conditions.
Although many studies demonstrate the efficacy of knee
orthoses in prevention of excessive anterior excursion under
static conditions, to generalize these static results to dynamic
activity for patients with ACL-deficient knees is audacious.
Because an orthosis can provide a degree of stability for the
knee under static conditions does not guarantee that it can
also stabilize the knee during high demand, multiplanar
activity. The low load levels applied to knee ligaments dur­
ing static or cadaver model testing do not accurately reflect
load levels during functional and athletic activities. Decisions
to choose a particular orthosis based on this type of research
alone are not well informed.
The selection of a functional brace today is even more
challenging as third-party payers have dictated to the con­
sumer where and from what vendor they can get their brace,
either in a custom-made or off-the-shelf model. This limits
the choice and type of brace used and puts the patient in a
one-brace-for-all scenario.
Another dilemma that clinicians face is the aggressive
rehabilitation protocols for ACL reconstruction that are
­currently being used show close to normal range and strength
by the third to sixth month. The decision to have the patient
advance through the rehabilitation protocols and perform
activities such as jumping, hopping, turning, or twisting is a
complex decision that is based on many factors. These factors
include strength of the ACL graft, graft fixation, and known
biological factors that affect healing. A knee joint that is sta­
bilized by a strong isometric graft, has healthy tissue healing
capability, and goes through a controlled rehabilitation pro­
gram should not need a functional brace. The most impor­
tant part of the patient's return to activity/work is the physical
rehabilitation and/or surgery.
HINGE DESIGN
Hinge options for knee orthoses range from simple single-
axis (unicentric) designs to complex four-bar polycentric
designs. Most commercially available off-the-shelf FKOs have
hinges in one of three categories: (1) the single-axis hinge, (2)
the posterior offset hinge, or (3) the polycentric or genucen­
tric hinge.
All single-axis/unicentric hinges act as a simple hinge;
a unicentric hinge becomes incongruent with the ana­
tomic joint axis as the instantaneous axis of rotation of the
knee changes with movement through the range of motion.
Posterior offset designs attempt to improve the match
between orthotic and anatomical axis of motion by approxi­
mating the location of the sagittal radius of curvature of the
posterior femoral condyles as it articulates with the tibia in
flexion.66 Polycentric designs attempt to replicate the instan­
taneous axis of rotation of the anatomical knee joint, using
two geared surfaces that mechanically constrain motion into
a defined path.67 Theoretically, polycentric or genucentric
hinges are better able than unicentric hinge designs to match
the rolling and gliding of the tibiofemoral joint as the knee
flexes and extends. This closer match to physiological motion
is meant to reduce pistoning, discomfort, and slippage of the
orthosis on the limb during activity.
When considering which hinge design to select, consider
that the soft tissue of the knee between the orthosis and the
bone compromises the impact of any hinge on the kinematics
of the knee. The most important characteristic of the hinge is
its ability to transfer load during activity. Poorly designed or
constructed hinges, or those made of weak or pliable mate­
rials, cannot effectively accomplish this task, and abnormal
translations and rotations will not be well controlled. The
work of Lew and colleagues67 demonstrated greater variation
in the pistoning constraint forces in a particular joint design
than across designs when three orthoses were compared dur­
ing specific activities.
Regalbuto and colleagues68 evaluated the performance of
four hinge designs fit into a custom-fit knee orthosis in three
healthy subjects. Subjects wore the orthosis while performing
a squat, an 8-inch step-up, a stand-to-sit activity, and an open
chain knee extension exercise. The researchers found that
accurate hinge placement was a more important influence on
function and comfort than hinge kinematics. Differences in
kinematics among the four designs were masked by the com­
pliance of the soft tissues between the brace cuffs and the
bones of the knee.
FUNCTIONAL ORTHOSES FOR ANTERIOR
CRUCIATE LIGAMENT INSUFFICIENCY
Physical therapists are often involved in conservative and
in postsurgical rehabilitation for patients with ACL insuffi­
ciency. For more than 30 years, FKOs have been used to pre­
vent forward subluxation of the tibia on the femur for patients
with ACL insufficiency. A variety of designs have evolved to
be used for partial ACL tears or for complete ACL rupture
(Figure 11-14).
Biomechanical Performance of Functional Knee
Orthoses for Anterior Cruciate Ligament Insufficiency
For patients with an ACL tear and/or deficiencies, one of
the primary goals of bracing is to control the excessive ante­
rior drawer movement of the tibia. A number of research
studies have attempted to evaluate whether these orthoses

322
Section II  Orthoses in Rehabilitation
are ­effective in controlling tibial movement. One strategy
is to use cadaver models to evaluate the efficacy of func­
tional knee orthoses for support of the ACL.69,70 The major
drawback of this type of study, however, is the difference
between living and preserved tissue. Because active muscle
contraction and normal soft tissue compliance contribute
to strain on the ACL, the lack of active musculature and
compliance changes in soft tissue around the knee limit the
application of cadaver study findings. Similarly, the magni­
tude and sequence of muscle contraction alter the stiffness
between the brace and the soft tissue of the leg. It is not
possible to reproduce this dynamic relationship in cadav­
eric studies.
Another strategy is to compare forward excursion of the
tibia on the femur using clinical tests of knee instability per­
formed on a subject with and without bracing.21,48,71 Wojtys
and colleagues72,73 conducted two studies in which anterior
tibial translation was measured while subjects were seated
on an ischial support, in both braced and unbraced condi­
tions. Patients were instructed to stay relaxed throughout a
test in which the tibia was forced anteriorly. Reflexive con­
traction of the hamstrings, quadriceps, and gastrocnemius
muscles to this initial perceived force occurred more quickly
in the braced than the unbraced condition. However, these
muscles reacted more slowly in the braced condition when
patients were told to actively resist this movement as soon
as they perceived it. Beynnon and colleagues74 found no
­significant improvement in subjects’ ability to detect passive
anterior ­tibial translation in braced conditions when subjects
were tested in a seated position. Also, the use of a functional
knee brace in patients with ACL deficiency has been shown
to improve hamstring reflex, but not as the muscle fatigues
with activity.75
In a randomized controlled clinical trial by Birmingham
and colleagues76 the authors compared functional knee
bracing to use of a neoprene sleeve in patients following
an ACL reconstruction. At the patient's 6-week postopera­
tive visit, the patient received either a functional knee brace
or a ­neoprene sleeve. The authors found no significant dif­
ference in quality of life (ACL-QOL) and activity, KT-1000
arthrometer findings, or hop limb symmetry. The authors
concluded that use of a functional knee brace following ACL
reconstruction yields no better outcomes that using a neo­
prene sleeve.76 However, functional knee bracing after ACL
reconstruction has been found to have positive impacts in
proprioception.77
It is difficult to draw a clinical conclusion regarding the
effects of bracing on anterior tibial translation in patients
with ACL-deficient knees given the conflicting results of
these studies. Although the studies seem to indicate that
subjects’ ability to perceive passive anterior tibial motion
did not improve, one must also consider that subjects were
A
B
FIGURE 11-14  Examples of commercially available, custom-fit functional knee orthoses. A, The
Townsend Design Premier Series is marketed as both a custom functional knee brace and pro­
phylactic brace. B, CTi. (A, Reprinted with permission from Townsend Design, Bakersfield, CA.
B, Reprinted with permission from Ossür Americas, Foothills Ranch, CA.)

Chapter 11  Orthoses for Knee Dysfunction
323
tested in nonfunctional, non–weight-bearing conditions
versus dynamic situations. Additionally, the relationship
between static testing and actual physiological loading dur­
ing sport activity has not been well established. Noyes and
colleagues69 have demonstrated that manual examination
cannot duplicate the magnitude of force that is present dur­
ing activity.
Although static and cadaver studies have been the
first step in critically evaluating the efficacy of FKOs for
patients with ACL insufficiency, the most informative
research would be done in vivo. This is especially impor­
tant because static and cadaver studies cannot replicate the
real-life ­physiological loading that occurs in the knee during
activities.69,70,78–81
Soma and colleagues82 found that custom made braces did
a better job at preventing anterior tibial translation than off-
the-shelf functional knee braces.
The next challenge for clinical researchers is to develop meth­
odology to evaluate FKOs worn during functional activities.
Evidence of Efficacy of Functional Knee Orthoses for
Anterior Cruciate Ligament Insufficiency
In 1997, Kramer and colleagues26 published a review of
research conducted between 1982 and 1992, which sum­
marized the evidence regarding use of FKOs on dynamic
performance. Collectively, these studies did not provide
overwhelming evidence to support or refute the use of FKOs
by individuals with ACL-deficient knees. This review cited
16 maximal effort experimental situations in which sub­
jects’ performance in braced and unbraced conditions for
one-leg hop test, figure-of-eight runs, stair climbing, sprint­
ing, and agility was recorded. Results across the studies were
mixed: FKOs either improved, hindered, or had no effect on
performance.
Kramer and colleagues’ review26 also summarized the
results of several matched effort tests that measured bio­
mechanical variables. The variables assessed in these stud­
ies included ground reaction forces, range of motion, EMG,
joint moment, and power. These studies were difficult to
interpret whether FKO use provided wearers with advan­
tages or disadvantages because it was not assessed how
changes in the measured variables impacted overall perfor­
mance. Three of the matched effort studies demonstrated
that bracing subjects during testing resulted in detrimen­
tal effects on energy costs. Overall, this literature review
noted that five of the included studies indicated that many
of the subjects reported feeling more stable when wearing
the FKO. Given the mixed results of these studies, it is dif­
ficult to make a conclusive statement about whether or not
patients with ACL deficiency should expect enhanced per­
formance when wearing FKOs.
The ability of subjects to control anterior tibial transla­
tion during functional testing was examined by Ramsey and
colleagues.83 This study demonstrated that there was negli­
gible reduction in the anterior drawer movement of the tibia
between braced and unbraced conditions when patients per­
formed horizontal, one-legged jumps.
Another strategy is to evaluate muscle function when
subjects with ACL deficiency use a functional knee ortho­
sis. Branch and colleagues84 found little difference in
electromyographic firing patterns between in-brace and
out-of-brace testing. Because muscle activity was simi­
larly reduced under both conditions (as referenced to an
ACL intact limb), the researchers suggest that FKOs do not
have a significant proprioceptive influence on muscle func­
tion. A study by Wu and colleagues85 looked at 31 subjects
who had undergone a unilateral ACL reconstruction with
three bracing conditions: (1) a manufactured brace, (2) a
mechanical placebo brace, and (3) no brace. Using an iso­
kinetic machine to measure specific knee joint angles and
peak torques, they found that knee bracing can improve
static proprioception but not muscle function. The manu­
factured and mechanical placebo brace groups performed
better than the no brace group. The apparent improve­
ment in proprioception with knee bracing was not due
to the mechanical restraining action of the brace.85 Other
studies show similar results when measuring propriocep­
tive improvement on ACL reconstructed knees when doing
functionally relevant tasks.86,87
Nemeth and colleagues27 studied the effects of bracing and
not bracing on six downhill skiers who had ACL-deficient
knees during a series of downhill ski runs. Surface electrodes
were placed over the muscle bellies of vastus medialis, gas­
trocnemius medialis, biceps femoris, and semimembranosus
and semitendinosus muscles to record these muscles’ activ­
ity during skiing and determine whether there were differ­
ences in the patterns of muscle firing between the braced
and unbraced conditions. Statistical analysis did not reveal
significant differences between subjects’ muscle response in
either of these conditions. However, they found that subjects
with greater knee instability, compared with subjects with
less knee instability, had increased levels of lateral hamstring
muscle activity during knee flexion when they were braced.
In theory, this muscle activation may help control excessive
anterolateral shifting of the tibial plateau, thereby helping the
patient feel greater lower extremity stability. Despite the lack
of definitive results in this study, all subjects who wore the
FKO reported feeling more safe and stable during their ski­
ing activity.
Another study by Ramsey and colleagues88 examined
the muscle firing patterns of rectus femoris, semitendino­
sus, biceps femoris, and the lateral head of the gastrocne­
mius of four subjects with ACL-deficient knees who were
braced and not braced during one-legged jumps. They also
measured anterior tibial displacement during the testing
activity. Interestingly, their findings indicated that the sub­
jects who were braced demonstrated decreased levels of
hamstring activity and increased levels of quadriceps activity.
The braced condition resulted in small reductions of anterior
displacement in two subjects, no change in one subject, and
small increases in this translation for one subject.
Cook and colleagues89 compared the ability of sub­
jects with absent ACLs (n = 14) to perform running and
cutting maneuvers with and without a commercially

