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
to volitionally activate hip flexions and quadratus lumborum
(hip hikers) to initiate a step, persons with thoracic level SCI
can use Craig-Scott orthoses and Lofstrand crutches using a
two-point swing-through gait pattern.108
Conventional KAFOs are frequently used to preserve
upright mobility for children with Duchenne muscular
dystrophy (DMD).110 While initially perceived as a sign of
­disease-related decline, parents and children often come to
appreciate the continued mobility that KAFOs allow.111 Use
of a KAFO may provide limited household or community
ambulation ability for boys with DMD for 2 or more years.
Fitting for KAFOs may be challenging because of the primary
and compensatory deformities that develop as children with
DMD strive to remain upright as their disease progresses.112
A lightweight modular system that allows the orthotist to
adjust the length of the uprights and quickly replace out­
grown thigh or calf supports has been developed specifically
for children with DMD.113
Thermoplastic KAFOs
A molded thermoplastic KAFO (also known as a hybrid ther­
moplastic and metal orthosis) is designed to have an intimate
fit so that it can be worn under clothing and fits within the
patient's shoe (Figure 9-22). The distal component (a SAFO
or HAFO, depending on the individual's needs) and the prox­
imal thigh component are vacuum formed over a rectified
positive model of the patient's limb. The proximal component
often encases the thigh from greater trochanter to femoral
condyles, and is closed with a pair of anterior Velcro straps.
Orthotic knee joints and metal uprights (sidebars) connect
the proximal and distal shells. The intimate total contact fit
of molded thermoplastic allows significantly more effective
control of the limb. The forces necessary for stabilization of
the limb are distributed over a large surface area, reducing
the possibility of discomfort or skin irritation. Such problems
would arise only if the fit of the orthosis allows pistoning of
the limb within the components while walking, or if growth,
weight gain, or edema makes the fit too snug, such that tissue
is compressed and damaged while walking.
This design also controls the limb using a series of over­
lapping three-point force systems. Flexion/extension control
in the sagittal plane is the same one used in a conventional
KAFO, except that the posterior counterforces are distributed
over a wider surface area. The intimate fit provides more pre­
cise control in both the frontal and transverse planes; this is
particularly important when dealing with segmental devia­
tions arising from transverse plane rotation related to abnor­
mal tone or longitudinal rotational deformity.114
Because any movement of the knee joint occurs in mul­
tiple planes of motion, any varus or valgus problems at the
knee will necessarily have a rotatory component. Control of
rotation is better accomplished with the intimate fit, total
contact thermoplastic KAFO as compared to the double
upright system of conventional KAFOs. This intimate fit,
however, is problematic for persons with medical conditions
associated with fluctuating edema and changing limb ­volume
ADVANTAGES
• Strong
• Most durable
• Easily adjusted
DISADVANTAGES
• Heavy
• Must be attached to shoe or shoe insert
• Less cosmetic
• Fewer contact points reduce control
INDICATIONS
• When maximum strength and durability are needed
• For individuals with significant obesity
• For individuals with uncontrolled or fluctuating edema
(e.g., congestive heart failure, dialysis)
CONTRAINDICATIONS
• When issues of energy expenditure make weight of the
orthosis a factor
• When control of transverse plane motion is important
BOX 9-3  Advantages and Disadvantages of
Conventional Knee-Ankle-Foot Orthoses
FIGURE 9-21  The Craig-Scott orthosis is a modified version of a
conventional knee-ankle-foot orthosis, designed to be as lightweight
as possible and to capitalize on alignment stability to enhance ambu­
lation and upright activities in patients with low thoracic and lum­
bar spinal cord injury. Note that the individual wearing the orthosis
stands with hyperextended hips, exaggerated lumbar lordosis, and
backward lean of the trunk, “hanging” on his Y ligaments to main­
tain upright position. (Reprinted with permission from DG Shurr,
TM Cook. Prosthetics and Orthotics. Norwalk, Conn: Appleton &
Lange, 1990. p. 141.)

Chapter 9  Principles of Lower Extremity Orthoses
243
(e.g., congestive heart failure, kidney dialysis), as well as
those who cyclically gain and lose weight.
Similar to most thermoplastic AFOs, the use different pairs
of shoes (as long as heel height is constant) can also occur
with thermoplastic KAFOs. One of the downsides of using
thermoplastics, however, is keeping cool while wearing them.
As lightweight as they are, the large contact area inherent in
thermoplastic KAFOs compromises dissipation of body heat;
they may be uncomfortably warm for wearers who are very
active or who live in hot climates. Advantages and disadvan­
tages of thermoplastic KAFOs are summarized in Box 9-4.
Carbon Composite KAFOs
Recently, carbon composite materials have begun to be
used in place of thermoplastics in KAFOs for persons with
residual impairment following polio (postpolio syndrome)
for whom fatigue is a major concern (Figure 9-23).115 On
average, because CC-KAFOs are as much as 30% lighter
in weight than other materials, the energy cost of walking
with CC-KAFOs may be up to 10% less (as measured by
VO2 max and physiological cost index).116,117 In addition,
CC-KAFOs have been deemed to be cosmetic by users,
persevered or increased walking speed, improved kinetic
characteristics of walking, and demonstrated exceptional
FIGURE 9-22  Schematic diagram of the components and sagittal
plane force systems that are necessary to control knee flexion/exten­
sion. Because the point of force application is distributed over the
entire posterior surface of the intimately fitting orthotic shell, more
precise and more comfortable control of the limb is possible.
ADVANTAGES
• Lightweight
• Interchangeability of shoes
• Greater cosmesis worn under clothing
DISADVANTAGES
• Can be hot to wear
INDICATIONS
• Intimate/total contact fit makes maximum limb con­
trol possible
• When energy expenditure makes weight of the ortho­
sis an issue
• When control of transverse plane motion is needed
CONTRAINDICATIONS
• Intimacy of fit is difficult when the individual is sig­
nificantly obese
• Intimacy of fit is compromised when the individual
has uncontrolled or fluctuating edema
BOX 9-4  Advantages and Disadvantages of
Thermoplastic Knee-Ankle-Foot
Orthoses
FIGURE  9-23  This carbon composite knee-ankle-foot orthosis
(CC-KAFO) has a posterior proximal shell, uses a stance control
knee unit, an anterior tibial shell, and a foot component similar to
that of a hinged AFO. Because CC-KAFOs are much lighter than
thermoplastic and conventional KAFO designs, they are well suited
for individuals with post-polio syndrome, reducing energy cost of
gait by improve most gait parameters. They are, however, much
more expensive to fabricate.

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Section II  Orthoses in Rehabilitation
durability.116,117 It is important to note, however, that the
cost of CC-KAFOs may be nearly double that of a custom-
molded thermoplastic KAFO.116,117
Controlling the Ankle
The ankle joints used in KAFOs are the same as those that
are available for AFOs: either nonarticulating solid (rigid)
designs that hold the ankle in a fixed position (i.e., SAFO)
or hinged orthotic joints that allow dorsiflexion (for forward
progression of the tibia over the foot in stance) block plan­
tarflexion, provide dorsiflexion assistance (to enhance swing
phase clearance), or allow free dorsiflexion and plantarflexion
within a specific range of motion.
The key question to consider in deciding which ankle
control system is appropriate for a given individual is how
orthotic control at the ankle and the GRF will impact knee
function and forward progression during stance phase. If a
locked ankle is necessary, the orthotist may opt to set the
orthosis in several degrees of dorsiflexion to minimize com­
promise of forward progression and to allow the individual
to achieve the stable hips-forward trunk-back stance posi­
tion quickly (i.e., to achieve stability with the GRF pass­
ing anterior to the knee and posterior to the hip as soon
as possible during stance) (see Figure  9-21). When ankle
motion must be constrained to protect the joint, to control
the impact of abnormal tone, or because of fixed deformity,
the orthotist may use a rocker sole on the patient's shoe to
simulate the normal rockers of gait. This strategy facili­
tates forward progression during stance by reducing the
toe lever of the orthosis, improving the smoothness of the
patient's gait and reducing the likelihood of compensatory
gait deviations.
An articulating or hinged orthotic ankle joint that allows
some plantarflexion enhances the transition from initial con­
tact to loading response (although the locked knee may com­
promise the shock absorption function of loading response).
Similarly, a hinged orthotic ankle joint that permits move­
ment into dorsiflexion during stance enhances forward pro­
gression of the body over the foot during stance, especially
when the orthotic knee is also locked.
Controlling the Knee
Historically, if a patient with motor control or muscle perfor­
mance impairment was unable to keep the knee stable in stance
by using their quadriceps or alignment of limb segments (i.e.,
hanging on the Y ligament at the hip), and an AFO was not
able to provide the necessary stability, the only option was a
KAFO with knee joints that remained locked at all times while
walking.118,119 This created a challenge for limb advancement in
swing, and often resulted in compensatory patterns such as cir­
cumduction or lateral leaning to the opposite side in an effort to
clear the swinging leg. While compensatory strategies accom­
plished the goal of limb clearance, they also markedly increased
the energy cost of walking. Those who had functional motor
control and muscle performance who required a KAFO to pro­
tect a mechanically unstable knee from extreme valgus or varus
may be able to use unlocked single axis orthotic knee joints.
There are a number of options for orthotic knee joints
that provide mechanical stability. The recent development of
various SC-KAFO knee joints that allow free knee motion in
swing but lock into extension during stance has had signifi­
cant impact of KAFO prescription and use.120,121 A brief over­
view of the mechanical joints is provided, and the impact of
SC-KAFOs is considered in more detail. See Table 9-3 for a set
of general guidelines for choosing the conventional orthotic
knee joints, based on the knee control they provide.
Single-Axis Knee Joints
The single-axis knee orthotic knee joint (straight knee joint
without drop lock or a free knee) is, essentially, a simple hinge
that allows full flexion and extension to neutral in the sagit­
tal plane (most designs prevent hyperextension) while pro­
viding mediolateral stability (Figure 9-24A). It is important
that the medial and lateral orthotic joints be positioned at
the approximate axis of the anatomical knee joint. Given the
polycentric structure of the anatomical knee versus the ­single
axis structure of the orthotic knee joint, a small torque is
likely, even if the single axis orthotic joints are correctly posi­
tioned. For the majority of persons using the orthosis, this
is not problematic. This knee joint is appropriate for those
who have sufficient muscle performance resource to achieve
knee stability in stance but need a KAFO to ­minimize or pre­
vent recurvatum, protect a structural (mediolateral) unstable
knee, or prevent excessive varus or valgus in stance.121
Single-Axis Locking Knee
When a locking mechanism is added to maintain knee exten­
sion, the KAFO with a single-axis knee joint becomes rigidly
stable in all planes. A locked knee has traditionally been used
for those whose motor control or muscle performance defi­
cits make them unable to control the knee effectively during
stance phase, such that they need additional external stability
to prevent knee flexion as body weight is transferred onto the
limb during stance.118
The most commonly used locking mechanism is a sim­
ple ring or drop that captures the halves of the orthotic joint
when fully extended, blocking subsequent movement into
flexion or hyperextension (see Figure  9-24B). A small ball
bearing in the upright holds the drop lock in position until
the individual or caregiver purposefully unlocks the orthosis.
Optimally, there is a drop lock on both the medial and lat­
eral uprights of the orthosis. Note that the knee must be fully
extended for the lock to be engaged or disengaged; this can be
challenging when transitioning between standing and sitting,
especially for persons with limited hand function, significant
lower extremity spasticity, or dependence on assistive devices
when standing.
An alternative lock that may be considered is a spring-
loaded bail lock (also known as pawl or Swiss lock)
(Figure 9-25). The posterior bail connects the medial and
lateral locks so that they can be locked or unlocked simul­
taneously. To unlock the KAFO when returning to sitting,
the individual backs up against the edge of a seating sur­
face (e.g., wheelchair, mat table, kitchen, or desk chair) and

Chapter 9  Principles of Lower Extremity Orthoses
245
TABLE 9-3  Indications and Contraindications for Orthotic Knee Joint Designs
Orthotic Knee Design
Desired Knee Control
Single Axis Unlocked
Single Axis Locked
Offset Unlocked
Offset Locked
Variable Position Locked
Stabilization of flail knee with knee
extension moment and free knee
joint motion
Contraindicated
Contraindicated
Indicated
Contraindicated
Contraindicated
Stabilization of flail knee without use
of knee extension moment and free
knee joint motion
Contraindicated
Indicated
Contraindicated
Indicated
Unnecessary
Control of genu recurvatum
Contraindicated
Indicated if orthosis will only
be locked when ambulating
Indicated
Indicated when individual
will lock knee intermittently
Contraindicated
Reduction of knee flexion contracture
Contraindicated
Lacks adjustability
Contraindicated
Lacks adjustability
Indicated
Control of genu valgum
Indicated
Indicated Use of lock optional
Indicated
Indicated Use of
lock optional
Unnecessary
Control of genu varum
Indicated
Indicated Use of lock optional
Indicated
Indicated Use of lock optional
Unnecessary
Modified from Short Course in Orthotics and Prosthetics—Course Manual. Dallas, Texas: University of Texas, Southwestern Medical Center, 1993. pp. 8-22.

246
Section II  Orthoses in Rehabilitation
pushes the posterior bar into the seat to disengage the lock.
This option is best used for persons with enough upper
body strength and coordination to control the descent into
sitting. There is a risk that the lock will disengage if the
bail behind the knee is inadvertently bumped, and a fall
will occur.
Offset Knee Joint
The offset knee joint (also known as a posteriorly offset, free
knee) is aligned with its axis posterior to the axis of the ana­
tomic knee (see Figure 9-24C). In early stance, during dou­
ble support, the ground reaction passes nearer to the axis of
the orthotic joint, reducing the magnitude of the external
flexion moment that is acting to flex the limb. With forward
progression toward midstance, the GRF moves anterior to
the orthotic joint, creating an extensor force that mechani­
cally augments stance phase stability during single limb
support. To be effective, however, the alignment between
ankle and knee must be finely tuned. Transitions between
sitting and standing become less problematic if the knee
does not have to be unlocked. A drop lock or other lock­
ing mechanism can be added, however, to stabilize the knee
when the individual using the orthosis will be standing for
long periods of time or when additional stability is advis­
able (e.g., when the patient is walking on uneven ground).
An offset knee joint is often most suitable for those with
lower motor neuron disease (e.g., poliomyelitis) or low
thoracic upper lumbar SCI.118,121
Variable Position Orthotic Knee Joint
The variable position locking orthotic knee joint (dial
lock, adjustable locking knee joint, serrated knee lock) (see
Figure  9-24D) is used for those who are unable to fully
extend the knee during stance because of knee flexion
contracture. When there is a knee flexion contracture of more
than 10 degrees, the GRF remains posterior to the anatomic
knee joint during all of stance phase, and it becomes signifi­
cantly more difficult for those with weakness or motor con­
trol impairment to generate the necessary muscle force for
stance stability. For these individuals, the variable position
knee joint is locked in the most extended position possible,
providing an external mechanical stability.16,118
Stance Control Orthotic Knee Joints
The initial SC options for KAFO orthotic knee joints
were intended for individuals with a history of poliomy­
elitis who were coping with ineffective quadriceps activ­
ity as well as postpolio syndrome.122–124 Use of SC-KAFO
FIGURE  9-25  A pawl and bail-locking mechanism allows the
medial and lateral locks to be disengaged at the same time by a poste­
rior pressure, as against the edge of the seating surface. This mecha­
nism is often used for patients with paraplegia who must maintain
bilateral upper extremity support via crutches for stability. (Reprinted
with permission from O'Sullivan S, Schmitz TJ [eds]. Physical
Rehabilitation, 5th ed. Philadelphia: FA Davis, 2007. p. 1224.)
FIGURE  9-24  Orthotic knee joints historically used in conven­
tional and thermoplastic knee-ankle-foot orthoses. A, A single-
axis, or free, knee allows full flexion and extension while providing
mediolateral and rotational stability to the knee joint. B, A drop lock
holds the knee in extension in standing, providing stability in all
planes. It must be unlocked for knee flexion to occur when return­
ing to sitting position. C, Because the axis of the offset orthotic knee
joint is positioned behind the anatomical knee axis, biomechanical
stability of the orthosis is enhanced. It is available with and without
a locking mechanism. D, A variable position, or adjustable, orthotic
knee joint permits the orthotist to accommodate for changing range
of motion or for fixed contracture at the knee.

Chapter 9  Principles of Lower Extremity Orthoses
247
has been extended to persons with stroke, brain tumor,
acquired brain injury, incomplete SCI, spinal degenerative
diseases, muscular dystrophy, multiple sclerosis, myopa­
thy, radicular and peripheral nerve injury, and polyneu­
ropathy.125–127 A variety of mechanisms (i.e., mechanical,
hydraulic, or computer microchip electronic joints) are
available (Figure  9-26).128–130 All are designed to lock
the orthotic knee joint in extension at initial contract
and during most of stance, while unlocking the knee on
heel rise during the third rocker, in the transition from
terminal stance to preswing.131 Hydraulic and electronic
SC orthotic joints add resistance to knee flexion when the
limb is loaded in less than a fully extended position, which
potentially improves function when the wearer is ascend­
ing stairs or walking on uneven surfaces. Most SC orthotic
knee joints are placed on the lateral upright of the KAFO.
Pneumatic orthotic knee joints to assist with knee exten­
sion during swing are also available, added onto the media
or lateral uprights of the KAFO.126 Many of the SC knee
units can be incorporated into KAFOs based on metal
uprights, thermoplastic thigh and AFO components, or
laminated designs. Characteristics of some of the commer­
cially available SC and swing assist knee units are summa­
rized in Table 9-4.
Most prescription guidelines for SC-KAFO indicate
that the individual must demonstrate muscle strength of
at least 3/5 on manual muscle testing at hip extensors and
flexors, and full extension of the anatomical knee joint.125–
127 Contraindications for SC-KAFO use include fixed hip
or knee flexion contracture, fixed plantarflexion contrac­
ture, significant spasticity, leg length discrepancy greater
than 3 inches (8 cm), valgus or varus deformity greater
than 10 degrees, and excessive body weight (above 220 to
265 pounds).125–127 Persons with cognitive impairment may
not be able to comprehend how to safely use or maintain
a SC-KAFO; SC options must be used with caution when
cognitive ability and judgment are impaired.
The positive impact of SC knee joints on kinematics
of walking is well documented. In addition to improving
self-selected walking speed, cadence, and stride length,
use of these orthotic knee joint improves symmetry of gait,
reduces compensatory movement, and allows safer man­
agement of inclines and obstacles when compared with
KAFOs with locked knees.120,122–124,128 Persons who have
used traditional KAFOs with locked knees for long peri­
ods before adopting SC designs benefit from additional
functional training to be able to take full advantage of
the mobility that a SC-KAFO provides.132 The few studies
that have examined wearers’ experience with SC-KAFOs
indicate better acceptance and general satisfaction
with the devices in terms of effectiveness in improving
mobility, dependability, and performance of the device and
A
B
C
FIGURE  9-26  A, The Becker UTX is a mechanical stance-control knee-ankle-foot ortho­
sis (SC-KAFO): The knee unit contains a cable-driven ratchet that locks the knee as it extends in
terminal swing in preparation for stance phase, and unlocks it at terminal stance to allow knee flex­
ion necessary for limb clearance during swing phase. Note the lightweight lateral upright, medial
cable, anterior padded cuffs, and Velcro-closing posterior straps. B, The Becker E-knee is an exam­
ple of a microchip-controlled and battery-powered SC-KAFO. A pressure-sensing footplate signals
the microprocessor to lock the knee joint when the limb is loaded (regardless of knee position), and
unlock the unit when unloaded in late stance. C, The Becker Load Response SC-KAFO also con­
tains a torsional spring that mimics controlled knee flexion for shock absorption in loading response.
(Reprinted with permission from Becker Orthopedic, Troy, Mich.)

