Handbook of Pediatric Neurosurgery

46 Surgical Management of Childhood Epilepsy:
Corpus Callosotomy and Vagal Nerve Stimulation
Oguz Cataltepe
46.1 Introduction
Resective surgical procedures in epilepsy fre-
quently provide seizure-free outcome and they are
accepted as best surgical option for patients with
epilepsy. However, resective surgery may not pro-
vide satisfactory seizure control in many patients.
More significantly, resective surgery may not be
feasible or preferable because of the location,
extent, or multifocality of the epileptogenic focus.
Resective surgical procedures are even not consid-
ered as an option in some cases such as atonic or
multifocal, nonlocalizable seizures. Palliative epi-
lepsy surgery techniques play significant role in
the management of these patients. Although, pal-
liative surgical interventions may not provide seiz-
ure-free outcome, they may still help the patient
to have a better seizure control and improved
quality of life. Corpus callosotomy (CC) and vagal
nerve stimulation (VNS) are two most commonly
used palliative epilepsy surgery interventions and
we will review these techniques here.
46.2 Corpus Callosotomy
Corpus callosum is the largest and most critical
commissure in propagation and generalization of
the epileptogenic discharges to the contralateral
hemisphere. Bilateral synchronization of epilepti-
form discharges, which is critical for generalization
of seizures, also occurs primarily via corpus cal-
losum. These anatomophysiological characteristics
of corpus callosum makes it a very attractive surgi-
cal target to prevent atonic and secondarily gener-
alized seizures and it is one of the oldest epilepsy
surgery procedures.
46.2.1 History
Corpus callosotomy is used in treatment of intract-
able epilepsy first time by Van Wagenen and
Herren in 1940.1 Then Bogen et al published their
corpus callosotomy series in 1960s, and Luessen-
hop et al and Wilson et al reported their experien-
ces in several articles in 1970s.2,3,4,5 Wilson et al
have many contributions to this technique includ-
ing introducing operating microscope to this pro-
cedure.4,5 Surgical technique that was used initially
included division of not only corpus callosum but
also hippocampal and anterior commissures. Then,
Wilson modified this technique in mid-70 s and
started not to divide anterior commissure and for-
nix and to leave the ependymal lining intact to
avoid related complications. Then, he further
modified his technique by applying two-stage sec-
tioning of the corpus callosum with a few months
interval.4,5 Gradually, two-thirds anterior callosot-
omy became a standard CC technique and com-
plete callosotomy was performed only if seizure
control with two-thirds anterior callosotomy is
not satisfactory. Although the early series had high
morbidity and mortality rates, CC gradually
became a safe, e ective, and well-established pro-
cedure with the introduction and refinement of
modern microsurgical techniques.6,7,8,9,10 However,
the number of CC surgeries dramatically decreased
during the following decades in parallel to increas-
ing popularity of vagal nerve stimulator placement
procedures.
46.2.2 Anatomy and Physiology
Corpus callosum is the largest commissure and
principal anatomical and neurophysiological con-
nection pathway between the two hemispheres
and consists of 180 to 200 million axons. Although
it mostly links homotopic areas together, it also
connects heterotopic areas.7,11,12 Corpus callosum
is frequently divided into four sections: rostrum,
genu, body, and splenium. Anterior half of cal-
losum (rostrum, genu, and anterior half of the
body) includes decussation fibers from premotor,
motor, anterior insular, and anterior cingulate
cortical areas. Anterior half of corpus callosum is
essential for the generalization of tonic, tonic–
clonic seizures, and atonic drop attacks. The poste-
rior half of the callosum includes posterior half of
callosal body and splenium. Its fibers connect pari-
etal, occipital, posterior insular, primary auditory
area, and caudal portions of parahippocampus.
46.2.3 Surgical Indications
Corpus callosotomy is considered as a treatment
option for patients with medically intractable gen-
eralized (primary or secondary) seizures that may
358

frequently cause serious injuries secondary to drop
attacks. Lennox–Gastaut is the most responsive
epilepsy syndrome to callosotomy. The patients
with atonic seizures, infantile spasms, unclear-
onset epileptogenic abnormality with secondary
widespread generalization, di use cortical malfor-
mations with generalized seizures might also be
good candidates for CC.9,13,14,15,16 CC may also have
a diagnostic utility to define the seizure focus in
patients with rapid generalization of epileptogenic
activity.17 In these patients, CC may be helpful to
determine the focus of ictal onset by isolating the
hemispheres and providing an opportunity for fur-
ther diagnostic work-up to find a focus, which may
be amenable for resective surgery.
46.2.4 Preoperative Assessment
Preoperative assessment of these patients is simi-
lar to other epilepsy surgery patients. First goal
during the assessment of the patient is ruling out
any lateralizable and localizable epileptogenic
abnormality with a complete investigative work-
up including brain magnetic resonance imaging
(MRI), MR venography, video/electroencephalog-
raphy (EEG) monitoring, and neuropsychological
assessment. Video/EEG monitoring would provide
a critical information regarding seizure semiology
and electrophysiological characteristics of epilep-
togenic abnormalities. MRI is helpful to assess the
structural abnormalities and MR venogram pro-
vides significant information for surgical planning
of CC by showing location and distribution of para-
sagittal veins. Neuropsychological assessment is
especially significant in these cases because pres-
ence of mixed cerebral dominance in complete CC
cases may cause significant postoperative language
deficits.
46.2.5 Surgical Technique
CC procedure has been generally performed as
anterior two-thirds CC. Complete callosotomy is
performed as a second step only if the patient does
not benefit from the initial procedure.
The patient is placed in supine position and the
head is secured with a pin head holder. Right-
sided approach is used unless the patient has a
pathology on the left hemisphere or has a right
hemispheric dominance. The neck is flexed 20
degrees and is slightly tilted to right to use gravity
for retraction during the procedure. A 6-cm length,
lazy-S incision is marked 2 cm anterior and parallel
to the coronal sutures. The incision crosses the
midline to the left side about 2 cm. Two burr holes,
2 cm anterior and 3 cm posterior to coronal suture,
are placed over the sagittal sinus and one burr hole
is placed over the coronal suture about 4 cm lateral
to midline. A triangular-shaped craniotomy flap is
removed. Right-sided edge of the sagittal sinus is
exposed and covered with Surgifoam and cotto-
noids. Dura is tented through the drill holes on
surrounding bone edges. Intravenous mannitol can
be administered at this point if needed. We do not
use lumbar drain in these cases. Then the dura is
opened U-shape and reflected over the sagittal
sinus. MR venogram is reviewed carefully before
surgery to determine the location of large bridging
veins and/or dural venous lacuna. If there are large
draining veins or venous lacuna, dural opening is
made accordingly by leaving dural patches on
them to work around these structures. Arachnoid
granulations are gently dissected from the dura
and sagittal sinus wall, then dural flap is further
retracted, and interhemispheric fissure as well as
falx are exposed. Cottonoid pledgets are placed
over the exposed cortex. At this stage, surgical
microscope is brought into the field and the
remaining part of the surgery is continued under
the microscope. If there are major bridging veins
entering to the sagittal sinus, their arachnoid
sleeves can be dissected as far lateral as possible to
minimize their stretch during the retraction and
surgical procedure can be carried out around these
veins using separate surgical corridors anterior
and posterior to them. However, if the bridging
veins are well anterior to coronal suture and not
draining from eloquent cortex, then they can be
sacrificed if needed. Then the cortex is gently
retracted away from the falx using a single retrac-
tor blade on the mesial frontal cortex. Arachnoid
adhesions extending from cortex to sagittal sinus
or falx can be easily dissected with bipolar and
microscissors while sliding the retractor blade
down. The inferior edge of the falx can also be seen
at this stage. Then the retractor blade is gently
slided further downward along a cottonoid until
cingulate gyrus is seen. At this stage, arachnoid
membrane over the mesial frontal cortex in inter-
hemispheric fissure may be opened at a few
separate points using a fine bipolar forceps and
cerebrospinal fluid (CSF) is drained by suctioning
it through the cotton balls. This maneuver pro-
vides a much relaxed exposure and the retractor
can be removed at this stage and only used as
needed to avoid unnecessary pressure over the
cortex. Then dissection is further advanced down-
ward to fully expose the cingulate gyri. Separation
Surgical Management of Childhood Epilepsy: Corpus Callosotomy and Vagal Nerve Stimulation
359

of cingulate gyri from each other can be di cult in
some cases because of arachnoid adhesions and
interdigitation of gyri. After finding a relatively
free part, dissection of the cingulate gyri can be
performed easily using bipolar forceps and Pen-
field # 4 dissector. At this point, underlying glisten-
ing white corpus callosum is encountered with a
very distinctive appearance and consistency. Next,
the cortical ribbon is repositioned and further CSF
drainage is obtained through supracallosal cistern.
Then, flu y small cotton balls are placed down-
ward just over corpus callosum at both ends of the
exposed area to keep cingulate gyri separated and
to expose corpus callosum better. At this stage,
pericallosal arteries are also seen. They frequently
travel very close to each other with some tiny
bridging vessels and sometimes they may even
override. Then pericallosal arteries are mobilized
and separated to have a wider exposure of the cor-
pus callosum. This will provide a satisfactory expo-
sure for performing planned CC. Corpus callosum
division should be done between pericallosal
arteries by staying strictly on the midline. Dividing
corpus callosum lateral to pericallosal artery may
cause injury to perforating vascular structures in
the pericallosal sulcus and cause ischemic damage
and edema. Corpus callosum is divided longitudi-
nally using microdissectors and bipolar forceps.
When the division of corpus callosum is deepened,
a grayish color of the ependymal lining can be
easily appreciated. Opening the ependyma and
entering into ventricle should be avoided if possi-
ble to decrease the risk of chemical meningitis. CC
is continued anteriorly around the genu until the
visualization of anterior commissure between the
fornices. Anterior commissure should be left intact.
Then dissection continues posteriorly on the ros-
trum and anterior body of the corpus callosum.
Posterior end of the callosotomy is determined
based on surgical planning. If anterior two-thirds
is aimed, then the length can be measured preop-
eratively using midsagittal MRI images. The meas-
urement is translated onto the surgical field using
a ruler or by using the thickness of the ribbon as
measuring tool. Another practical and more reli-
able tool to use for this purpose is neuronavigator.
After completing callosotomy as planned, meticu-
lous hemostasis is obtained and the layers are
closed appropriately.
If the goal is performing posterior callosotomy
or completing the anterior two-thirds craniotomy
to a complete callosotomy, a second incision, par-
allel to the first one, is placed at vertex level. The
incision crosses the midline 2 cm to the left and
the surgical field is exposed with self-retaining
retractors. Targeted exposed area in midline
extends from 4 cm anterior to lambda to just over
or 1 cm behind the lambda posteriorly. The burr
holes in midline are placed on sagittal sinus and
the lateral burr hole is placed 4 cm lateral to mid-
line on the right to remove a free bone flap. Using
the same surgical technique described above, the
dura is opened and the dissection is continued
toward the posterior body of the callosum and
splenium by following falx. It is very critical to stay
on midline during this part of the procedure to
avoid any injury to fornices. Neuronavigator would
be very helpful in these cases. The division of the
corpus callosum ends with the exposure of the
arachnoid membranes covering the vein of Galen.
46.2.6 Surgical Complications
and Side E ects
Complication rates for CC procedure have been
reported 3 to 10% in di erent series. Most com-
mon complications are cerebral edema, infarction,
meningitis (septic/aseptic), hydrocephalus, ische-
mia, and subdural/epidural hematoma originating
from parasagittal veins.8,9,18,19 Another well-know,
although rare, issue is disconnection-related syn-
dromes. This is closely related to the extent of cal-
losotomy. Anterior two-thirds callosotomy may
cause decreased spontaneity of speech that gener-
ally persists between a few days or weeks. In some
cases, left-sided neglect, apraxia, various degrees
of left leg paresis, hemiparesis, left-sided or bilat-
eral forced grasp reflexes, bilateral extensor plan-
tar responses, and urgency incontinence may be
also seen.8,9,18 Symptoms typically improve over
days to weeks. Surgical retraction-related brain
edema on nondominant parasagittal cortex, sup-
plementary motor area, or premotor cortex might
be responsible from these findings.
On the other hand, posterior callosotomy causes
interhemispheric somatosensory, auditory, and
visual disconnection syndromes, which are fre-
quently temporary. However, permanent interhe-
mispheric sensory disconnection can also develop
and especially sectioning of splenium can result in
visual and sensory disconnection syndromes with
inability to describe the objects presented visually
or tactilely on the nondominant side.6,7,13,18
Complete corpus callosotomy–related side
e ects include both anterior and posterior callos-
otomy–related findings which are described above.
It may also infrequently cause interhemispheric
Functional Disorders
360