324
Section II  Orthoses in Rehabilitation
­available ­orthosis. Subjects’ performance with the orthosis
was objectively and subjectively better. In a similar study
that compared the performance of subjects with ACL
deficiency in several orthoses, Marans and colleagues90
reported improved performance in two of the six orthoses
evaluated.
A number of studies have examined the metabolic cost
using dynamic analysis of orthotic use to test the valid­
ity and reliability of functional knee braces on ACL-
insufficient knees.31,91 Whether the slight increase in
energy requirements noted is offset by protection and
improved function while wearing the orthosis is not yet
understood.
The authors in these studies that examined the effects of
bracing subjects with ACL-deficient knees during dynamic
test conditions suggest that there may be afferent inputs from
knee proprioceptors and the brace-skin-bone interface to the
central nervous system. This neural input may evoke adap­
tive motor responses when patients wear the knee brace dur­
ing functional activities. The number of subjects used in each
of these studies is fewer than 10, making it difficult to draw
conclusions if one is to consider each study independently.
Collectively, however, the results of each of the studies are
similar, which may help the physical therapist formulate an
opinion about the merits of using a brace on patients with an
ACL-deficient knee.
CASE EXAMPLE 2
Individual with History of ACL Tear
B. J. is a 23-year-old female alpine ski racer who is 6 months
postop ACL reconstruction with a patellar tendon-bearing
graft to her left knee. B. J. has worked diligently in her post­
operative rehabilitation. She denies pain, but still reports
limited agility and quickness.
B. J. is anxious to return to the ski slopes and resume ski
racing. You have been in communication with her orthopedic
surgeon who recommends that B. J. can only return to skiing
if she wears a knee brace. B. J. asks you what benefits the brace
will provide as she relates that she has heard conflicting infor­
mation about whether or not knee braces were beneficial. B. J.
wonders if a specialized knee brace will help her maintain the
stability of her knee during her alpine ski races. Also, she is
concerned that the extra weight of a knee brace will slow her
down on the slopes. She wants advice from the physical thera­
pist about the merits of obtaining such a brace.
The therapist wanted to find evidence to support whether
or not B. J. should invest in an FKO brace to enhance her
knee stability. The clinical question that will direct review
of the evidence is, “Will a brace designed for patients with
ACL-deficient knees enhance the control and stability of the
knee during recreational activities?”
Questions to Consider
• Given this patient's history and current presentation,
what additional tests and measures would provide help­
ful information to use in your evaluation process?
• What is your movement dysfunction-related diagnosis
for this patient?
• What is B. J.'s prognosis?
• What are your rehabilitation goals?
• How long to do you think it will take to achieve the goals
that you and B. J. agree upon?
• What is the role of exercise and/or FKO in the manage­
ment of a patient like B. J. following ACL reconstruction?
• What evidence is available in the clinical research litera­
ture about the efficacy of FKO to protect the integrity of
the ACL following reconstruction?
• Based on B. J.'s goals and expectations, your understand­
ing of the underlying disease process, and evidence from
the clinical research literature, what recommendations
would you make for intervention at this point in time?
• Is the evidence convincing enough, given the level of
impairment that B. J. demonstrates and her prognosis,
that you would recommend she purchase an FKO to
wear during recreational activities?
• Would you recommend an off-the-shelf or custom-made
FKO?
• Of the various FKO designs available, which might be
most appropriate for B. J. following ACL reconstruction
and accelerated rehabilitation?
• How will you assess whether B. J.'s rehabilitation goals
have been met?
• What type of follow-up would you recommend for this
patient?
Recommendations for the Patient Following Anterior
Cruciate Ligament Reconstruction
After reviewing the evidence, the physical therapist dis­
cusses what she has discovered with B. J., that the research
to support or refute the use of an FKO is equivocal. There is
evidence to suggest that some patients feel more stable when
they wear a brace, but it is unknown whether patients’ feel­
ings of enhanced stability are due to biomechanical or neu­
romuscular changes that are the result of FKO wear. Specific
to skiers, there is evidence that the use of an FKO may help
reduce the risk for reinjury.29 The therapist recommends
that B. J. rehabilitate her knee through participation in a
dynamic, sport-specific exercise program before she con­
siders returning to Alpine ski racing.

Chapter 11  Orthoses for Knee Dysfunction
325
The Role of Exercise in ACL Rehabilitation
There is literature to support the premise that hamstrings and
gastrocnemius muscles assist in stabilizing ACL-deficient
knees as well as evidence to support that patients with ACL-
deficient knees benefit from closed kinetic chain exercise pro­
grams and perturbation training.92–96 If the patient perceives
the need for an FKO after participating in a rehabilitation
program, the therapist can direct the patient to braces that are
available while cautioning that the patient must continue with
a home strengthening program.
ORTHOSES FOR OSTEOARTHRITIS
Narrowing of the medial or lateral compartment of the knee
is a common source of discomfort and pain for many adults.
OA is a condition in which the collagen fibers of the articular
cartilage are compromised. The breakdown of the articular
cartilage in the medial or lateral compartment will result in
the uneven distribution of the load forces.97 There are cur­
rently five general methods of management for OA:
1. Pharmaceuticals
2. Surgery: unicompartmental or total knee arthroplasty (TKA)
3. Foot orthoses
4. Injections
5. Use of valgus or varus knee orthoses
Valgus/varus knee bracing evolved in the early 1990s with
the theory that by unloading the medial or lateral compart­
ment, pain could be altered enough to ward off surgery and
prolong the function of an osteoarthritic knee.
Most individuals with OA of the knee demonstrate func­
tional losses and report pain when the knee is loaded during
the stance phase of gait, beginning at heel strike and end­
ing with toe-off. Biomechanical analysis on healthy subjects
reveals that loading in the knee is 62% on the medial side and
38% on the lateral side during stance; in those with a varus
deformity associated with medial joint OA, the medial com­
partment loading can increase to 100% of the total compres­
sive load on the knee joint during this phase of gait.98 Based on
this premise, the conservative and surgical strategy in treat­
ing these individuals is to reduce the load on the medial side
of the joint to reduce the painful symptoms that the patient
experiences.99
Valgus (unloading) orthoses (Figure 11-15) are designed
to unload the medial knee compartment noted to have degen­
erative changes and provide a similar type of advantage as
realignment osteotomy.98 These orthoses unload the medial
compartment of the knee through use of adjustable tension
straps crossing the lateral aspect of the knee joint, lateral con­
dylar pads, or lateral hinge systems, which are fixed to a brace
shell at the calf and thigh.98–100
A
B
FIGURE  11-15  Examples of unloader knee orthoses designed to unload medial compartment
of the knee for individuals with painful osteoarthritis (OA). A, The CTi OA brace from Ossür 2.
B, The Single Upright Premier Series OA Knee Brace from Townsend Design. (A and B, Reprinted
with ­permission from Ossür Americas, Foothills Ranch, CA.)