248
Section II  Orthoses in Rehabilitation
TABLE 9-4  Stance-Control Knee-Ankle-Foot Orthosis Characteristics
Name
Manufacturer
Control System
Orthotic Components
Other Characteristics
Stance-control
orthosis
Horton
Little Rock, Ark.
Mechanical
Pushrod and cam system
Thermoplastic stirrup at ankle causes pushrod
to engage cam into friction ring to lock knee
at initial contact unloading in late stance
re-positions Pushrod
to disengage cam from friction ring, allowing
free knee flexion during swing
Dual uprights
Three settings: locked, automatic, unlocked
Lightweight, but bulky
May require larger shoe size to accommodate nested
thermoplastic stirrup and AFO
Most effective at constant walking speed and consistent
stride length (not cadence responsive)
Free Walk
Otto Bock Healthcare
Duderstadt, Germany
Mechanical
Cable driven pawl lock system
Spring-loaded pawl locks the knee when
in full extension during stance
Unit unlocks with dorsiflexion of ankle in late
stance to allow free knee flexion during swing
Single lateral upright with medial cable
Very light weight
Requires full knee extension to engage the lock, although
uprights can be contoured to accommodate up to 10
degrees of knee flexion contracture
Requires at least 5 degrees of mobility at ankle
Requires at least 3⁄5 hip flexion and extension strength
for safe and effective use
Not appropriate for those with varus > 10 degrees
UTX
Becker Orthopedic
Mechanical
Swing Phase
Lock 2
Fillauer
Chattanooga, Tenn.
Mechanical
Gravity-activated pendulum system with
weighted pawl lock
Weighted pawl causes knee to lock when hip
flexion in late swing Moves thigh anterior to
body in preparation for initial contact in
late stance, when thigh is posterior to body,
weight pawl moves to unlocking position
Dual-upright, with SC gravity system in lateral upright
Swing control spring to control/assist knee extension
during swing phase can be incorporated into medial
knee unit
No cables or pushrods
Not effective on stairs, inclines, uneven ground
Four settings controlled by a remote push button
switch: manual lock, manual unlock, automatic,
or free swing
E-Knee




Becker




Microchip




Electromechanical system with pressure
sensitive footplate that feeds information
to micro processor to engage/disengage
locking mechanism

Dual-uprights
Can be used with thermoplastic and laminated materials
Lithium battery must be charged daily
Provides locking in increments of 8 degrees at any angle
of knee flexion at initial contract
No minimum strength or ROM requirements
Load Response


Becker


Mechanical


Spiral torsional spring designed to mimic shock
absorption during loading response

Locking mechanism responsive for 0 to 18 degrees of knee
flexion at initial contract
Not effective for persons with fixed knee flexion contracture
or valgus > 15 degrees

Chapter 9  Principles of Lower Extremity Orthoses
249
GX-Knee
Becker
Mechanical and
pneumatic
Pneumatic spring on lateral joint provides
assistance with knee extension during
swing phase
Does not provide mechanical stability in stance phase
Requires 4⁄5 hip flexion and extension strength for safe use
Full Stride
Becker
Mechanical
Cable-driven system
Requires full-knee extension to engage lock, although uprights
can be contoured to accommodate knee flexion contracture
< 10 degrees
Requires 5 degrees of ankle motion to achieve necessary cable
excursion to operate locking mechanism
Safety Stride
Becker Orthopedic
Mechanical
Cable-driven system
Resists knee flexion in stance regardless of knee angle
No minimum strength or ROM requirements
GX swing assist system can be incorporated
Sensor Walk


Otto Bock Healthcare


Electromechanical


Unidirectional wrap-spring clutch-actuated
by pressure sensors in heel and forefoot and
motion sensor at knee
Heavy-duty custom KAFO
accommodates up to 15 degrees of knee flexion contracture
Powered by lithium-ion battery
Locks knee joint when footplate indicates a stumble
AFO, ankle-foot orthosis; KAFO, knee-ankle-foot orthosis; ROM, range of motion; SC, stance control.
Adapted from Operating instructions for the E-Mag and Free Walk orthosis, Ottobock Germany. Available at:
walk.pdf; Stance Control Overview Guide II, Becker Orthopedic Troy, Mich. Available at: MO25-SPL Manual, Fillauer,
Chattanooga Tenn. Available at: Yakimovich T, Lemaire ED, Kofman J. Engineering design review of stance-control knee-ankle-foot orthoses.
J Rehabil Res Dev. 2009;46(2):257-267.

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Section II  Orthoses in Rehabilitation
enhancing the wearer's sense of well-being.133,134 The major
concerns raised by wearers include ease of donning and
doffing, weight of the orthosis, and cosmesis.133,134
Medially Linked Bilateral KAFO Designs
For persons with mid to low thoracic and lumbar SCI, sev­
eral options have been developed to link a pair of conven­
tional KAFOs in an effort to allow reciprocal gait without
having to brace about the hip in a conventional HKAFO
(Figure 9-27). The Walkabout Orthosis, and the Moorling
Medial Linkage Orthosis, both of which use a single axis
hinge between the two medial uprights of the KAFOs, are
most effective for individuals with some residual volitional
hip flexion who have sufficient thoracolumbar spinal mobil­
ity, especially into lateral flexion.135–137 In both of these sys­
tems, the linkage system limits abnormal abduction of the
limbs during gait. Preparation for swing limb advancement
begins with an exaggerated lateral lean for weight shift onto
the stance limb; the wearer then initiates swing using resid­
ual hip hiking or hip flexion ability. When compared with
reciprocal gait HKAFO (see later), medially linked KAFOs
provided better ability (less assistance required) to accom­
plish sit to stand transitions, but walking speed tended to
be slower, management of inclines more problematic, and
performance on measures of balance somewhat less effec­
tive.138,139 In addition, persons with SCI who wore both
devices over a 3-month period reported that both were use­
ful for standing and there was no functional advantage of
medially linked KAFOs over reciprocal gait HKAFOs in
terms of mobility.140 Hybrid systems, consisting of medially
linked KAFOs and functional electrical stimulation (FES),
have also been used as an approach to improve the ability to
walk for persons with SCI.141
KAFO DELIVERY AND FUNCTIONAL TRAINING
Once fabrication is completed, the orthotist inspects the
KAFO to ensure that selected components work as intended,
that finish work of plastic edges and metal components are
effective, that the placement and contours are appropriate to
the individual's limbs, and that orientation of the axis of the
orthotic ankle and knee match anatomical joint axis. This ini­
tial fitting process not only identifies the fit of the orthosis in
its intended functional upright and weight-bearing positions
but also closely examines potential for soft tissue irritation in
vulnerable areas of the person's skin. Length of the uprights
as well as position and alignment of components are carefully
inspected. The goal is a comfortable standing position, with
no discomfort or skin irritation. If minor problems are iden­
tified, the orthotist often makes simple adjustments of fit and
alignment before functional training. The team then evaluates
the ability of the orthosis to meet the functional goals of the
orthotic prescription.
If the team determines that fit is acceptable and that
orthotic goals (a combination of joint protection, structural
stability, especially in stance, and functional mobility) have
been met, functional training then begins. In most cases,
especially if a patient is new to the use of an orthosis, a wear­
ing schedule is developed, tailored to the patient's specific
needs and physical condition, in which the patient gradually
increases to full-time wear.
Whether the orthosis is of conventional KAFO design or is
a SC-KAFO, physical therapy programs should include:
• exercises to strengthen muscle groups that control hip,
knee, and core (trunk) (concentric, eccentric, and holding
contractions) to maximize ability to use the device;
• practice donning/doffing the device;
• rising to standing and returning to sitting;
• activities to facilitate anticipatory and reactionary postural
control and balance;
• gait training in parallel bars (emphasizing weight accep­
tance in early stance, single limb stability in midstance,
and swing limb clearance), progressing to over-ground
activities, and (for SC-KAFO) on treadmill training to
improve gait speed and other gait kinematics;
• practice on stairs, uneven surfaces, and inclines;
• functional activities in open environments where the indi­
vidual is called upon to adjust speed and avoid obstacles in
relation to others who are moving around within the same
space.
Walking speed would be an appropriate and powerful out­
come indicator for physical therapy intervention.
Training should also focus on developing a clear under­
standing of the fit of the orthosis on the limb, proper
adjustment of stabilizing straps, education about appropri­
ate footwear, and management of the locking mechanisms
and function of the knee unit. Wearers and their caregivers
must understand the care and maintenance of the ortho­
sis, which is a mechanical device with moving parts that
requires regular cleaning and occasional lubrication of its
mechanical parts.
FIGURE 9-27  The Walkabout Orthosis connects a pair of conven­
tional thermoplastic knee-ankle-foot orthoses with a single axis joint
attached to the proximal edge of the medial uprights. (Reprinted with
permission from Middleton JW, Yeo JD, Blanch L, Vare V, Peterson
K, Brigden K. Clinical evaluation of a new orthosis, the `Walkabout,'
for restoration of functional standing and short distance mobility in
spinal paralysed individual. Spinal Cord. 1997;35:574-579.)

Chapter 9  Principles of Lower Extremity Orthoses
251
CASE EXAMPLE 3
An Individual with Poliomyelitis-Related Impairment
T. C., a 63-year-old man who survived acute poliomyelitis as
a 7-year-old, has been living with longstanding atrophy and
weakness of his right lower extremity since that time. Until
recently, he used a conventional KAFO with drop locks to
maintain knee stability in stance. He used a combination of
circumduction of the right lower extremity and vaulting on
the left lower extremity to achieve right swing limb clearance.
In his home, on level surfaces, he is able to ambulate without
assistive device, touching furniture or wall surfaces to occa­
sionally provide additional stability. Until recently, when he
began to have difficulty with back pain, he had been using
either a straight cane or single forearm (Lofstrand) crutch
for mobility outside and for long distances. He recently read
about SC-KAFOs and made an appointment at the orthotic
clinic of a nearby rehabilitation center to determine whether
this would be an appropriate option. He has two goals: (1)
improve his mobility (both quality and distance) and (2)
reduce the intensity of his back pain when walking.
Examination reveals a fairly fit and active man with
marked atrophy of anterior thigh and calf muscles. There
is a 5-degree hip flexion contracture noted bilaterally using
Thomas test, and slightly exaggerated lumbar lordosis is
noted in stance. There is no restriction in knee range of
motion, and all knee ligaments are intact, although there
is mild valgus noted, along with moderate knee hyperex­
tension passively and in stance. No rotational or torsional
deformities are apparent. Ankle dorsiflexion (0 to 7 degrees)
and plantarflexion (0 to 10 degrees) are limited by long­
standing soft tissue tightness.
Right lower extremity muscle performance per MMT is
as follows:
Hip flexion and rotation: 3+/5
Hip extension and abduction: 4/5
Knee extension (quadriceps): 2/5
Knee flexion (hamstrings): 4/5
Dorsiflexion: 3+/5
Plantarflexion: 2+/5
Sensation: exteroception and kinesthesia (vibration)
appear to be intact
Questions to Consider
• What are the major benefits and tradeoffs associated with
a conventional locked-knee KAFO versus a SC-KAFO?
• What are the minimum requirements for muscle strength,
range of motion, and limb alignment that an individual must
have to use the various SC-KAFO designs currently available?
• Is T. C. a suitable candidate for a SC-KAFO? Why or why not?
Which of the SC joints would be most appropriate for him?
Why would you recommend this particular orthotic option?
• Given that T. C. has used a conventional KAFO with a locked
knee for most of his life, what challenges do you expect him
to encounter as he learns to use a SC-KAFO and its improved
mobility? How might you structure a physical therapy exer­
cise and functional training intervention to help him quickly
learn to trust and effectively use his new orthosis?
CASE EXAMPLE 4
An Individual with L1 Traumatic Spinal Cord Injury
K. G. is a 19-year-old woman who sustained traumatic
complete SCI in a motor vehicle accident 3 months ago.
She underwent surgical fusion of T10 to L2 spinal ver­
tebrae and wore a thoracolumbar orthosis for 8 weeks.
She has completed her inpatient rehabilitation, is no
longer required to wear the spinal orthosis, and func­
tions independently indoors in a solid frame wheel­
chair, needing minimal assistance for ramps and curbs.
Her rehabilitation continues on an outpatient basis, and
she wants to “give walking a try.” She is referred to the
Gait & Orthotics Clinic at the rehabilitation center for
evaluation.
At present, K. G. presents with 3/5 hip flexion strength
on the right and 2/5 hip flexion strength on the left. Reflexes
at the knee and ankle are “0” with flaccid paralysis and com­
plete sensory loss below the L1 neurological level. She has
hip and knee flexion contractures of 10 degrees bilaterally.
Skin is intact at the moment, although a grade 3 sacral decu­
bitus ulcer has recently healed. Upper extremity and upper
body strength and flexibility are sufficient for ambulation
with an appropriate assistive device.
Questions to Consider
• What additional information is important for the clinic
team to gather as they prepare to make recommenda­
tions about orthotic options for K. G.? What additional
tests and measures might be important to use?
• Given her current level of function, as well as her lower
motor neuron SCI, what orthotic options are the team
likely to consider for K. G.?
• If the team opts for a KAFO, which design would you rec­
ommend using: conventional thermoplastic KAFO, with
or without FES, a pair of SC-KAFOs, a pair of Craig-Scott
orthoses, a set of linked orthoses such as the Walkabout,
conventional HKAFOs, a parawalker, or hip guidance
orthosis? What are the benefits or tradeoffs of each? Why
have your chosen the orthosis that you are recommending?
• In addition to learning to ambulate with the orthoses,
what additional motor tasks will K. G. have to master to
use them functionally?
• How will the team evaluate the effectiveness and effi­
ciency of K. G.'s ability to walk with the orthoses as she
becomes more adept at using them?

252
Section II  Orthoses in Rehabilitation
WHEN IS AN HKAFO INDICATED?
There is much less evidence available in the clinical research
literature to guide prescription and selection of HKAFOs than
for selecting AFOs and KAFOs. Because HKAFO encompass
the hip, pelvis, and sometimes the trunk, they tend to be much
more cumbersome to use, more challenging to don and doff,
more expensive to fabricate, and require more maintenance
than AFOs and KAFOs. HKAFOs only partially restore func­
tional mobility, often with high energy cost. The additional
control of joint motion achieved by moving proximally with
a hip joint and pelvic band or an attached lumbosacral ortho­
sis must be balanced against the practical challenges that the
wearer will face when using the device.
Persons who use HKAFOs for standing and the limited
mobility that they provide typically have much more neu­
romotor system impairment that those who use AFOs and
KAFOs. These orthoses are most often prescribed for chil­
dren with myelomeningocele and individuals with SCI but
may also be appropriate for those with progressive neuro­
muscular disorders; in effect for any person for whom the
ability to stand may not only enhance function for some func­
tional tasks, but also contribute to bone health, skin integrity,
efficacy of digestion, urinary and bowel health, respiratory
capacity, cardiovascular fitness and exercise response, and
the psychological benefit that that comes from being upright
when interacting with peers.142 Children, with their lower cen­
ter of mass, may not be quite as concerned about the conse­
quences of a fall, but for adults, upright standing in HKAFOs
may be made more challenging by concerns about the poten­
tial to fall, the risk of being injured, or the thought of being
stranded on the ground due to inability to get back up.143
HKAFO DESIGN OPTIONS
As in the case of AFOs and KAFOs, HKAFOs can be fabricated
with many different materials (e.g., metals, thermoplastics,
carbon composites) and orthotic ankle, knee, and hip com­
ponents. Historically, during the years immediately follow­
ing the polio epidemic until the mid to late 1980s, orthotists
fabricated HKAFOs by adding a hip joint and pelvic band to
conventional KAFOs. To better meet the developmental and
educational needs of children with myelomeningocele (spina
bifida), conventional HKAFO designs evolved into standing
frames, parapodiums, and swivel walkers. Building on this,
a number of HKAFOs specifically designed to mechanically
facilitate reciprocal gait were developed to meet the needs of
persons with SCI.
Conventional HKAFOs
Figure  9-28 illustrates the configuration of conventional
HKAFOs. These devices are designed to hold both lower
extremities in a stable extended position for upright stand­
ing; persons wearing this orthosis use either a hop-to gait
with walkers or a swing-through gait with a pair of crutches
for ambulation. On rare occasions, a single HKAFO might
be used for persons with neuromuscular or musculoskeletal
impairment affecting one lower extremity. Even after the
incorporation of lightweight thermoplastic or carbon com­
posite materials, the energy cost of ambulation with con­
ventional HKAFOs is significant and often functionally
prohibitive. With rare exception, HKAFOs are used in the
parallel bars, or on level surfaces with bilateral crutches or
solid frame or reciprocal (nonrolling) walker.
The most distal component of the HKAFO is usually a
solid ankle or dorsiflexion assist articulating ankle AFO.
These are typically set in a few degrees of dorsiflexion to
direct the tibia forward enough that the individual's weight
line falls anterior to the knee and posterior to the hip in
when in tripod standing position with crutches or a walker.
Traditionally, the orthotic knee joint is locked into exten­
sion, although for persons with incomplete SCI capable of
reciprocal gait, a stance control knee joint might be con­
sidered. Thermoplastic thigh cuffs are effective in resist­
ing torsional forces that would otherwise act on the limb in
standing. A variety of commercially available orthotic hip
A
B
FIGURE 9-28  A, Example of a traditional metal and leather hip-
knee-ankle-foot orthosis (HKAFO), with its pelvic band, orthotic
hip joints and locks, proximal and distal thigh bands, orthotic knee
joints and stabilization pads, proximal and distal calf bands, ankle
joints, and stirrups. B, Themoplastic HKAFOs, typically lighter in
weight than conventional HKAFOs, also have a pelvic band and
orthotic hip and knee joints. Because they distribute forces over a
wider thigh and calf band, an anterior knee stabilization pad may
not be necessary. Many incorporate a solid-ankle or articulating
ankle ankle-foot orthosis design, fitting inside the shoe rather than
in an external stirrup.