antagonism. Split-brain syndrome can develop
after complete callosotomy which involves lan-
guage impairment, hemisphere competition, and
disordered attention-memory sequencing. These
findings generally improve with time.7
46.2.7 Outcome
One of the largest reviews on corpus callosotomy
included 563 patients from multiple centers.20 This
study reported that 60.9% of the patients had
worthwhile improvement with rare seizures, 7.6%
of the patients had seizure-free outcome, and
31.4% had no improvement. Some other large ser-
ies also provided similar results.18,21
The outcome of the corpus callosotomy has also
been reviewed based on the extent of callosot-
omy.8,10,17,22,23 Spencer et al reported better out-
come with complete corpus callosotomy than
partial callosotomy (80 vs. 50% satisfactory
improvement).21 Roberts and Siegel reported these
rates as 81 and 38% in their series.8 Some other
authors also reported better outcome with com-
plete corpus callosotomy in comparison to partial
corpus callosotomy.10,19,23,24,25,26,27,28 On the other
hand, Jea et al reported that children in both ante-
rior two-thirds and complete callosotomy groups
achieved comparable improved seizure control, 80
and 87.5%, respectively.16 Again, Fuiks et al did not
find any significant di erence between the two
approaches.22 Tanriverdi et al reported a large
series that includes 95 patients and stated that
complete callosotomy was not necessary at least
initially and it should be reserved as a second stage
in those cases in which anterior two-thirds resec-
tion fails.29
Outcome assessments based on seizure type
were reported in several series. Roberts and Siegel
published a detailed outcome analysis based on
the seizure types.8 They reported that atonic seiz-
ures responded best to corpus callosotomy with
72% significant improvement rate, 21% of them
being seizure free. These authors observed 34%
seizure freedom and 24% significant improvement
(> 50% reduction in seizure frequency) in patients
with generalized major motor seizures and 42%
seizure freedom and 20% significant improve-
ments in patients with complex partial seizures.
The worst outcome was seen in the focal motor
seizure group. According to Pinard et al, the best
outcomes were associated with drop attacks with
dramatical reduction in frequency in 90% of the
children.10 In another series, Kawai et al reported
complete resolution of drop attacks in 80% of their
patients.14 In Tanriverdi et al series, the best res-
ponse was achieved in generalized tonic–clonic
seizures (77.3%), followed by drop attacks (77.2%),
and generalized tonic seizures and simple partial
seizures (71.4%).29
Overall, best response to corpus callosotomy is
seen in patients with generalized tonic–clonic
seizures with drop attacks, and patients with com-
plex partial seizures with or without secondary
generalization. Atypical absence seizures consti-
tute the worst outcome group.15,29
46.3 Vagal Nerve Stımulatıon
VNS therapy has been used in the treatment of
refractory epilepsy since 1988. Its e ectivity and
safety profile extensively tested since then and its
e ciency is consistently demonstrated in many
trials and series. Currently, VNS is one of the most
commonly used adjunctive treatment modalities
in epilepsy.
46.3.1 History
First study on the e ect of VNS on cerebral activity
was performed by Bailey and Bremer in 1938 in an
animal model.30 They demonstrated VNS-related
changes in cortical EEG patterns using various ani-
mal models. Then in 1952, Zanchetti used a chemi-
cally induced seizure model in cats to demonstrate
reduction in interictal epileptic activities by
intermittent stimulation of vagal nerve.31 Several
decades later, Zabara conducted a series of animal
studies to assess the e ect of VNS on seizure con-
trol and published his findings in 1985.32 Then,
Zabara and Reese developed first vagal nerve stim-
ulator model and then, first VNS implantation pro-
cedure in a patient was performed by Bell and
Penry in 1988.33,34 This was followed by a series of
pilot studies with VNS Therapy System (Cyberonics
Inc., Houston, Texas). VNS Study Group conducted
five multicenter VNS clinical trials, the final one
being in 1996, and published their results in a
series of articles.33,35,36,37
European community
approved VNS therapy for epilepsy in 1994 and
Food and Drug Administration (FDA) approved it in
1997.33 Finally, American Academy of Neurology’s
Therapeutics and Technology Assessment Subcom-
mittee reported that “su cient evidence exists to
rank VNS for epilepsy as e ective and safe, based
on a preponderance of Class I evidence.”38,39
Surgical Management of Childhood Epilepsy: Corpus Callosotomy and Vagal Nerve Stimulation
361

46.3.2 Vagus Nerve Anatomy
Vagus nerve is a mixed cranial nerve with both
a erent and e erent fibers. A erent fibers consti-
tute approximately 80% of the vagus nerve which
is composed of myelinated A, B, and nonmyeli-
nated C fibers. Vagus nerve receives somatic sen-
sory, visceral sensory, and special sensory a erent
fibers and reaches to many parts of the brain with
extensive projection fibers. Nucleus tractus solitar-
ius (NTS) is the main recipient of the majority of
a erent sensory fibers. Di use pathways originat-
ing from NTS are connected to dorsal raphe, locus
coeruleus, the nucleus ambiguous, and reaches with
extensive projection fibers to wide areas in the brain
including cerebellum, hypothalamus, thalamus, and
limbic structures. This anatomical and physiological
characteristic of vagus nerve makes it a perfect
pathway for neuromodulation.40,41
46.3.3 Mechanism of Action
Precise mechanism of seizure suppression of VNS
therapy is still not completely understood. It was
demonstrated that vagal nerve projections extend
noradrenergic and serotonergic neuromodulatory
systems of the brain via NTS through locus coeru-
leus and raphe nuclei. Some studies using animal
models documented that activation of noradrener-
gic and serotonergic neurons has antiepileptic
e ects. It has also been demonstrated that VNS sti-
mulation increases neuronal c-fos protein expres-
sion, increases regional blood flow in some areas
such as thalamus, putamen, and cerebellum and
again causes local or regional increase in GABA
levels and decrease in glutamate aspartate lev-
els.40,41,42,43,44,45 Therefore, it is possible that action
of VNS might be related to noradrenergic and sero-
tonergic neuromodulatory systems, modulation of
excitatory and inhibitory neurotransmitters, and
also possibly by modified cerebral electrical activ-
ity through thalamocortical pathways.
46.3.4 Safety and E ectiveness
Series of large multicenter studies are conducted
and many series are published to assess the safety
and e ectiveness of VNS since the first pilot study
in 1998.45,46,47,48,49,50,51,52,53 VNS Study Group con-
ducted three open-label and two double-blind
randomized controlled trials and results were
published separately and also as a meta-analysis of
five studies.35,36,37,38,39
It was reported that
although only 1 to 2% of patients became seizure
free, many patients had significant long-term ben-
efit from VNS with an average 50% seizure reduc-
tion in 43% of patients at 3 years after VNS
placement. Although, there is no prospective,
randomized controlled trial in pediatric age group,
many pediatric series also consistently demon-
strated sustained, long-term improvement in
seizure control and quality of life after VNS place-
ment.46,50,51,52,53
46.3.5 VNS Therapy System
Components
The VNS Therapy System (Cyberonics Inc.,
Houston, Texas) composed of an implantable, pro-
grammable pulse generator and a bipolar lead.
Nonimplantable components of the system are a
programming wand and a handheld computer
with software. The pulse generator delivers a
biphasic current to the vagal nerve through the
bipolar lead with cycles between on and o peri-
ods. Current generators are model 102/102 R 105
and 106 (25 g, 6.9-mm thickness) and smaller one,
model 103 (16 g, 6.9-mm thickness) (Fig. 46.1).
There are two lead sizes (2- and 3-mm helix inner
diameters). VNS lead has three helical (two elec-
trodes and one anchor tether), which are wrapped
around the vagal nerve and an extension cable
ending with a connector pin for insertion into gen-
erator47 ( Fig. 46.2 and Fig. 46.3).
46.3.6 Indications
VNS is used as an adjunctive therapy in patients
with medically refractory epilepsy who are not
candidates for resective epilepsy surgery or who
Fig. 46.1 Various VNS pulse generators: the models
102,103, and 105. (Reproduced with permission from
Cyberonics.)
Functional Disorders
362

have not responded to previous resective surgical
interventions satisfactorily. Its e ectiveness is
demonstrated in generalized epilepsy, Lenox–
Gastaut syndrom e, and partial-onset seizures.38,45,
46,47,48,49,50,53
46.3.7 Preoperative Assessment
The patients have standard epilepsy surgery work-
up. It needs to be demonstrated that patients’ seiz-
ures are medically refractory and no resectable
epileptogenic focus is present. History of cardiac
dysfunction, apnea, and swallowing di culties
should also be questioned because of the possibil-
ity of worsening on these problems with VNS
placement.
46.3.8 Surgery
VNS placement is typically performed under gen-
eral anesthesia. Left vagal nerve is used for VNS
placement because right vagal nerve innervates
sinoatrial node and stimulation of left vagal nerve
is less likely cause any cardiac problem.
The patient is placed in supine position with a
shoulder role under the neck to give some exten-
sion. Head stays in neutral position or slightly
turns to right. Left-sided neck and chest are
prepped and draped as usual sterile manner. Intra-
venous antibiotic is given before skin incision. Sur-
gery is performed under optic magnification. Two
skin incisions on the left side are marked: one over
the neck and the other is on chest. Neck incision is
placed at midpoint of a line between mastoid tip
and medial edge of the clavicula. A transverse,
2- to 3-cm length incision, preferably on a skin
fold, is marked by centering the medial border of
sternocleidomastoid muscle (SCM). Chest incision
is placed on anterior axillary line and the length is
determined based on the generator size. While a
small, 2 cm, incision might be su cient for model
103 generators, a larger incision will be needed for
models 101, 102/102 R. Neck incision is fashioned
first. After skin incision on neck, platysma is
sharply opened and undermined superiorly and
inferiorly. Then cervical fascia is opened along the
medial border of sternocleidomastoid muscle. Dis-
section continues along the medial border of SCM
toward the neurovascular bundle. Carotid pulse is
palpated to guide the dissection. After reaching
the carotid sheath, it is opened sharply parallel to
vascular structures. Internal jugular vein and caro-
tid artery are easily exposed and gently separated
by dissecting bluntly and holding separated with
handheld retractors. Vagus nerve is generally
located between these vessels posteriorly and fre-
quently closer to jugular vein, although variations
on the location of vagus nerve is not uncommon.
Then about 3-cm length segment of vagus nerve is
dissected proximally and distally and a vessel loop
is passed underneath. Then chest incision is fash-
ioned to create an appropriate size subcutaneous
pocket for generator. This pocket is prepared in
subclavicular area at left upper chest by exposing
pectoralis fascia. Then a tunneler was inserted
from chest incision and exited from neck incision.
Lead cable is placed subcutaneously through the
tunneler. Then helical electrodes and anchor tether
are wrapped around vagal nerve one by one. First
anchoring electrode, then positive electrode, and
lastly negative electrode is placed. Anchor helix
should be located farthest away from head and
Fig. 46.3 Configuration of implanted VNS system.
(Reproduced with permission from Cyberonics.)
Fig. 46.2 VNS lead with helical electrodes. (Repro-
duced with permission from Cyberonics.)
Surgical Management of Childhood Epilepsy: Corpus Callosotomy and Vagal Nerve Stimulation
363