326
Section II  Orthoses in Rehabilitation
Evidence of Efficacy of Valgus/Unloading Orthoses
Research over the past 10 years has attempted to validate
manufacturer's claims that valgus/varus bracing will achieve
significant reductions in the amount of pain and swelling
in the involved joint region. Pollo101 looked at nine subjects
(mean age 46 ± 11 years) with a varus mechanical alignment
of 0 to 10 degrees. Each subject was tested during walking
with and without a commercially available brace. Kinematic
and kinetic data were recorded using a video-based six-
camera Motion Analysis System in conjunction with two
Bertec force platforms. Comparisons were made at the ini­
tial test and at the 3-month follow-up. There was a statis­
tically significant improvement in pain and function along
with a reduction in the external varus moment about the
knee when wearing the commercially available brace. Other
authors have found similar results with unicompartmental
OA and the improved function that the valgus brace affords
to the patients.102
A study by Katsuragawa and colleagues102 demonstrated
an increase in bone mineral density more in the lateral tibial
condyle than the medial condyle due to the transfer of forces
across the knee joint from the medial to the lateral side after
use of a valgus orthosis. Research by Horlick and colleagues103
demonstrated a significant reduction of pain when wearing
a valgus brace, but did not find a change in functional status
or in the femoral-tibial angle and joint space as viewed via
radiographs.
Self and colleagues98 examined the effects of valgus knee
bracing on the varus moment at the knee during level gait on
five patients who had confirmed medial compartment knee
arthrosis. The varus moment causes greater loading on the
medial compartment and may be responsible for the pain that
patients with medial knee arthrosis experience. The research­
ers collected kinematic data on subjects’ patterns of walking
with and without their orthoses. The use of a valgus brace
reduced the net varus moment on the medial compartment
of the knee during the time when this moment was typically
at its maximum load.98 Lindenfeld and colleagues99 examined
the pain intensity and function scores for subjects with con­
firmed medial compartment knee arthrosis and persistent
pain during ambulation. They hoped to determine whether
valgus knee bracing altered the loads at the knee joint. Most
patients who wore the prescribed brace had excellent clinical
responses in terms of increased function and decreased pain,
and demonstrated medial compartment unloading ­during
radiographic testing.99
In patients with medial compartment knee OA,
Birmingham and colleagues104 found proprioception was
improved in patients during use of a custom-fit brace.
However, patients did not show a significant increase in pos­
tural control.
Finally, Hewett and colleagues100 examined the effects of
valgus bracing on a group of 19 adults with chronic medial
knee joint pain, which limited their ability to participate in
sports or perform activities of daily living (ADLs). Study
participants were assessed after 9 weeks and again after
about 1 year of orthotic wear to determine whether there
were changes in their symptoms and function. Fifteen of
18 ­subjects reevaluated after 9 weeks reported reduction in
their pain symptoms and/or an increase in walking tolerance.
Thirteen patients continued to wear the brace for an average
of a year. Ten of these patients felt an improvement in pain or
function after using the brace. The most dramatic improve­
ments were related to the amount of time participants were
able to walk before onset of pain. Wearing the orthosis did not
have much impact on returning participants to sports activi­
ties. Despite the improvements in symptoms and function
for many patients, gait analysis did not reveal any changes in
loading at the varus moment or any gait adaptations during
brace wear.100
Furthermore, Nadaud and colleagues105 performed an
in  vivo study examining the effectiveness of five commer­
cial types of functional knee braces across five subjects. They
found variability among the average amount of medial condy­
lar separation among braces but found consistent off-loading
of the knee upon heel-strike during gait and decreased ability
to off-load at midstance.105
These studies, reviewed independently, include relatively
small numbers of subjects. However, the conclusions in all of
the studies regarding patients who wore valgus braces to con­
trol the detrimental effects of medial tibiofemoral arthrosis
were similar. If pain associated with medial joint compart­
ment arthritis is related to varus loading of the knee joint,
it appears that valgus bracing can be effective in controlling
some of the painful symptoms that are associated with this
pathology.
The impact of valgus bracing on function and gait kine­
matics is not as clear. Despite the conflicting evidence
regarding the influence that these braces have on gait kine­
matics and joint loading, there does seem to be evidence to
support the notion that patients may benefit from valgus
brace wear to diminish pain and increase function if these
individuals do not want to consider surgery as an immedi­
ate option.
There is clear evidence that weakness of the quadri­
ceps muscle is related to osteoarthritic conditions at the
knee joint.106,107 Ramsey and colleagues108 found that, in
subjects with medial compartment OA that decreased
muscle, ­co-contraction of the vastus lateralis and ­lateral
hamstrings resulted in decreased pain while using an
unloader brace.108 In a review of research related to guide­
lines for management of OA in the knee, Hochberg and
­colleagues109 cite the need for patients to participate in
quadriceps strengthening and range of motion exercises as
well as aerobic conditioning exercises. In their review of
the literature, Raja and Dewan110 cited the lack of homoge­
neity of studies analyzing the use of knee bracing for OA,
which did not allow for a conclusive statement supporting
the use of knee braces. However, the authors do mention
that use of knee braces and foot orthoses may prove to be
less costly than other interventions.110
Divine and Hewett111 suggest that clinicians should pre­
scribe a knee brace on a trial basis in order to provide lower
extremity biomechanical changes to decrease pain.

Chapter 11  Orthoses for Knee Dysfunction
327
ORTHOSES FOR PATELLOFEMORAL
DYSFUNCTION
Just as evidence to support prophylactic and functional ortho­
ses for tibiofemoral joint instability is inadequate, research
support for the efficacy of patellofemoral taping and brac­
ing is lacking. Nevertheless, orthotic management of patel­
lofemoral dysfunction has become widespread in athletic
and in nonathletic practice environments. The need for well-
designed clinical research studies is pressing.
Physical therapy interventions for patients with patello­
femoral stress syndrome (PFSS) are most often directed at
optimizing patellofemoral mechanics, while reducing symp­
toms. Interventions may include pain relief modalities such as
iontophoresis and phonophoresis, patellofemoral taping, soft
tissue stretching and mobilization to enhance medial patella
gliding, and extensibility of the soft tissue along the lateral
aspect of the patella. An exercise program, guided by the
patient's tolerance, typically focuses on restoring appropriate
tissue length and suppleness, as well as strengthening exer­
cises (especially eccentric) for the quadriceps muscle group.
Patellofemoral orthoses (Figure 11-16) are often used as
adjuncts to exercise to do the following112:
1. Provide pain relief and improve function for patients with
patellofemoral pain syndrome
2. Prevent or control patellar subluxation or dislocation in
patients with patellar tracking problems
3. Provide pain relief and support tissue healing for patients
with irritation of the quadriceps or patellar tendon (e.g.,
patellar tendinopathy or Osgood-Schlatter disease)
4. Manage patients with chondromalacia and other symptom­
atic degenerative articular changes of the patellofemoral joint
There are a variety of knee orthoses directed at control­
ling the pain associated with PFSS. Typically these braces con­
sist of an elasticized or neoprene sleeve worn over the knee
CASE EXAMPLE 3
Patient with Osteoarthritis of the Knee
R. P. is a 55-year-old man who has completed 8 weeks of
physical therapy (PT) with the goal of managing his right
knee pain. An orthopedic surgeon referred R. P. for PT with a
diagnosis of degenerative joint disease. Radiographs of R. P.'s
right knee showed medial compartment tibiofemoral OA. R.
P. has a 1-year history of increasing knee pain, concentrated
around the medial joint line. The symptoms had worsened to
the point where he felt compromised in his ADLs. R. P.'s past
medical history is significant for a right partial medial menis­
cectomy 4 years before the onset of his knee pain.
Functionally, R. P. reported that he could not stand for
more than 10 minutes or walk more than 30 minutes. His
goals were to walk 60 minutes on a level surface for exer­
cise and stand for 45 minutes. R. P. came to the PT clinic
three times per week; his program emphasized quadriceps
strengthening and exercises to maintain his knee range of
motion. At the conclusion of 4 weeks of therapy, R. P. felt that
there had been little change in his function. The referring
physician recommended surgery because R. P.'s symptoms
had not changed. R. P., however, did not want to consider
surgery, based on the length and intensity of postoperative
rehabilitation. He asked if there were any other interven­
tions that might be considered to manage his knee pain.
Questions to Consider
• Given R. P.'s history and current presentation, what addi­
tional tests and measures would provide helpful informa­
tion to use in your evaluation process?
• What is your movement dysfunction-related diagnosis
for this patient?
• What is R. P.'s prognosis?
• What are physical therapy goals for R. P.?
• How long to do you think it will take to achieve the goals
that you and R. P. agree upon?
• Based on R. P.'s goals and expectations, as well as your
understanding of the underlying disease process, what
recommendations would you make for intervention
at this point in time? What evidence from the clinical
research literature supports your recommendations?
Why have you chosen and/or prioritized these possible
interventions?
• How will you assess whether the patients and rehabilita­
tion goals have been met?
• What type of follow-up would you recommend for this
patient?
Recommendations for a Patient with Osteoarthritis
of  the Knee
After reviewing the evidence, and in light of the R. P.'s
goals for intervention, the physical therapist recommends
that wearing a valgus brace may diminish RP's knee pain
and improve his functional activities, such as standing
and walking. R. P. and the physical therapist consult with
an orthotist to select the most appropriate orthosis. The
physical therapist and orthotist caution R. P., but there is
little evidence to suggest how long the potentially posi­
tive effects of this brace wear will last. The physical thera­
pist encourages R. P. to continue exercising on a regular
basis because there is clear evidence that weakness of the
quadriceps muscle is related to osteoarthritic conditions
at the knee joint. The physical therapist and R. P. agree on
a home exercise program that includes range of motion,
aerobic, and quadriceps resistive exercise, and they dis­
cuss appropriate intensity. The physical therapist helps
R. P. understand that brace wear and exercise should not
induce increased pain or swelling or loss of function, and
instructs him to return to his physician, , or orthotist for
follow-up.

328
Section II  Orthoses in Rehabilitation
(see Figures 11-2 and 11-16). Most have a circular opening to
accommodate the patella and a semicircular crescent-shaped
buttress that is sewn in place or held by Velcro closures and
reinforcing straps. The purpose of the buttress and straps is to
stabilize the position of the patella as it slides in the intracondy­
lar groove during knee motion.14 The goal of the PFSS orthosis
is to control the undesirable, excessive lateral movement of the
patella that is thought to be the underlying cause of PFSS. Some
of these braces have a hinge system that, theoretically, resists
knee extension, thereby reducing the potential for the unfa­
vorable coupling effect of knee extension and excessive lateral
patella excursion.42 Other braces allow the buttress to be posi­
tioned in a number of positions around the patella, depending
on the type of patella malalignment the patient demonstrates.4
Another design uses a curved vinyl-covered strap worn snugly
at the patellar tendon to support and elevate the patella ­during
activity for more efficient tracking.113 Normalization of track­
ing can, theoretically, minimize abnormal compressive forces
on the articular surfaces, reduce the likelihood of further
degenerative changes, and provide relief of symptoms.114
Biomechanics of Patellofemoral Orthoses
The mechanism for pain in those who suffer PFSS is unclear.
Various theories propose that pain can be caused from patellar
maltracking, tightness of the surrounding soft tissues, and/or
less than optimal firing of various aspects of the quadriceps.115
Based on these assumptions, several studies have examined
the effect of patellofemoral orthoses on the biomechanic
function of the patellofemoral joint. Powers and colleagues115
studied 10 female subjects with 12 symptomatic patellae, all of
whom had a kinematic procedure done with magnetic reso­
nance imaging (MRI), which documented lateral subluxation
in their knees. The subjects performed resisted knee exten­
sion during an MRI, which recorded patella movement in
braced and unbraced conditions. The patellofemoral orthosis
used in this study had no significant effect on patella tracking
(i.e., patellar tilt or medial/lateral displacement) from 45 to 0
degrees of knee flexion. The research did show a subtle patel­
lar position change in the sulcus angle of the patella such that
the patella moved to a more shallow portion of the trochlear
groove when the knees were braced.114
Timm116 used a Protonics orthosis, a brace that can be
set to offer resistance to the knee flexor and extensor muscle
groups while subjects perform functional activities, such as
walking. There was a reduction in patellofemoral pain and
improvement in patellofemoral congruence for patients who
wore the brace as much as possible for 4 weeks.116 A system­
atic review by D'hondt and colleagues117 concluded in 2003
that the strength of the scientific evidence to support the use
of patellofemoral orthoses is limited. The authors stated that
one must take clinicians’ clinical expertise and patient prefer­
ences into account when prescribing a knee orthosis.
A
B
FIGURE  11-16  Examples of orthoses used for patellofemoral stress syndrome and/or patellar
tracking problems. A, The Q Baby Patella Tendon infrapatellar strap from BioSkin. B, The Mueller
#6479 Max Knee Strap. (A, Reprinted with permission, Cropper Medical, Inc/Bioskin, Ashland, OR.
B, Reprinted with permission, Mueller Sports Medicine, Prairie du Sac, WI.)