Chapter 9  Principles of Lower Extremity Orthoses
253
joints include various single axis designs that can be used in
locked position, allow free motion when unlocked, or allow
motion only within a limited range (Figure 9-29). The axis
of motion (center) of the orthotic hip joint must be posi­
tioned just proximal and anterior to the greater trochanter to
best match the anatomical axis of motion of the hip. Because
orthotic hip joints are fixed to the pelvic band and to lateral
uprights of the thigh section, they effectively restrict abduc­
tion/adduction and rotation of the limb as well. Single axis
hip joints meet the needs of most individuals who require
HKAFOs to stand and to ambulate. There are also several
types of dual-axis hip joints with separate mechanical con­
trol systems for flexion/extension and for abduction/adduc­
tion. The proximal pelvic band is positioned between the
trochanter and iliac crest. The pelvic band provides solid
support from a position slightly medial to the anterior supe­
rior iliac spines (ASIS) and around the posterior pelvis. The
pelvic band can be fabricated from metal, laminated compo­
nents, or thick thermoplastic, and is typically closed anteri­
orly by a belt or webbing with Velcro fastener.
For stability in standing, the individual typically stands
in a tripod position, with crutch tips diagonally 12 to 18
inches forward and a slightly exaggerated lumbar lordosis.
This position ensures that the individual's center of gravity
(weight line) falls posterior to the hip joint, creating an exten­
sion moment at the hip, achieving stability by alignment. To
achieve forward motion, the individual uses the “head-hips”
principle with shoulder joints a pivot point. (Figure 9-30)
A quick forceful “pike” (chin tuck and forward inclination of
the trunk) while pushing downward through the handles of
the assistive device elevates the lower extremities from the
ground. This is immediately followed by head, neck, and back
extension to “throw” the lower extremities forward for the
next initial contact. As soon as the feet contact the ground,
the individual quickly advances the crutches to once again
reach the stable “tripod” position.
To effectively use HKAFOs, hip and knee joints of the
lower extremity must be flexible enough to be positioned in
extension. Although exaggerated lumbar lordosis may com­
pensate for mild hip flexion contracture in achieving upright
position, over time and with repeated forceful loading of
swing through gait, this lordosis will likely contribute to
development of disabling low back pain. Prevention of flexion
contracture or deformity of the hips and knees is a key com­
ponent of physical therapy intervention, especially for grow­
ing children with myelomeningocele
Parapodiums, Standing Frames, and Swivel Walkers
This group of HKAFOs emerged to meet the developmen­
tal needs of children with myelomeningocele and cerebral
palsy. As a group, these devices allow a young child to main­
tain upright standing posture and provide limited mobility
for home and classroom use. Many include components to
address alignment and control thoracic spine. Most can be
used without an ambulatory assistive device (i.e., walker or
crutches), allowing individuals to use their hands during
activity. Cost may be lower than for conventional HKAFOs,
because many can be fabricated from commercially available
components and kits.
The simplest in this group of orthoses are standing frames.
Prone standers primarily support the anterior surface of the
body and can be positioned against a counter or table work
surface so that the child can use the upper extremities for
functional activities (Figure 9-31A). Some versions of prone
standers incorporate wheels that children can use to propel
themselves from place to place. Fully upright standing frames
(see Figure 9-31, B) have restraining straps anterior to the
knee and posterior to the pelvis, and provide circumferential
support for the trunk. A lever is used to unlock the orthotic
knee and hip joints of the device so the individual can move
from standing to sitting.
Standers are used for children who are not developmen­
tally ready to walk and for those with impairments so sig­
nificant that the ability to walk is unlikely. Standing frames
are most often prescribed to allow children with significant
mobility impairment to participate in activities typically
done in standing position in school and home settings.144
Some children may fear falling and be reluctant to use full
upright standers. Routine use of standing frames appears
to limit severity of knee and hip flexion contracture, as
A
B
FIGURE 9-29  A, Examples of a single-axis hip joint. A drop lock
holds the hip in extension in standing, but when pulled upward to
disengage, allows free hip flexion for sitting. B, This hip joint allows
controlled flexion and extension within a limited range of motion
while limiting abduction/adduction and rotation.

254
Section II  Orthoses in Rehabilitation
well as decrease level of assistance needed and/or difficulty
­performing transfers and activities of daily living.145 Standing
frames provide an opportunity for children with mobil­
ity impairment to interact with peers at eye level, empow­
ering them to participate more fully in academic and social
activities.
Standing frames have also been adapted and developed for
adults with neuromuscular impairments such as SCI, severe
stroke, traumatic brain injury, and other diseases that com­
promise motor control such that independent standing is
no longer possible. The benefits for adult users are the same
as for children: better physiological function of many body
structures and systems, enhanced ability to perform tasks
usually performed in standing position, and the psychologi­
cal benefits of being upright at one's full height.146–148 Some
specialized wheelchairs (both manual and powered versions)
may have a built-in standing function.149
There are constraints to consider, however, when decid­
ing if standing frames would be appropriate: (1) getting into
and out of a standing frame may require considerable assis­
tance; (2) the frame may not be easily mobile such that it
should be pre-positioned before donning, (3) the frame may
need adjustment or replacement as the child grows, and (4)
the frame may require maintenance, mechanical hydrau­
lic components, or replacement of worn straps and locking
mechanisms.
FIGURE 9-30  Illustration of the head-hips principle in swing through gait using bilateral KAFOs
and lofstrand crutches, with shoulder joints acting as the fulcrum for movement. A, Resting position
is a stable hips forward, shoulders back posture, with a tripod formed by the individuals feet and the
tips of the crutches. B, Mobility is initaited with a quick and forceful chin tuck that C, is combined
with downard pressure through the crutches to unweight the feet. D, A backward head movement
then propels the lower body forward until E, the hips are forward and shoulders back to once again
assume a stable inverted tripod position. Finally F, the individual quickly propels off of the crutches
to move them anteriorly to the stable starting position. (From Sisto SA, et al. Spinal Cord Injuries:
Management and Rehabilitation. St. Louis: Mosby, 2009, p. 388.)

Chapter 9  Principles of Lower Extremity Orthoses
255
The Parapodium (Ontario Crippled Children's Center
in Toronto) and the Swivel Walker (Orthotic Research and
Locomotor Assessment Unit, Oswestry, England), first
introduced in the 1980s, are essentially standing frames
with mobile attachment to a solid base (Figure 9-32).150–152
Limited mobility is achieved by a combination of weight
shifting and arm swing. While both are also available in
adult sizes, they are primarily used for young children with
myelomeningocele and cerebral palsy as an early aid to standing
and mobility.153,154
HKAFOs for Reciprocal Gait
A number of lumbosacral-HKAFO systems have been devel­
oped for persons with high level (above T10 neurological
level) spinal cord dysfunction (congenital and traumatic)
who do not have motor function at the hip or higher. All use
a lateral weight shift from one limb to the other as the basis
for orthotic-assisted reciprocal gait. The hip guidance ortho­
sis (HGO) was developed for children with myelomeningo­
cele at the Orthotic Research and Locomotor Assessment
Unit, Edinburgh, Scotland.155,156 The ORLAU Parawalker
uses similar principles to enable ambulation for adults with
SCI.157 The reciprocating (reciprocation, reciprocal) gait
orthosis (RGO), developed at Louisiana State University
assists walking using a dual cable-driven orthotic system.158
The Advance Reciprocating Gait Orthosis (ARGO) with its
simplified cable system was introduced in the 1990s.159,160
The underlying goal for all of these orthoses was to achieve
mobility with a lower energy cost than expended in a typi­
cal swing through gait pattern.161 Many persons fitted with
these devices use them primarily for exercise or activities
in standing, finding that wheelchairs are more efficient for
mobility tasks.162 The complexity of these systems contrib­
ute to relatively frequent need for adjustment and repair
A
B
FIGURE 9-31  A, Example of a prone standing frame with adjustable angle of inclination. This device
supports the anterior surface of the body to allow a child to work at a counter or table. Safety straps
hold the pelvis and thighs against the anterior supports. B, Standing frame orthosis developed at
Gillette Children's Hospital. The tubular frame has hip and knee joints, allowing the child to transfer
into the device and then raise into standing. The fulcrum of the three-force system used to ensure hip
extension is the broad posterior pelvic pad (at the center, without Velcro straps), with counterforces
delivered by the anterior thoracic corset and the anterior kneepads. (A, Courtesy Rifton Equipment,
Rifton, N.Y.)

256
Section II  Orthoses in Rehabilitation
with consistent use. Individuals who used the devices at
least several times a week over long periods of time were
less likely to develop serious decubitus ulcers or sustain
fractures than their peers who discontinued use of this type
of orthosis.163,164
Hip Guidance Orthosis and Parawalker
The HGO and the ORLEAU Parawalker allow individu­
als with impaired muscle performance (those unable to
accomplish the lifting of body weight needed for swing
through gait pattern with crutches) to “walk” with crutches
with a lateral weight shift (Figure  9-33). The HGO and
Parawalker require the use of an ambulatory assistive
device; training usually begins in the parallel bars and
progresses to over ground level surfaces using a rolling
walker or bilateral Lofstrand crutches. The HGO's orthotic
hip joint is stable when weight is borne through the lower
extremity during stance but allows a pendular swing of
the unweighted extremity for swing clearance. This occurs
because of the rigid support that the HGO provides during
single limb stance, keeping the limbs parallel in the coronal
plane, which enhances swing limb clearance as the oppo­
site limb advances.165,166 In the original evaluation of the
HGO prescribed for children with myelomeningocele, the
ability to sit unsupported (hands free) for extended peri­
ods was the best predictor of successful use of the HGO.156
The Parawalker, similar in design, provides more proximal
support to the thorax and trunk (making it even more
rigid) and uses a smaller orthotic hip joint. Because of its
higher proximal trim line, the Parawalker can be used for
standing and limited mobility (i.e., therapeutic walking)
for persons with SCI at upper thoracic levels.167–169
Reciprocal Gait Orthoses
The LSU RGO, originally designed for children with myelo­
meningocele and now used for adults with traumatic SCI,
extends a pair of thermoplastic KAFOs upward to include
a pelvis and thoracic bands (Figure 9-34); providing rigid
stability for stance, it uses a cable-coupling system to pro­
vide hip joint motion for swing phase.170,171 Its dual cable
system operates by reinforcing extension of the stance limb
as the swing limb flexes forward when unloaded by lat­
eral weight shift. This reciprocal dual cable also reduces
risk of “jack-knifing” during ambulation by preventing
FIGURE 9-33  The hip guidance orthosis, usually worn over cloth­
ing, provides a rigid support system for the stance limb. Advancement
of the swing limb occurs with its unweighting when the patient leans
or shifts laterally onto the stable stance limb.
FIGURE 9-32  A young child with myelomeningocele, upright in
an Orthotic Research and Locomotor Assessment Unit (ORLAU)
swivel walker. The ankles are stabilized in a neutral position against
the footplate, with knees in extension by a padded anterior bar, hips
in extension by a broad pelvic band, and the trunk supported by a
broad chest strap. Some versions have orthotic joints at the knee and
hip that allow the child to sit but lock when the child is assisted into
standing. The child learns to use reciprocal movement of the arms to
shift weight from side to side, alternately advancing one of the swivel
pads under the footplate.

Chapter 9  Principles of Lower Extremity Orthoses
257
both hips from flexing at the same time. Like the HGO and
Parawalker, the RGO requires the person to use an assis­
tive device (rolling walker, bilateral Lofstrand crutches,
bilateral canes), relying on upper extremity motor control
and muscle performance to a large degree to operate the
system. The ARGO is an adaptation of the design, using
a single cable, and engineered to allow standing with uni­
lateral or no upper extremity support.172,173 A prototype for
an adjustable AGRO has been described; this would pro­
vide opportunity for a trial of ambulation with ARGO dur­
ing rehabilitation to assist decision making about capacity
to use the device before a custom ARGO is fabricated.174
There is some evidence that persons with neuromuscu­
lar conditions who consistently use an RGO or ARGO for
therapeutic walking are less likely to develop ­significant
secondary complications (i.e., contractures, decubitus
ulcers, and/or scoliosis) than those with similar conditions
who do not.158
Hybrid Orthoses: Functional Electrical Stimulation
The most recent investigations of reciprocal orthoses for
persons with upper motor neuron SCI have added FES
to HGO/Parawalker and RGO/ARGO designs.175,176 SC
orthotic knee joints (described in the section on KAFOs)
have also been incorporated in hybrid RGO-FES systems, to
afford a more natural pattern of swing limb advancement.177
The major benefit of hybrid RGO-FES systems appears to be
in greater distance covered, lower energy cost (as measured
by physiological cost index), and somewhat faster walking
speed.174–176 It is important to note that, while such hybrid
systems are promising, they do not fully restore the ability to
walk at preinjury levels. Walking speeds with hybrid devices
have been reported to be between 0.20 and 0.45 m/sec, while
limited community walking becomes possible when walk­
ing speed is above 0.6 m/sec, and usual waking speed for
healthy adults ranges from 1.0 to 1.3 m/sec, depending on
height.176–178
IMPLICATIONS FOR REHABILITATION
When the rehabilitation team considers whether an ortho­
sis that would facilitate therapeutic reciprocal walking
would be appropriate for an individual with paralysis, the
costs and benefits need to be weighed carefully. The indi­
vidual and/or their caregivers must clearly understand
that these devices cannot fully restore the ability to walk
at what would be considered community level. They must
explore and embrace the goals of therapeutic walking:
enhancement of bone health, cardiovascular condition­
ing, digestive and urinary health, among others. For many
individuals, gaining the motor skills necessary for safe
use of the device may require substantial time and effort;
training times reported in the literature range from 45 to
80 hours over a period of weeks to months. They must be
ready to adhere to stretching protocols to ensure sufficient
range of motion at hip, knee, and ankle so that the device
will both fit and operate optimally. They must be prepared
to work to improve muscle performance and postural con­
trol of trunk and upper extremities so that they can use the
orthosis most effectively. They must be willing to main­
tain a stable weight so that the orthosis will fit over many
months or years. They must have the postural control nec­
essary to (eventually) don and doff the orthosis without
substantial assistance. They must understand the design of
the orthosis and the function of its components enough
to recognize when maintenance, adjustment, or repair is
necessary. This is quite a bit to commit to; it is often wise
to have the person interested in pursuing use of such an
orthosis interact with someone else who has successfully
used one to get a clear sense of what is required and what
the potential outcomes are.
FIGURE 9-34  The reciprocal gait orthosis uses a dual cable system
to couple flexion of one hip with extension of the other. This cou­
pling assists forward progression of the swing limb while ensuring
stability of the stance limb.

258
Section II  Orthoses in Rehabilitation
CASE EXAMPLE 6
An Adult with Traumatic Spinal Cord Injury
L. F. is a 20-year-old man who sustained multiple gun­
shot wounds to his abdomen during an armed robbery of
the convenience store where he worked. He was airlifted
to a regional level 1 trauma center for initial evaluation.
He underwent several surgeries to repair internal organs,
remove his spleen, and stabilize burst fractures of T-9 to
T-11 vertebral bodies with fusion. Once stable, L. F. was
transferred to a rehabilitation center wearing a TLSO for a
4-week stay. He is now living at home and the TLSO has
been discontinued. L. F. has continued his rehabilitation on
an outpatient basis for the past 3 months. He is independent
in wheelchair mobility on level surface, ramps, and curbs.
He has been actively involved in an FES program using
the ERGYS cycle ergometer for the past 2 months. He has
expressed interest in walking for cardiovascular fitness exer­
cise, perhaps combining an orthosis with FES.
At present, there is no apparent neuromuscular or sen­
sory function below the level of T-9. Deep tendon reflexes
are +3 at knee and +4 at ankle, with occasional spasm of
lower extremities, typically a sign of bladder infection or
skin irritation. Range of motion is within normal limits at
ankle and knee, but there are hip flexion contractures of 10
degrees bilaterally.
Questions to Consider
• What additional information would be important for
the clinic team to gather as they prepare to make rec­
ommendations about orthotic options for L. F.? What
additional tests and measures might be important to
use?
• Given L. F.'s current level of function and his upper
motor neuron deficit, what orthotic options are the
team members likely to consider: KAFO or HKAFO?
Why?
• If the team opts for an HKAFO, which design would
you recommend they use: a conventional thermoplastic
HKAFO with locked hip and knees or an HKAFO that
would allow reciprocal gait? What are the benefits and
tradeoffs of each? Why have you chosen the one that you
are recommending?
• In addition to learning to stand and ambulate with his
new HKAFO, what other motor tasks must L. F. master
to use his orthosis functionally?
• How will the team evaluate the effectiveness and effi­
ciency of the orthosis as L. F. becomes more adept at
using it?
CASE EXAMPLE 5
A Young Child with Myelomeningocele
J. B. is an 18-month-old girl with myelomeningocele at L1
neurological level. Her spinal defect was surgically repaired
the day after her birth. A ventriculoperitoneal shunt was
placed to control hydrocephalus when she was 2 months
old. She has attended a spinal bifida clinic at a regional chil­
dren's hospital, 2 hours from her home, and participated in
a home-based “birth to three” program since birth.
Currently, there is no active contraction of muscle in either
lower extremity and no evidence of withdrawal response to
painful stimuli at or below the L1 dermatome or myotome.
J. B. has consistently worn night splints to prevent plantarflex­
ion contractures at the ankle. At 14 months of age, she sus­
tained a midfemoral fracture while playing on the floor with
her brothers; the fracture was managed by immobilization in
a spica cast for 6 weeks. She has developed soft tissue tightness
such that her lower extremities are in a somewhat abducted
and externally rotated position at the hip. Knee range of
motion is sufficient for sitting and supported standing.
J. B.'s primary means of mobility is by an upper extrem­
ity powered commando crawl when playing with her brothers
and similar-aged peers. For longer distances, she is wheeled
in a stroller by a family member. Recently, her behavior sug­
gests she is frustrated by her inability to pull into standing and
her limited mobility. Her family and therapists have returned
to the spina bifida clinic for evaluation of her readiness for
orthotic intervention that would allow her to stand and walk.
Questions to Consider
• What additional information would be important for
the clinic team to gather as they prepare to make rec­
ommendations about orthotic options for J. B.? What
additional tests and measures might be important to
use?
• Given her current level of function and her lower motor
neuron deficit, what orthotic option is the team likely to
consider: KAFO or HKAFO? Why?
• If the team opts for an HKAFO, which design would
you recommend: a thermoplastic HKAFO, standing
frame, parapodium, swivel walker, or HKAFO designed
for reciprocal gait? What are the benefits and tradeoffs
of each? Why have you chosen the one you are recom­
mending for J. B.?
• In addition to learning to stand and perhaps to ambu­
late with her HKAFO, what other motor tasks will J.
B. and her family have to master to use the HKAFO
functionally?