other two electrodes should be closer to head. All
three helical electrodes should be coiled around
vagal nerve segment below where the superior
and inferior cardiac branches separate from the
vagus nerve. All electrodes have attached sutures
at the end and all manipulations during electrode
placement should be done by holding these
sutures, but not electrodes itself, with fine forceps.
It is also very significant not to stretch or to devas-
cularize vagus nerve or its branches during coiling
the electrodes. Vagus nerve also should be kept
moist throughout the procedure. After wrapping
all three coils around the vagus nerve, it should be
verified that lead cables exiting from coils are at
the same direction and parallel to each other as
well as to vagus nerve. After wrapping all three
coils around the vagus nerve, coiled nerve is
placed back to its original anatomical location
without any stretch. Then a strain relief loop was
created at the distal end by turning the cable
upward. The lead is secured to deep fascia with a
tie-down and nonabsorbable suture. Then another
strain relief loop is created above the SCM and
again it is secured to fascia with another tie-down.
Then lead connector pin is inserted into pulse
generator and connection is locked down by tight-
ening the set screw with hex screwdriver. First
intraoperative diagnostic testing of the system is
performed at this stage to ensure the system integ-
rity. Then pulse generator is inserted into subcuta-
neous pocket and extra lead is coiled and placed to
the side of the generator. The generator is secured
to pectoralis fascia with a silk suture. Surgical sites
are irrigated with antibiotic-containing saline.
Then all layers, platysma, subcutaneous tissue, and
skin incision are closed with absorbable sutures.
Second intraoperative diagnostic testing is again
performed after skin closure using programming
wand and handheld computer to confirm that the
lead impedance is correct and the generator func-
tions normally.
46.3.9 Surgical Complications
and Side E ects
VNS procedure has relatively low rate of complica-
tions. Complications include infection, hoarseness
of voice, temporary vocal cord paralysis, and,
although much rare, nerve damage, vascular
injury, bradycardia, asystole. Side e ects typically
occur during stimulation and improves over time.
Most common side e ects are voice alteration/
hoarseness, throat paresthesia, cough, shortness of
breath, and less frequently, drooling, and sleep
apnea. Side e ects can be frequently eliminated
with some changes in stimulation parameters such
as reducing the pulse width or signal frequency
even without changes in output current.36,37,38,45,46,
50,51,52,53,54
46.3.10 Postoperative Care
VNS system is generally activated 2 weeks after
implantation to give some time to recover. Initial
setting is typically 0.25-mA output current, 20- to
30-Hz frequency, 250 to 500 microseconds pulse
width, on for 30 seconds, o for 5 minutes. The sti-
mulation setting is readjusted by epileptologist
over the weeks based on the patient’s response
and degree of side e ects. The goal is obtaining
maximum seizure control with minim al side
e ect.
Long-term follow-up is performed in epilepsy
clinic with periodic diagnostic checks to determine
the status of generator. Approximate battery life of
the pulse generator is 5 to 6 years, depending on
set stimulation parameters as well as extent of
magnet use. It is always preferable to replace the
generator before it is depleted.
46.3.11 Precautions
Patients with VNS should not receive shortwave
diathermy or microwave diathermy. Again, thera-
peutic radiation therapy, external defibrillation,
extracorporeal shockwave lithotripsy, or electro-
surgery may damage the pulse generator. MRI
can be performed with certain conditions. It
should not be performed with MRI body coil in
transmitter mode. 1.5 Tesla brain MRI with trans-
mit-and-receive type head coils is considered as a
safe procedure. The patient’s VNS generator output
current should be set to 0 mA before MRI and it
should be tested and reprogrammed to original
setting after MRI. Diagnostic ultrasound is a safe
procedure for patients with VNS.47
46.3.12 Outcome
All published outcome studies regarding VNS in
pediatric age group shows satisfactory benefit on
seizure control.36,37,38,45,46,50,51,52,53,55 Several large
series reported about 50% responder rate with,
again, about 50% decrease in overall seizure fre-
quency. Elliott et al reported 56% seizure reduction
and 64% responder rate in a series of 436
patients.56 These rates were 51 and 59% (n:138
Functional Disorders
364

patients) in De Herdt, 51 and 59% (n: 269 patients)
in Labar, 44% and 43% (n:440 patients) in Morris,
58% and 57% (n: 125 patients) in Helmers et al ser-
ies.37,57,58,59 It has been also consistently demon-
strated in all these studies that response to VNS
therapy improves with tolerance to side e ects
over time and is also sustains long term.
46.3.13 Failure and Removal
When necessary, both generator and lead can be
removed. While generator removal is a simple pro-
cedure, removal of the lead is a challenging proce-
dure with certain risks because of scarring of coil
electrodes to vagus nerve and even to adjacent
vascular structures. If removal of coil electrodes is
not feasible, the lead might be removed by cutting
the lead to leave only coils in place. In that case, no
more than 4 cm of the lead wire should be left
remaining.
46.4 Conclusions
Both corpus callosotomy and VNS therapy are
e ective palliative treatm ent options for patients
w ith m edically refractory epilepsy. Callosotomy
is associated with greater e cacy in patients
w ith drop attacks and Lennox–Gastaut syndro-
m e, but it has higher risk for complications than
VNS. Safety and e ectiveness of VNS therapy
have been confirm ed w ith m any studies includ-
ing several random ized controlled trials and it
has been used w idely both in adult and pediatric
patients. VNS becam e m ost com m only used pal-
liative surgical procedure today. Although VNS
has comparable results in m ost of the cases, cor-
pus callosotomy is still a viable option in the
patients with drop attacks and Lennox–Gastaut
syndrom e and also in patients w ho did not
respond to vagal nerve stim ulator. In general,
VNS is considered as the initial approach in vast
m ajority of cases because of better adverse event
profile than corpus callosotomy which is still the
m ore e cient treatm ent option for drop attacks
and Lennox–Gastaut syndrom e.24,25,26,27
46.5 Common Clinical
Questions
1. What is the most common corpus callosotomy
technique and which parts of the corpus
callosum are divided?
2. Describe the most common complications of
corpus callosotomy.
3. Which patient group responds better to corpus
callosotomy?
4. What is the mechanism of action of VNS
therapy?
5. Describe the most common complications and
side e ects of VNS therapy.
46.6 Answers to Common
Clinical Questions
1. Partial or anterior two-thirds corpus
callosotomy is the most common callosotomy
technique today. Genu, rostrum, and anterior
half of callosal body is divided and posterior
end of the callosal body with splenium is spared
in this technique.
2. Cerebral edema, meningitis (septic/aseptic),
hydrocephalus, ischemia/infarction, subdural/
epidural hematoma, and disconnection
syndromes are most commonly seen
complications of corpus callosotomy
procedures.
3. Patients with generalized tonic–clonic seizures
with drop attacks and Lennox–Gastaut
syndrome respond better to corpus
callosotomy.
4. We do not know the precise mechanism of
action of VNS therapy. However, mechanism of
action of VNS most likely related to
noradrenergic and serotonergic
neuromodulatory systems, modulation of
excitatory and inhibitory neurotransmitters,
and also possibly related to modification of
cerebral electrical activity through
thalamocortical pathways.
5. Voice alteration/hoarseness, throat paresthesia,
cough, shortness of breath, and less frequently,
drooling, and sleep apnea.
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[36] Handforth A, DeGIorgio CM, Schachter SC, et al. VNS therapy
for partial-onset seizures: a randomized active control trial.
Neurology. 1998; 51:48–55
[37] Morris GL, Mueller WM. Long-term treatm ent with VNS in
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[38] Schachter SC. Vagus nerve stim ulation therapy summary:
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[39] Fisher RS, Handforth A. Reassessment: VNS for epilepsy: a
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[40] Fanselow EE. Central mechanisms of cranial nerve
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[43] Naritoku DK, Terry WJ, Helfert RH. Regional induction of fos
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Surgical Management of Childhood Epilepsy: Corpus Callosotomy and Vagal Nerve Stimulation
367

47 Surgical Management of Pediatric Spasticity
Michael M. McDowell, Michelle Q. Phan, Richard C.E. Anderson
47.1 Introduction
Spasticity is a condition of hypertonia, causing
hyperactive reflexes, poor coordination, and weak-
ness that can greatly a ect a child’s comfort level
and ability to perform daily activities. Spasticity is
distinguished from other forms of childhood
hypertonia, such as rigidity and dystonia, in that it
is defined as hypertonia with velocity-dependent
resistance to externally imposed movements.1
47.2 Epidemiology and
Pathophysiology
In children, the most common cause of spasticity
and motor disability is cerebral palsy. Cerebral
palsy is not a discrete disorder, but a range of non-
progressive syndromes of movement and posture
due to static injuries to the developing fetal or
infant central nervous system (CNS). Cerebral palsy
is estimated to occur in 2 to 3 of every 1,000 live
births, and in premature infants born before 28
weeks’ gestational age, the incidence rises up to 100
per 1,000.2
Advances in neonatal care have
improved the survival in newborns of low birth
weight and there has been a corresponding increase
in the incidence of cerebral palsy.3 Other factors
that are linked to the development of cerebral palsy
include multiple births, chorioamnionitis, antepar-
tum vaginal bleeding, second stage of labor lasting
longer than 4 hours, perinatal asphyxia, and perina-
tal infection.2,4,5,6,7,8 Following cerebral palsy, com-
mon causes of childhood spasticity are traumatic
brain injury, spinal cord injury, meningitis, ence-
phalitis, stroke, and pediatric multiple sclerosis.
Spasticity can result from any disease process
that impairs the upper motor neurons within the
CNS, causing a decrease in descending inhibitory
corticospinal and reticulospinal input to short-
latency stretch reflexes and a loss of functionally
important long-latency reflexes. Disinhibition of
short-latency reflex arcs leads to the hyperexcit-
ability of simple stretch reflexes. Combined with
reduced facilitation of functional, polysynaptic, or
long-latency reflexes, this results in a profound
alteration of proprioception.9 Initial maladaptive
hypertonic movement patterns, with reduced pro-
prioceptive feedback, lead to secondary viscoelas-
tic changes in muscle fiber, collagen tissue, and
tendon properties that propagate cycles of paresis,
contracture, and spasticity (Fig. 47.1).10,11,12
Untreated, these changes can progress to joint and
muscular contractures, bony deformations, joint
subluxations and dislocations, and permanent loss
of joint mobility, contributing to weight loss, skin
breakdown, and chronic pain.10,11,13,14,15,16
47.3 Diagnosis and
Examination
The clinical evaluation of spasticity requires a
thorough accurate history with input from patient,
caretakers, and therapists. The history should
inquire about possible gestational and perinatal
events, the patient’s motor and cognitive mile-
stones, potential triggers of spasticity, family his-
tory of motor disorders, patient’s quality of life
and functional limitations.17,18 There are a variety
of complementary global and specific functional
measurement instruments; the gross motor per-
formance measure and pediatric evaluation of
disability index are generally considered the best
standard measures of function.19
The physical examination should include assess-
ments of motor power, muscle tone, active and
passive range of motion (PROM) and joints, deep
tendon reflexes, station, presence of limb deform-
ities or contractures, and spinal alignment.
Spasticity is di erentiated from other causes of
hypertonia by characteristic features including
velocity dependence, the clasp-knife phenomenon,
stroking a ect, and di erential distribution with
antigravity muscles.13,20 Spasticity can be quanti-
fied by rating systems such as the modified Ash-
worth scale, Tardieu scale, and pendulum test. The
modified Ashworth scale is the most widely used
in clinical practice and as an end point in clinical
trials, it does not require additional instruments
and is simple to administer (Box 47.1); however, it
does not di erentiate resistance due to spasticity
and fibrotic changes in muscle.21,22
Supplementary testing may involve imaging
studies such as cranial ultrasound, computed
tomography (CT), or magnetic resonance imaging
(MRI) in order to evaluate for hemorrhage, hydro-
cephalus, or other structural abnormalities of the
CNS. A majority of cerebral palsy patients have MR
368