Chapter 11  Orthoses for Knee Dysfunction
329
Sleeve type braces and wrap braces have been shown to
make positive changes in patellofemoral contact area.118,119
Evidence of Efficacy of Patellofemoral Orthoses
There have been a number of studies that have examined the
effectiveness of these braces. It has been difficult to make
comparisons of the research because different braces have
been used and the measured outcomes also vary within these
studies.
In a longitudinal study of 25 patients with unilateral retro­
patellar pain syndrome, Reikeras120 found patellofemoral brac­
ing to be minimally effective for symptom relief and for return
to functional activities. In contrast, comprehensive conser­
vative management of chondromalacia and of patellofemo­
ral pain staged for acute symptom management, exercises to
build flexibility and strength, maintenance exercise for eccen­
tric control and muscular endurance, and return to activity
using patellofemoral bracing were effective for 77% to 82%
of patients.121,122 A preliminary report by Crocker and Stauber
demonstrated that use of a patellar stabilizing brace enabled
four of five subjects to generate normal strength curves and
increased power during isokinetic testing.123 Subjects in this
study also experienced improved performance in functional
and sport activities when wearing the patellofemoral brace.
In a larger study, 59 of 62 patients with diagnoses of patel­
lar subluxation, patellofemoral arthritis, or Osgood-Schlatter
disease were able to perform activities that typically pro­
voked symptoms (pivoting, running, stair climbing, and long-­
distance walking) when wearing a patellofemoral brace.14
Powers and colleagues found that the use of a patello­
femoral knee orthoses improved patellofemoral joint contact
area and decreased pain in women with PFSS.119 In a cadav­
eric study, Bohnsack and colleagues124 found that the use of
a patellar brace decreased patellofemoral contact area and
decreased pressure of infrapatellar tissue. Additionally, Selfe
and colleagues125 found that the use of a patellofemoral brace
could reduce coronal plane alterations and torsional angles.
Although some of these results are encouraging, the use of
a patellofemoral brace as the primary intervention for patients
with patellofemoral pain is not well supported. Conservative
management strategies with established efficacy include
activity modification, limited use of nonsteroidal antiinflam­
matory medications, and strengthening and flexibility exer­
cises. Further clinical research to evaluate carefully the added
benefit of patellofemoral bracing in the conservative manage­
ment of patellofemoral dysfunction is necessary.
The literature regarding the appropriate rehabilitation
protocol for management of PFSS is not consistent. A system­
atic review by Crossley and colleagues,126 which examined the
efficacy of a number of nonpharmacological and nonsurgi­
cal physical interventions for PFSS, illustrates this notion.
The recommendation made by the authors based on the evi­
dence from studies included in this review, is that stretching
exercises, patient education, and quadriceps strengthening,
including eccentric exercises, should be included in a physi­
cal therapy program. However, the evidence to support these
protocols is inconclusive.126
A study by Finestone and colleagues127 demonstrated that
a group of Army recruits having patellofemoral pain had
diminished symptoms with use of a simple elastic sleeve or
an elastic sleeve with a silicone patella ring compared with
symptoms in a control group that did not have any brace.
However, 80% of the recruits who did not receive a brace
were found to be asymptomatic at a 2-month follow-up
visit.127 In a study by Greenwald and colleagues,128 subjects
who wore a brace with a neoprene undersleeve and plastic
exoskeleton with an extension stop reported that use of this
brace significantly reduced the frequency and severity of
their pain. BenGal and colleagues129 demonstrated that there
may be some evidence to support the use of a knee brace to
prevent anterior knee pain.
Strengthening of the joints proximal and distal to the
patellofemoral joint have been shown to result in decreased
pain, function, and biomechanics with PFPS.130
CASE EXAMPLE 4
Patient with Patellofemoral Stress Syndrome
B. G. is a 25-year-old woman referred for PT with a diag­
nosis of left PFSS. She reports that 4 months ago, she began
training for a marathon, and that she has experienced a
diffuse ache around her anterior left patella for the last 2
months. She had increased her mileage gradually to the
point that she was jogging 3 to 7 miles, four times per
week. After 1 month of participation in the program, B. G.
was experiencing left knee pain after completing her jog.
This pain resolved within about 1 hour after stopping the
activity. B.G.continued to jog, but noticed that her pain
got progressively worse over the next 2 months. Currently,
B. G. reports that she experiences pain in her left knee if
she sits with her knee flexed for more than 45 minutes,
when ascending and descending stairs, and when she runs
more than 1 mile.
Examination reveals that B. G. has pain on palpation of
the posterolateral aspect of the left patella. She also has a
positive Ely's test, a measurement of rectus femoris tight­
ness.131 On visual inspection, the patella orientation was
consistent in demonstrating some malalignments. At 20
degrees of knee flexion, B. G.'s patella was sitting 10 mm
closer to the lateral femoral epicondyle than the medial fem­
oral epicondyle. When B. G. is positioned in supine with
her knee extended, the medial border of the patella is higher
than the lateral border. These patterns of patella alignment
may contribute to the symptoms of PFSS.132
Continued

330
Section II  Orthoses in Rehabilitation
SUMMARY
This chapter reviews the normal structure and function
of the tibiofemoral and patellofemoral joints, with special
focus on arthrokinematics and osteokinematics of the knee
joint. The different categories of knee orthoses for the knee
complex are rehabilitation orthoses, functional orthoses,
prophylactic orthoses, unloader orthoses, and patello­
femoral orthoses. A review of the research literature offers
some support to the use of knee orthoses. However, there
appears to be a gap between what many of the braces are
designed to do and evidence of their efficacy. This chapter
identifies research strategies that are most frequently used
in the study of knee orthoses and discusses problems with
research design, methods, and generalizability to patients
and athletes involved in dynamic activities. Similar prob­
lems exist when the role of patellofemoral orthoses in
sports medicine and rehabilitation are considered. It is
important for clinicians to realize that although there is a
lack of clear consensus supporting the use of knee ortho­
ses, that knee orthoses should be a consideration as an
intervention for a patient who presents with knee pain.
Despite the lack of consensus amongst evidence-based
data, the subjective reports of patients can always give the
most important information about whether a knee ortho­
sis may be beneficial.
This chapter is intended to give health care profession­
als the ability to better evaluate the intent and design of knee
orthoses and to ask for clinically applicable evidence of effi­
cacy from brace designers and manufacturers. This chapter
is also intended to encourage clinicians to contribute to the
understanding of knee orthoses in rehabilitation and long-
term management of patients with ligamentous instability by
participating in clinical research.
REFERENCES
1. Cawley PW. Is Knee Bracing Really Necessary? A Review of
Current Research on Brace Function, the Natural History of Graft
Remodeling, and Physiologic Implications. Carlsbad, CA: Smith &
Nephew Donjoy Biomechanics Research Laboratory; 1989.
2. Trautman P. Lower limb orthoses. In: Redford JB, Basmajian JV,
Trautman P, eds. Orthotics: Clinical Practice and Rehabilitation
Technology. New York: Churchill Livingstone; 1995:13–54.
3. Drez D, DeHaven K, D'Ambrosia R. Knee Braces Seminar Report.
Chicago: American Academy of Orthopaedic Surgeons; 1984.
4. Paluska SA, McKeag DB. Knee braces: current evidence and
clinical recommendations for their use. Am Fam Physician.
2000;61(2):411–418, 423–424.
5. Chew KT, Lew HL, Date E, et al. Current evidence and clini­
cal applications of therapeutic knee braces. Am J Phys Med
Rehabil. 2007;86(8):678–686.
6. Nordin M, Frankel VH. Biomechanics of the knee. In: Nordin M,
Frankel VH, eds. Basic Biomechanics of the Musculoskeletal
System. 3rd ed. Philadelphia: Lippincott Williams & Wilkins;
2001.
7. Levangie PK, Norkin CC. The knee complex. In: Joint Structure
and Function: A Comprehensive Analysis. 3rd ed. Philadelphia:
FA Davis; 2001.
8. Neumann DA. Knee. In: Neumann DA, ed. Kinesiology of the
Musculoskeletal System: Foundations for Rehabilitation. 2nd ed.
St. Louis: Mosby Elsevier; 2010.
9. Antich TJ. Orthoses for the knee: the tibiofemoral joint. In:
Nawoczenski DA, Epler ME, eds. Orthotics in Functional
Rehabilitation of the Lower Limb. Philadelphia: Saunders;
1997:57–76.
10. Terry GC, Hughston JC, Norwood LA. Anatomy of the iliopatel­
lar band and iliotibial tract. Am J Sports Med. 1986;14(1):39–45.
11. Greenfield BH. Functional anatomy of the knee. In: Greenfield
BH, ed. Rehabilitation of the Knee: A Problem Solving Approach.
Philadelphia: Davis; 1993:1–42.
Questions to Consider
• Given this patient's history and current presentation,
what additional tests and measures would be helpful
information in your evaluation process?
• What is your movement dysfunction-related diagnosis
for this patient?
• What might the prognosis be for this patient? What are
the patient's goals for intervention? What are your reha­
bilitation goals? How long to do you think it will take to
achieve the goals that you and the patient agree upon?
• Based on the patient's goals and expectations, as well as
your understanding of the underlying disease process,
what recommendations would you make for interven­
tion at this point in time?
• What evidence from the clinical research literature sup­
ports your recommendations? Why have you chosen
and/or prioritized these possible interventions?
• How will you assess whether the patients and rehabilita­
tion goals have been met?
• What type of follow-up would you recommend for this
patient?
Recommendations for a Patient with Patellofemoral
Stress Syndrome
B. G. states that her pain decreased after her course of
therapy. She had greater sitting tolerance, can ascend and
descend stairs with no pain, and has resumed running.
However, she runs 3 miles 4 days a week. She experienced
mild discomfort at the end of her run, but this resolved
after 30 minutes. B. G.'s goal was to increase her jogging
distance to that of her original exercise program; how­
ever, she was concerned that her symptoms would recur.
She asked the therapist whether wearing a knee ortho­
sis during exercise would be beneficial. The therapist
recommended a patellofemoral brace with a lateral but­
tress for long-­distance running. This orthosis would help
minimize B. G.'s excessive lateral patella tracking and,
hopefully, reduce her pain. The therapist also strongly
recommended that B. G. continue with her exercise pro­
gram for soft tissue work, strengthening her hip abduc­
tors, external rotators, and quadriceps muscle, even as her
running time and distance increases.