Chapter 9  Principles of Lower Extremity Orthoses
259
OUTCOME MEASURES IN ORTHOTIC
REHABILITATION
How do the health care team, the individual using an ortho­
sis and their caregivers, and the payers of the health care sys­
tem determine successful use of a lower extremity orthosis,
whether it be as simple as a UCBL insert for a child with mild
diplegic cerebral palsy, an adult using an articulating AFO,
a person with postpolio syndrome using a SC-KAFO, or a
person with SCI using an ARGO? Initial criteria to consider
might include:
• Can the person don and doff the orthosis independently?
• Does the person understand how the orthosis should fit on
the limb, and can the person recognize signs that fit may
not be appropriate (especially for growing children and for
adults with peripheral or central sensory impairment)?
• Can the person transition from sitting to standing and back
to sitting safely, independently, and with reasonable effort?
• Does the person have sufficient postural control to use the
device not only on level nonresistant surfaces (e.g., tile or
wood floors) but also on other surfaces (e.g., carpet, grass,
inclines, stairs), which are likely to be encountered in the
course of daily life?
• Children often play on the floor, and adults are often quite
concerned about being stranded on the floor if they fall.
Can the person transition from the floor to standing safely,
independently, and with reasonable effort? If not, can the
person direct those who would offer assistance?
• Does the person know how to manage his or her body and
assistive devices in case of a fall?
• Does the person understand the care and maintenance
requirements of the device?
These questions, while ensuring that the individual is able
to use the orthosis safely, do not sufficiently address the effi­
cacy of the orthosis in enhancing the individual's ability to
walk. While observational gait analysis might allow the ortho­
tist and physical therapist to evaluate changes an orthosis
effects at each subphase of the gait cycle, this description
of the quality of walking is not enough evidence to justify
orthotic intervention. The ceiling effects and poor ecological
validity of the distance criteria for independent locomotion
of measures such as Functional Independence Measure are
likewise insufficient.179 A variety of outcome measures must
be used to address efficacy of an orthosis and the physical
therapy intervention that facilitates its use.
Walking Speed
Probably the most robust indicator of the ability to walk is
walking (gait) speed. Although technology such as motion
analysis and the GAITRite system provide precise data about
gait velocity, walking speed can be quickly and easily captured
using a stopwatch over a known distance.178,180 There is clear
evidence for validity, reliability, and responsiveness of walk­
ing speed (measured over 10 m or over 4-m distances), as well
as information about typical walking performance values, and
criteria for limited versus full community ambulation ability
for most of the medical diagnoses in which a lower extremity
orthosis may be prescribed (stroke, SCI, cerebral palsy, trau­
matic brain injury, among others).181–189 Documenting com­
fortable and maximum walking speed at intervals without and
with the orthosis at time of delivery, and change in walking
speed over the course of physical therapy intervention, along
with discussion of the change in walking speed with respect to
age-base and disease-reference norms provide powerful infor­
mation about efficacy of intervention.
Endurance During Walking
The ability to sustain walking over a period of time is also a key
outcome of orthotic and physical therapy intervention. The
most frequently used measure of endurance while walking
is the 6-minute walk test (6 MW), in which the distance that
an individual walks (with rests as needed) during a 6-minute
period is measured. Originally developed for persons unable
to perform treadmill or cycle ergometer stress tests because
of congestive heart failure, the 6 MW has been used for many
of the groups of patients who would benefit from orthoses.190
Clinometric properties of the 6 MW have been evaluated
for persons with stroke, SCI, cerebral palsy, traumatic brain
injury, myelomeningocele, and chronic poliomyelitis.191–196
A self-report indicator of effort of physical activity that
has also been used extensively in the clinical research liter­
ature is Rating of Perceived Exertion (RPE). In his original
work, Borg presented a scale ranging from 6 (no effort) to 20
(maximum effort)197; a modified version, which uses a 1 to
10 scale (for adults) or color-coded schematic pictures of the
face (for children and those with cognitive dysfunction) may
be more interpretable for patients.198,199 The question that use
of RPE scale addresses is, “Does the orthosis reduce the per­
ceived work (effort) of walking?” RPE scales have been used
to assess efficacy of therapeutic intervention for persons with
stroke, brain injury, SCI, and cerebral palsy.176,200–202
Mobility and Balance While Walking
The ability to change direction and transition between sur­
faces (i.e., sit to stand) is also a key aspect of successful use
of a lower extremity orthosis. During the Timed Up-and-Go
(TUG) test, an individual must rise from a seated position,
walk forward over a 10-m distance, turn around, walk back
to the chair, and return to sitting, either at a usual pace or as
quickly as safely able.203 Because most lower extremity ortho­
ses constrain joint movement, and many of those who use
them have neuromuscular impairments that place them at
risk for falling, the TUG may provide a snapshot of dynamic
postural control during walking with an orthosis. The TUG
has been successfully used to assess functional status and
predict outcomes in persons with stroke, in children with
cerebral palsy, brain injury, and myelomeningocele, and in
persons with SCI.193,204–209
SUMMARY
This chapter explores the biomechanical design and compo­
nent options of lower extremity orthoses used to facilitate the
ability to walk for persons with a variety of neuromuscular

260
Section II  Orthoses in Rehabilitation
impairments, and at various ages and developmental stages
of the life span. We have discovered that no orthosis can
make walking “normal,” although an appropriate orthosis
can make walking more functional and less energy costly.
We now can evaluate how an orthosis will impact each of
the rockers of stance phase, as well as the ability to clear
the limb during swing phase. We now have ideas about how
footwear, such as an athletic shoe that provides a cushion
heel and a rocker bottom, may compensate if an orthosis
limits forward progression over the foot during stance. We
have discovered that the selection of an appropriate ortho­
sis involves input from many members of the rehabilita­
tion team, not the least being the person who will wear the
orthosis and his or her caregivers. We certainly have gained
an appreciation that there is no “one size fits all” when it
comes to choosing an orthosis, but that orthotic prescrip­
tion requires thoughtful deliberation about both the func­
tional benefits and tradeoffs, as well as the financial cost of
the device. We have learned that using an orthosis effec­
tively requires much more than simply putting it on; there
must be adequate time filled with appropriately challeng­
ing activities so that motor practice can build skill, postural
control, and endurance necessary for functional walking.
Finally, we have begun to consider strategies to assess out­
comes of orthotic and physical therapy interventions for
persons who require an AFO, KAFO, or HKAFO to accom­
plish their mobility goals.
ACKNOWLEDGMENTS
The author would like to recognize professional colleagues
Robert S. Lin, CPO (Director of Pediatric Clinical Services
and Academic Programs, Hanger Orthopedic Group at the
Connecticut Children's Medical Center, Hartford, Conn.),
Thomas V. DiBello, BS, CO (President, Dynamic Orthotics
and Prosthetics, Inc., Houston, Texas), and James H.
Campbell, PhD, CO (Director of Research and Development,
Engineering and Technical Services, Becker Orthopedic,
Troy Mich.), whose excellent chapters on ankle-foot orthoses,
knee-ankle-foot orthoses, and hip-knee-ankle-foot orthoses
in the previous editions of this text provided a solid founda­
tion for the this integrative chapter.
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266
10
MOVEMENT IMPAIRMENT IN NEUROLOGICAL
AND NEURNEUROMUSCULAR PATHOLOGY
Pathologies of the neuromuscular system manifest in a
sometimes confusing array of clinical signs and symp­
toms. To select the most appropriate therapeutic interven­
tion, be it exercise to promote neuroplasticity and recovery,
­functional training, or the use of various orthoses and
assistive devices to accommodate for impairment of a body
system or structure, the clinician must develop a strategy
to “classify” the movement disorder that has produced
the observed impairments and functional limitations.1
The clinician must understand the medical prognosis and
potential progression of the disease process, as well as the
lifestyles and risk factors that might contribute to second­
ary impairments that limit function over time (even if the
disease is “nonprogressive”) and their impact on the indi­
vidual's growth and development.1–3
Health professionals use a number of organizational
strategies as frameworks for decision making during reha­
bilitation of individuals with pathologies leading to neu­
romuscular dysfunction. Many neurologists use a medical
differential diagnosis process to locate the lesion as being
within the central nervous system (CNS) or involving struc­
tures of the peripheral nervous system (PNS) or the muscle
itself.4 They do this by triangulating evidence gathered by
examining tone and deep tendon reflexes, observing pat­
terns of movement and postural control, and looking for
specific types of involuntary movement.5,6 They may also
interpret results of special tests such as nerve conduction
studies, electromyography (EMG), computed tomography
(CT), and magnetic resonance imaging (MRI).7,8 These tests
might pinpoint areas of denervation, ischemia, or demyelin­
ization and help the health professionals arrive at a medical
diagnosis.
Rehabilitation professionals are most interested in the func­
tional consequences associated with the various neuromotor
conditions. They examine the ways in which abnormal tone
(hypertonicity—excessive tone; hypotonicity—insufficient
tone; or flaccidity—absence of tone) affects mobility and loco­
motion, postural control, motor planning and motor control
during movement, coordination (error control), and muscle
performance during functional activities.9,10 Rehabilitation
professionals are not only concerned about function at the
present time but also consider the long-term impact of neu­
romotor impairment on the person's joints and posture, espe­
cially in children who are growing with abnormal tone and
postures.11,12
Orthotic Decision Making in Neurological and Neuromuscular
Disease
Michelle M. Lusardi and Donna M. Bowers
10
LEARNING OBJECTIVES
On completion of this chapter, the reader will be able to:
1. Describe the contribution of the major components of the
central nervous system (CNS) and the peripheral nervous
system (PNS) to functional, goal- directed movement.
2. Describe the impact of CNS and PNS pathologies com­
monly encountered in physical therapy and orthotic
practice on functional, goal-directed movement.
3. Explain the continuum of muscle tone and of muscle per­
formance and their interactive effect on goal-directed,
functional movement.
4. Describe the characteristics of muscle tone in the CNS
and PNS pathologies most commonly encountered in
physical therapy and orthotic practice and how altered
tone impacts on functional movement.
5. Describe the contributions of various CNS and PNS compo­
nents to, and key determinants of, effective postural control.
6. Describe the contributions of various CNS components
to, and key determinants of, mobility and coordination
during functional activity.
7. Discuss the roles of orthopedic and neurosurgical pro­
cedures, central and peripherally acting pharmacological
agents, and various orthotic options for the management
of hypertonicity.
8. Describe strategies used by rehabilitation professionals to
reduce the risk of developing secondary musculoskeletal
impairments in persons with hypertonicity.
9. Plan a strategy for examination and evaluation of persons
with CNS and PNS dysfunction to determine the need
for an orthosis or adaptive equipment.
10. Describe a strategy for clinical decision making in the
selection of an appropriate orthosis for individuals with
neurological and neuromuscular pathologies.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
267
This chapter considers the ways that key components of
the CNS and PNS contribute to functional movement. We
explore the concepts of muscle tone and muscle performance,
considering how their interaction influences an individual's
ability to move. We investigate how abnormalities of tone
resulting from CNS and PNS pathologies are described in
clinical practice. We consider the determinants of postural
control and of coordination and how CNS and PNS pathol­
ogies might lead to impairments of balance and movement.
We provide an overview of the ways that commonly encoun­
tered CNS pathologies impact muscle tone, muscle perfor­
mance, postural control, movement, and coordination as a
way of understanding how an orthosis or adaptive equipment
might help improve an individual's ability to walk and par­
ticipate in meaningful activities and roles. We consider how
the physical therapy examination contributes to the determi­
nation of a need for an orthosis or adaptive equipment. We
also explore the clinical decision-making process by asking
key questions about how an orthosis might help (or hinder)
function. Finally, we apply what we have learned using five
clinical cases to develop orthotic prescriptions.
DIFFERENTIAL DIAGNOSIS: WHERE IS THE
PROBLEM?
Most neurological and neuromuscular diseases affect either
the CNS or the PNS; only a few diseases, such as amyo­
trophic lateral sclerosis, affect both CNS and PNS. Diseases
of the CNS and of the PNS may contribute to motor or sen­
sory impairment; however, there are patterns and character­
istics of dysfunction that are unique to each. Selection of the
appropriate orthosis, seating/wheelchair system, or assistive
devices is facilitated when the therapist, orthotist, members
of the rehabilitation team, patient, and patient's family under­
stand the normal function and consequences of the disease
process of the neurological subsystem that is affected.
The Central Nervous System
The CNS is a complex of dynamic and interactive subsys­
tems that mediates purposeful movement and postural con­
trol, vital autonomic vegetative and physiological functions,
and learning of all types.13 Readers are encouraged to refer
to a recent neuroanatomy or neuropathology textbook to
refresh their understanding of CNS structure and function.
Knowledge of the roles of various CSN structures and their
interactions (for perception, problem solving, motor plan­
ning, and coordination) is foundational for clinical decision
making when considering orthoses for individuals with neu­
romuscular dysfunction.
Some diseases affect a single CNS system or center (e.g.,
Parkinson's disease affects the function of the basal ganglia
in regulating agonist/antagonist muscle activity; a lacunar
stroke in the internal capsule may interrupt transmission only
within the pyramidal/corticospinal pathway) leading to a spe­
cific array of signs/symptoms characteristic of that system or
center. Other pathologies disrupt function across several sys­
tems: a thromboembolic stroke in the proximal left middle
cerebral artery may disrupt volitional movement and sensation
of the right side of the body, as well as communication and vision.
Several exacerbations of multiple sclerosis (MS) may lead to
plaque formation in the cerebral peduncles/pyramidal system,
superior cerebellar peduncle/error control system, restiform
body/balance system, and fasciculus gracilis/lower extremity
sensation; in this case, it can be challenging but imperative to
sort through the various types of impairments that may result
in order to select the most appropriate therapeutic or orthotic
intervention for the individual.
Pyramidal System
The pyramidal system is responsible for initiation of voli­
tional movement and plays a major role in the development
of skilled and manipulative activities. The cell bodies of pyra­
midal neurons are located in the postcentral gyrus/primary
motor cortex. The motor cortex in the left cerebral hemi­
sphere influences primarily the right side of the body (face,
trunk, and extremities); the right cortex influences the left
body. The axons of pyramidal neurons form the corticobul­
bar and corticospinal tracts, projecting toward α motor neu­
rons in cranial nerve nuclei and anterior horn of the spinal
cord. To reach their destination, these axons descend through
the genu and posterior limb of the internal capsule, the cere­
bral peduncles, the basilar pons, the pyramids of the medulla,
and finally the opposite lateral funiculus of the spinal cord.
A lesion at any point in the pyramidal system has the poten­
tial to disrupt volitional movement. The degree of disruption
varies with the extent and functional salience of the struc­
tures that are damaged, manifest on a continuum from mild
weakness (paresis) to the inability to voluntarily initiate and
direct movement (paralysis).
Immediately following insult or injury of the pyramidal
system, during a period of neurogenic shock, there may be
substantially diminished muscle tone and sluggish or absent
deep tendon reflexes.14 As inflammation from the initial
insult subsides, severely damaged neurons degenerate and
are resorbed, while minimally damaged neurons may repair
themselves and resume function.15,16 The more neurons that
are destroyed, the greater the likelihood that hypertonicity
will develop over time due to the altered balance of descend­
ing input of pyramidal and extrapyramidal systems. As the
recovery period continues, individuals may begin to move in
abnormal synergy patterns whenever volitional movement is
attempted.17,18 When the damage to the system is less exten­
sive, individuals may eventually recover some or all volitional
motor control; the more extensive the damage to the system,
the more likely there will be residual motor impairment.15,18
Extrapyramidal System
The extrapyramidal system is made up of several subcortical
subsystems that influence muscle tone, organize patterns of
movement from among the many possible movement strat­
egies, and make both feedforward adjustments (in anticipa­
tion of movement) and refining feedback adjustments (in
response to sensations generated as movement occurs) dur­
ing performance of functional tasks.19 The motor planning

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Section II  Orthoses in Rehabilitation
subsystem is a series of neural loops interconnecting the
premotor and accessory motor cortices in the frontal lobes,
the nuclei of the functional basal ganglia (caudate, putamen,
globus pallidus, substantia nigra, subthalamus), and several
nuclei of the thalamus. Damage to the premotor and acces­
sory motor cortex leads to apraxia, the inability to effectively
sequence components of a functional task and to understand
the nature of a task and the way to use a tool in performance
of the task.20 If there is damage to the caudate and putamen
(also called the corpus striatum), underlying muscle tone may
fluctuate unpredictably (athetosis) and involuntary dancelike
movements (chorea) are likely to occur.21 Damage to the sub­
thalamic nuclei can lead to forceful, often disruptive, invol­
untary movement of the extremities (ballism) that interrupts
purposeful activity.22 Damage to the substantia nigra char­
acteristically leads to resting tremor, rigidity of axial and
appendicular musculature (hypertonicity in all directions),
and bradykinesia (difficulty initiating movement, slow move­
ment with limited excursion during functional tasks), which
are most commonly seen in persons with Parkinson's dis­
ease.23 Motor impairments resulting from damage to the ven­
tral anterior nucleus and related thalamic nuclei are less well
understood but may contribute to less efficient motor plan­
ning, especially when the individual is learning or perform­
ing novel tasks.24
Extrapyramidal structures influence muscle tone and
readiness to move via a network of interconnections among
motor centers in the brainstem. The reticulospinal tracts,
originating in the lower pons and medulla, are thought to
influence tone by acting on γ motor neurons and their associ­
ated muscle spindles. They play a major role in balancing the
stiffness required for antigravity position and the flexibility
necessary for movement of the limbs through space during
functional activity and are likely the effectors for tonic hind­
brain reflexes.19,25 The vestibulospinal tracts, also originating
from the pons and medulla, influence anticipatory postural
adjustment in preparation for movement and reactionary
postural adjustments as movement occurs. These tracts are
thought to be the “effectors” for postural control and bal­
ance.19,26 The tectospinal tracts, originating in the collicular
nuclei of the dorsal midbrain, influence linkages between the
head and extremities (especially arms and hands) so that the
visual and auditory systems can be used effectively to orient
the head and body during tasks that require visual (eye-hand)
and auditory (ear-hand) guidance.16,27
Coordination Systems
The error control, or coordination subsystem, has several
interactive components.28 Feedforward information (how
movement is likely to occur) from the forebrain's motor cor­
tex is relayed through the thalamus to the deep nuclei of the
cerebellum via the middle cerebellar peduncle (brachium
pontis). Feedback information generated by movement trav­
els from the muscle spindle and anterior horn of the spinal
cord via the inferior cerebellar peduncle (restiform body), as
does sensory information from static and dynamic vestibu­
lar receptors (head position and movement in space) and
the vestibular nuclei in the brainstem. Through interaction
of Purkinje cells in the cerebellar cortex and neurons in the
deep cerebellar nuclei, the cerebellum judges how “in sync”
these various types of information are (essentially asking the
questions, “Did the movement occur as planned? Was the
outcome of the movement as intended?”) and suggests refine­
ments for more precise and coordinated movement.29 These
adjustments are relayed to the red nucleus in the midbrain via
the superior cerebellar peduncle (brachium conjunctiva) and
are forwarded back to the thalamus and the motor cortex, as
well as to the spinal cord via the rubrospinal tract. The rubro­
spinal tract is thought to be essential for refinement and cor­
rection of direction and control of movement as it occurs.29
Somatosensory and Perceptual Systems
The somatosensory system is composed of a set of ascend­
ing pathways, each carrying a specific sensory modality from
the spinal cord and brainstem to the thalamus and post­
central gyrus of the cerebral cortex, reticular formation, or
cerebellum. The anterolateral (spinothalamic) system car­
ries exteroceptive information from mechanoreceptors that
monitor protective senses (e.g., pain, temperature, irritation
to skin and soft tissue).30 This tract originates in the dorsal
horn (substantia gelatinosa) of the spinal cord and the spi­
nal trigeminal nucleus, crosses the midline of the neuraxis to
ascend in the lateral funiculus of the spinal cord to the con­
tralateral ventral posterior thalamus, and then continues to
the postcentral gyrus. The dorsal column/medial lemniscus
carries information from encapsulated receptors that serve
as internal monitors of body condition and motion.31 This
tract ascends from the spinal cord to reach the nuclei gracilis
and cuneatus in the medulla of the brainstem, then crosses
midline to ascend to the contralateral ventral posterior thal­
amus and on to the posterior central gyrus. The postcentral
gyrus (somatosensory cortex) is organized as a homunculus,
with each region of the body represented in a specific area.32
Sensation from the lower extremities (lumbosacral spinal
cord) is located at the top of the gyrus near the sagittal fis­
sure. Moving downward toward the lateral fissure, the next
area represented is the trunk (thoracic spinal cord), followed
by upper extremities and head (cervical spinal cord), and
finally face, mouth, and esophagus (trigeminal nuclei) just
above the lateral fissure. A lesion such as an MS plaque in
one of the ascending pathways may result in a discrete area of
loss of exteroception or of conscious proprioception in one
area of the body; a lesion on the somatosensory cortex can
lead to a more profound, multimodality impairment on the
opposite side of the body.
Although sensory information is logged in at the postcen­
tral gyrus, the location of the somatosensory cortex, inter­
pretation and integration of this information occurs in the
somatoperceptual system in the parietal association areas,
with specialization in the right hemisphere.32 These associa­
tion areas give meaning to the sensations that are generated
as people move and function in their environments. This is
where people understand the relationships among their var­
ious extremities and trunk (body schema), as well as their