abnormalities, with general patterns of gyral
anomalies, periventricular leukomalacia, and water-
shed cortical or deep gray nuclear damage.23,24
Preoperative MR findings may help predict post-
operative improvement, in particular, after selective
dorsal rhizotomy.25
47.4 Nonsurgical Management
The goal of management is to reduce spasticity
and halt the progression of contractures or
deformities in order to improve the ease of care-
giving, decrease pain, and increase quality of life.
47.4.1 Nonpharmacological
Therapy
Nonpharmacological therapy is used to maximize
range of motion, strengthen muscles, inhibit spas-
tic agonist muscles, and encourage adaptive motor
development. While controlled trials are limited,
physical and occupational therapy are mainstays
in the treatment of spasticity and are requisite for
surgical and medical interventions to achieve their
maximal benefit.26,27,28 Specific exercises that have
been shown to help reduce spasticity include
cycling, strengthening exercises, and treadmill
training.29,30,31,32,33 Static weight-bearing exercises
Fig. 47.1 Diagram depicting the cascade of mechanisms contributing to spastic movement disorders.
Surgical Management of Pediatric Spasticity
369

like standing with the assistance of tilt tables and
standing frames can reduce spasticity, improve
bone mineral density, prevent hip dislocation, and
improve bowel and urinary functions. In contrast,
passive stretching remains largely evidence-free
despite its widespread popularity.34,35,36
Con-
straint-induced therapy, in which temporary
splinting or casting is used to encourage utilization
and strengthening of less dominant muscle
groups, has received renewed attention in the past
decade due to positive results in adult stroke ther-
apy; constraint in cerebral palsy patients showed
better quality movements and structural neuro-
plastic changes.37,38 While the evidence of upper
extremity orthoses in children with cerebral palsy
is inconclusive, ankle–foot orthoses are commonly
used to treat dynamic equinus in cerebral palsy
and can reduce ankle excursion and increase dor-
siflexion in foot strike.39,40 The use of orthotics for
neurodevelopmental retraining are particularly
important during the periods of weakness follow-
ing botulinum toxin treatment.41
47.4.2 Oral Antispasticity Drugs
Oral antispasticity drugs can be used alongside an
e ective physical program or more invasive thera-
pies. Use of these drugs is patient-centered as the
drugs have di erent side e ect profiles. Baclofen,
diazepam, tizanidine, dantrolene, and gabapentin
are the most prescribed oral antispastic drugs
(Table 47.1).
Baclofen is the most widely used antispastic drug
in clinical practice, although most research involving
oral use has been conducted in adults. Baclofen
should be started at the lowest possible dose to
minimize side e ects such as sedation, somnolence,
and vertigo. It must be carefully tapered when start-
ing and discontinuing use in order to avoid central
side e ects of rebound spasticity, hallucinations,
hyperthermia, and seizures.42,43
Diazepam is e ective for short-term treatment
of spasticity, but there are no studies formally
addressing whether it improves motor function,
and caution of physical dependence with pro-
longed use has limited its long-term use.44 Clona-
zepam has been found to be particularly useful in
treating nocturnal spasms.13
Sodium dantrolene is the only major antispastic
drug that works at the muscle, rather than in the
nervous system. Although it has been shown to
Table 47.1 Oral medications utilized in the treatment of spasticity
Drug

Mechanism of action

Adverse effects
Baclofen

GABA agonist

Drowsiness, respiratory depression, ataxia, confusion
Diazepam

Benzodiazepine receptor agonist

Lethargy, rapid tolerance and dependence
Dantrolene
Blocks calcium efflux from muscle sarcoplasmic
reticulum

Weakness, hepatotoxicity, rash
Tizanidine

α2 adrenergic agonist

Sedation, dizziness, hypotension
Gabapentin

Alters voltage-gated calcium channel traffic

Dizziness, somnolence, nystagmus
Cannabinoids Cannabinoid receptor agonist
Palpitations, altered mentation, gastrointestinal
distress
Abbreviation: GABA, γ-aminobutyric acid.
Box 47.1 The modified Ashworth
scale, measuring the relative
spasticity in an individual muscle
group
The individual muscle group scores and mean
score for lower or upper extremities are fre-
quently used both in clinical practice and
research studies to approximate the objective
outcome of spasticity-reducing operations.
0 = No increase in muscle tone.
1 = Slight increase in muscle tone.
1 + = Slight increase in muscle resistance
throughout the range.
2 = Moderate increase in muscle tone through-
out the range of motion; passive movement is
easy.
3 = Marked increase in muscle tone throughout
the range of motion; passive movement is
di cult.
4 = Marked increase in muscle tone; a ected
part is rigid.
Functional Disorders
370

reduce spasticity in children with cerebral palsy, it
is infrequently used chronically due to hepatotox-
icity.43,45
Tizanidine has been found to be able to reduce
spasticity in studies with adults with multiple
sclerosis and spinal cord injury and in small stud-
ies with children with cerebral palsy. While
muscle weakness may be seen less with tizanidine
than baclofen, tizanidine may have cardiovascular,
CNS, and hepatotoxic e ects that must be taken
into account.46
Gabapentin has been shown in small studies to
have good tolerability and benefits for spasticity,
but has mostly been investigated in the context of
spinal cord injury or multiple sclerosis.47 Cannabi-
noids have been of interest recently as a treatment
for pain and spasticity in adults with multiple scle-
rosis, but have not been used in children.47
47.4.3 Intramuscular Injections
Intramuscular injections of alcohol, phenol, and
botulinum toxin produce neuromuscular block-
ades that can help treat focal spasticity or manage
problem muscle groups in more generalized spas-
ticity.
Five to seven percent phenol or 45% alcohol
injections perineurally or into the motor point of
selected muscles induce necrosis of axons in
hyperexcitable anterior horn cells. This produces a
reduction in limb tone that can last up to 12
months when phenol is used and 2 to 5 months
when alcohol is used. The sustained reduction in
tone and relative low cost of phenol injections are
balanced with side e ects including pain and dys-
esthesia due to necrosis of secondary axons in the
peripheral nerve, lethargy, and nausea due to sys-
temic absorption, and potential necrosis at the
injection site. Both treatments are rarely used
today due to the advent of botulinum toxin
therapy.43
Botulinum toxin acts to inhibit the release of
acetylcholine at the neuromuscular junction, and
today, it is the most commonly used pharmacolog-
ical injection for the management of spasticity.
The e ects of botulinum toxin generally begin 1 to
3 days, peaking at 21 days, and dissipating by 3 to 4
months. It is licensed for the treatment of dynamic
equinus foot in pediatric cerebral palsy, and there is
good evidence for its use at calf, hip, adductor, ham-
string, and upper limb levels.48,49,50,51,52 Botulinum
toxin is well tolerated, but has rare side e ects
that include respiratory infection, seizures,
m uscle atrophy, im m unoresistance, and transient
pain at injection site.53,54,55 General dosing guide-
lines are 2 to 6 U/kg and should take into account
the child’s m uscle bulk and degree of spasticity.
The use of electromyography, m uscle stim ulators,
or direct ultrasound guidance for the correct
adm inistration to targeted areas is increasingly
com m on.56 Postinjection care should include a
comprehensive physiotherapy and follow-up for
repeated or m ultilevel injections to accelerate
functional outcom es and m inim ize the need for
orthopedic intervention.41,50,57
47.4.4 Complementary Medicine
Complementary medicine, including hyperbaric
oxygen, craniospinal osteopathy, and acupuncture
has been used internationally for the management
of spasticity in children; these treatments have
been found to be useful in individual cases, but for
most, there is little supportive evidence.58,59
47.5 Surgical Indications
A wide array of surgical options is available for the
treatment of spasticity, allowing for various options
based on the patient’s clinical characteristics and
the goals of treatment. Spasticity reducing opera-
tions will not resolve already established orthopedic
issues such as contractures, joint subluxation, dislo-
cation, or bony deformity. Early reduction in tone
has been shown to reduce the development of
orthopedic issues and, thus, operations to reduce
tone should be considered prior to the onset of
orthopedic problems when possible.60,61
Younger patients with the greatest amount of
spasticity in the lower extremities are most likely
to obtain the greatest functional benefit from
selective dorsal rhizotomy (SDR), but functional
benefit can be obtained at older ages as well.61,62
Studies have also demonstrated that patients can
have a reduction in spasticity and functional
improvement in the upper extremities after SDR,
but to a lesser extent than in the lower extrem-
ities.63,64,65,66
Intrathecal baclofen (ITB) pumps are most
clearly indicated in patients with severe spastic
quadriplegia that are dependent on caregivers.
This therapy is also e ective in older adolescents.67
At some centers, patients being considered for
baclofen therapy undergo a trial injection of 50 to
100 µg intrathecally. Antispastic e ects are typi-
cally seen within 2 to 4 hours after lumbar punc-
ture and wear o by 8 hours. A reduction in tone
Surgical Management of Pediatric Spasticity
371

by one point or more on the Ashworth scale is con-
sidered a positive response, and is seen in the vast
majority of patients undergoing trials.17,68 Impor-
tantly, patients and caregivers can temporarily
assess the realistic level of tone reduction and bene-
fit from ITB on spasticity and joint mobility.
Patients in whom function-impairing spasticity is
located to a single or a few muscle groups in an
extremity may choose botulinum toxin injections as
the best option.52,69 There are few side e ects due to
its localized delivery, with the primary risk being an
allergic reaction.70,71 Botulinum toxin injections and
baclofen pumps have largely supplanted the older
technique of selective neurotomy. However, in
contrast to botulinum toxin injections, selective
neurotomy o ers a longer-lasting reduction in
tone and can also be performed to provide partial
denervation of the muscle group based on intraope-
rative neurophysiologic monitoring and stimulation,
allowing for a balance between spasticity and motor
weakness.72,73
47.5.1 Surgical Technique
Selective Dorsal Rhizotomy
The patient is positioned prone and draped to allow
adequate exposure of the lower back. Although this
procedure is often performed with a five-level lami-
nectomy or laminoplasty to expose the roots as they
exit the spinal canal, we prefer the SDR through a
single laminectomy as popularized by Park et al
(Fig. 47.2).74 A single-level laminectomy at the L1
level is performed and access to the conus cauda
Fig. 47.2 Illustration of key steps during selective dorsal rhizotomy. (a) The innervation pattern of each dorsal root is
examined using electrophysiogical stimulation using a threshold voltage. (b) The dorsal root is subdivided into three to
seven smaller rootlets. (c) Each rootlet is tested to determine the relative level of spasticity generated with stimulation.
(d) Rootlets to be preserved are placed behind the Silastic sheet. (e) Rootlets with the greatest spastic responses are
sectioned. (f) The remaining dorsal roots to be examined are kept above the Silastic sheet. Section rootlets are displaced
laterally. Spared rootlets are meticulously kept below the sheet. (Reproduced with permission from Oxford University
Press.)
Functional Disorders
372