Chapter 11  Orthoses for Knee Dysfunction
331
12. Cox AJ. Biomechanics of the patello-femoral joint. Clin
Biomech (Bristol, Avon) 1990;5:123–130.
13. Grabiner MD, Koh TJ, Draganich LF. Neuromechanics of the
patellofemoral joint. Med Sci Sports Exerc. 1994;26(1):10–21.
14. Palumbo PM. Dynamic patellar brace: a new orthosis in the
management of patellofemoral disorders. Am J Sports Med.
1981;9(1):45–49.
15. Van Kampen A, Huiskes R. The three-dimensional tracking
pattern of the human patella. J Orthop Res. 1990;8(3):372–382.
16. Larson RL, Cabaud HE, Slocum DB, et al. The patellar com­
pression syndrome: surgical treatment by lateral retinacular
release. Clin Orthop. 1978;34:158–167.
17. Wiberg G. Roentgenographic and anatomic studies on the
femoropatellar joint: with special references to chondromala­
cia patellae. Acta Orthop Scand. 1941;12:319–409.
18. Ward SR. Biomechanical applications to joint structure and
functio n. In: PK Levangie, CC Norkin, eds. Joint Structure and
Function: A Comprehensive Analysis. 5th ed. Philadephia: FA
Davis; 2011.
19. Muller W. The Knee: Form, Function, and Ligament
Reconstruction. Berlin: Springer-Verlag; 1985.
20. Regalbuto MA, Rovic JS, Walker PS. The forces in a knee brace
as a function of hinge design and placement. Am J Sports Med.
1989;17:535–543.
21. Bassett GS, Fleming BW. The Lenox Hill brace in anterolateral
rotatory instability. Am J Sports Med. 1983;11(5):345–348.
22. Branch TP, Hunter RE. Functional analysis of anterior cruciate
ligament braces. Clin Sports Med. 1990;9(4):771–797.
23. Nicholas JA. Bracing the anterior cruciate ligament deficient
knee using the Lenox Hill derotation brace. Clin Orthop.
1983;172:137–142.
24. Beets CL, Clippinger FW, Hazard PR, et  al. Orthoses
and the dynamic knee: a basic overview. Orthot Prosthet.
1985;39(2):33–39.
25. DeCoster LC, Vailas JC. Functional anterior cruciate liga­
ment bracing: a survey of current brace prescription patterns.
Orthopedics. 2003;26(7):701–706.
26. Kramer JF, Dubowitz T, Fowler P, et  al. Functional knee
braces and dynamic performance: a review. Clin J Sports Med.
1997;7:32–39.
27. Nemeth G, Lamontagne M, Tho KS, et al. Electromyographic
activity in expert downhill skiers using functional knee braces
after anterior cruciate ligament injuries. Am J Sports Med.
1997;25(5):635–641.
28. Fleming BC, Renstrom PA, Beynnon BD, et al. The influence
of functional knee bracing on the anterior cruciate ligament
strain biomechanics in weightbearing and nonweightbearing
knees. Am J Sports Med. 2000;28(6):815–824.
29. Sterett WI, Briggs KK, Farley T, et al. Effect of functional bracing
in skiers with anterior cruciate ligament reconstruction: a pro­
spective cohort study. Am J Sports Med. 2006;34(10):1581–1585.
30. Stephens DL. The effects of functional knee braces on speed in
collegiate basketball players. JOSPT. 1995;22(6):259–262.
31. Highgenboten CL, Jackson A, Meske N. The effects of knee
brace wear on perceptual and metabolic variables during hori­
zontal treadmill running. Am J Sports Med. 1991;19(6):639–643.
32. Wojtys EM, Kothari SU, Huston LJ. Anterior cruciate lig­
ament functional brace use in sports. Am J Sports Med.
1996;24(4):539–546.
33. Grace TG, Skipper BJ, Newberry JC, et al. Prophylactic knee
braces and injury to the lower extremity. J Bone Joint Surg.
1988;70A(3):422–427.
34. Styf JR, Nakhostine M, Gershuni DH. Functional knee braces
increase intramuscular pressures in the anterior compartment
of the leg. Am J Sports Med. 1992;20(1):46–49.
35. Styf J. The effects of functional knee bracing on muscle func­
tion and performance. Sports Med. 1999;(2):77–81.
36. Sforzo GA, Chen NM, Gold CA, et al. The effect of prophy­
lactic knee bracing on performance. Med Sci Sports Exerc.
1989;1:254–257.
37. Styf JR, Lundin O, Gershuni DH. Effects of a functional
knee brace on leg muscle function. Am J Sports Med.
1994;22:830–834.
38. McDevitt ER, Taylor DC, Miller MD, et al. Functional brac­
ing after anterior cruciate ligament reconstruction: a pro­
spective, randomized, multicenter study. Am J Sports Med.
2004;32(8):1887–1892.
39. Black KP, Raasch WG. Knee braces in sports. In: Nicholas JA,
Hershman EB, eds. The Lower Extremity and Spine in Sports
Medicine. 2nd ed. St. Louis: Mosby; 1995:987–998.
40. Erickson AN, Yasuda K, Beynnon B. An in vitro dynamic eval­
uation of prophylactic knee braces during lateral impact load­
ing. Am J Sports Med. 1993;21:26–35.
41. Garrick JG, Requa RK. Prophylactic knee bracing. Am J Sports
Med. 1987;15(5):471–476.
42. France PE, Paulos LE. Knee bracing. J Am Acad Orthop Surg.
1994;2(5):281–287.
43. Edelstein JE, Bruckner J. Orthotics: A Comprehensive Clinical
Approach. Thorofare, NJ: Slack Inc; 2002:59–71.
44. Baker BE, VanHanswyk E, Bogosian SP, et al. The effect of knee
braces on lateral impact loading of the knee. Am J Sports Med.
1989;17(2):182–186.
45. Baker BE, VanHanswyk E, Bogosian SP. A biomechanical study
of the static stabilizing effect of knee braces on medial stability.
Am J Sports Med. 1987;15:566–570.
46. France EP, Paulos LE, Jayaraman G, et al. The biomechanics
of lateral knee bracing. Part II: Impact response of the braced
knee. Am J Sports Med. 1987;15(5):430–438.
47. Paulos LE, France EP, Rosenberg TD, et al. The biomechanics
of lateral knee bracing. Part I: Response of the valgus restraints
to loading. Am J Sports Med. 1987;15(5):419–429.
48. Paulos LE, Cawley PW, France EP. Impact biomechanics of lat­
eral knee bracing. The anterior cruciate ligament. Am J Sports
Med. 1991;19(4):337–342.
49. Hewson GF, Mendini RA, Wang JB. Prophylactic knee bracing
in college football. Am J Sports Med. 1986;14(4):262–266.
50. Rovere GD, Haupt HA, Yates CS. Prophylactic knee bracing in
college football. Am J Sports Med. 1987;15(2):111–116.
51. Sitler M, Ryan J, Hopkinson W, et al. The efficacy of a pro­
phylactic knee brace to reduce injuries in football. A pro­
spective, randomized study at West Point. Am J Sports Med.
1990;18(3):310–315.
52. Teitz CC, Hermanson BK, Kronmal RA, et al. Evaluation of the
use of braces to prevent injury to the knee in collegiate football
players. J Bone Joint Surg. 1987;69A(1):2–9.
53. Albright JP, Powell JW, Smith W, et al. Medial collateral lig­
ament knee sprains in college football. Am J Sports Med.
1994;22(1):12–18.
54. Borsa PA, Lephart SM, Fu FH. Muscular and functional perfor­
mance characteristics of individuals wearing prophylactic knee
braces. J Athletic Training. 1993;28(4):336–342.
55. Liggett CL, Tandy RD, Young JC. The effects of prophy­
lactic knee bracing on running gait. J Athletic Training.
1995;30(2):159–161.