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
269
­relationship to and position within our physical environment.
Damage to the parietal lobes leads to problems ranging from
left-right confusion to the inability to recognize and monitor
the condition of a body part (neglect, agnosia), depending on
how much of the association area is involved.33,34
Visual and Visual-Perceptual Systems
The visual system begins with processing of information
gathered by the rods and cones in the multiple layers of spe­
cialized neurons in the retina, located in the posterior cham­
ber of the eye. Axons from retinal ganglion cells are gathered
into the optic nerve, which carries information from that eye
toward the brain. At the optic chiasm there is reorganization
of visual information, such that all information from the left
visual field (from both eyes) continues in the right optic tract
and that from the right field continues in the left tract. This
information is relayed, through the lateral geniculate body of
the thalamus, via the optic radiations, to the primary visual
cortex on either side of the calcarine fissure of the midsagit­
tal occipital lobe.35 Damage to the retina or optic nerve results
in loss of vision from that eye. Damage to the optic chiasm
typically leads to a narrowing of the peripheral visual field
(bitemporal hemianopsia); a lesion of one of the optic tracts
or radiations leads to loss of part or all of the opposite visual
field (homonymous hemianopsia). Damage to the visual cor­
tex can result in cortical blindness, in which visual reflexes
may be intact but vision is impaired.36
Visual information is interpreted in the visual association
areas in the remainder of the occipital lobe.37 The visual asso­
ciation areas in the left hemisphere are particularly important
to interpretation of symbolic and communication informa­
tion, while spatial relationships are of more interest in the
right hemisphere. Specific details about the environment,
especially about speed and direction of moving objects with
respect to the self and of the individual with respect to a rela­
tively stationary environment, are important contributors to
functional movement and to the development of skilled abili­
ties.38 Interconnections between the parietal and occipital
association areas serve to integrate visual and somatic/kines­
thetic perception and provide important input to motor plan­
ning and motor learning systems.39
Effective visual information processing is founded on
three interactive dimensions: visual spatial orientation, visual
analysis skills, and visual motor skills.40 Developmentally,
visual spatial orientation includes spatial concepts used to
understand the environment, the body, and the interaction
between the body and environment that are part of func­
tional activity (e.g., determining location or direction with
respect to self, as well as respect to other objects or persons
encountered as people act in their environment). Visual anal­
ysis skills allow people to discriminate and analyze visually
presented information, identify and focus on key character­
istics or features of what people see, use mental imagery and
visual recall, and respond or perceive a whole when presented
with representative parts. The visual motor system links what
is seen to how the eyes, head, and body move, allowing one
to use visual information processing skills during skilled,
purposeful ­activities. This also provides the foundation for
fine manipulative skills requiring eye-hand coordination.37
Executive Function and Motivation
The ability to problem solve, consider alternatives, plan and
organize, understand conceptual relationships, multitask, set
priorities, and delay gratification, as well as the initial com­
ponents of learning are functions of the frontal association
areas of the forebrain.41,42 These dimensions of cognitive func­
tion are often described by the phrase higher executive func­
tion. Quantitative and other analytical skills are thought to
be primarily housed in the frontal association areas of the
left hemisphere, while intuitive understanding and creativ­
ity may be more concentrated in the right hemisphere. Most
people tap the resources available in both hemispheres (via
interconnections through the corpus callosum) during daily
life, although some may fall toward one end or another of the
analytical-intuitive continuum. Individuals with acquired
brain injury involving frontal lobes often exhibit subtle defi­
cits that have a significant impact on their ability to function
in complex environments, as well as under conditions of high
task demand; difficulty in these areas certainly compromises
functional efficiency and quality of life.43,44
The neuroanatomical structures that contribute to the
motivational system include the nuclei and tracts of the lim­
bic system, prefrontal cortex, and temporal lobes; all play
major roles in managing emotions, concentration, learn­
ing, and memory.45 The motivational system not only has
an important impact on emotional aspects of behavior but
also influences autonomic/physiological function, efficacy
of learning, interpretation of sensations, and preparation for
movement (Figure  10-1).46 Dimensions of limbic function
that influence motivation and the ability to manage chal­
lenges and frustration include body image, self-concept, and
self-worth as related to social roles and expectations, as well
as the perceived relevance or importance (based on reward or
on threat) of an activity or situation.47,48 Central set is a phrase
used to describe the limbic system's role as a motivator and
repository of memory on readiness to move or act.46 Central
set helps people predict movement needs relevant to a given
situation or circumstance (considering both the physical and
affective dimensions of the environment in which they are
acting) from past experience.49
Consciousness and Homeostasis
The ability to be alert and oriented when functioning in a
complex environment is the purview of the consciousness
system and is a function of interaction of the brainstem's
reticular formation, the filtering system of thalamic nuclei,
and the thought and problem solving that occur in the asso­
ciation areas of the telencephalon, especially in the frontal
lobes.50 The reticular activating system, found in the inferior
mesencephalon and upper pons of the brainstem, is the locus
of sleep-wake and level of alertness.51 The thalamus and the
reticular formation help people habituate to repetitive sen­
sory stimuli while they focus on the type of sensory informa­
tion that is most germane to the task at hand.52 The frontal

270
Section II  Orthoses in Rehabilitation
Interconnections between Sensory, Limbic, and Motor Systems
Limbic System
Motivational Centers
Olfactory cortex
Septal area
Entorhinal
Olfactory pathway
Olfactory tract
Olfactory bulb
Visual
association
Brodmann’s (18,19)
Angular gyri (39)
Visual pathway
Visual cortex (17)
Optic radiations
LGB
Optic tract
Optic chiasm
Optic nerve
Retina
Auditory
association
Wernicke’s (40,42)
Angular gyri (39)
Sensory stimulus
Information from environment
Information generated by movement
Intrafusal muscle activation
Extrafusal muscle activation
Smooth muscle behavior
Task-specific motor behaviors
Auditory path
Auditory cortex (41)
MGB
Inferior colliculus
Lateral lemniscus
Superior olive N.
D & V cochlear N
8th CN & cochlea
Primary motor cortex
(4)
Motor planning cortex (6)
&
Functional basal ganglia
Extrapyramidal systems
Reticulospinal tracts (tone)
Vestibulospinal tracts
(equilibrium/postural control)
Rubrospinal tracts
(error control)
Tectospinal tracts
(head-body coordination)
Gamma motor neurons
Pyramidal
system
Corticospinal
tracts
Apha motor
neurons
(esp. distal
extremity)
Muscle
Red nucleus
Cerebellum
Vestibular nuc.
8th CN
SSC, S&U
DSCT (actual)
VSCT (intended)
Muscle spindle
Med
Lemniscus
N Gracilis (LE)
N Cuneus (UE)
Dorsal columns
Anterior-lateral
Spinothalamic
(exteroception)
SC lat.
Funiculus
Somatosensory association
Parietal lobe (5,7)
Somatic sensory pathways
Postcentral gyrus (3,1,2)
VPL & VPM
Amygdala
&
Hypothalamus
Brainstem
Parasympathetic
Thoracic
Sympathetic
Lumbosacral
Parasympathetic
Peripheral
Autonomic ganglia
Motor centers
FIGURE 10-1  A conceptual model of the interactions and interconnections among sensory, limbic, and motor systems that influence functional movement.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
271
association areas add content to one's consciousness: the abil­
ity to reason and to adapt to challenges encountered as one
moves through daily life.53 Alteration in quality and level of
consciousness and behavior are indicators of evolving prob­
lems within the CNS.54 Increasing intracranial pressure, the
result of an expanding mass or inflammatory response fol­
lowing trauma or ischemia, may be initially manifest by con­
fusion or agitation; progression into a state of lethargy, stupor,
or unresponsiveness (coma) indicates deteriorating compro­
mise of the CNS structures.55
Homeostasis and the ability to respond to physiological
stressors are functions of the components of the autonomic
nervous system.56 The nuclei of the hypothalamus serve as the
command center for parasympathetic and sympathetic ner­
vous system activity via projections to parasympathetic cra­
nial nerve nuclei in the brainstem, the sympathetic centers
of the intermediate horn in the thoracic spinal cord, and the
parasympathetic centers in the lumbosacral spinal cord. The
hypothalamus has extensive interconnections with the lim­
bic system, bridging physiological and emotional/psychologi­
cal aspects of behavior and activity.57 The hypothalamus also
integrates neural-endocrine function through interconnec­
tions with the pituitary gland.58 Clearly, this relatively small
area of forebrain plays a substantial integrative role in physi­
ological function of the human body. Damage or dysfunction
to this area therefore has significant impact on physiological
stability and stress response.
Peripheral Nervous System
The PNS serves two primary functions: to collect informa­
tion about the body and the environment and to activate
muscles during functional activities. Afferent neurons col­
lect data from the various sensory receptors distributed
throughout the body and transport this information to the
spinal cord and brainstem (sensory cranial nerves) for initial
interpretation and distribution to CNS centers and structures
that use sensory information in the performance of their var­
ious specialized roles.33 The interpretation process can have a
direct impact on motor behavior at the spinal cord level (e.g.,
deep tendon reflex) or along any synapse point in the sub­
sequent ascending pathway (e.g., righting and equilibrium
responses) as sensory information is transported toward its
final destination within the CNS.59 Efferent neurons (also
described as lower motor neurons or, more specifically, α and
γ motor neurons) carry signals from the pyramidal (volun­
tary motor) and extrapyramidal (supportive motor) systems
to extrafusal/striated and intrafusal (within muscle spindle)
muscle fibers that direct functional movement by enacting
the CNS's motor plan.26,60,61
The cell bodies of these α and γ motor neurons live in the
anterior horn of the spinal cord and in cranial nerve somatic
motor nuclei. In the spinal cord, α and γ axons project through
the ventral root, are gathered into the motor component of
a spinal nerve, and (in cervical and lumbosacral segments)
are reorganized in a plexus before continuing toward the tar­
geted muscle as part of a peripheral nerve. In the brainstem, α
and γ axons project to target muscles via motor cranial nerves
(oculomotor, III; trochlear, IV; motor trigeminal, V; abdu­
cens, VI; facial, VII; glossopharyngeal, IX; spinal accessory,
XI; hypoglossal, XII).62 When α and γ axons reach their target
set of muscle fibers (motor unit), a specialized synapse—the
neuromuscular junction—triggers muscular contraction.63
Pathologies of the PNS can be classified by considering
two factors: the modalities affected (only sensory, only motor,
or a combination of both) and the anatomical location of the
problem (at the level of the sensory receptor, along the neu­
ron itself, in the dorsal root ganglion, in the anterior horn,
at the neuromuscular junction, or in the muscle itself).64,65
Poliomyelitis is the classic example of an anterior horn cell
disease; Guillain-Barré syndrome is a demyelinating infec­
tious-autoimmune neuropathy that impairs transmission
of electrical impulses over the length of motor and sensory
nerves. The polyneuropathy of diabetes (affecting motor, sen­
sory, and autonomic fibers) is the classic example of a meta­
bolic neuropathy. Radiculopathies (e.g., sciatica) result from
compression or irritation at the level of the nerve root, while
entrapment syndromes (e.g., carpal tunnel) are examples of
compression neuropathies over the more distal peripheral
nerve. Myasthenia gravis, tetanus, and botulism alter func­
tion at the level of the neuromuscular junction. Myopathies
and muscular dystrophies are examples of primary muscle
diseases.65
DETERMINANTS OF EFFECTIVE MOVEMENT
Regardless of the underlying neurological or neuromuscular
disease, rehabilitation professionals seek to understand the
impact of the condition on an individual's underlying muscle
tone and motor control (ability to initiate, guide, sustain, and
terminate movement), muscle performance (strength, power,
endurance, speed, accuracy, fluidity), and postural control and
balance (ability to stay upright, to anticipate how to make pos­
tural adjustment during movement, and to respond to unex­
pected perturbations) in order to move effectively during
goal-directed, functional movement necessary for daily life.
Muscle Tone and Muscle Performance
Effectiveness of movement is determined by the interaction
of underlying muscle tone and muscle performance. Muscle
tone can be conceptualized as the interplay of compliance and
stiffness of muscle, as influenced by the CNS. Ideally the CNS
can set the neuromotor system to be stiff enough to align and
support the body in functional antigravity positions (e.g., pro­
vide sufficient baseline postural tone) but compliant enough
in the limbs and trunk to carry out smooth and coordinated
functional movement and effectively respond to changing
environmental conditions or demands as daily tasks are car­
ried out.66,67 At the center of the tone continuum, the inter­
play of stiffness and compliance is optimal, such that motor
performance is well supported (Figure 10-2, horizontal con­
tinuum). At the low-tone end of the continuum, where there is
low stiffness and high compliance, individuals are challenged
by inadequate postural control and inability to support anti­
gravity movement. At the high tone end of the continuum,

272
Section II  Orthoses in Rehabilitation
where there is high stiffness and low compliance, freedom
and flexibility of movement are compromised. Among indi­
viduals, postural tone varies with level of consciousness, level
of energy or fatigue, and perceived importance (salience) of
the tasks they are involved with at the time.68,69
Effective movement occurs when muscle performance
meets the demands of the task. The components of muscle
performance are the ability to (1) generate sufficient force
(strength); (2) at the rate of contraction required for the task
at hand (speed and power); (3) to sustain the concentric,
holding/isometric, or eccentric contraction necessary to meet
task demands (muscle endurance); (4) to ramp up or dampen
force production in response to task demands (accuracy);
and (5) coordinate mobility and stability of body segments to
complete the task (fluidity). Muscle performance can also be
conceptualized as having a continuum with optimal control
of its components around the center and inadequate control
on either side: hypokinesis (little movement) at one extreme
and hyperkinesis (excessive movement) at the other (see
Figure 10-2, vertical continuum).
While muscle tone and muscle performance are distinct
contributors to movement, they are certainly interactive.70,71
Movement is most effective and efficient if an individual's
resources fall at the center of each continuum. A problem
with muscle tone, or with muscle performance, or a combina­
tion of both leads to abnormal and less efficient movement.
Consider what will happen if there is a combination of low
tone and inadequate hypokinetic muscle performance: indi­
viduals will have difficulty with force production and power,
as well as with eccentric and isometric control, such that
movement tends to occur in shortened ranges. For example,
an infant with Down syndrome (with low tone) struggles to
sustain an upright head in prone on elbows position in order
to visually interact or reach for a toy (hypokinesis).
In the presence of low tone and hyperkinetic muscle per­
formance, movement is fast but imprecise, with bursts of
power that cannot be sustained. For example, a toddler with
Down syndrome (with low tone) who is beginning to walk
takes rapid and inconsistent steps (hyperkinesis). In con­
trast, the presence of high tone and hypokinetic muscle per­
formance, movement is slow and stiff, with inadequate force
production, compromised segmentation, impaired eccen­
tric control (difficulty letting go), and constrained range. For
example, an individual with Parkinson's disease takes short
steps and has little reciprocal arm swing when walking.
In the presence of high-tone and hyperkinetic muscle per­
formance, there tends to be “all or nothing” force production,
with somewhat ballistic and inaccurate movement occurring
between the extremes of ranges. For example, a child with
spastic quadriplegic cerebral palsy (CP) rising from sitting to
standing often employs rapid mass extension (lower extrem­
ity and trunk), compromising his or her ability to move
toward flexion in order to effectively rise; the child would also
have difficulty lowering back into sitting without ­collapsing.
MUSCLE PERFORMANCE CONTINUUM
Inadequate
Hyperkinetic
(Problematic)
Excessive extensibility
Excessive fluidity
Quick, imprecise movement
Burst of power with difficulty
sustaining force
Tendency to move through the
extremes of range
Optimal
Muscle Tone
Excessive force production
Excessive power, but with
difficulty adapting or dampening
force
“All or nothing” force with
ballistic tendency
Poor accuracy and precision
Optimal
Muscle Performance
EFFECTIVE
MOVEMENT
Optimal
Muscle Performance
Inadequate
Hypokinetic
(Problematic)
Difficulty generating adequate
force
Difficulty with eccentric and
isometric control
Tendency to move only within a
shortened range
Optimal
Muscle Tone
Inadequate force production
Slow movement
Difficulty with segmentation
(dissociation) and fluidity
Poor eccentric control
Tendency to move within a
shortened range
MUSCLE TONE CONTINUUM
Low Tone
Low Stiffness
High Compliance
(Problematic)
High Tone
High Stiffness
Low Compliance
(Problematic)
FIGURE 10-2  A conceptual model of the interrelationship of muscle tone and muscle performance as they interact to influence functional
abilities. The muscle tone ranges from excessively compliant (easily extensible on passive movement) to excessively stiff (resistant to passive
movement). The muscle performance continuum ranges from hypokinetic (exhibiting minimal movement during task activity) to hyperki­
netic (exhibiting excessive and poorly controlled movement during task activity). Movement is most effective at the intersection of optimal
muscle tone and optimal muscle performance.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
273
Although muscle performance, especially the ability to gen­
erate force, does tend to decline with aging, the impact of
inactivity is even more profound; all aspects of muscle per­
formance can improve with appropriate training, even in the
very old.72–74
Traditionally, an individual's muscle tone has been
described clinically as hypertonic or spastic, rigid, hypotonic
or low, flaccid, or fluctuating.
Hypertonus
Hypertonus is a term used to describe muscles that are influ­
enced to be too stiff or are excessively biased toward support­
ing antigravity function. Spasticity is a type of hypertonus that
typically occurs when there is damage to one or more CNS
structures of the pyramidal motor system and is encountered
as a component of many neuromuscular pathologies.75–79
Decrements in underlying tone and muscle performance, in
bipedal humans with impairment of the pyramidal system,
most often occurs in a decorticate pattern: The upper extrem­
ity is typically biased toward flexion, such that the limb can
be easily moved into flexion but not into extension (decreased
compliance of flexors). The lower extremity is biased toward
extension, such that the impaired compliance of extensors
makes movement into flexion difficult (Figure 10-3).80 In per­
sons with severe acquired brain injury the entire body may
be biased toward extension, a condition or posture described
as decerebrate pattern spasticity (Sherrington originally
described this phenomenon as decerebrate rigidity).80 Both
decorticate and decerebrate conditions are unidirectional in
nature; there is an increase of muscle stiffness and resistance
to passive elongation (impaired compliance) in one group
of muscles (agonists) with relatively normal functioning of
opposing muscle groups (antagonists).
Spasticity is a velocity-dependent phenomenon. Under
conditions of rapid passive elongation, spastic muscle groups
“fight back” with increased stiffness, a result of a hypersen­
sitive deep tendon reflex loop (Figure 10-4). This has been
described as clasp-knife spasticity, in which the spastic limb
“gives” after an initial period of resisting passive movement in
the way that a pocket knife initially resists opening when near
its initially closed position but then becomes more compliant
once moved past a threshold position as it is opened. Growing
evidence indicates that the stiffness encountered during pas­
sive movement has both neurological (spasticity) and mus­
culoskeletal (changes in muscle and associated soft tissue)
components that combine to increase the risk of contracture
development.81,82
Given the unidirectional nature of severe hypertonus, it
is common for persons with severe hypertonus to develop
chronic abnormal postures. The limb or body segment
assumes an end-range position that the limb would not nor­
mally be able to assume (e.g., extreme equinovarus with
marked supination in an individual with severe acquired
brain injury, equinovalgus with marked pronation in a child
with CP).80,81 If persistent, these fixed postures are associ­
ated with a significant likelihood of secondary contracture
development.83
Hypertonicity is also associated with deficits in muscle
performance, most notably diminished strength, diminished
ability to produce power (generate force quickly), diminished
ability to effectively isolate limb and body segments, dimin­
ished excursions of movements within joints (i.e., moving
within a limited range of motion [ROM]), and inefficiency
with altering force production or timing of contractions to
meet changing (fluid) demands of tasks.84–86 Muscle per­
formance deficits can contribute to an imbalance of forces
around a joint that leads to habitual abnormal patterns of
movement. These habitual patterns are often biomechani­
cally inefficient and, over time, contribute to the development
of secondary musculoskeletal impairments such as adaptive
shortening or lengthening of muscles and malalignment of
joints.83 Strengthening exercises can have a positive impact on
function, even in the presence of hypertonicity.85–87
Rigidity
Individuals with Parkinson's disease and related neurologi­
cal disorders often demonstrate varying levels of rigidity: a
bidirectional, co-contracting hypertonicity in which there is
resistance to passive movement of both agonistic and antago­
nistic muscle groups.88 Co-contraction of flexor and extensor
muscles of the limbs and trunk creates a bidirectional stiff­
ness that interferes with functional movement. Rigidity is
often accompanied by slowness in initiating movement (bra­
dykinesia), decreased excursion of active ROM, and altered
resting postures of the limbs and trunk (Figure 10-5). The
rigidity of Parkinson's disease can be overridden under cer­
tain environmental conditions: Persons with moderate to
A
B
FIGURE  10-3  Decorticate pattern hypertonicity following cere­
brovascular accident. A, The affected upper extremity is held in a
flexed posture, while the extensor bias in the lower extremity pro­
vides stability at midstance and permits swing limb advancement of
the less-involved extremity. B, The extensor pattern hypertonus in
the affected lower extremity precludes swing-limb shortening nor­
mally accomplished by hip and knee flexion; instead, the individual
uses an abnormal strategy such as pelvic retraction and hip hiking to
advance the involved limb.