equina junction is confirmed via ultrasound prior to
opening the dura.74 Nerve roots are isolated and
tested using electrical stimulation and neurophysio-
logical monitoring. Ventral roots are separated from
dorsal roots and each dorsal root is separated into
four to eight rootlets. Individual dorsal rootlets are
then stimulated to determine which should be
transected based on the relative severity of the spas-
ticity elicited. Stimulated sensory rootlets that dem-
onstrate sphincter innervation or normal responses
are preserved, while rootlets demonstrating spastic
responses when stimulated are transected. Intra-
operative palpation of muscle groups during rootlet
stimulation by a physical and occupational therapy
team or physiatrist is helpful in providing physiolog-
ical feedback when determining which rootlets
to transect based on the degree of spasticity elicited.
With the single-level laminectomy surgical
approach, ventral roots are easily identified via elec-
trophysiological stimulation.75 Many centers per-
form transection of 40% or less of rootlets due to
concerns such as iatrogenic neurological deficits.76,
77,78,79,80 However, other centers including ours sup-
port aggressively transecting up to 70% of rootlets
based on data suggesting that relief of spasticity is
proportional to the percent of dorsal nerve tissue
transected.63,78,81
Intrathecal Baclofen Pump
The appropriate surgical techniques for ITB have
been previously described.82 Briefly, the patient is
positioned in the lateral decubitus position to
allow for both implantation of the pump in the
anterior abdominal wall and insertion of the cath-
eter tip into the subarachnoid space. The side of
pump placement should be dictated by patient
preference and existence of coexisting hardware
such as a percutaneous gastrostomy tube. Both
subcutaneous or subfascial placement are possible,
with the latter favored in patients with low tissue
volume that will be more prone to hardware ero-
sion.83 The abdominal incision is made and a sub-
cutaneous plane is dissected and expanded for
subcutaneous placement, if desired. For subfascial
placement, the external oblique fascia and rectus
abdominis fascia are identified and an incision is
made followed by blunt dissection to develop a
space between the fascial and muscle layers.
The location of catheter placement is dependent
on the distribution of spasticity, with higher place-
ment being indicated in the setting of increased
upper extremity tone. For spastic diplegia, the
catheter is threaded from insertion at L3–L4 or L4–
L5 to rest in the region of T10–T12. For spastic
quadriparesis, the catheter can be threaded further
upward to C5–T2.82 Confirmation of placement is
performed using fluoroscopic guidance. Flexible
tubing is tunneled subcutaneously around the
flank to the lumbar spine to connect the catheter
and pump. Intermittent refilling is generally
required every 2 to 6 months based on dosing
parameters.
Selective Neurotomy
The patient is draped and positioned based on the
muscle groups in question. Ideally, the limb being
operated is sterilized and draped in such a way to
allow intraoperative assessment of tone by the
surgeon. Localization of the nerve is performed
using anatomical landmarks and refined based on
neurophysiological testing with a sharp probe
(Table 47.2). Temporary anesthetic blocks may
be performed to determine the contribution of
spasticity versus orthopedic complications for a
given joint in order to determine the likely func-
tional benefit of neurotomy.84 Subsequent to inci-
sion and subcutaneous dissection, an operative
microscope is used to identify individual motor
nerve fibers. Nerve stimulation is then used to
determine the most spastic fibers, which are then
obliterated.
47.5.2 Complications
Selective Dorsal Rhizotomy
Selective dorsal rhizotomy is a well-tolerated
procedure with a very low risk of permanent mor-
bidity. Urinary retention from nerve root manipu-
lation may be seen transiently, but permanent
urinary dysfunction is rare.85,86,87,88 Urinary cathe-
terization from nerve room manipulation and
anesthesia may be seen transiently. Transient dys-
esthesia and hypoesthesia are also frequently
reported within the first few postoperative weeks,
but permanent neurological complaints after SDR
occur in less than 5% of patients. An even smaller
percentage of patients have any type of functional
decline after SDR.88,89,90,91,92 Older studies have
drawn attention to the possibility of an increased
incidence of scoliosis after SDR.93,94 As this is a
common finding in children with spasticity without
SDR, it is unclear what role SDR plays in the devel-
opment of scoliosis and whether this relationship
exists in the era of single-level laminectomy rather
Surgical Management of Pediatric Spasticity
373

Table 47.2 Indication, location of incision, and key anatomical landmarks for common nerves targeted with selective
neurotomy
Nerve

Indication

Incision location

Nerve anatomical
landmarks
Lateral pectoral
nerve
Spasticity of shoulder with
internal rotation and
adduction
Curvilinear incision over infra-
clavicular fossa in medial part
of deltopectoral groove
Deep to partially reflected
clavipectoral fascia and pec-
toralis major
Teres major nerve

Spasticity of shoulder with
internal rotation and
adduction
Incision along inner border of
teres major from lower border
of posterior head of deltoid to
lower extremity of scapula
In space separating teres ma-
jor from teres minor and other
infraspinatus muscles
Midway between long portion
of triceps brachii above and
insertions of teres major on
infraspinatus aponeurosis
below
Musculocutaneous
nerve
Spasticity of elbow with
flexion
Longitudinal incision from in-
ferior edge of pectoralis ma-
jor, medial to biceps brachii
muscle
Anterior and medial to bra-
chialis muscle
Median nerve

Spasticity of forearm with
pronation deformity, flexion
deformity in wrist, swan-neck
deformity of fingers
Curvilinear incision above
flexion line of elbow, medial
to biceps brachii tendon,
through elbow and before
junction of upper and middle
third of anterior forearm
Medial to brachial artery, deep
to lacertus fibrosus
Recurrent branch of
median nerve
Thumb-in-palm deformity

Curvilinear carpal incision

Deep to transverse carpal
ligament
Ulnar nerve

Spastic wrist flexion, adduc-
tion/flexion deformity of
thumb
Longitudinal or arched inci-
sion between two heads of
flexor carpi ulnaris
Medial to medial epicondyle
between heads of flexor carpi
ulnaris proximally
Obturator nerve

Spasticity of adductor
muscles, diplegic children
with scissoring, facilitation of
perineal toileting and self-
catheterization
Longitudinal incision ex-
tended distally from point just
below groin over belly of
adductor longus
Transverse incision in hip
flexion fold centered on
prominence of adductor lon-
gus tendon (aesthetically
preferred)
Anterior branch is lateral to
adductor longus
Posterior branch is deep and
should be spared to preserve
stabilizing muscles
Sciatic nerve

Spastic diplegia with flexion
deformity of knees
Longitudinal straight incision
on posterior thigh between
ischial tuberosity and tip of
femoral greater trochanter
Deep to gluteus maximus and
biceps femoris
Femoral nerve

Spasticity of quadriceps,
limited knee flexion during
swing phase of gait
Horizontal incision in hip flex-
ion fold, medial to sartorius
muscle
Nerve to rectus femoris
muscle is superficial to nerve
to vastus intermedius
Tibial nerve

Spastic varus plantar flexion
with or without claw toes
Z-shaped incision over popli-
teal fossa
Deep to popliteal fascia,
superficial to popliteal artery
and vein
Sensory medial cutaneous
nerve is encountered first and
should be spared
Superior soleus nerve is mid-
line and posterior to tibial
nerve
Functional Disorders
374

than multilevel laminectomies. In addition, SDR
does not eliminate the need for future orthopedic
surgery. Approximately 34% of patients who are
operated on between the ages of 2 and 5 years may
ultimately still require surgery for orthopedic com-
plications within 7.5 years after SDR.95,96 However,
this is in contrast to the approximately 60% of
patients with spasticity at birth who without SDR
will require an orthopedic procedure by the age of
8.95,97
Intrathecal Baclofen Pump
The body habitus and disability of patients under-
going pump placement contributes to a postopera-
tive wound infection rate of 5 to 36%. More than
half of these wound infections are severe enough
to require removal of the pump hardware.98,99,100
Cerebrospinal fluid (CSF) leakage occurs fre-
quently, but can typically be resolved without
operative repair or removal of the hardware.98
Pump failure requiring replacement occurs in 5
to 10% of cases and failure of the catheter itself
may occur as much as in 35% of early cases,
though increased use and quality of the devices
has lowered this to less than 10% in more recent
studies.98,99,101,102,103,104
ITB infusions also harbor some risk. Most com-
monly, baclofen is often associated with mild seda-
tion, which is easily resolved by lowering the does.
More serious symptoms such dizziness, blurred
vision, nausea, confusion, and slurred speech have
also been reported on occasion.102 Baclofen with-
drawal is a serious condition resulting in rebound
spasticity, tachycardia, hyperthermia, itching,
paresthesias, and seizures. It is best managed
through extensive education to the patient and
family.105,106 New-onset seizure or increased seiz-
ure frequency has been reported but typically
resolve with repair of any device malfunction and
short-term seizure prophylaxis.101,107 Severe respi-
ratory, neurological, or cardiovascular depression
can occur during overdose scenarios and often are
accompanied by weakness, flaccidity, and areflexia
in all extremities. Reduction of the baclofen dose
while supporting the patient’s cardiovascular and
respiratory status allows for continuation of the
therapy after the crisis.101
Selective Neurotomy
Postoperative complications vary based on the
specific location and nerve, but are typically
transient in nature. Hematoma formation, infec-
tion, hypoesthesia, and weakness of the a ected
limb have been reported with rates ranging from 0
to 5%.84,108,109
47.5.3 Postoperative Care
Postsurgical pain from surgical exploration and
pump implantation as well as laminectomy and
nerve root manipulation is common. For postope-
rative pain following SDR, intravenous, epidural,
and transthecal approaches to pain management
have been reported, with morphine or fentanyl
typically being the medication of choice in a sur-
vey of 59 centers worldwide. In more than half of
cases, continuous infusion can be discontinued in
1 to 4 days, but may be required for up to 1 week
followed by several additional days of oral opioids.
The duration of pain management has not been
found to be associated with drug of choice or
mechanism of delivery.110 In our center, we have
had excellent results with the combination of
intravenous toradol and diazepam, with additional
morphine for breakthrough pain.17,111
As well as pain management, the primary goal
of postoperative care is to maximize the long-term
benefit from reduced spasticity and improved
function.26,76,112 Existing data suggest that patients
may benefit from physiotherapy beyond the post-
operative period.26 Appropriate therapy is best
obtained in conjunction with trained therapists
who can accurately assess the physical presenta-
tion and key barriers to function, set appropriate
goals, choose the appropriate intervention, and
reassess following implementation.113 These inter-
ventions typically focus on muscle lengthening,
muscle strength, and motor memory, and plan-
ning. Temporary splinting and casting may assist
patients in muscle lengthening between sessions
when deemed necessary, as severely spastic
children may require hours of stretching daily to
prevent progression to contracture.114 As well as
traditional muscle strengthening exercises, high
activity levels in daily life tapered to physical and
mental disabilities should also be encouraged.115
47.5.4 Outcomes
Selective Dorsal Rhizotomy
There have been a number of excellent long-term
outcome studies for selective dorsal rhizotomy.
The outcome measures examined include muscle
Surgical Management of Pediatric Spasticity
375

tone, flexibility, gait pattern, functional position-
ing, and the ability of the child to deal with his or
her environment. Nearly all studies investigating
SDR have demonstrated a significant and persis-
tent decrease in spasticity without a return of
hypertonicity over time. Improved function and
ambulation are commonly seen regardless of the
preoperative abilities.116,117,118 After SDR, 50 to
78% of patients with impaired ambulation have
been found to improve to a higher level of inde-
pendence (e.g., walk with assistance to walk with
walker alone).119 More recently, long-term out-
come data for children with spastic diplegia who
underwent SDR in Capet own have been pub-
lished.117 In this prospective cohort study, the data
demonstrated that significant improvements in
both range of motion and quality of gait (cadence
and step length) persisted over a 20-year period.
Importantly, SDR did not abolish the need for sub-
sequent orthopedic surgery, as approximately half
of these children still required lengthening of the
rectus femoris, hamstrings, and/or Achilles’ tendon.
McLaughlin et al reported a comparative analy-
sis and meta-analysis of three randomized clinical
trials in 2002.77,78 Eighty-two children with spastic
diplegia received either SDR and physiotherapy or
physiotherapy alone. Outcome measures were
used for spasticity (Ashworth’s scale) and function
(gross motor function measure) and applied at a
12-month follow-up visit. Overall, selective dorsal
rhizotomy with physical therapy was more e ec-
tive than physical therapy alone in reducing spas-
ticity and improving overall function in children
with spastic diplegia.
Although many studies have documented the
e cacy of SDR and ITB therapy on the treatment
of spasticity, only recently has information com-
paring these treatments directly become avail-
able.118 Kan and colleagues reported a consecutive
series of 71 children who underwent SDR for spas-
ticity and compared them with another group of
71 children who underwent ITB therapy matched
by age and preoperative score on the gross motor
function classification system (GMFCS).118 At 1
year postoperatively, both SDR and ITB therapy
decreased tone, increased PROM, and improved
function. Compared with ITB therapy, however,
SDR provided a significantly larger magnitude of
improvement in tone, PROM, and gross motor
function. In addition, fewer patients in the SDR
group required subsequent orthopedic procedures
(19.1 vs. 40.8%).
SDR has typically been only used for children
with spastic diplegia due to the unpredictable
e ects of SDR on the upper extremities. However,
numerous examples of suprasegmental improve-
ments in the upper extremities have now been
reported in patients with spastic quadriplegia
undergoing SDR.63,120 Most recently, Gigante et al
demonstrated that over 90% of patients with upper
extremity spasticity had a reduction in tone and
over 70% had an increase in motor control or spon-
taneous movement of the upper extremities after
SDR.63
Intrathecal Baclofen Pump
Multiple clinical trials have demonstrated that ITB
therapy is e ective at decreasing spasticity and
improving functional outcome.68,99,121,122
The
degree of ambulation was found to be improved in
28 to 43% of patients.123,124,125 In the original mul-
ticenter randomized controlled trial, 100% of
patients randomized into the baclofen group were
found to have at least a 1 point reduction on the
mean Ashworth scale for their lower extrem-
ities.122 This was subsequently supported in a pre-
dominantly pediatric trial of quadriplegic patients,
all of which met the same criteria for reduced
spasticity in upper and lower extremities on long-
term follow-up. Further, it was found that, in all
age groups, the required amount of baclofen
needed to maintain this reduced spasticity tended
to titrate upward toward twice the original dose
during the initial 2 postoperative years, followed
by a leveling o and stabilization of the dose.121
Perhaps the greatest benefit for ITB therapy is
that it is a nondestructive procedure for which
dosing can be adjusted to fit each patient’s needs.
However, vigilant maintenance is required with
ITB therapy; as discussed above, patients may have
a higher risk of complications and need for reope-
rations, particularly in patients under the age of 10
or with a mean Ashworth score of 3 or greater.98
Selective Neurotomy
Selective neurotomy is e ective at increasing the
postoperative passive and active range-of-motion
of joints, and allows for a greater utilization of
function of the limb, and reduces spasticity of the
associated muscle groups.72,84
However, most
available data are in the form of small cohorts lack-
ing in long-term follow-up. In contrast to SDR,
there may be a higher rate of recurrence of spastic-
ity following neurotomy. Approximately 15% of
adult cases witness a partial or complete return of
spasticity at 6 months and 37% at 17 months.84,126
Functional Disorders
376