332
Section II  Orthoses in Rehabilitation
56. Osternig LR, Robertson RN. Effects of prophylactic bracing on
lower extremity joint position and muscle activation during
running. Am J Sports Med. 1993;21(5):733–737.
57. Van Horn DA, Makinnion JL, Witt PL. Comparison of the
effects of the Anderson knee stabler and McDavid knee guard
on the kinematics of the lower extremity during gait. JOSPT.
1988;9(7):254–260.
58. Veldhuizen JW, Koene FM, Oostvogel HJ. The effects of a sup­
portive knee brace on leg performance in healthy subjects. Int J
Sports Med. 1991;12(6):577–580.
59. Deppen RJ, Landfried MJ. Efficacy of prophylactic knee brac­
ing in high school football players. JOSPT. 1994;20(5):243–246.
60. Greene DL, Hamson KR, Bay RC, et  al. Effects of protec­
tive knee bracing on speed and agility. Am J Sports Med.
2000;28(4):453–459.
61. Sforzo GA, Chen NM, Gold CA, et al. The effect of prophy­
lactic knee bracing on performance. Med Sci Sports Exerc.
1989;21(3):254–257.
62. Borsa PA, Lephart SM, Fu FH. Muscular and functional perfor­
mance characteristics of individuals wearing prophylactic knee
braces. J Athletic Train. 1993;28(4):336–344.
63. Liggett CL, Tandy RD, Young JC. The effects of pro­
phylactic knee bracing on running gait. J Athletic Train.
1995;30(2):159–161.
64. Martin TJ, Committee on Sports Medicine and Fitness.
American Academy of Pediatrics. Technical Report: knee brace
use in the young athlete. Pediatrics. 2001;108(2):503–507.
65. Sanders MS, Cates RA, Baker MD, et al. Knee injuries and the
use of prophylactic knee bracing in off-road motorcycling:
results of a large-scale epidemiological study. Am J Sports Med.
2011;39(7):1395–1400.
66. Gardner HF, Clippinger FW. A method for location of pros­
thetic and orthotic knee joints. Artif Limbs. 1979;13:31–35.
67. Lew WD, Patrnchak CM, Lewis JL, et  al. A comparison of
pistoning forces in orthotic knee joints. Orthot Prosthet.
1984;36(2):85–95.
68. Regalbuto MA, Rovick JS, Walker PS. The forces in a knee
brace as a function of hinge design and placement. Am J Sports
Med. 1989;17(4):535–542.
69. Noyes FR, Grood ES, Butler DL, et al. Clinical laxity tests and
functional stability of the knee: biomechanical concepts. Clin
Orthop. 1980;146:84–89.
70. Wojtys EM, Loubert PV, Samson SY, et al. Use of a knee-brace
for control of tibial translation and rotation. J Bone Joint Surg.
1990;72A(9):1323–1329.
71. Colville MR, Lee CL, Ciullo JV. The Lenox Hill brace. An eval­
uation of effectiveness in treating knee instability. Am J Sports
Med. 1986;14(4):257–261.
72. Wojtys E, Kothari W, Huston L. Anterior cruciate liga­
ment functional brace use in sports. Am J Sports Med.
1996;24(2):539–546.
73. Wojtys E, Huston L. “Custom-Fit” versus “Off-the-Shelf” ACL
functional braces. Am J Knee Surg. 2001;14(3):157–162.
74. Beynnon B, Ryder S, Konradsen L, et al. The effect of anterior
cruciate ligament trauma and bracing on knee proprioception.
Am J Sports Med. 1999;27(2):150–155.
75. Lam RY, Ng GY, Chien EP. Does wearing a functional knee
brace affect hamstring reflex time in subjects with anterior cru­
ciate ligament deficiency during muscle fatigue? Arch Phys Med
Rehabil. 2002;83:1009–1012.
76. Birmingham TB, Bryant DM, Griffin JR, et al. A randomized
controlled trial comparing the effectiveness of functional knee
brace and neoprene sleeve use after anterior cruciate ligament
reconstruction. Am J Sports Med. 2008;36(4):648–655.
77. Birmingham TB, Kramer JF, Kirkley A, et al. Knee bracing after
ACL reconstruction: effects on postural control and proprio­
ception. Med Sci Sports Exerc. 2001;33(8):1253–1258.
78. Beck C, Drez D, Young J, et al. Instrumented testing of func­
tional knee braces. Am J Sports Med. 1986;14(4):253–256.
79. Beynnon BD, Pope MH, Wertheimer CM, et al. The effect of
functional knee-braces on strain on the anterior cruciate liga­
ment in vivo. J Bone Joint Surg. 1992;74A(9):1298–1312.
80. Jonsson H, Kärrholm J. Brace effects on the unstable knee in 21
cases. A roentgen stereophotogrammetric comparison of three
designs. Acta Orthop Scand. 1990;61(4):313–318.
81. Mishra DK, Daniel DM, Stone ML. The use of functional knee
braces in the control of pathologic anterior knee laxity. Clin
Orthop. 1989;241:213–220.
82. Soma CA, Cawley PW, Liu S, et al. Custom-fit versus premanu­
factured braces. Orthopedics. 2004;27(3):307–310.
83. Ramsey D, Lamontagne M, Wretenberg P, et al. Assessment of
functional knee bracing: an in  vivo three-dimensional kine­
matic analysis of the anterior cruciate deficient knee. Clin
Biomech (Bristol, Avon). 2001;16:61–70.
84. Branch TP, Hunter RE, Donath M. Dynamic EMG analysis of
anterior cruciate deficient legs with and without bracing dur­
ing cutting. Am J Sports Med. 1989;17(1):35–41.
85. Wu GK, Ng GY, Mak AF. Effects of knee bracing on the sen­
sorimotor function of subjects with anterior cruciate ligament
reconstruction. Am J Sports Med. 2001;29(5):641–645.
86. Moller E, Forssblad M, Hanson L, et al. Bracing versus nonbrac­
ing in rehabilitation after anterior cruciate ligament reconstruc­
tion: a randomized prospective study with 2-year follow-up.
Knee Surg Sports Traumatol Arthrosc. 2001;9(2):102–108.
87. Wu GK, Ng GY, Mak AF. Effects of knee bracing on the func­
tional performance of patients with anterior cruciate liga­
ment reconstruction. Arch Phys Med Rehabil. 2001;82(2):
282–285.
88. Ramsey D, Wretenberg P, Lamontagne M, et  al. Electro­
myographic and biomechanic analysis of anterior cruciate lig­
ament deficiency and functional knee bracing. Clin Biomech
(Bristol, Avon). 2003;18:28–34.
89. Cook FF, Tibone JE, Redfern FC. A dynamic analysis of a func­
tional brace for anterior cruciate ligament insufficiency. Am J
Sports Med. 1989;17(4):519–524.
90. Marans HJ, Jackson RW, Piccinin J, et al. Functional testing of
braces for anterior cruciate ligament–deficient knees. Can J
Surg. 1991;34(2):167–172.
91. Zetterlund AE, Serfass RC, Hunter RE. The effect of wearing
the complete Lenox Hill derotation brace on energy expen­
diture during horizontal treadmill running at 161 meters per
minute. Am J Sports Med. 1986;14(1):73–76.
92. Yanagawa T, Shelburne K, Serpas F, et al. Effect of hamstrings
muscle action on stability of anterior cruciate ligament-defi­
cient knee in isokinetic extension exercise. Clin Biomech
(Bristol, Avon). 2002;17(9–10):705–712.
93. Giove TP, Miller 3rd SJ, Kent BE, et al. Higher levels of sports
participation in patients whose hamstring strength was equal
to or greater than quadriceps. J Bone Joint Surg. 1983;65A(2):
184–192.
94. Lass P, Kaalund S, LeFevre S, et  al. Muscle coordina­
tion following rupture of anterior cruciate ligament.
Electromyographic studies of 14 patients. Acta Orthop
Scand. 1991;62(1):9–14.

Chapter 11  Orthoses for Knee Dysfunction
333
95. Kirst J, Gillquist J. Sagittal plane knee translation and electro­
myographic activity during closed and open kinetic chain exer­
cise in anterior cruciate ligament-deficient patients and control
subjects. Am J Sports Med. 2001;29(1):72–82.
96. Chmieleski TL, Rudolph KS, Snyder-Mackler L. Development
of dynamic knee stability after acute anterior cruciate ligament
injury. J Electromyogr Kinesiol. 2002;12(4):267–274.
97. Loomer R, Horlick S. Valgus knee bracing for medial gonar­
throsis. Clin J Sport Med. 1993;3:251–255.
98. Self B, Greenwald RM, Pflaster D. A biomechanical analy­
sis of a medial unloading brace for osteoarthritis in the knee.
Arthritis Care Res. 2000;14(4):191–197.
99. Lindenfeld T, Hewett T, Andriacchi TP. Joint loading with val­
gus bracing in patients with varus gonarthrosis. Clin Orthop
Relat Res. 1997;344:290–297.
100. Hewett TE, Noyes FR, Barber-Westin SD, et  al. Decrease in
knee joint pain and increase in function in patients with medial
compartment arthrosis: a prospective analysis of valgus brac­
ing. Orthopedics. 1998;21(2):131–138.
101. Pollo FE, Otis JC, Wickiewicz TL, et al. Biomechanical analysis
of valgus bracing for the osteoarthritic knee. Presentation at
the first North American clinical gait lab conference, Portland,
Oregon; 1994.
102. Katsuragawa Y, Fukui N, Nakamura K. Change of
bone density with valgus knee bracing. Int Orthop.
1999;23(3):164–167.
103. Horlick SG, Loomer RL. Valgus knee bracing for medial gonar­
throsis. Clin J Sports Med. 1993;3(4):251–255.
104. Birmingham TB, Kramer JF, Kirkley A, et  al. Knee brac­
ing for medial compartment osteoarthritis: effects on pro­
prioception and postural control. Rheumatology (Oxford).
2001;40(3):285–289.
105. Nadaud MC, Komistek RD, Mahfouz MR, et al. In vivo three-
dimensional determination of the effectiveness of the osteoar­
thritic knee brace: a multiple brace analysis. J Bone Joint Surg
Am. 2005;87:114–119.
106. Slemenda C, Brandt KD, Heilman DK, et al. Quadriceps weak­
ness a primary risk factor for knee pain. Ann Intern Med.
1997;127(2):97–104.
107. Hurley MV. The role of muscle weakness in pathogenesis of
osteoarthritis. Rheum Dis North Am. 1999;25(2):283–298.
108. Ramsey DK, Briem K, Axe MJ, et  al. A mechanical the­
ory for the effectiveness of bracing for medial compart­
ment osteoarthritis of the knee. J Bone Joint Surg Am.
2007;89:2398–2407.
109. Hochberg MC, Altman RD, Brandt KD, et al. Guidelines for
the medical management of osteoarthritis. Arthritis Rheum.
1995;38(11):1541–1546.
110. Raja K, Dewan N. Efficacy of knee braces and foot orthoses in
conservative management of knee osteoarthritis: a systematic
review. Am J Phys Med Rehabil. 2011;90:247–262.
111. Divine JG, Hewett TE. Valgus bracing for degenerative knee
osteoarthritis: relieving pain, improving gait, and increasing
activity. Phys Sports Med. 2005;33(2):40–46.
112. Belyea BC. Orthoses for the knee: the patellofemoral joint.
In: Nawoczenski DA, Eppler ME, eds. Orthotics in Functional
Rehabilitation of the Lower Limb. Philadelphia: Saunders;
1997:31–56.
113. Levine J, Splain S. Use of the infrapatellar strap in the treatment
of patellofemoral pain. Clin Orthop. 1979;139:179–181.
114. Levine J. A new brace for chondromalacia patella and kindred
conditions. Am J Sports Med. 1978;6(3):137–140.
115. Powers CM, Shellock FG, Beering TV, et al. Effect of bracing on
patellar kinematics in patients with patellofemoral joint pain.
Med Sci Sports Exerc. 1999;31(12):1714–1720.
116. Timm K. Randomized controlled trial of Protonics on patel­
lar pain, position, and function. Med Sci Sports Exerc.
1998;30(5):665–670.
117. D'hondt NE, Struijs PA, Kerkhoffs GMJ, et al. Orthotic devices
for treating patellofemoral pain syndrome (Cochrane Review).
In: The Cochrane Library. Issue 2, 2003.
118. Wilson NA, Mazahery BT, Koh JL, et al. Effect of bracing on
dynamic patellofemoral contact mechanics. J Rehabil Res Dev.
2010;47(6):531–542.
119. Powers CM, Ward SR, Chan LD, et al. The effect of bracing
on patella alignment and patellofemoral contact area. Med Sci
Sports Exerc. 2004;36(7):1226–1232.
120. Reikeras O. Brace with a lateral pad for patellar pain: 2 year
follow-up of 25 patients. Acta Orthop Scand. 1990;61:319–320.
121. DeHaven KE, Lolan WA, Mayer PJ. Chondromalacia patel­
lae in athletes: clinical presentation and conservative manage­
ment. Am J Sports Med. 1979;7(1):5–11.
122. Malek M, Mangine R. Patellofemoral pain syndromes: a com­
prehensive and conservative approach. J Orthop Sports Phys
Ther. 1981;2(3):108–116.
123. Crocker B, Stauber WT. Objective analysis of quadriceps force
during bracing of the patella: a preliminary study. Aust J Sci
Med Sport. 1989;21:25–28.
124. Bohnsack M, Halcour A, Klagen P, et al. The influence of patel­
lar bracing on patellar and knee load-distribution and kinemat­
ics: an experimental cadaver study. Knee Surg Sports Traumatol
Arthrosc. 2008;16:135–141.
125. Selfe J, Richards J, Thewlis D, et al. The biomechanics of step
descent under different treatment modalities used in patello­
femoral pain. Gait Posture. 2008;27:258–263.
126. Crossley K, Bennell K, Green S, et al. A systematic review of
physical interventions for patellofemoral pain syndrome. Clin J
Sport Med. 2001;11(2):103–110.
127. Finestone A, Radin EL, Lev B, et al. Treatment of overuse patel­
lofemoral pain. Prospective randomized controlled clinical trial
in a military setting. Clin Orthop Relat Res. 1993;293:208–210.
128. Greenwald AE, Bagley AM, France P, et al. A biomechanical
and clinical evaluation of a patellofemoral knee brace. Clin
Orthop Relat Res. 1996;324:187–195.
129. BenGal S, Lowe J, Mann G, et al. The role of the knee brace in
the prevention of anterior knee pain syndrome. Am J Sports
Med. 1997;25(1):118–122.
130. Earl JE, Hoch AZ. A proximal strengthening program improves
pain, function, and biomechanics in women with patellofemo­
ral pain syndrome. Am J Sports Med. 2011;39(1):154–163.
131. Magee DJ. Hip. In: Orthopedic Physical Assessment. New York:
Saunders; 2002: 632.
132. McConnell J. Management of patellofemoral problems. Man
Ther. 2000;1(2):60–66.
ADDITIONAL RESOURCES
Bellamy MM. Controversy faces braces. Sportcare Fitness. 1988;
Sept/Oct:17–24.
Burns GS, Hull ML, Patterson HA. Strain in the anteromedial bun­
dle of the anterior cruciate ligament under combination loading.
Orthop Res. 1992;10:167–176.
Cawley PW. Postoperative knee bracing. Clin Sports Med.
1990;9(4):763–770.