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Section II  Orthoses in Rehabilitation
FIGURE 10-4  Diagram of the deep tendon reflex loop: stimulation of the annulospiral receptor within muscle spindle of the quadriceps (A)
and biceps brachii (B) (via “tap” on the patellar tendon with a reflex hammer) activates 1a afferent neurons, which in turn assist motor neurons
in the anterior horn of the spinal cord. These motor neurons project to extrafusal muscle fibers in the quadriceps, which contract, predictably,
as a reflex response. Sensitivity of muscle spindle (threshold for stimulation) is influenced by extrapyramidal input, reaching γ motor neurons
in the anterior horn, which project to intrafusal muscle fibers within the muscle spindle itself.
Quadriceps
muscle
Peripheral
nerve
A
Patellar
tendon
Pyramidal
tracts
Extrapyramidal tracts
Anterior
horn
DRG
MN
MN
Ia
Condyle of
femur
Muscle spindle
annulospiral
ending
Descending
pyramidal
tracts
Descending
extrapyramidal
tracts
MN
Muscle
spindle
(enlarged)
Ia
afferent
B
Dorsal root ganglion
MN
MN

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
275
severe disease can suddenly run reciprocally if they perceive
danger to themselves or a loved one; once this initial limbic
response has dissipated, they will resume a stooped and rigid
posture, with difficulty initiating voluntary movement, lim­
ited active ROM, and bradykinesia. Because rigidity creates a
situation of excessive stability of the trunk and limbs, ortho­
ses are not typically a component in the plan of care for per­
sons with Parkinson's disease.89
Hypotonus
Hypotonus (low muscle tone) describes a reduced stiffness
of muscle that does not effectively support upright posture
against gravity or to generate force during contraction; as a
result, hypotonic muscles are more compliant than they are
stiff.90 In children, hypotonia can arise from abnormal function
within the CNS (approximately 75%) or from problems with
peripheral structures (peripheral nerve and motor units, neu­
romuscular junction, the muscle itself, or unknown etiology).91
Hypotonia can be congenital (seen as “floppy” infants), tran­
sient ( e.g., in preterm infants), part of the clinical presentation
of CP, Down syndrome and other genetic disorders, as well as
Autism spectrum disorders.91–96
Hypotonic muscles are considerably more compliant
on rapid passive elongation (i.e., less resistant to passive
stretch) than muscles with typical tone, as well as those with
hypertonus/spasticity. Because their postural muscles are
less stiff, individuals with hypotonicity often have difficulty
when assuming and sustaining antigravity positions.97 To
compensate for their reduced postural tone, persons with
hypotonicity may maintain postural alignment by relying
on ligaments and connective tissue within joint capsule and
muscle to sustain upright posture (Figure 10-6). With over­
reliance on ligaments in extreme ends of range, further deg­
radation to joint structures often occurs.
In addition to postural control dysfunction, individu­
als with hypotonia often have difficulty with coordination
of movements. This may be due to the decreased efficacy of
afferent information collected by a lax muscle spindle during
movement execution.98 Children with hypotonia often have
impaired control of movements at midrange of muscle length,
suggesting that kinesthetic information is not being used
efficiently to guide movement or that the ability to regulate
force production throughout movements is compromised.
In either case, muscle performance is notably less efficient,
especially in activities that require eccentric control (e.g., con­
trolled lowering of the body from a standing position to sit­
ting on the floor).97 Individuals with hypotonia have difficulty
regulating force production and collaboration between ago­
nists and antagonists is not well coordinated.97
Immediately after an acute CNS insult or injury there is
often a period of neurogenic shock in which the motor sys­
tem appears to shut down temporarily, with apparent loss of
voluntary movement (paralysis) and markedly diminished or
absent deep tendon reflex responses.98–100 This phenomenon
is observed following cervical or thoracic spinal cord injury
and early on following significant stroke. During this period,
individuals with extreme levels of hypotonus are sometimes
(erroneously) described as having flaccid paralysis. Most
individuals with acute CNS dysfunction will, within days
to weeks, begin to show some evidence of returning mus­
cle tone; over time, many develop hyperactive responses to
deep tendon reflex testing and other signs of hypertonicity.99
If they continue to have difficulty activating muscles volun­
tarily for efficient functional movement, these individuals are
described as demonstrating spastic paralysis.
FIGURE  10-5  Typical standing posture in individuals with
Parkinson's disease, with a forward head, kyphotic and forward
flexed trunk, and flexion at hip and knees. Upper extremities are
often held in protracted and flexed position. The altered position of
the body's center of mass, when combined with rigidity and brady­
kinesia, significantly decreases the efficacy of anticipatory postural
responses during ambulation, as well a response to perturbation.
FIGURE 10-6  Postural control is often inefficient in children (and
adults) with hypotonicity or low tone. This 10-month-old child
has insufficient muscle tone to maintain her head and trunk in an
upright position and uses her upper extremities to reach or manipu­
late, visually track objects in her environment, or safely transition
into and out of a sitting position. (Modified from Stokes M. Physical
Management in Neurological Rehabilitation. Edinburgh: Mosby,
2004. p. 322.)

276
Section II  Orthoses in Rehabilitation
Flaccidity
The term flaccidity is best used to describe muscles that can­
not be activated because of interruption of transmission or
connection between lower motor neurons and the muscles
they innervate.101 True flaccidity is accompanied by signifi­
cant atrophy of muscle tissue, well beyond the loss of mus­
cle mass associated with inactivity; this is the result of loss
of tonic influence of lower motor neurons on which muscle
health is based.102
The flaccid paralysis seen in persons with myelomenin­
gocele (spina bifida) occurs because incomplete closure of
the neural tube during the early embryonic period (soon
after conception) prevents interconnection between the
primitive spinal cord and neighboring somites that will
eventually develop into muscles of the extremities.103 The
flaccid paralysis observed in persons with cauda equina
level spinal cord injury is the result of damage to axons of
α and γ motor neurons as they travel together as ventral
roots to their respective spinal foramina to exit the spinal
column as a spinal nerve.104 After acute poliomyelitis, the
loss of a portion of a muscle's lower motor neurons will
lead to marked weakness; the loss of the majority of a mus­
cle's lower motor neurons will lead to flaccid paralysis.65
In Guillain-Barré syndrome, the increasing weakness and
flaccid paralysis seen in the early stages of the disease are
the result of demyelination of the neuron's axons as they
travel toward the muscle in a peripheral nerve.105 After
injection with botulinum toxin, muscle tone and strength
are compromised because of the toxin's interference with
transmitter release from the presynaptic component of the
neuromuscular junction.106
Fluctuating Tone: Athetosis and Chorea
Athetosis is the descriptor used when an individual's under­
lying muscle tone fluctuates unpredictably.107 Athetosis is
characterized by random changes in postural tone, with vari­
ations from hypertonus to hypotonus. Athetosis, although
less common than spastic CP, can have as significant (and
often more pronounced) an impact on daily function.108
Although etiology of athetosis is not well understood, it is
most frequently described as a type of basal ganglia or tha­
lamic dysfunction associated with bilirubin toxicity or sig­
nificant perinatal anoxia.107 Persons with athetosis typically
demonstrate truncal hypotonia, with fluctuating levels of
hypertonus in antigravity musculature and the extremities.
In some individuals, movements appear to have a writhing
dancelike quality (choreoathetosis) in addition to the tonal
influences. Others may compensate for postural instabil­
ity by assuming end-range positions, relying on mechani­
cal stability of joints during functional activity. Although
persons with athetosis are less likely to develop joint con­
tracture than those with long-standing hypertonicity, they
are more likely to develop secondary musculoskeletal com­
plications that compromise stability of joints, a result of
extreme posturing, imbalance of forces across joint struc­
tures, and the need to stabilize in habitual postural align­
ment patterns for function.109
Postural Control
Postural control has three key dimensions: (1) Static postural
control is defined as the ability to hold antigravity postures
at rest; (2) dynamic anticipatory postural control is the ability
to sustain a posture during movement tasks that shift (inter­
nally perturb) the center of mass; and (3) dynamic reaction­
ary postural control is the ability to be able to withstand or
recover from externally derived perturbations without loss of
balance.110 One has functional postural control if the center of
mass (COM) can be maintained within one's base of support
(BOS) under a wide range of task demands and environmen­
tal conditions. This requires some level of ability across the
triad of static, anticipatory, and reactionary control.
The key interactive CNS systems involved in postural con­
trol include extrapyramidal and pyramidal motor systems,
visual and visual-perceptual systems, conscious (dorsal
column/medial lemniscal) and unconscious (spinocerebellar)
somatosensory systems, the vestibular system, and the cer­
ebellar feedback/feedforward systems.111,112 Clinical measures
used to assess efficacy of static postural control include tim­
ing of sitting or standing activities and measures of center of
pressure excursion in quiet standing.113 The Clinical Test of
Sensory Interaction and Balance sorts out the contribution
of visual, vestibular, and proprioceptive systems’ contribution
to balance, as well as the individual's ability to select the most
relevant sensory input when there is conflicting information
collected among these systems.114
Measures of anticipatory postural control consider how
far the individual is willing to shift his or her center of mass
toward the edge of his or her sway envelope.115,116 Clinically,
anticipatory postural control is often quantified by measur­
ing reaching distance in various postures.117–119 Measures of
dynamic reactionary postural control consider the individu­
al's response to unexpected perturbations (e.g., when pushed
or displaced by an external force, when tripping/slipping in
conditions of high environmental demand).120,121 Although
these three dimensions of postural control are interrelated,
competence in one does not necessarily ensure effective
responses in the others.122
Many individuals with neuromuscular disorders demon­
strate inefficiency or disruption of one or more of the CNS
subsystems necessary for effective postural control and bal­
ance.123 An individual with mild to moderate hypertonicity or
spasticity often has difficulty with anticipatory and reaction­
ary postural control, especially in high task demand situa­
tions within a complex or unpredictable open environment.124
Difficulty with muscle performance, such as impairment of
control of force production or the imbalance of forces acting
across a joint, might constrain anticipatory postural control
in preparation for functional tasks such as reaching or step­
ping. Impairment of the ability to segment trunk from limb
or to individually control joints within a limb may affect the
individual's ability to react to perturbations in a timely or
consistent manner.125
Persons with hypotonicity, on the other hand, often have
difficulty with sustaining effective postural alignment in
antigravity positions such as sitting and standing. They are

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
277
likely to demonstrate patterns of postural malalignment
such as excessive lumbar lordosis and thoracic kyphosis.97
Because of difficulty with muscle force production (espe­
cially in midrange of movement), individuals with hypoto­
nia also have difficulty with anticipatory postural control.90
A lack of on-demand motor control contributes to difficulty
moving within one's postural sway envelope; this may be
observed as a tendency to stay in one posture for long peri­
ods of time, with infrequent alterations in position during
tasks.94 Reactionary control may also be altered, particularly
with respect to the use of equilibrium reactions and the reli­
ability of protective responses. Individuals with hypotonia
have difficulty when a task requires them to absorb small-
amplitude perturbations; they must use equilibrium or bal­
ance strategies more frequently than persons with adequate
muscle tone.90 Additionally, a lack of stability in joints, from
both tonal and ligamentous laxity, contributes to an inability
to safely stop an accelerating body part as it comes into con­
tact with a surface during a loss of balance episode.94
Movement and Coordination
Many functional activities require us to move or transport
the entire body (e.g., mobility or locomotion) or a segment
of the body (e.g., using one's upper extremity to bring a cup
toward the mouth to take a drink) through space.126,127 The
locomotion task that receives much attention in rehabilita­
tion settings is bipedal ambulation—the ability to walk. For
full functional ability, individuals must be able to manage a
variety of additional locomotion tasks: running, skipping,
jumping, and hopping.128 To fully understand an individ­
ual's functional ability, therapists and orthotists must also
consider the environmental context in which ambulation is
occurring.129 What are the physical characteristics of the sur­
face on which the individual needs to be able to walk or tra­
verse? Is it level, unpredictably uneven, slippery or frictional,
or structurally unstable? Is the ambulation task occurring
where lighting is adequate for visual data collection about
environmental conditions? Does it involve manipulation of
some type of object (e.g., an ambulatory assistive device, a
school backpack, shopping bags, suitcases)? Is it occurring in
a familiar and predictable environment (e.g., at home) or in a
more unpredictable and challenging open environment such
as a busy school, supermarket, mall, or other public space?
The task demands of locomotion in complex and challeng­
ing environments create more demand on the CNS struc­
tures involved in motor control (perceptual-motor function,
motor planning, cerebellar error control), as well as on the
musculoskeletal effectors (muscles and tendons, joints, liga­
ments, and bones) that enact the motor plan necessary for
successful completion of the task that relies on body trans­
port. Individuals with neurological and neuromuscular
system problems related to muscle tone, muscle performance,
and postural control are typically less efficient, less adaptable,
and more prone to fall when walking, especially if there are
competing task demands and the environment is complex
and challenging.130
The use of a limb segment can also be defined by the nature
of the task and the circumstances in which the movement is
performed. Upper extremity functional tasks can involve one
or more components: reaching, grasping, releasing, manipu­
lating, or any combination of these four purposes.126 Upper
extremity tasks can also be defined by considering the func­
tion to be accomplished by the movement: grooming, dress­
ing, meal preparation, self-care, or writing. Many upper
extremity mobility tasks are founded on effective postural
control (e.g., making appropriate anticipatory postural adjust­
ments as the COM shifts while throwing, lifting, lowering, or
catching an object).126 Complex mobility tasks require simul­
taneous locomotion and segmented use of extremities (e.g.,
reaching for the doorknob while ascending the steps toward
the front door, throwing or catching a ball while running dur­
ing a football or baseball game). For individuals with neuro­
logical and neuromuscular system dysfunction, the ability to
safely and efficiently perform complex mobility tasks is often
compromised due to abnormal muscle tone, impaired muscle
performance, and poor postural control.130
Coordination can be thought of as the efficacy of execution of
the movement necessary to complete a task. A well-coordinated
movement requires effective simultaneous control of many dif­
ferent dimensions of movement: the accuracy of a movement's
direction and trajectory; the timing, sequencing, and precision
of muscle activation; the rate and amplitude of force production;
the interaction of agonistic and antagonistic muscle groups; the
ability to select and manage the type of contraction (concen­
tric, holding, or eccentric) necessary for the task; and the abil­
ity to anticipate and respond to environmental demands during
movement.131 Coordination can be examined by considering
the individual's ability to initiate movement, sustain movement
during the task or activity, and terminate movement according
to task demands.132
For movement and coordination to be functional, one must
have muscle performance that is flexible/adaptable to varying
demands.133 Mobility or transport tasks cannot be performed
independently (safely) unless the individual is able to (1) tran­
sition into and out of precursor positions (e.g., getting up from
the floor into a standing position, rising from a chair), (2) ini­
tiate or begin the activity (e.g., take the first step), (3) sustain
the activity (control forward progression with repeated steps),
(4) change direction as environmental conditions demand
(e.g., step over or avoid an obstacle), (5) modulate speed as
environmental conditions demand (e.g., increase gait speed
when crossing the street), and (6) safely and effectively stop
or terminate the motion, returning to a precursor condition or
position (quiet standing, return to sitting).133
For individuals with neuromuscular disorders who have dif­
ficulty with muscle performance, abnormal underlying tone, or
poor postural control, coordination of functional movement
can be compromised in several ways. In order to approach and
complete a movement task, the individual might rely on abnor­
mal patterns of movement with additional effort and energy
cost.134 Many individuals with hypertonicity initiate movement
with strong bursts of muscle contractions but have difficulty sus­
taining muscle activity and force of contraction through the full

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Section II  Orthoses in Rehabilitation
ROM necessary to perform a functional movement.98,108 Deficits
in timing and sequencing of muscle contractions, as well as diffi­
culty with dissociation of limb and body segments, also contrib­
ute to difficulty with performance of functional tasks.135 An adult
with hemiplegia following a cerebrovascular accident may be
able to initiate a reach toward an object but not be able to bring
the arm all the way to the target.136 The same individual may
have difficulty with timing and segmentation, leading to inabil­
ity to open the hand before reaching the target in preparation
for grasping the object.137,138 The muscle performance of many
children with CP is compromised by inappropriate sequencing
of muscle contractions when activation of synergists and antago­
nists happens simultaneously.108 Conversely, an individual with
hypotonus who has difficulty with stabilization often moves
quickly with diminished accuracy and coordination.90
The following tables provide an overview of incidence/
prevalence, etiology and risk factors, clinical presentation,
and impact on muscle tone, muscle performance, postural
control, and movement for of the most common pathologies
that might include use of an orthosis: stroke (Table 10-1), CP
(Table 10-2), spina bifida (Table 10-3), MS (Table 10-4), and
spinal cord injury (Table 10-5).
When considering an upper or lower extremity orthosis
or a seating system to support the trunk for individuals with
TABLE 10-1  Stroke
Also known as
Brain attack, cerebrovascular accident (CVA)
Incidence
Approximately 610,000 per year in the U.S.*
Prevalence
2.6% of total US population have had stroke*
8.1% of US population over age 65 have had stroke*
ETIOLOGY AND RISK FACTORS
Ischemic Stroke (88%)
Thrombus
Hypertension, hypercholesterolemia, diabetes and metabolic syndrome, overweight and
obesity, smoking, sedentary lifestyle*
Embolism
Atrial fibrillation, atherosclerosis in carotid/vertebral arterial systems; previous embolic stroke
Hemorrhagic Stroke (12%)
Intracranial hemorrhage
Uncontrolled hypertension, ruptured aneurysm
STROKE SYNDROMES (BY ARTERY)
Middle cerebral (most common)
Contralateral hemiparesis/hemiplegia, lower face, UE > LE
Contralateral sensory loss of lower face, UE > LE
Contralateral homonymous hemianopia (optic tract)
Possible dysarthria and dysphagia
R hemisphere: visual-spatial or somatic perceptual impairment
L hemisphere: communication impairment (various aphasias)
Lenticulo-striate (lacunar MCA)
Contralateral hemiparesis/hemiplegia, lower face, UE = LE
Cortical functions (perception, communication) intact
Anterior cerebral
Contralateral hemiparesis/hemiplegia LE > UE
Sensation often intact or only mildly impaired (contralateral)
Incontinence
“Alien hand” syndrome (involuntary/unintended movement)
Motor (nonfluent/Broca's) aphasia may occur
Posterior cerebral
Contralateral homonymous hemianopsia (optic radiations)
Visual inattention
L hemisphere: alexia (unable to read), with ability to write preserved
Thalamogeniculate (lacunar PCA)
Contralateral sensory loss, often severe
Sensory ataxia (uncoordinated movement due to lack of proprioception)
Thalamic pain and hyperpathia syndrome
Basilar (complete)
Loss of consciousness, coma
High mortality
Superior cerebellar



Ipsilateral ataxia, falling to side of lesion
Intention tremor
Contralateral loss of pain temperature sensation from body
Contralateral loss of proprioception
Ipsilateral Horner's syndrome (meiosis, ptosis, anhydrosis)