Patients undergoing repeat neurotomy seem to
benefit a similar degree as first time cases.84 Data
are lacking to support the widespread utility of
this operation in children, in whom long-term
reduction of spasticity is crucial given the number
of years of expected life, and thus this technique is
generally reserved for a highly select group of
patients with focal spasticity.
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Functional Disorders
380

IX
Section IX
Trauma
48 Neonatal Brachial Plexus
Injury

382
49 Pediatric Spine Trauma

390
50 Pediatric Peripheral Nervous
System Trauma

397
51 Management of Pediatric
Head Trauma

409
52 Abusive Head Trauma

423

48 Neonatal Brachial Plexus Injury
Jonathan Pindrik
48.1 Introduction
Neonatal brachial plexus injury (nBPI) occurs
within 0.4 to 4 newborns per 1,000 live births
annually.1,2,3 Shoulder dystocia indicates trapping
of the anterior shoulder below the pelvic rim dur-
ing delivery. While several obstetric maneuvers
ameliorate passage of the neonate through the
birth canal, mechanical or stretching forces jeop-
ardize the structural and functional integrity of
the brachial plexus. Temporary deficits that
resolve completely represent a neurapraxia. Other
injuries result in prolonged deficits that may
improve with surgical intervention and/or sponta-
neous neural regeneration. The severity of nBPI
typically relates to the number of nerves involved,
degree of structural damage and functional
impairment, and duration of neurological deficits.3
● Perinatal risk factors for nBPI: Fetal macrosomia,
prior delivery history of nBPI, multiparity, and
breech or complex deliveries (including those
requiring vacuum or forceps assistance).1,2
● Nearly one-third of infants with mild nBPI
exhibit incomplete recovery by 6 months of
age.1,2,3
● Over 80% of infants with severe nBPI exhibit
residual deficits by 6 months of age.3
● Neuropathological grading of nBPI severity is
based on the Sunderland classification: I—
neurapraxia; II—axonotmesis with myelin
damage; III—axonotmesis with endoneurial
damage; IV—axonotmesis with perineurial
disruption; V—neurotmesis with nerve
discontinuity.1,4
● Clinical grading system for nBPI severity:
Narakas’ classification3 ( Table 48.1).
● Less severe nBPIs show a greater propensity for
spontaneous neural regeneration and functional
recovery.3 More severe nBPIs typically result in
permanent deficits and require surgical
intervention.2
48.2 Anatomy
Originating from roots C5–T1, the brachial plexus
represents an organized network of peripheral
nerves ultimately innervating sensory derma-
tomes and muscle groups associated with the
upper extremity. Most nBPIs occur proximally at
the level of roots or trunks and a ect the upper
trunk (C5–C6) as in Erb–Duchenne palsy. The mid-
dle trunk (C7) also may sustain damage. Lower
trunk (C8–T1) injuries, consistent with Klumpke’s
palsy, rarely occur in isolation but may appear in
severe nBPI extending to the lower plexus.2 Mild
nBPIs involve stretch or traction injury with transi-
ent conduction impairment, while more severe
nBPIs may result in neuroma formation or nerve
root avulsion. A neuroma represents a focal collec-
tion of fibrosis and misdirected sprouting axons
along the course of an injured peripheral nerve.4
● The proximal portion of the brachial plexus
traverses the posterior cervical triangle,
bordered by the sternocleidomastoid, trapezius,
and clavicle.
● The hierarchical structure of the brachial plexus
from proximal to distal: Roots →trunks →
divisions →cords →branches ( Fig. 48.1).
Table 48.1 Narakas’ classification for neonatal brachial plexus injury (nBPI) severity
Narakas’ grade Description of injury

Comment
I

Involves upper trunk (C5, C6)

- Classic Erb–Duchenne palsy1,2
- Most common and least severe type1
- Most favorable prognosis1
II

Involves upper and middle trunks (C5, C6, C7)

- Less severe than type III or IV lesions
- Second most common type of nBPI1
III

Involves full plexus (C5–T1) with global impairment - Type III and IV lesions account for nearly 25%
of nBPIs
IV

Involves full plexus (C5–T1) with arm flaccidity and
possible Horner’s syndrome
- Most severe type of nBPI
- Suggests presence of preganglionic nerve root
avulsions1
Source: Data from Foad SL, Mehlman CT, Foad MB, Lippert WC. Prognosis following neonatal brachial plexus palsy: an
evidence-based review. J Child Orthop 2009;3(6):459–463.
382

● The nerve roots of the brachial plexus travel
between the anterior and middle scalene muscles
to form the upper, middle, and lower trunks.
● From their respective trunks, divisions and cords
run inferolaterally between the clavicle and first
thoracic rib into the axilla.
● The lateral, medial, and posterior cords are
named anatomically with respect to the axillary
artery.
● Inferior to the clavicle, the cords pass deep to the
pectoralis major and minor muscles.
48.3 Examination
Physical examination of infants with nBPI evalu-
ates passive and active movement and any asym-
metries or deformities associated with the upper
extremity. Examination involves observation of
spontaneous activity and intentional reaching or
grasping of presented objects.1 Most nBPIs involve
deficits of shoulder external rotation or abduction
and elbow flexion. Middle trunk injury addition-
ally impairs extension about the elbow, wrist, and/
or fingers. Lower trunk involvement causes deficits
in hand or finger movement.
● Assessing the passive range of motion about the
shoulder and elbow may reveal contractures.
● Palpation of the pectoralis major, latissimus
dorsi, and teres major muscles may reveal
tightness.1
● Glenohumeral subluxation or instability should
be assessed visually and tactilely during rest and
passive range of motion exercises.1
● Active movement about the shoulder, elbow,
wrist, forearm, and fingers should be thoroughly
assessed without and with gravity. Findings can
be graded and recorded using the Toronto
Obstetric Brachial Plexus Active Movement Scale
(AMS).
● Examination of other systems may reveal
neurological deficits. For instance,
approximation of the diaphragmatic height or
chest radiography may reveal hemidiaphragm
elevation due to phrenic nerve dysfunction.
Fig. 48.1 Anatomical diagram of the brachial plexus. (Reproduced with permission from Figure 1–44. Brachial Plexus.
Page 80. Comprehensive Neurosurgery Board Review by Citow, Macdonald, Kraig, Wollmann. Thieme 2000.)
Neonatal Brachial Plexus Injury
383

● Lesions extending inferiorly to the lower trunk
may cause an incomplete Horner’s syndrome
with ptosis and myosis. This often suggests
preganglionic nerve root avulsion of C8 and/or
T1.1
48.4 Nonsurgical Management
Initial patient evaluation within 2 weeks of deliv-
ery helps establish a neurological baseline for later
comparison in nBPI. The next follow-up appoint-
ment should occur at 3 months of age. Depending
on the severity of nBPI and management strategy,
reevaluation may occur at age 6 to 9 months or
sooner. These serial examinations help track the
progression of neurological deficits and functional
impairment. Patients that exhibit adequate func-
tional recovery (at least partial antigravity
strength) in motion about the shoulder, elbow,
and/or hand may be managed nonoperatively.1
Clinic visits provide the opportunity to link the
patient and family with specialists trained in phys-
iotherapy or physical medicine and rehabilitation.
Physiotherapy exercises focus on passive range of
motion and stimulation to encourage activity
of the a ected extremity. Furthermore, parents or
caretakers may be coached regarding appropriate
positioning strategies and activities to mobilize
the a ected extremity. Supervised home therapy
may help reduce contracture formation about the
shoulder or elbow, promote shoulder stability, and
help prevent neglect of the paretic limb.1,2 Physio-
therapy and rehabilitative care also represent
important adjuncts to operative management.
48.5 Surgical Indications
Serial evaluations and monitoring of nBPI allow
su cient time to observe spontaneous neural
regeneration.1 Inadequate functional recovery in
shoulder external rotation or abduction, elbow
flexion, and/or hand movement by age 3 months
prompts surgical consideration during the 3- to 6-
month age range.1,2,5 Some peripheral nerve sur-
geons prefer surgical intervention at 9 months of
age to allow longer observation periods for sponta-
neous recovery.1 When nerve root avulsions are
present, surgical intervention should occur at the
earliest time point.
● Inadequate performance on objective measures
such as the Toronto Obstetric Brachial Plexus
Active Movement Scale (AMS) and the Cookie
test may corroborate surgical decision making.
● The presence of Horner’s syndrome on follow-up
examination at age 3 months indicates severe
nBPI likely spanning the full plexus. Extensive
nBPIs usually require early surgical intervention.
● Additional diagnostic studies help investigate
the severity of injury and corroborate surgical
decision making. Cervical spine magnetic
resonance imaging (MRI) may reveal
pseudomeningoceles suggesting nerve root
avulsion.
● Other ancillary studies include
electromyography and nerve conduction studies,
performed at or beyond 3 months of age.2,4
These studies help identify the presence of
regenerating motor units and conducting action
potentials.
48.6 Surgical Technique
Most operative explorations and repairs of nBPI
require a supraclavicular approach. Extension of
the traumatic injury or neuroma along the divi-
sions and cords may require the addition of an
infraclavicular approach. Following exposure of
normal anatomy, the injured elements of the bra-
chial plexus can be identified through direct visu-
alization and nerve stimulation. Depending on the
extent of injury and function of donor nerves, vari-
ous methods of repair may be employed. Di erent
types of peripheral nerve repair include neurolysis,
neuroma resection and grafting, and nerve transfers
(with or without bridging grafts). The goals of sur-
gery revolve around promoting neural regeneration
and muscular reinnervation to improve elbow flex-
ion and shoulder stability, abduction, and external
rotation. Additional approaches target hand and fin-
ger functional recovery. For all nBPI explorations
and repairs, anesthetic paralytic agents should be
avoided.
● Patient position: Supine, head rotated
contralaterally, with a rolled sheet or bump
under the upper torso to elevate the
supraclavicular region.
● Special lucent drapes or sterile preparation of
the a ected extremity within the surgical field
allow intraoperative nerve stimulation and
observation of muscular contractions.
● One or both lower extremities should be sterilely
prepared from the popliteal fossa to lateral
malleolus if surgical planning involves sural
nerve harvesting.
● Skin incision for supraclavicular approach:
Parallel to and one to two finger-breadths above
Trauma
384

the clavicle, extending laterally toward the
anterior border of the trapezius and medially
along the posterior border of the
sternocleidomastoid (as needed).6
● Skin incision for infraclavicular approach:
Vertically oblique line along the deltopectoral
groove, curving medially toward the clavicle.
● Relevant anatomical landmarks: See
Table 48.2.
● Brachial plexus exposure requires careful
division of the anterior scalene while protecting
the phrenic nerve.
● Division of the anterior scalene first exposes the
upper trunk and C5–C6 nerve roots. Gentle
retraction of the upper trunk exposes the
underlying middle and lower trunks.
● Fibrotic scarring and neuroma formation in nBPI
may complicate plexus exploration. Neuroma
formation typically occurs along the upper or
middle trunks.
● Nerve stimulation and observation of muscle
contraction aid identification of plexus elements
and help investigate the presence of conduction
across a neuroma or region of trauma.
● After identification of a neuroma or
nonfunctioning plexus elements, several
di erent methods of repair may be employed
(Table 48.3).
● Common examples of nerve grafting include
cables between the C5 or C6 nerve roots and
anterior or posterior divisions of the upper trunk
or lateral cord, following neuroma resection.
Table 48.2 Anatomical landmarks in neonatal brachial plexus injury (nBPI) surgery
Anatomical structure

Location

Relevance/comments
Platysma mm.