334
Section II  Orthoses in Rehabilitation
Cawley PW, France EP, Paulos LE. The current state of functional
knee bracing research. A review of the literature. Am J Sports
Med. 1991;19(3):226–233.
France EP, Cawley PW, Paulos LE. Choosing functional knee braces.
Clin Sports Med. 1990;9(4):743–750.
Fuss FK. Anatomy of the cruciate ligaments and their function in extension
and flexion of the human knee joint. Am J Anat. 1989;184(2):165–176.
Gray HG. Gray's Anatomy. Philadelphia: Running Press; 1974: 274–276.
Henry JH. The patellofemoral joint. In: Nicholas JA, Hershman EB,
eds. The Lower Extremity and Spine in Sports Medicine. 2nd
ed.Philadelphia: Mosby; 1995:940–970.
Hofmann AA, Wyatt RWB, Bourne MH, et  al. Knee stability in
orthotic knee braces. Am J Sports Med. 1984;12(5):371–374.
Houston ME, Goemans PH. Leg muscle performance of athletes
with and without knee support braces. Arch Phys Med Rehabil.
1982;63(9):431–432.
Liu SH, Daluiski A, Kabo JM. The effects of thigh soft-tissue
stiffness on the control of anterior tibial displacement by
functional knee orthoses. J Rehabil Res Dev. 1995;32(2):
135–140.
Seebacher JR, Inglis AE, Marshal JL. The structure of the posterolat­
eral aspect of the knee. J Bone Joint Surg. 1982;64(4):536.
Sell KE. On the field again: knee bracing options. Adv Rehabil. 1996:
March:51–53.
Silbey MB, Fu FH. Knee injuries. In: Fu FH, Stone DA, eds. Sports
Injuries. Mechanisms, Prevention, Treatment. Baltimore: Williams
& Wilkins; 1994:949–976.
Terry GC. The anatomy of the extensor mechanism. Clin Sports
Med. 1989;8(2):163–177.
Warren LF, Marshall JL. The supportive structures and layers on the
medial side of the knee. An anatomical analysis. J Bone Joint Surg
1979;61(1):56.

335
Orthoses in Orthopedic Care and Trauma
Michelle M. Lusardi, William J. Barringer, Melvin L. Stills, Joshua L. Carter,
and Mark Charlson
Orthoses play a significant role in orthopedic and rehabilitative
care of individuals with many different types of musculoskel­
etal pathologies and impairments. Dysfunction of the musculo­
skeletal system can be the result of congenital or developmental
disorders or can be acquired as a result of overuse injury, sys­
temic disease, infection, neoplasm, or trauma at any point in the
life span. This chapter focuses on the use of orthoses to man­
age congenital and developmental musculoskeletal problems in
children and fractures of long bones of the lower extremity.
The understanding of how orthoses are helpful in the care
of those with musculoskeletal impairments is founded on
knowledge of the development and physiology of musculo­
skeletal tissues (bone, cartilage, ligaments, menisci, ­muscles,
and their tendons or aponeuroses); the kinesiological relation­
ships among these tissues; and an understanding of how these
tissues remodel in response to physical stressors (forces).1,2
This chapter begins with an overview of the anatomy of
bone, its growth and remodeling, and the principles behind
the rehabilitation (examination and intervention) of persons
with disorders of bone. Then the authors look specifically at
­disorders of the hip joint and orthotic/orthopedic strategies
for limb fractures.
BONE STRUCTURE AND FUNCTION
In anatomy classes and texts, students learn that the mature
adult human skeleton is composed of 206 bones (Figure 12-1),
ranging from the long bones of the extremities, the blocklike
vertebrae of the spine, the encasing protective ribs and skull,
and the multiarticulating carpals and tarsals of the wrist and
ankles that enable positioning of the hands and feet for
functional ­activities.3,4 Bony prominences formed during
­development from the force of muscle contraction at tendinous
origins and insertions are identified.1 Students scrutinize articular
surfaces to understand how joints move, consider the hyaline carti­
lage that protects the joint from repeated loading and shear dur­
ing activity, and learn to examine the ligaments that maintain
alignment for normal joint function. From a skeletal model
or examination of bone specimens in anatomy laboratory, it is
not intuitively apparent that living bone is a dynamic and meta­
bolically active tissue serving multiple purposes and physiolog­
ical roles.5 These include storage and homeostasis of calcium,
phosphate, magnesium, sodium, and carbonate (via ongoing
osteoblastic and osteoclastic activity in conjunction with kid­
ney function); production of erythrocytes, granular leukocytes,
and platelets in the marrow; physical growth and development
(by responsiveness to the pituitary's hormones at the epiphyseal
plate); provision of a protective and functional frame for the
organs of the thorax and abdomen (how would people breathe
without ribs?); and body weight support when the body is either
at rest or in motion during functional activities.6
Bone is a dense, regular, connective tissue derived from
embryonic mesoderm. It contains a combination of special­
ized cells (osteoblasts, osteocytes, osteoclasts) embedded in a
matrix of minerals (70%), protein (22%), and water (8%). The
many bones of the human body can be described as long or
short tubular bone (e.g., the femur, tibia, metatarsals, phalan­
ges), flat bone (e.g., the pelvis or skull), irregular bone (e.g.,
the tarsals and carpals), sesamoid bone embedded within ten­
dons (e.g., patella), or accessory bones (e.g., ossicles of the
middle ear). Alternatively, they can be classified as primarily
cortical (dense) or cancellous (trabecular) bone on the basis
of the density and arrangement of their components. Long
bones are subdivided into regions, each of which has its own
blood supply (Figure 12-2). The diaphysis (shaft) is supplied
by one or more nutrient arteries that penetrate the layers of the
bony cortex, dividing into central longitudinal arteries within
the marrow cavity. The flared metaphyses serve as an area of
transition from cortical to cancellous bone and are supplied
by separate metaphysical arterioles. The epiphyses are meta­
bolically active areas of cancellous bone with ­supportive tra­
beculae, with an extensive capillary network derived from
12
LEARNING OBJECTIVES
On completion of this chapter, the reader will be able to:
1. Describe the most common musculoskeletal injuries that
occur at various points in the life span.
2. Describe orthotic intervention for congenital and growth-
related musculoskeletal impairments.
3. Classify fracture of bone by type and severity and describe
the interventions most often used by orthopedists and
orthopedic surgeons on the basis of fracture type.
4. Delineate the roles of health care team members in the
rehabilitation and orthotic management of individuals
with congenital and acquired musculoskeletal impairment.

336
Section II  Orthoses in Rehabilitation
epiphyseal arteries. The epiphysis is actively remodeled over
the life span in response to weight bearing and muscle con­
traction during activity.7 In childhood and adolescence, before
skeletal maturation, the bony metaphyses and epiphyses are
connected by cartilaginous epiphyseal (growth) plate, which
calcifies and fuses throughout various periods of ­development.
The ­periosteum is a layer of less dense, vascularized connec­
tive tissue that overlies and protects the external surface of all
bone and houses osteoblastic cells necessary for bone depo­
sition and growth. The periosteum is replaced by articular
(hyaline) cartilage within the joint capsule. The endosteum,
a thin connective tissue lining of the marrow cavity of long
FIGURE 12-1  The bones of the human skeleton. A, Anterior view.
A
Coccyx
Sternum
Ribs
Vertebral column
Coxal (hip) bone
Ilium
Sacrum
Frontal bone
Zygomatic
bone
Maxilla
Manubrium
Clavicle
Scapula
Xiphoid process
Costal cartilage
Humerus
Ulna
Radius
Carpals
Metacarpals
Phalanges
Femur
Patella
Tibia
Fibula
Tarsals
Metatarsals
Phalanges
Orbit
Nasal bone
Mandible
Greater
trochanter
Pubis
Ischium

Chapter 12  Orthoses in Orthopedic Care and Trauma
337
bones and the internal spaces of cancellous bone of the mar­
row space, also houses osteoblasts. Both linings are active as
part of osteogenesis during growth and fracture healing.
Cortical bone is the most highly mineralized type of bone
found in the shafts (diaphyses) of the long bones of the body
and serves as the outer protective layer of the metaphysis
and epiphysis of tubular bone, as well as the external layers
of flat, irregular, and sesamoid bones. Most of the bones in
the human skeleton (80% to 85%) are primarily cortical with
cancellous/trabecular bone in the metaphyseal and epiphy­
seal region. Cross section of a long tubular bone reveals three
layers of cortical bone: the inner or endosteal region next to
B
Parietal bone
Acromion process
Clavicle
Cervical vertebrae (7)
Scapula
Lumbar
vertebrae (5)
Thoracic
vertebrae (12)
Humerus
Ulna
Radius
Coccyx
Carpals
Metacarpals
Phalanges
Femur
Tibia
Fibula
Tarsals
Calcaneus
Metatarsals
Phalanges
Occipital bone
Ribs
Coxal
(hip) bone
Sacrum
Ischium
Axial skeleton
Appendicular
skeleton
FIGURE 12-1—cont'd  B, Posterior view. (From Thibodeau GA, Patton KT. Anatomy and Physiology.
5th ed. St. Louis: Mosby, 2003.)