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
279
neurological or neuromuscular dysfunction, the therapist
and orthotist must clearly define what they hope the ortho­
sis will accomplish (e.g., management of abnormal tone,
provision of stability for a limb segment in the presence of
impaired muscle performance or motor control, or enhanc­
ing positioning to allow more efficient function and move­
ment). They must also consider the impact of the orthosis
on postural control, overall mobility, and ability to adapt to
environmental demands. There is no perfect orthosis that will
address all dimensions of movement dysfunction; there are
always trade-offs that must be taken into account.
MANAGEMENT OF NEUROMUSCULAR
IMPAIRMENTS
Effective care of persons with movement dysfunction second­
ary to neurological and neuromuscular pathologies requires
collaboration of health professionals from many ­disciplines:
neurologists, orthopedist, physiatrists, physical and occu­
pational therapists, and orthotists, among others.139–141
Physicians and surgeons manage spasticity and correct
orthopedic deformity with medication and surgery. Nurses
are involved in wellness care, as well as medical and surgical
management. Rehabilitation professionals facilitate return of
function after an acute event and provide functional train­
ing and postoperative rehabilitation for individuals across the
spectrum of neurological and neuromuscular pathologies.
Orthotists contribute their knowledge of orthotic options to
improve gait and function. The multidisciplinary approach
leads to greater satisfaction with care and less risk of aban­
donment of orthoses and assistive devices by the person they
were made for.142
Medical and Surgical Care
Medical management of CNS dysfunction often includes pre­
scription of pharmacological agents. Physicians can select
from a range of centrally acting tone-inhibiting medications
(e.g., baclofen [Lioresal]) or pharmacological interventions
that target lower motor neurons, peripheral nerves, or mus­
cle (e.g., botulinum toxin injection, intrathecal baclofen) for
Anterior-inferior cerebellar
Ipsilateral facial paralysis (both upper and lower face)
Ipsilateral loss of pain and temperature of entire face
Contralateral loss of pain and temperature from body
Loss of taste sensation, loss of corneal reflex, ipsilateral hearing loss, nystagmus, vertigo, nausea
Ataxia and incoordination of limb movement
Ipsilateral Horner's syndrome (meiosis, ptosis, anhydrosis)
Vertebral
Contralateral loss of pain, temperature sensation from body
Posterior-inferior cerebellar (Wallenberg's
syndrome) (lateral medullary syndrome)
Ipsilateral loss of pain and temperature sensation from face
Ipsilateral Horner's syndrome (meiosis, ptosis, anhydrosis)
Dysphonia, dysphagia, dysarthria, diminished gag reflex
Nystagmus, diplopia, vertigo, nausea
Ipsiversive falling (toward side of lesion), incoordination, ataxia
PROGNOSIS
Ischemic: severity depends on site of occlusion within arterial tree and the size of the area that
is without blood flow
Embolic: risk of recurrence is higher than in thrombosis; risk of hemorrhage at site of embolism
Hemorrhagic: highest morbidity and mortality
Static event, with evolving symptoms in weeks/months following initial damage, due to initial
inflammatory response and subsequent tissue remodeling/healing.
MUSCLE TONE
Initial hypotonus (sometimes appearing to be flaccid) due to neurogenic shock. Some
individuals remain hypotonic, most develop various levels of hypertonus in weeks/months
following event. Hyperactive deep tendon reflexes evolve over time.
MUSCLE PERFORMANCE
Upper extremity often biased toward flexion, with lower extremity biased toward extension.
Impaired force production, speed and power, eccentric/isometric control, accuracy, and fluidity.
POSTURAL CONTROL
Frequently impaired, especially if lesion included gray matter of R hemisphere, with
perceptual dysfunction.
MOBILITY AND COORDINATION

Asymmetry in ability to use trunk, limbs during functional .activity; tendency to move in
abnormal “synergy” (flexion UE, extension LE). Frequently require AFO and ambulatory
device.
AFO, ankle-foot-orthosis; L, left; LE, lower extremity; MCA, middle cerebral artery ; PCA posterior cerebral artery, ; R, right; UE, upper extremity.
*American Heart Association Risk Factors for Stroke. Available at:
Article.jsp; accessed 8/9/11.
TABLE 10-1  Stroke—cont'd

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Section II  Orthoses in Rehabilitation
TABLE 10-2  Cerebral Palsy
Incidence
Approximately 11,500 new cases diagnosed per year*
Prevalence
764,000 children and adults in the U.S.; 3.3 per 1000*
Etiology
Unknown in most instances
Risk factors
Prematurity, high-risk pregnancy, low birth weight, perinatal or neonatal respiratory distress/
anoxia, mother's substance abuse while pregnant
TYPES OF CEREBRAL PALSY
Spastic (85%-93%)*,†
Quadriplegia/tetraplegia: global impact on both gray and white matter structures in forebrain.
Some individuals have concomitant cognitive impairment and seizure disorders.
Diplegia: usually due to damage of white matter of internal capsule/corona radiate, impacting
on motor and sensory systems more than perceptual.
Hemiplegia: may be due to intracerebral hemorrhage or ischemia affecting one hemisphere.
Dyskinetic (5%-10%)*,† (choreoathetoid)
May be related to perinatal damage of basal ganglia
Unpredictably fluctuating tone of head/neck, trunk, and extremities; may be associated with
perinatal bilirubin toxicity
Ataxic/cerebellar (5%)
May be related to perinatal damage of cerebellar cortex, nuclei, or peduncles
PROGNOSIS
Static event occurring at or around the time of birth. Signs and symptoms become
apparent over first 2 years of life as motor developmental delay. High risk of secondary
musculoskeletal deformity due to impact of abnormal tone during periods of growth and
repetitive impact of muscle imbalance on movement. Level of disability often becomes more
pronounced as child moves into middle childhood, adolescence, and young adulthood due
to increasing body size and weight.
MUSCLE TONE
Spastic
Initial hypotonus in premature and low-birth-weight infants common. Hypertonus develops
over time; severity of hypertonus varies depending on extent of central nervous system
damage. Hypertonus may increase in times of growth, or in times of excitement and stress.
Hyperactive deep tendon reflexes, as well as abnormal tonic developmental reflexes.
Dyskinetic
Unpredictable fluctuation of muscle tone (from very low tone to significant hypertonus),
affecting muscles of limbs, axial skeleton, respiration, and phonation. Often appears
as writhing motions of trunk and extremity. Response to tendon reflexes varies due to
changing tone.
Ataxic
Frequently hypotonic with hyperflexible joints in both appendicular and axial skeleton. At risk
for secondary overuse injury with habitual and long-term hyperflexibility during movement
and in static postures. Often pendular deep tendon reflexes.
MUSCLE PERFORMANCE
Spastic
May be hypokinetic (small excursion of movement) or hyperkinetic (large excursion of
movement) with difficulty modulating force; force production can be great (strong forceful
unrelenting contraction) or small (inability to sustain contraction for functional movements);
difficulty with eccentric and isometric control, poor accuracy and precision of movement.
Dyskinetic
May be hypokinetic (slow and minimal movement) or hyperkinetic (movements can be
random and/or repetitive with minimal purpose); force production, speed, and timing of
contractions do not match task demands; poor accuracy.
Ataxic
May be hypokinetic or hyperkinetic; tasks demanding greater accuracy lead to faster and greater
excursions, with worsening accuracy; tasks demanding less accuracy lead to slower and lesser
excursions with some accuracy. Timing of agonist and antagonist sequencing is impaired.
POSTURAL CONTROL
Spastic
Often impaired, due to influence of persistent tonic reflexes, and less efficient development of
righting and equilibrium responses in trunk and affected limbs.
Dyskinetic
May be significantly impaired; fluctuating tone challenges ability to attain and hold positions
or move dynamically through space.

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
281
Ataxic
Sitting and standing postures may be “floppy,” as child relies on soft tissue structures of the
musculoskeletal system to support upright position because of inadequate antigravity
postural control.
MOBILITY AND COORDINATION
Spastic
Frequently employ movement strategies based on atypical and less variable patterns/synergies;
over time may develop rotational deformity of lower extremity as well as joint contracture
due to combination of preferred abnormal positions/patterns of movement and hypertonus.
Often require ankle-foot-orthosis, assistive devices, or wheelchair for locomotion. Those
with significant trunk and upper extremity involvement may require adaptive equipment
for feeding, communication, and activities of daily living. Orthoses or resting splints may be
used as a means of managing abnormal tone, minimizing risk of musculoskeletal deformity,
or after orthopedic surgery to correct deformity.
Dyskinetic
Often depend on external support for stability during functional tasks and locomotion. May
benefit from use of ambulatory device, adaptive equipment, seating systems, or upper and
lower extremity orthoses.
Ataxic


Depending on severity of impairment, may have difficulty with trunk stability during
functional tasks using upper extremity (activities of daily living), and lower extremity
(walking). May use ankle-foot orthosis to provide external support/positioning during
functional task.
*Centers for Disease Control and Prevention: Cerebral Palsy Accessed 8/11/11.
†Kirby RS, Wingate MS, Van Naarden Braun K. Prevalence and functioning of children with cerebral palsy in four areas of the United States
in 2006: a report from the Autism and Developmental Disabilities Monitoring Network. Res Dev Disabil. 2011;32(2):462-469.
TABLE 10-2  Cerebral Palsy—cont'd
TABLE 10-3  Spina Bifida
Incidence
.05 per 1000 live births; approximately 3000 per year in the U.S.*†‡
Prevalence
1.9 to 3.1 per 10,000 children 0-19 years in the U.S.a,b,c
Etiology
Unknown
Risk factors§¶
Folate deficiency
Advanced maternal age
Genetic tendency/previous pregnancy or family member with spina bifida
Taking valproic acid or carbamazepine for seizures
Having high temperatures early in pregnancy
TYPES OF SPINA BIFIDA||
Occulta
Abnormal formation of lumbar or sacral vertebrae, with intact spinal cord and spinal nerves, and full
skin coverage. May be a progressive deterioration of function in late childhood into adulthood.
Meningocele
Vertebral defect such that meninges and cerebrospinal fluid protrude but spinal cord, cauda equina,
and spinal nerves remain within the spinal column. Vertebral defect may or may not be covered by
skin. Often associated with minor to mild impairment of motor and sensory function.
Myelomeningocele
Defect such that meninges and incompletely closed spinal cord protrude; associated with lower motor
neuron dysfunction (flaccid paralysis) and complete sensory loss below level of lesion; may have
spasticity of muscles innervated by spinal nerves just proximal to level of lesion. Urinary and fecal
incontinence common, risk of neuropathic wounds high; risk of osteoporosis of lower extremities high.
PROGNOSIS






Incomplete closure of neural tube soon after conception; leading to flaccid paralysis and total sensory
impairment of all structures innervated at and below level of lesion. May be concurrent with
hydrocephalus, often managed by ventriculoperitoneal shunt.
Static, nonprogressive condition; however level of disability often becomes more pronounced as child
moves into middle childhood, adolescence, and young adulthood due to increasing body size and weight.
High risk of secondary musculoskeletal deformity (e.g., osteoporosis, fracture, contracture) due to
combination of motor and sensory impairment.
Depending on level of lesion, voluntary bladder and bowel control may also be impaired or absent.
(Continued)

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Section II  Orthoses in Rehabilitation
TABLE 10-4  Multiple Sclerosis
Incidence
10,000 new cases of MS are diagnosed yearly in the U.S.*
Prevalence
between 350,000 and 400,000 people living with MS; 1 in 750 people, 90 per 100,000*†
Etiology
Unknown; CNS demyelinating disease affecting CNS subsystem
Risk factors
May be exposure to slow virus, environmental toxin, possible autoimmune components, risk higher
among siblings, more common in women than men, more common among persons in northern
latitudes; more common among Caucasians. Most commonly diagnosed in early to mid adulthood.
CLASSIFICATIONS OF MS‡
Possible MS
an individual experiences a clinically isolated syndrome (CIS): a single neurologic episode that lasts
at least 24 hours, and is caused by inflammation/demyelination in one or more sites in the central
nervous system, especially if lesions are present on MRI.
Relapsing remitting (85%)
cycle of exacerbations (new signs/symptoms) followed by partial to complete recovery during which
there is no apparent worsening of the disease process
Progressive
steadily worsening of symptoms from time of diagnosis, with incomplete recovery between exacerbations.
PROGNOSIS










Unpredictable exacerbations result from inflammation and destruction of myelin around pathways
within the CNS.
Residual impairments are the consequence of slowed transmission of neural impulses across plaques
interrupting connections between CNS structures.
May impact on any subsystem within CNS (voluntary motor, postural control, coordination, memory,
perception, sensation).
Definitive diagnosis made if there have been at least two different episodes of impairment, involving two
different neurological subsystems, affecting two different parts of the body, at two different periods of time.
Variable course, with many different types of impairment accruing over time with repeated
exacerbations.
Typically onset of initial symptoms in young and mid-adulthood. Often diagnosis by exclusion; when
neurological signs/symptoms cannot be attributed to other disease processes.
MUSCLE TONE
Typically flaccid paralysis with absent deep tendon reflexes. May have spotty hypertonicity of muscle
innervated by nerve roots proximal to level of lesion.
MUSCLE PERFORMANCE
No muscle activity below level of lesion
POSTURAL CONTROL
Normal righting reactions and equilibrium responses above level of lesion; with absence of righting
and equilibrium responses in trunk and limbs below level of lesion. Postural control in sitting
influenced by how much of trunk and pelvis is innervated. At risk of developing hypermobility of
spinal column around level of lesion.
MOBILITY AND
COORDINATION



Impairment and functional limitation proportional to level of lesion. Those with sacral or low lumbar
level lesions may be able to ambulate with ankle-foot orthosis, with or without assistive devices.
Those with mid to high lumbar lesions may use knee-ankle-foot orthosis or hip-knee-ankle-foot
orthosis for limited mobility. Many individuals with lumbar and higher levels opt, over time, to
use seating and wheelchair systems for functional mobility. Orthoses and splints may be used after
orthopedic surgeries to repair fracture or correct deformity.
*Shin M, Besser LM, Siffel C, et al. Prevalence of spina bifida among children and adolescents in 10 regions in the United States. Pediatrics.
2010;126(2):274-279.
†Boulet SL, Gambrell D, Shin M, Honein MA, Matthews TJ. Racial/ethnic differences in the birth prevalence of spina bifida—United States,
1995-2005. JAMA. 2009;301(21):2203-2204.
‡Racial/ethnic differences in the birth prevalence of spina bifida—United States, 1995-2005. MMWR Morb Mortal Wkly Rep.
2009;57(53):1409-1413.
§Bowman RM, Boshnjaku V, McLone DG. The changing incidence of myelomeningocele and its impact on pediatric neurosurgery: a review
from the Children's Memorial Hospital. Child Nervous Syst. 2009;25(7):801-806.
¶
|| Accessed 8/11/11.
TABLE 10-3  Spina Bifida—cont'd

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
283
MUSCLE TONE
Varies, depending on location and size of residual plaque. Some individuals may exhibit normal tone
and deep tendon reflexes, in the presences of perceptual, postural, or coordination impairment. Others
may demonstrate hypertonus and hyperactive reflexes is various muscles. Others may have hypotonus
and impaired muscle performance.
MUSCLE PERFORMANCE
Varies, depending on location of MS plaque. If in pyramidal system, may have weakness, impaired
muscle endurance, poor eccentric control, among others. If in cerebellar systems, may demonstrate
ataxia, intention tremor, among others.
POSTURAL CONTROL
Postural control and equilibrium responses may be impaired due to a combination of pyramidal and/or
extrapyramidal motor system impairment, sensory impairment or somatosensory, spinocerebellar, or
visual pathways, or damage of major integrative while matter structures such as the corpus callosum,
or medial longitudinal fasciculus
MOBILITY AND
COORDINATION


Mobility and locomotion may be impaired, along with postural control, depending on location of lesion.
Some individuals with impaired muscle performance benefit from AFOs (for support and positioning
of lower extremity in gait) associated with weakness or hypertonicity. Many choose to use ambulatory
aides and assistive devices for function and safety. Some with significant multisystem impairment
benefit from seating and wheeled mobility systems.
AFO, ankle-foot orthosis; CNS, central nervous system; MRI, magnetic resonance imaging; MS, multiple sclerosis.
*Rumrill PD. Multiple sclerosis: medical and psychosocial aspects, etiology, incidence, and prevalence. J Vocat Rehabil. 2009;31(2):75-78.
†
‡National MS Society. About MS. Available at: Accessed 3/9/12.
TABLE 10-4  Multiple Sclerosis—cont'd
TABLE 10-5  Spinal Cord Injury
Incidence
11,000 new cases in the U.S. per year,* 4.5 per 100,000†
Prevalence
Nearly 250,000 persons in the U.S. are living with spinal cord injury (SCI)*
Etiology
Usually traumatic, sometimes infectious (e.g., transverse myelitis) or ischemic (e.g., complication of
abdominal aortic aneurysm repair)
Risk factors
Young age, male gender, drunk driving, participation in extreme sports, all terrain vehicle accidents,
military injury
SCI SYNDROMES
Complete upper motor
neuron (UMN)
Quadriplegia (cervical cord injury) or paraplegia (thoracic cord injury) with spastic paralysis.
Consequence of compression, contusion, or ischemia of spinal cord as a result of vertebral fracture or
dislocation sustained in fall, collision, diving, gunshot wound, or other high-impact event.
Exacerbated by resultant inflammatory process.
Spinal cord below level of lesion survives but is unhooked from brain and brainstem, only able to operate
reflexively (e.g., neurogenic bladder and bowel function).
Incomplete (>60%)‡
Similar mechanism of injury but with sparing of one or more areas of spinal cord such that there is
some volitional motor function and sensation along with more typical UMN (for cervical and thoracic
vertebral lesions) or lower motor neurons (LMN) (for lumbosacral vertebral lesions) (e.g., central cord
syndrome: upper extremity involvement > lower extremity involvement, often with preserved volitional
bladder and bowel function).
Becoming more common with advances in emergency care on newly injured persons.
Complete LMN
Paraplegia consequence of compression, contusion of lumbosacral nerve roots (cauda equina) within the
lower spinal canal, resulting in flaccid paralysis and sensory loss below the level of lesion.
Prognosis
Improved emergency and acute medical management often results in incomplete lesion, with varying
combinations of return of function and spastic paralysis.
MUSCLE TONE
Complete UMN



Initial hypotonicity during period of neurogenic shock. Many develop significant hypertonicity in the
months after injury; some may have muscle spasm needing pharmacological intervention. Sudden
increase in resting tone may signal unrecognized skin irritation, bladder distention or infection, or bowel
impaction. At risk of secondary musculoskeletal deformity (contracture) due to longstanding abnormal
tone and limited mobility.
(Continued)

284
Section II  Orthoses in Rehabilitation
individuals with significant hypertonicity.143–149 A host of med­
ications have become available to reduce likelihood of exac­
erbation, delay disease progression, and manage fatigue for
persons with MS.150,151 Many individuals with CNS disorders
also must cope with seizure management; many antiepileptic
drugs affect tone, arousal, and ability to learn.152 It is impor­
tant for physical therapists and orthotists to be aware of the
potential impact of neuroactive medications on an individual's
ability to concentrate and learn, overall health status, and neu­
romotor control.153,154 A summary of pharmacological agents
used in the management of hypertonicity resulting from CNS
disease, in the management of MS, and for seizure disorders is
presented in Table 10-6.
Alternatively, physicians may recommend various
neurosurgical procedures and orthopedic surgeries to
correct deformity, improve flexibility, or reduce level of
abnormal tone, with the goal of enhancing mobility and
improving performance of functional tasks. Neurectomy
and neurotomy, for example, may be used to manage
severe equinovarus and upper extremity spasticity after
stroke and for children with CP.155–159 Selective dorsal
rhizotomy effectively reduces problematic hypertonicity
for children with CP but does not seem to reduce future
risk of developing deformity, which would then require
orthopedic surgery.160–162 Intrathecal baclofen pumps
have been used as a strategy to manage severe spasticity
in persons with traumatic brain injury, stroke, spinal cord
injury, and CP.163–165
Despite pharmacological and positioning interventions,
musculoskeletal deformities can still develop, particu­
larly in the growing child. Surgical interventions are used
to correct musculoskeletal defaults of the spine and limbs,
realign joints for better mechanical advantage, improve ease
of caregiving and hygiene management, promote cosmesis,
or reduce and prevent pain. Tendon lengthenings or trans­
fers are commonly used to correct contractures and provide
Incomplete
Also may demonstrate hypotonicity in the days immediately following injury. Some volitional muscle
function may be apparent early on; spasticity may develop in other muscles over time. Muscles with
spasticity similar to complete UMN injury.
Complete LMN
Considered a lower motor neuron lesion with flaccid paralysis and absence of deep tendon reflexes at and
below level of lesion.
MUSCLE PERFORMANCE
Complete UMN
Impaired and inadequate; reflexive function only.
Incomplete
Muscles that remain innervated often initially weak; responsive to interventions to enhance force
production, muscle endurance, power.
Complete LMN
No muscle function and areflexic below level of lesion.
POSTURAL CONTROL
Complete UMN
Disconnection of lower motor neuron pool below level of lesion results in loss of volitional movement,
as well as automatic postural responses, despite hypertonus. Deep tendon reflexes are often brisk,
sometimes resulting in sustained clonus.
Incomplete
Varies from significantly impaired to minimally impaired, depending on location and extent of lesion.
Complete LMN
Postural control of trunk intact, although flaccid paralysis of lower extremities limit stability in standing
without external support of orthoses.
MOBILITY AND COORDINATION
All Types
May temporarily use spinal orthosis (CO, CTO, TLSO) until surgical stabilization of damaged vertebrae is
well healed. Often require seating and wheelchair systems for mobility.
Persons with cervical level lesions may require upper extremity splints and adaptive equipment for
activities of daily living, or resting splints or orthoses to manage abnormal tone and prevent contracture.
Complete LMN