First layer of mm. deep to skin during
supraclavicular
approach
Separated during exposure and
reapproximated during closure
Sternocleidomastoid mm. (SCM) Deep to platysma, along medial aspect
of exposure
Dividing the lateral one-third of this mm.
enhances exposure of the plexus
Supraclavicular fat pad

Deep to platysma, along inferior aspect
of exposure
Careful dissection or retraction of the fat
pad allows better visualization of deep
structures
Omohyoid mm.

Inferior belly lies within lower region of
neck, deep to the SCM
Division or retraction of this mm. helps
expose deeper structures
Anterior scalene mm.

Deep to SCM and omohyoid, along
medial aspect of exposure
● Brachial plexus travels between
anterior and middle scalene mm.
● Division of anterior scalene mm.
exposes the proximal plexus
Phrenic n.

Ventral surface of the anterior scalene
mm., running from lateral to medial as it
descends
● Stimulation with low amplitude
produces diaphragmatic contractions
● Requires careful protection while
dividing the anterior scalene mm.
Subclavian a. and v.

● Subclavian a. lies between anterior
and middle scalene mm.
● Subclavian v. lies ventral to anterior
scalene mm.
● Both lie near lower trunk and C7
transverse process
● Damage to either structure may
require assistance from vascular
surgery team
Clavicle

● Located between manubrium of the
sternum and acromion of the scapula
● Typically hinders visualization and
manipulation of underlying divisions or
proximal cords of the plexus
Pectoralis major mm.

● Origin: medial clavicle, sternum, costal
cartilage, aponeurosis of external
oblique mm.
● Insertion: proximal humerus
● Separation of fibers during an infra-
clavicular approach allows exposure of
underlying pectoralis minor mm. and
distal brachial plexus
Pectoralis minor mm.

● Deep to pectoralis major mm.
● Origin: ribs 3–5 (anterior surface)
● Insertion: scapula (coracoid process)
● Division of this mm. exposes distal
brachial plexus (cords, proximal
branches)
Abbreviations: a., artery; mm., muscle(s); n., nerve; v., vein.
Neonatal Brachial Plexus Injury
385

● Synthetic nerve guides help reduce operative
times and eliminate donor-site morbidity, but
have shown encouraging results only for short
gaps up to 30 mm in length.7,8
● Several options for nerve transfers
(neurotization) exist depending on the function
of plexus elements (Table 48.4).
● Common targets of neurotization include the
suprascapular, musculocutaneous, and axillary
nerves. Ulnar nerve targeting helps recover hand
function in nBPI involving the lower trunk.
● Complete nBPI with preganglionic avulsions
m ay benefit from contralateral C7 nerve root
transfer targeting elbow flexion or hand
m ovem ent. This m ay additionally require a
vascularized ulnar nerve graft due to large gap
distances.1,3,5
● Grafting and neurotization require neurolysis to
expose healthy-appearing fascicles in
preparation for coaptation. Coaptation can be
performed in end-to-end, end-to-side, or side-
to-side fashion.
Table 48.3 Methods of repair neonatal brachial plexus injury (nBPI)
Method of repair

Description

Applicability/comments
Neurolysis

Dissection along the longitudinal axis of a
nerve to expose fascicles
● Applicable to neuroma or fibrotic scarring
along the course of a nerve
● Release of scar tissue may enhance periph-
eral nerve regeneration
Neuroma resection Division of a nerve segment proximal and distal
to a region of obvious scarring and dysfunction
● Applicable to any neuroma, especially with
poor conduction along the nerve
● Requires grafting across the resultant defect
Nerve grafting

● Bridging the gap between proximal and
distal portions of damaged nerve
● Autologous grafts include MABCN and sural
nerves
● Artificial grafts include synthetic nerve
guides typically approved for defects up to
30 mm in length7,8
● Applicable to gap between proximal and
distal nerve stumps created by neuroma
resection or nerve root avulsion
● May also parallel a nonresected neuroma
when affixed to nerve segments proximal
and distal to the site of injury
Nerve transfer or
neurotization
● Promotes neural regeneration by adjoining
proximal end of functioning nerve to distal
end of nonfunctioning nerve
● Decrements the function of donor nerve,
while favoring regeneration of damaged
target motor nerves
● Applicable to nonfunctioning nerves distal to
the level of injury (beyond a nerve root
avulsion or neuroma)
● Useful in preganglionic nerve root avulsions
when proximal nerve ends are not available
for grafting5
Abbreviation: MABCN, medial antebrachial cutaneous nerve.
Table 48.4 Di erent examples of nerve transfer for neonatal brachial plexus injury (nBPI)
Common nerve transfers

Ultimate goal

Comments
Spinal accessory n. →suprascapular n.

Shoulder stability, arm
abduction
Spinal accessory n. is dissected along
anterior border of trapezius mm.
Radial n. (triceps branch) →axillary n.

Shoulder stability, arm
abduction
Usually requires dorsal approach to
shoulder within quadrilateral space5
Ulnar n. →musculocutaneous n. (biceps
branch)
Elbow flexion

Classic Oberlin technique1,2,5
Median n. →musculocutaneous n. (brachialis
branch)
Elbow flexion

Modified Oberlin technique1,2,5
Intercostal n. →musculocutaneous n. (biceps
branch)
Elbow flexion

Typically requires at least 3 intercostal
nerve donors5
Medial pectoral n. →musculocutaneous n. or
axillary n.
Elbow flexion or shoulder
stability
Abbreviations: mm., muscle; n., nerve(s).
Trauma
386

● Nerve grafts or transfers are secured with
adhesive glue at the site of nerve coaptation. The
junction can be reinforced with one to two low-
caliber epineurial sutures prior to gluing.
● Free gracilis muscle transfers are employed in
delayed fashion during secondary surgery to
recapitulate elbow flexion. This technique
requires neurotization from intercostal, spinal
accessory, or ulnar nerves to the preserved
recipient obturator nerve.3,5
● Other examples of secondary surgery for nBPI
include attempts to improve shoulder stability
with trapezius or latissimus dorsi tendon
transfers or osteotomies.
48.7 Complications
Complications of nBPI exploration and repair may
occur intraoperatively or postoperatively. Surgical
risks include damage to nearby vasculature or
nerves. Injury to the subclavian vessels may
require assistance from a vascular surgeon, while
trauma to the phrenic nerve may result in respira-
tory compromise or hemidiaphragm elevation. In
more complicated repairs, harvesting intercostal
nerves may cause violation of the pleura and
pneumothorax. Occurrence of these latter events
can be evaluated with plain chest radiography.
Postoperative complications include delayed surgi-
cal site hematoma, wound infection or dehiscence,
lack of functional recovery in targeted muscle
groups, or decrement of function in a donor nerve
used for neurotization.
48.8 Postoperative Care
Postoperative care for nBPI repair involves a com-
bination of early immobilization to protect nerve
grafts or transfers, wound monitoring, and even-
tual rehabilitative therapy. For the first 2 to 3
weeks following surgery, upper extremity immo-
bilization and sling support ensure the continuity
of nerve coaptations. Postoperative follow-up
within 10 to 14 days allows adequate wound
inspection and investigation of muscle groups
potentially a ected by nerve donor usage in neu-
rotization. After immobilization, physiotherapy
and rehabilitation represent important adjuncts in
the management of nBPI. Patients and caretakers
should be seen regularly for physiotherapy and
guidance with passive and active motion exercises
or rehabilitative devices.
48.9 Outcomes
The length of peripheral nerve regeneration
required to reinnervate target muscles determines
the anticipated duration of recovery.2
Since
peripheral nerve growth and regeneration occur at
a rate of 1 mm/day, observing functional recovery
requires prolonged follow-up.4 Full realization of
functional improvement may require up to 2 years
following surgery due to the necessity of physio-
therapy and adaptation following neurotization.
Surgical success rates of functional recovery
depend on the type of repair and vary between 67
and above 90%, with lower rates (<50%) for con-
tralateral C7 transfers.2,5
Long-term morbidity
most commonly relates to shoulder weakness or
instability, a ecting over one-third of nBPI
patients.1 Complications associated with the gle-
nohumeral joint include contracture, subluxation,
and deformity requiring surgical correction.
Surgical outcomes are influenced by location of
the injury and timing of surgical intervention.
While upper trunk injuries carry the best progno-
sis for functional recovery, lesions involving the
lower trunk exhibit worse outcomes.1 Additional
poor prognostic factors include pan plexopathy
and preganglionic avulsions.1 Regarding timing,
early surgical intervention maximizes recovery
time. Surgical intervention for nBPI at 3 to 6
months of age typically o ers better chances of
functional recovery.1 Primary exploration or repair
in nBPI beyond 9 to 12 months of age may portend
worse outcome due to target muscle fibrosis and
scarring. Ideally, reinnervation of target muscle
groups should occur by 18 months to provide the
best chance for functional recovery.4,7 Patients
with unimproved deficits following primary sur-
gery, failed conservative management, or delayed
presentation may benefit from secondary surgery
involving free muscle (e.g., gracilis) transfers.
48.10 Surgical Pearls
● Identification of a dorsal root ganglion (DRG)
distal to its normal location within the neural
foramen implies nerve root avulsion.
● The suprascapular nerve represents an
important early branch of the plexus whose
origin helps confirm the identity of the upper
trunk.
● Vascular loops placed without tension around
identified nerves help organize the surgical field.
Neonatal Brachial Plexus Injury
387