338
Section II  Orthoses in Rehabilitation
the marrow cavity, the metabolic intracortical or haversian
region with its haversian canals surrounded by concentric
layered rings (osteons) and Volkmann's canals containing a
perpendicularly arranged anastomosing capillary network,
and the dense outer periosteal region (Figure 12-3).
Cancellous (trabecular) bone with its honeycomb or
spongy appearance is much more metabolically active and
much less mineralized than cortical bone. Cancellous bone is
composed of branching bony spicules (trabeculae) arranged
in interconnecting lamellae to form a framework for weight
bearing (Figure  12-4A). In the vertebral bodies, for exam­
ple, trabeculae are arranged in an interconnecting horizontal
and vertical network oriented perpendicular to the lines of
weight-bearing stress into a boxlike shape (see Figure 12-4B).
In contrast, trabeculae in the proximal femur form an arch­
like structure to support weight-bearing forces between the
hip joint and femoral shaft (see Figure 12-4C). In living bone,
cavities between trabeculae are filled with bone marrow.
Three types of cells are embedded within the various com­
partments of bone. Osteoblasts, bone building cells, synthesize
and secrete the organic matrix of bone (osteoid) that mineral­
izes as bone matures. They are located under periosteum and
endosteum and are active in times of bone growth and repair.
Osteocytes are matured and inactive osteoblasts that have
become embedded within bone matrix. Osteocytes remain
connected to active osteoblasts via long dendritic processes
running through the canaliculi (small channels) within the
bone matrix. Both osteoblasts and osteocytes are responsive
to circulating growth hormones, growth factors, and cyto­
kines, as well as mechanical stressors and fluid flow within
the bone itself.8,9 Osteocytes are thought to be involved in
mineral exchange, detection of strain and fatigue, and control
of mechanically induced remodeling.10 Osteoclasts, derived
from precursor cells in bone marrow, are macrophage-like
cells that can move throughout bone to resorb bone by releas­
ing minerals from the matrix and removing damaged organic
components of bone.11,12
The epiphyses of long bones, the vertebrae, and large flat
bones house nociceptors and mechanoreceptors and a net­
work of afferent sensory neurons that contribute to extero­
ceptive (primarily pain) pathways.13 The periosteum has a
particularly rich neural network with branches that continue
along with penetrating nutrient arteries into the haversian
canals into the diaphysis.
BONE GROWTH AND REMODELING
OVER THE LIFE SPAN
During childhood and adolescence, growth occurs through
the process of modeling, in which bones increase in length
and diameter and are reshaped until the epiphyseal plates
calcify and skeletal maturity is achieved (­typically in
Epiphyseal
vessel
Metaphyseal
vessel
Periosteal
vessel
Nutrient
artery
Periosteum
Epiphyseal
plate
Epiphysis
Metaphysis
Diaphysis
FIGURE 12-2  Diagram of the regions (epiphysis, epiphyseal plate,
metaphysis, and diaphysis) of a long bone and their arterial vascular
supply. (Modified from Lundon K. Orthopedic Rehabilitation Science,
Principles for Clinical Management of Bone. Boston: Butterworth
Heinemann, 2000.)
blood vessels
outer circumferential
lamellae
periosteum
inner circumferential
lamellae
endosteum
Haversian canal
Volkmann's canal
A
B
osteon
interstitial lamellae
N. Kupiec 1999
FIGURE 12-3  A, A cross section through the diaphysis of a long bone, with the external periosteal layer,
the middle haversian/intracortical layer, the inner endosteal layer, and the marrow cavity. B, Diagram
of a cross section through the diaphysis of a long bone. (From Lundon K. Orthopedic Rehabilitation
Science: Principles for Clinical Management of Bone. Boston: Butterworth-Heinemann, 2000.)

Chapter 12  Orthoses in Orthopedic Care and Trauma
339
­mid-adolescence for females and early adulthood for males).14
In adulthood, bone health is maintained by the ongoing
­process of remodeling, in which there is a balance and cou­
pling between osteoblastic deposition of new bone sub­
stance and osteoclastic resorption of existing bone.15 This
ongoing process of turnover means that the internal archi­
tecture of living bone is actively restructured and replaced
at a rate of approximately 5% per year in cortical bone and
up to 20% per year in cancellous bone.5 The rate of bone
formation, resorption, and turnover is influenced by both
systemic hormones and other substances (e.g., parathyroid
hormone, calcitonin, vitamin  D from the kidney, growth
hormone, adrenocorticosteroids, estrogen, progesterone,
androgens); local cell-derived growth factors; and avail­
ability of essential nutrients (calcium, fluoride, vitamin A,
vitamin D, and ­vitamin E).16–18 These substances, along with
blood or urinary levels of certain enzymes active during
turnover and metabolites of bone resorption, are monitored
as biomarkers to track progression of bone diseases asso­
ciated with high rates of bone resorption (e.g., Paget's dis­
ease, osteoporosis, hyperparathyroidism) and to determine
efficacy of medical-pharmaceutical interventions for these
diseases.19–21
In the prenatal period and in infancy, the flat bones of
the skull develop as the fetal mesenchyme that forms as
the periosteum begins to ossify (intramembranous ossifi­
cation). Most long bones, as well as the vertebrae and pel­
vis, develop from a cartilaginous framework or template.
In this process of endochondral bone formation, cartilage
cells mature and eventually ossify.7 During childhood and
adolescence, bones grow in both length and diameter and
are dynamically modeled toward their mature configura­
tions.22 During puberty, accumulation of bone mass accel­
erates; by the end of puberty, as much as 90% of mature
bone mass is established.23 For young children with abnor­
mal skeletal development, orthoses attempt to capitalize
on the dynamic modeling process, applying external forces
to influence bone shape and length.24 For approximately
15 years following puberty, after closure of the epiphyseal
plates of the long bones, bone mass continues to increase—
a process described as consolidation.22 Gender differences
in peak bone mass have been well documented: Average
peak bone mass in women is approximately 20% less
than that of men. Early in the midlife period, both men
and women enter a period of gradual endochondral bone
loss that appears to be genetically determined; the rate of
A
B
C
FIGURE  12-4  A, Scanning electron microscope view
of cancellous/trabecular bone. B, The trabecular pat­
tern in a healthy lumbar vertebra demonstrates bone tis­
sue's response to vertical and horizontal forces during
upright activity. C, The relationship of form and function
is demonstrated by the arched bridgelike trabecular pat­
tern in this cross section of the proximal femur. (From
Lundon K. Orthopedic Rehabilitation Science: Principles
for Clinical Management of Bone. Boston: Butterworth
Heinemann, 2000.)

340
Section II  Orthoses in Rehabilitation
bone loss is also influenced by hormonal status, nutrition,
­smoking and alcohol use, and activity level.25–28 It is esti­
mated that males will lose between 15% and 40% of cancel­
lous bone mass and 5% to 15% of cortical bone mass over
their lifetime. In women, menopause accelerates the rate
of bone loss; there may be up to a 50% decrease from peak
cancellous bone mass and 30% decrease in cortical bone
mass over their lifetimes.29 Significant loss of bone mass is
associated with increasing vulnerability to fracture, espe­
cially among postmenopausal women.
ORTHOSES IN THE MANAGEMENT OF HIP
DYSFUNCTION
Hip orthoses are important in the management of hip dis­
orders in infants and children, as well as in the postsurgical
care of children and adults. An understanding of the designs
of and indications for various hip orthoses is essential for
physicians and rehabilitation professionals working with
individuals who have orthopedic problems of the pelvis, hip
joint, or proximal femur. For children with developmental
dysplasia of the hip (DDH) or Legg-Calvé-Perthes disease
(LCPD), hip orthoses are the primary intervention for pre­
vention of future deformity and disability. Hip orthoses are
essential elements of postoperative care and rehabilitation
programs for children with musculoskeletal and neuromus­
cular conditions who have had surgical intervention for bony
deformity or soft tissue contracture. Hip orthoses can also be
major postoperative interventions for adults who have had
repair of a traumatic injury or a complex total hip arthro­
plasty. The efficacy of orthotic intervention is influenced by
patient and caregiver adherence: The key to successful use
of these orthoses is clear, and open communication exists
among the physician, ­therapist, orthotist, and family con­
cerning the primary goals of the orthosis, its proper appli­
cation and wearing schedule, and the possible difficulties
that may be encountered. Positive health care outcomes and
happy patients and families are contingent on the ability of
the health care team to communicate.
When are Hip Orthosis Indicated?
Most nontraumatic hip joint dysfunction or pathology occurs
either in childhood or in late adult life and is frequently
related to one or more of the four following factors:
1. Inadequate or ineffective development of the acetabulum
and head of the femur in infancy
2. Avascular necrosis of the femoral head associated with
inadequate blood supply during childhood
3. Loss of cartilage and abnormal bone deposition associated
with osteoarthritis
4. Loss of bone strength and density in osteoporosis
Orthotic intervention is an important component in the
­orthopedic management of many of these conditions. Most often,
hip orthoses are used to protect or position the hip joint by lim­
iting motion within a desirable range of flexion/extension and
­abduction/adduction. It is important to note that hip orthoses
alone are not effective in controlling internal/external rotation
of the hip joint. If precise rotational control is desired, a hip-
knee-ankle-foot orthosis (HKAFO) must be used.
Hip Structure and Function
The hip (coxofemoral) joint is a synovial joint formed by the
concave socketlike acetabulum of the pelvis and the rounded
ball-like head of the femur (Figure  12-5). Because of the
unique bony structure of the hip joint, movement is possible
in all three planes of motion: flexion/extension in the sagittal
plane, abduction/adduction in the frontal plane, and inter­
nal/external rotation in the transverse plane. Most functional
activities blend movement of the femur on the pelvis (or of
the pelvis on the femur) across all three planes of motion.
The hip joint has two important functions. First, it must
support the weight of the head, arms, and trunk during func­
tional activities (e.g., erect sitting and standing, walking, run­
ning, stair climbing, transitional movements in activities of
daily living). Second, it must effectively transmit forces from
the pelvis to the lower extremities during quiet standing, gait,
and other closed chain activities.30
The acetabulum is formed at the convergence of the pubis,
ischium, and ilium. Its primary orientation is in the vertical,
facing laterally, but it also has a slight inferior inclination and
an anteverted, or anterior-facing tilt. Developmentally, the
depth of the acetabulum is dynamically shaped by motion of
the head of the femur during leg movement and weight bear­
ing. The acetabulum is not fully ossified until late adoles­
cence or early young adulthood. The articular surface of the
acetabulum is a horseshoe-shaped, hyaline cartilage–covered
area around its anterior, superior, and posterior edges. A space
along the inferior edge, called the acetabular notch, is nonartic­
ular, has no cartilage covering, and is spanned by the transverse
acetabular ligament. The acetabular labrum is a fibrocartilagi­
nous ring that encircles the exterior perimeter of the acetab­
ulum, increasing joint depth and concavity. The center of the
acetabulum, the acetabular fossa, contains fibroelastic fat and
the ligamentum teres, and is covered by synovial membrane.
The femoral components of the hip joint include the fem­
oral head, the femoral neck, and the greater and lesser tro­
chanters. The spherical articular surface of the femoral head
is covered with hyaline cartilage. Because the femoral head is
larger and somewhat differently shaped than the acetabulum,
some portion of its articular surface is exposed in any position
of the hip joint. The femur and acetabulum are most congru­
ent when positioned in a combination of flexion, abduction,
and external rotation. The proximal femur, composed pri­
marily of trabecular bone, is designed to withstand ­significant
loading while also permitting movement through large excur­
sions of range of motion. The orientation of the femoral head
and neck in the frontal plane, with respect to the shaft of the
femur, is described as its angle of inclination (Figure 12-6).
In infancy the angle of inclination may be as much as
150 degrees but decreases during normal development to
approximately 125 degrees in mid-adulthood and to 120
degrees in later life.31 The orientation of the proximal femur
to the shaft and condyles in the transverse plane, called the
angle of anteversion, is also a key determinant of hip joint