Persons with low thoracic and lumbosacral lesions may use AFO, KAFO, or HKAFO along with assistive
device (rolling walker, crutches) for ambulation, either as part of rehabilitation or of fitness program;
energy cost of ambulation for community distances often high enough to be impractical.
AFO, ankle-foot orthosis; CO, cervical orthosis; CTO, cervical thoracic orthosis; TLSO, thoraco-lumbo-sacral orthosis; HKAFO, hip-ankle-
foot orthosis; KAFO, knee-ankle-foot orthosis.
*Sipski ML, Richards S. Spinal cord injury rehabilitation. Am J Phys Med Rehabil. 2006;85(4):310-342.
†Hirtz D, Thurman DJ, Gwinn-Hardy K, et al. How common are the "common" neurologic disorders? Neurology. 2007;68(5):326-337.
‡Wyndaele M, Wyndaele J. Incidence, prevalence and epidemiology of spinal cord injury: what learns a worldwide literature survey? J Spinal
Cord. 2006;44(9):523-529.
TABLE 10-5  Spinal Cord Injury—cont'd

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
285
TABLE 10-6  Pharmacological Interventions for Individuals with Neurological and Neuromuscular System Impairments
Trade Names
Generic Name (class)
Administration
Indications
Adverse Effects
MANAGEMENT OF DYSTONIA AND CENTRAL NERVOUS SYSTEM (CNS)-RELATED SPASM
NeuroBloc
Myobloc
botulinum B toxin
(neurotoxin)
Intramuscular
Facial spasm, spasmodic torticollis,
blepharospasm
Pain at injection site, ptosis, eye irritation, weakness
of neck muscles, dysphagia, dry mouth, heartburn
MANAGEMENT OF HYPERTONICITY, CLONUS, AND TICS
Botox
Dysport
botulinum A toxin
(neurotoxin)
Intramuscular or perineural
injection, intrathecal
Chronic severe spasticity or dystonia
Pain or bruising at injection site, muscle weakness,
tiredness, drowsiness, nausea, anxiety
Catapres
clonidine
(antihypertensive)
Oral or
transdermal
Spasticity in MS
Dry mouth, gastrointestinal disturbances, fatigue,
headache, nervousness, insomnia, skin irritation
(transdermal)
Ceberclon
Klonopin
Rivotril
Valpax
clonazepam
(benzodiazepine)
Oral
Spasticity in CP, dystonic, chorea,
akathisia
(also for seizures, panic attacks)
Sedation, dizziness, unsteadiness, incoordination,
memory problems, muscle or joint pain, blurred
vision, frequent urination
Dantrium
dantrolene sodium
(skeletal muscle relaxant)
Oral or injection
Chronic severe spasticity of UMN orgin
Drowsiness, dizziness, generalized weakness,
malaise, fatigue, nervousness, headache
Ethanol
ethyl alcohol
(neurotoxin)
Intramuscular or perineural
injection
Severe spasticity, with serial casting
follow-up
Neuritis, hyperesthesia, or parasthesia
Lioresal
baclofen
(skeletal muscle relaxant)
Oral, injection, or intrathecal
Chronic severe spasticity for conditions
including SCI, ABI, MS; not effective in CP
Sedation, confusion, hypotension, dizziness,
ataxia, headache, tremor, nystagmus, paresthesia,
diaphoresis, muscular pain or weakness,
insomnia, behavioral changes
Neurontin
gabapentin
Oral
Adjunct to other antispasticity
medications for SCI and MS
Drowsiness, dizziness, ataxia, fatigue, nystagmus,
nervousness, tremor, diplopia, memory
impairment
Phenol
phenol
Intramuscular or perineural
injection
Severe lower limb spasticity (with serial
casting follow-up) pain control
Damage to other neural structures
Robaxin
methocarbamol
Oral or injection
Short-term relief of muscle spasm or
spasticity
Sedation, drowsiness, lightheadedness, fatigue,
dizziness, nausea, restlessness
Valium
diazepam
Oral or injection
Short-term relief of muscle spasm or
spasticity
Sedation, drowsiness, fatigue, ataxia, confusion,
depression, diplopia, dysarthria, tremor
Zanaflex
Sirdalud
tizanidine
(skeletal muscle relaxant)
Oral
Spasticity from MS or SCI
Sedation, drowsiness, fatigue, dizziness, mild
weakness, nausea, hypotension, GI irritation
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286
Section II  Orthoses in Rehabilitation
Trade Names
Generic Name (class)
Administration
Indications
Adverse Effects
MANAGEMENT OF MULTIPLE SCLEROSIS: ACUTE EXACERBATION
Aristocort
Aristo-Pak
Kenacort
triamcinolone
(corticosteroid)
Oral
Acute exacerbation
Electrolyte disturbances, CHF, hypokalemia,
weakness, myopathy, osteoporosis, seizures,
papilledema, vertigo, headache
Decadron
Hexadrol
Maxidex
Mymethasone
dexamethasone
(corticosteroid)
Oral, injection, or intravenous Acute exacerbation
Electrolyte disturbances, weakness, atrophy,
osteoporosis, seizure, high ICP, vertigo headache,
Cushing's syndrome
Depo-Medrol
Solu-Medrol
methylprednisolone
dexamethasone
(corticosteroid)
Oral, injection, or intravenous Acute exacerbation
Cushing's syndrome, hypertension, confusion,
muscle wasting, insomnia, psychosis, GI
irritation, osteoporosis, delayed wound healing
Deltasone
prednisone
(corticosteroid)
Oral
Acute exacerbation
Electrolyte imbalance, CHF, weakness, atrophy,
Achilles tendon rupture, osteoporosis,
papilledema, vertigo, headache
Delta-Cortef
prednisolone
Intravenous
Acute exacerbation
Electrolyte imbalance, CHF, weakness, atrophy,
Achilles tendon rupture, osteoporosis,
papilledema, vertigo, headache
Decadron
Medrol
dexamethasone
(corticosteroid)
Oral
Acute exacerbation
GI disturbance, headache, dizziness, insomnia,
restlessness, depression or anxiety, easy bruising
MANAGEMENT OF MULTIPLE SCLEROSIS: MANAGE DISEASE PROGRESSION
Actimmune
Avonex
Betaseron
Extavia
Rebif
beta-1a-interferon
beta-1b-interferon
Injection, every 2 to 7 days
To reduce frequency and severity of
exacerbations for relapsing/remitting MS
Injection site reaction, anxiety, convulsion, seizure
Azasan
Imuran
azathioprine
(chemotherapeutic)
Oral
To slow disease progression over time when
other medications are not effective
Nausea, vomiting, diarrhea, muscle aches,
cough, mouth sores, fatigue, loss of appetite, GI
disturbance, jaundice, flulike symptoms, blurred
vision
Copaxone
glatiramer
Daily injection
To reduce frequency, severity of
exacerbations for relapsing/remitting MS
On injection: flushing, chest pain, palpitation,
tachycardia, dyspnea
After Injection: nausea, edema, syncope, headache,
tremor, diaphoresis, hypotonia, arthralgia, seizure
Cytoxan
CTX
Neosar
cyclophosphamide
(chemotherapeutic)
Oral or injection

To slow disease progression over time when
other medications are not effective
Loss of appetite or weight gain, changes in skin
color, fatigue, dizziness, chills, shortness of breath,
edema, nausea, vomiting, GI or urinary bleeding
TABLE 10-6  Pharmacological Interventions for Individuals with Neurological and Neuromuscular System Impairments—cont'd

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
287
Gengraf
Neoral
Sandimmune
SangCya
cyclosporin-modified
(immunosuppressant)
Oral
To slow disease progression over time
Headache, GI disturbance, tremor, muscle or joint
pain, paresathesia, insomnia, nephrotoxicity,
hypertension, exacerbation when discontinued
Gammagard
Gammar-P IV
Gaminune N
Iveegam
Panglobulin
Sandoglobulin
Venoglobulin
intravenous
immunoglobulin
(antibody)
Intravenous
To slow disease progression over time when
other medications are not effective
Flulike symptoms immediately following infusion,
headache
Gilenya
fingolimod
(immunosuppressant)
Oral
To reduce frequency, severity of
exacerbations for relapsing/remitting MS
Bradycardia, headache, hypertension, weakness,
back pain, paresthesias, depression, fatigue,
dizziness, chest pain, nausea, vomiting, loss of
appetite, jaundice
Leustatin
Mylinax
2-CdA
cladribine
(chemotherapeutic)
Intravenous
To slow disease progression when other
medications are not effective
GI disturbance, loss of appetite, muscle or joint
pain, headache, insomnia, fatigue
MTX
Rheumatrex
Trexall
methotrexate
(chemotherapeutic)
Oral
To slow disease progression over time when
other medications are not effective
Dizziness, drowsiness, headache, loss of appetite,
blurred vision, seizures, confusion, weakness
Novantrone
mitoxantrone
(chemotherapeutic)
Intravenous, every 3 months
Severe advanced MS
Ventricular cardiac dysfunction, myelosuppression
(risk of leukemia)
Tysabri
natalizumab
(immunosuppressant)
Monthly, intravenous
To slow disease progression over time when
other medications are not effective
Headache, UTI, muscle and joint pain, GI
disturbance, fatigue, depression, allergic reactions,
liver dysfunction, risk of progressive multifocal
leukoencephalopathy
Zovirax
acyclovir
(antiviral)
Oral
To reduce frequency, severity of
exacerbations for relapsing/remitting MS
GI disturbances, dizziness, fatigue, agitation, joint
pain, changes in vision
MULTIPLE SCLEROSIS: MANAGEMENT OF DYSESTHESIA/NEUROPATHIC PAIN
Carbatrol
Epitol
Tegretol
Dilantin
Neurontin
Zonegran
Norpramin
carbamazepine

phenytoin
gabapentin
zonisamide
desipramine
(anticonvulsants)
Oral






Trigeminal neuralgia, pelvic pain, intense
episodic/lancinating/burning pain
Pins/needles, cramping, dysesthetic
extremity pain, tonic spasms, other
neurogenic pain, nocturnal spasms


See Seizure Medications






(Continued)

288
Section II  Orthoses in Rehabilitation
Trade Names
Generic Name (class)
Administration
Indications
Adverse Effects
Adapin
Sinequan
Triadapin
Zonalon
Elavil
Imavate
Janimine
Tofranil
Vivactil
doxepin
amitriptyline
imipramine
protriptyline (tricyclic
antidepressants)
Oral
Chronic neurogenic pain (e.g., dysesthetic
extremity pain such as burning, tingling)
Drowsiness, blurred vision, dizziness, GI and
urinary disturbances, tachycardia, hypotension,
weight gain, fatigue, headache
MULTIPLE SCLEROSIS: MANAGEMENT OF FATIGUE
Contenton
Symmetrel
Symadine
Topharmin
amantadine
(antiviral, Parkinson's)
Oral
To manage fatigue associated with chronic
MS, and drug-induced extrapyramidal
symptoms
Nervousness, restlessness, tremor, dizziness,
seizure, headache, blurred vision, GI disturbance,
edema, dry mouth, diaphoresis, tics
Provigil
modafinil
(CNS stimulant)
Oral
To manage fatigue associated with
chronic MS
Risk of dependence, allergic reaction, depression or
anxiety, hallucination, aggressiveness, arrhythmia,
dyspnea, back pain, GI disturbances
MANAGEMENT OF SEIZURES
Amytal
amobarbital
(barbiturate)
Intravenous
Status epilepticus
Sedation, nystagmus, ataxia, vitamin K and folate
deficiency
Ativan
lorazepam
(benzodiazepine)
Intravenous
Status epilepticus
Sedation, ataxia, changes in behavior
Atretol
Convline
Epitol
Macrepan
Tegretol
carbamazepine
(iminostilbene)
Oral
Complex partial seizures, tonic-clonic
seizures, trigeminal neuralgia, bipolar
disorder
Ataxia, diplopia, drowsiness, fatigue, dizziness,
vertigo, tremor, headache, nausea, dry mouth,
anorexia, agitation, rashes photosensitivity, heart
failure
Celontin
methsuximide
(succinimide)
Oral
Alternative to ethosuximide for absence
seizures
Nausea, vomiting, headache, dizziness, fatigue,
lethargy, dyskinesia, bradykinesia
Cerebyx
fosphenytoin
(hydantoin)
Intravenous
Status epilepticus
GI irritation, confusion, sedation, dizziness,
headache, nystagmus, ataxia, dysarthria
Depacon
Sodium valproate
(carboxylic acid)
Oral or injection
All types of seizures
Ataxia, tremor, sedation, nausea, vomiting,
hyperactivity weakness, incoordination,
risk of hepatotoxicity
TABLE 10-6  Pharmacological Interventions for Individuals with Neurological and Neuromuscular System Impairments—cont'd

Chapter 10  Orthotic Decision Making in Neurological and Neuromuscular Disease
289
Depakene


valproic acid
(carboxylic acid)

Oral


Absence seizures, as adjunct for other
seizure types

Nausea, sedation, ataxia headache nystagmus,
diplopia, asterixis, dysarthria, dizziness,
incoordination, depression, hyperactivity,
weakness, risk of hepatotoxicity
Depakote
divalproex sodium
(carboxylic acid)
Oral
Complex partial seizures, absence seizures,
as adjunct for other seizure types
Headache, asthenia, nausea, somnolence, tremor,
dizziness diplopia, risk of hepatotoxicity
Diamox
acetazolamide
(sulfonamide)
Oral
Absence seizures, myoclonic seizures
Drowsiness, dizziness
Dilantin
Diphen
Diphentoin
Dyantoin
Phenytex
phenytoin
(hydantoin)
Oral or injection
Status epilepticus, tonic-clonic seizures,
simple complex seizures
Ataxia, slurred speech, confusion, insomnia,
nervousness, hypotension, nystagmus diplopia,
nausea, vomiting
Felbatol
felbamate
(2nd generation)
Oral
Partial seizures, absence seizures
Used for severe seizure disorders
unresponsive to other medications
Aplastic anemia, liver failure, insomnia, headache,
dizziness, loss of appetite, nausea, vomiting
Gabitril
tiagabine
(2nd generation)
Oral
Partial seizures
Generalized weakness, dizziness, tiredness,
nervousness, tremor, distractibility, emotional
lability
Keppra
levetiracetam
(2nd generation)
Oral
Adjunct for partial seizures in adults
Sedation, dizziness, generalized weakness
Klonopin
Rivotril
clonazepam
(benzodiazepine)
Oral or injection
Myoclonic seizures, absence seizures,
kinetic seizures
Drowsiness, dizziness, ataxia, dyskinesia,
irritability, disturbances of coordination, slurred
speech, diplopia, nystagmus, thirst
Lamictal
lamotrigine
(2nd generation)
Oral
Partial seizures, tonic-clonic seizures
Dizziness, headache, ataxia, drowsiness,
incoordination, insomnia, tremors, depression,
anxiety, diplopia, blurred vision, GI disturbances,
agitation, confusion, rash
Luminol
Solfoton
phenobarbital
(barbiturate)
Oral or injection
Status epilepticus, all seizure types except
absence seizures
Drowsiness, lethargy, agitation, confusion, ataxia,
hallucination, bradycardia, hypotension, nausea
Mebaral
mephobarbital
(barbiturate)
Oral
Tonic-clonic seizures, simple and complex
partial seizures
Drowsiness, sedation, nystagmus, ataxia, folate and
vitamin K deficiency
Mesantoin
mephenytoin
(hydantoin)
Oral
Partial seizures, tonic-clonic seizures used
if Dilantin is not effective
Similar to Dilantin, but more toxic
Milontin
phensuximide
(succinimide)
Oral
Alternative to Zarontin for absence
seizures
Nausea, vomiting, headache, dizziness, fatigue,
lethargy, bradykinesia, dyskinesia
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290
Section II  Orthoses in Rehabilitation
Trade Names
Generic Name (class)
Administration
Indications
Adverse Effects
Mysoline
primidone
(barbiturate)
Oral
All seizure types except absence seizures,
essential tremor
Ataxia, vertigo, drowsiness, depression, inattention,
headache, nausea, visual disturbances
Nembutal
pentobarbital
(barbiturate)
Intravenous
Tonic-clonic seizures, simple and complex
partial seizures
Sedation, nystagmus, ataxia, vitamin K and folate
deficiency
Neurontin
gabapentin
(2nd generation)
Oral
Partial seizures in adults and children older
than 3 years, neuropathic pain
Drowsiness, dizziness, ataxia, fatigue, nystagmus,
nervousness, tremor, diplopia, memory
impairment
Peganone
ethotoin
(hydantion)
Oral
Tonic-clonic seizures; used if Dilantin is not
effective
Similar to Dilantin, but more toxic
Seconal
secobarbital
(barbiturate)
Intravenous
Tonic-clonic seizures, partial seizures
Sedation, nystagmus, vitamin K and folate
deficiency
Topamax
topiramate
(2nd generation)
Oral
Partial seizures, adjunct to tonic-clonic
seizures
Ataxia, confusion, dizziness, fatigue, paresthesia,
emotional lability, confusion, diplopia, nausea
Thosutin
Zarontin
ethosuximide
(succinimide)
Oral
Absence seizures
Drowsiness, headache, fatigue, dizziness, ataxia,
euphoria, depression, myopia, nausea, anorexia
Tranxene
clorazepate
(benzodiazepine)
Oral
Adjunct for partial seizures
Sedation, ataxia, changes in behavior
Trileptal
oxcarbazepine
(iminostilbene)
Oral
Partial seizures, tonic-clonic seizures
Ataxia, drowsiness, nausea, dizziness, headache,
agitation, memory impairment, asthenia, ataxia,
confusion, tremor, nystagmus
Valium
Valrelease
diazepam
(benzodiazepine)
Injection
Status epilepticus, severe recurrent seizures
Drowsiness, fatigue, ataxia, confusion, depression,
dysarthria, syncope, tremor, vertigo
Zonegran
zonisamide
(2nd generation)
Oral
Adjunct for partial seizures in adults
Sedation, ataxia, loss of appetite, fatigue
ABI, acquired brain injury; CHF, congestive heart failure; CNS, central nervous system; CP, cerebral palsy; GI, gastrointestinal; ICP, intracranial pressure; MS, multiple sclerosis; NMJ,
neuromuscular junction; SCI, spinal cord injury; UMN, upper motor neuron; UTI, urinary tract infection.
TABLE 10-6  Pharmacological Interventions for Individuals with Neurological and Neuromuscular System Impairments—cont'd