● Nerve conduction across a neuroma with
muscular contraction distally suggests some
degree of spontaneous reinnervation. In this
setting, less aggressive surgical techniques
include neurolysis, side-to-side cable grafting
along the neuroma, and/or distal nerve transfers.
However, many peripheral nerve surgeons
routinely advocate neuroma resection and
grafting.1
● Nerve coaptation in grafting and neurotization
should be accomplished without tension on the
nerve segments.
● Testing for excursion involves observing nerve
donor and recipient relative motion during
upper extremity movement to estimate the
length of nerve dissection required to prevent
tension or separation following coaptation.
● Intraoperative nerve stimulation, harvesting
nerve grafts, and division of nerves require
careful attention. Respect the common adage:
Measure/check twice, cut once.
● Specialized centers facilitating a
multidisciplinary approach with peripheral
nerve surgeons, pediatric neurologists,
physiotherapists, and specialists in physical
medicine and rehabilitation o er the best
management strategy for patients with nBPI.
48.11 Common Clinical
Questions
1. Describe the appearance of an upper extremity
in nBPI involving the upper trunk (classic Erb–
Duchenne palsy).
2. Which management strategy represents the
optimal approach in nBPI with evidence of
partial but incomplete biceps functional
recovery at 3 months of age?
3. In the context of preganglionic nerve root
avulsion, will the a ected peripheral nerve
conduct sensory nerve action potentials?
4. Can nerve grafting and transfers be combined
within the same procedure?
48.12 Answers to Common
Clinical Questions
1. Injuries confined to the upper trunk (C5–C6)
cause weakness in the supraspinatus,
infraspinatus, deltoid, biceps, and brachial
muscles.2 In this context, the upper extremity
appears adducted, internally rotated, extended at
the elbow, and pronated along the forearm.2
Additional middle trunk (C7) involvement causes
unopposed flexion of the wrist and fingers.2
2. The optimal treatment strategy in this situation
has not been determined. No randomized,
controlled clinical trial has compared
nonoperative and operative management for
incomplete functional recovery at 3 to 6 months
following nBPI. Many authors advocate surgical
intervention; however, case series have
reported spontaneous recovery without
operative intervention despite lack of elbow
flexion at 3 months age.2 Furthermore,
controversy exists between di erent surgical
approaches. Many peripheral nerve surgeons
advocate neuroma resection and grafting, while
newer approaches involve neurolysis or distal
nerve transfers.
3. Yes. In the context of nerve root avulsion,
sensory nerve action potentials may still
conduct along the involved peripheral nerve
due to continuity between axons and the
neuronal cell body within the DRG. The
di erentiation between preganglionic and post-
postganglionic injury represents an important
distinction in nBPI. The presence of
preganglionic nerve root avulsion carries
significant implications for anticipated recovery
and surgical planning. Without surgical
intervention, spontaneous reinnervation will
not occur in the distribution of avulsed nerves.
To promote functional recovery, brachial plexus
exploration and repair should be planned early
(after 3 months of age). Without the presence of
proximal nerve stumps for grafting, several
types of nerve transfer can be employed.
4. Nerve grafting and transfers are commonly
employed in the same surgical approach to the
brachial plexus. These techniques can be
combined on the same nerve construct, as with
an ulnar or median nerve to musculocutaneous
nerve transfer with an interpositional bridging
nerve graft. The graft may be harvested from
the medial antebrachial cutaneous nerve or
sural nerve. Interpositional nerve grafts from a
proximal intercostal nerve stump have proven
less e ective; therefore, direct intercostal nerve
transfers to the musculocutaneous nerve are
favored currently.3,5 Alternatively, neurotization
may reinforce nBPI repair separate from the site
of grafting. For instance, nerve grafting from the
C5 nerve root to the suprascapular nerve
following neuroma resection can be
supplemented by distal Oberlin’s or modified
Trauma
388

Oberlin’s transfers. While the former approach
promotes shoulder abduction and stability, the
latter techniques provide for elbow flexion.
References
[1] Hale HB, Bae DS, Waters PM. Current concepts in the
management of brachial plexus birth palsy. J Hand Surg Am.
2010; 35(2):322–331
[2] Malessy MJA, Pondaag W. Obstetric brachial plexus injuries.
Neurosurg Clin N Am. 2009; 20(1):1–14, v
[3] Foad SL, Mehlman CT, Foad MB, Lippert WC. Prognosis
following neonatal brachial plexus palsy: an evidence-based
review. J Child Orthop. 2009; 3(6):459–463
[4] Belzberg AJ. Acute nerve injuries. Rengachary SS, Ellenbogen
RG, eds. Principles of Neurosurgery. 2nd ed. Philadelphia, PA:
Elsevier Mosby; 2005:387–395
[5] Shin AY, Spinner RJ, Bishop AT. Nerve transfers for brachial
plexus injuries. Oper Tech Orthop. 2004; 14:199–212
[6] Laurent JP. Supraclavicular approach to birth-related brachial
plexus injury. Albright AL, Pollack IF, Adelson PD, eds.
Operative Techniques in Pediatric Neurosurgery. New York,
NY: Thieme; 2001:219–225
[7] Siemionow M, Brzezicki G. Chapter 8: Current techniques
and concepts in peripheral nerve repair. Int Rev Neurobiol.
2009; 87:141–172
[8] Dornseifer U, Matiasek K, Fichter MA, et al. Surgical
therapy of peripheral nerve lesions: current status and
new perspectives. Zentralbl Neurochir. 2007; 68(3):
101–110
Neonatal Brachial Plexus Injury
389

49 Pediatric Spine Trauma
Douglas Brockmeyer
49.1 Introduction
Spine trauma is a common occurrence in the
pediatric age group. This chapter will outline com-
mon spinal injuries in children, as well as their
evaluation and management. Surgical approaches
to the treatment of unstable pediatric cervical
spine injuries are highlighted.
49.2 Epidemiology
Although less common than spinal trauma in other
age groups, pediatric spinal injuries are not rare.
The incidence of pediatric spine trauma within the
overall population of spinal injuries ranges from 1 to
11%.1,2,3 A reasonable estimate at most major pedia-
tric trauma centers is that 5% of spinal column and
spinal cord injuries will occur in the age group
between 0 and 16 years of age. Males more fre-
quently sustained spinal column and spinal cord
injuries than females.1 This statistic is influenced by
an increased likelihood of vertebral column injury
in adolescent males in the 10- to 16-year-old age
group. The pediatric spine can be subjected to every
pattern of force that its adult counterpart may see.
The actual type of injury responsible for the mecha-
nism varies according to the age of the patient.
● Di erences in referral patterns, injury grading,
and treatment and outcome measures between
physicians all mask the true incidence and
severity of pediatric spinal cord and spinal
column injury.
● The lack of a standardized nationwide database
for these injuries has hampered our
understanding of this disease process. Until
strict guidelines and a national database are
established, our understanding of injury
patterns and injury types will be incomplete.
49.3 Pathophysiology
● Pure forces of flexion, extension, rotation, axial
loading, and distraction have all been
documented and described, also combination
forces, such as flexion/distraction injuries.
● Spinal cord ischemia either by compression or
disruption has also been documented.
Compression of the spinal cord from blood clots,
fractured bones, bending or buckling of
ligaments, and angulation of the spinal column
also occurs.
● Underlying congenital or developmental
conditions of the patient, including os
odontoideum, Down syndrom e, Chiari
malformations, congenital bone abnorm alities,
rheumatoid arthritis, ankylosing spondylitis, and
other infections or tumors may contribute to the
risk of spinal injury.
● The youngest patients (0–10 years) have a high
incidence of falls and pedestrian/automobile
accidents, while older children have a higher
incidence of motor vehicle accidents, motorcycle
accidents, and sports-related injuries.
49.4 Anatomy
The pediatric spine demonstrates significant ana-
tomical and biomechanical di erences from the
adult spine. Many of the anatomical di erences
explain the di erent injury patterns seen in various
age groups. The infant spine is very flexible and
elastic because of its incomplete development.
Between the ages of 2 and 10 years, tremendous
changes occur in the supportive elements of the spi-
nal column. Gradually, the spinal anatomy develops
an adult configuration. Muscles and ligaments
strengthen, bones grow and reach a mature shape
and size, and areas of cartilage and soft bone are
replaced with normal calcified bone. In addition, the
body habitus changes so that the head is smaller in
proportion to the torso. These changes shift the
focus of injury from the upper cervical spine (skull-
C1–C2) to the lower cervical spine (C5–C6).
● The spine of infants between 0 and 2 years of
age has tremendous mobility and elasticity
because of underdevelopment of the neck
muscles; incompletely calcified, wedge-shaped
vertebrae; and shallow, horizontally oriented
facet joints. The relatively large head size in
young patients with respect to the torso
increases the likelihood of cervical spine injuries,
especially between the skull and first two
cervical vertebrae.
● Age-related maturation in the upper pediatric
cervical spine is usually completed by
approximately age 10, and the maturation of the
lower cervical spine occurs by approximately
age 14.
390

● The elasticity of the young spinal column
probably allows some protection against spinal
cord trauma that might cause fracture in older
patients. This mobility and elasticity in the
infant spine explains the relatively low incidence
of spinal column injuries and the
proportionately high incidence of spinal cord
injuries without radiographic abnormalities
(SCIWORA). In essence, the young spine will
stretch, but not break, but this places the spinal
cord at increased risk for stretching and
disruptive injuries.
49.5 Specific Injuries
As described above, di erent patterns of spinal
cord and spinal column injuries are seen in adult
and pediatric patients. This section will expand on
these di erences in light of specific injury types.
49.5.1 Fractures and Dislocations
Fractures encompass all types of disruption of the
bony vertebral column. Fracture types vary widely
from simple linear fractures a ecting the vertebral
bodies or posterior portion of the spine to complex
fractures involving several elements of the spine
or possibly several vertebral levels. Specific frac-
ture types, listed from least to most unstable,
include compression fractures, burst fractures, and
fracture/dislocations.
● A fracture may or may not make the spinal
column unstable, depending on its type and
severity. The AO/Orthopedic Trauma Association
classification of spine fractures4 developed for
adults is a good general starting point in
determining spinal stability, although it may not
be completely applicable in children. Fractures
may or may not compress the spinal cord and
cause spinal cord injury.
● Dislocation refers to abnormal position and
motion between vertebral levels in the spine.
Typically, dislocations are caused by injuries of
the bony–ligamentous complex that stabilizes
each vertebral level. In addition to ligamentous
injuries, intervertebral disk disruption may also
contribute to spinal dislocation. Obviously,
fractures and dislocations may exist either
independently or in combination with each
other.
● Complex fracture/dislocations are typically the
worst type of vertebral column injury and imply
both bony and ligamentous disruption. These
patients usually have the most severe
neurological injuries as well.
49.5.2 Injuries Seen in Young
Children
Young children (< 4 years of age) tend to sustain
soft tissue injuries without incurring “true frac-
tures,” a finding that reflects hypermobility and
skeletal immaturity. Most of the spinal injuries in
the first decade of life a ect the upper segments
of the cervical spinal column. Young children are
also prone to ligamentous injury without fracture.
In these instances, a higher rate of persistent
instability can occur than with fracture dislocation
injuries.
Young children sometimes have traumatic
growth plate fractures and separations, also
known as “synchondrosis fractures.” These frac-
tures are highly likely to heal with immobilization;
however, the chronic nonunion of an odontoid
synchondrosis fracture is thought to be a possible
etiological factor behind many cases of os odontoi-
deum. Os odontoideum may lead to chronic insta-
bility and confer an increased risk of spinal cord
injury.5 In young patients, a C2 synchondrosis frac-
ture is almost always treated with an external halo
orthosis, although surgical stabilization might be
needed in rare cases.6
49.5.3 Strains and Sprains
Muscular cervical sprains and strains are perhaps
the most common type of spinal injury in young
children but have been poorly documented
because of their “trivial” status. More serious liga-
mentous injuries also probably have a much
higher incidence than we realize, but are most
often self-limited.
Cervical strains and sprains may sometimes be
diagnosed using a combination of dynamic X-ray
imaging and magnetic resonance imaging (MRI),
although the diagnostic utility of these modalities
is suspect because of the high rate of false-positive
results, especially with MRI.7
49.5.4 Atlanto-Occipital
Dislocation
Atlanto-occipital dislocation (AOD) is an injury of
the supporting ligaments of the occipitocervical
joint. Flexion, distraction, and rotational mecha-
nisms are commonly involved. Unfortunately, a
Pediatric Spine Trauma
391

large proportion of AOD injuries are fatal; their
overall incidence is probably underreported.
● Although injuries in this area can result in
extreme instability at the craniocervical
junction, many are less severe and patients may
have little to no neurological deficit.
● Recently, the “condyle–C1 interval” (CCI) has
been recognized as a useful measurement for
diagnosing AOD.8 A CCI of greater than 4.0 mm is
generally accepted as diagnostic of AOD.
49.5.5 C1–C2 Injuries
Dislocations between C1 and C2 may occur alone
or in combination with an O–C1 injury. They may
sometimes be misdiagnosed as solely an AOD
injury. They are usually due to flexion–distraction
mechanisms and commonly occur when a young
child restrained in child safety seat is involved in a
motor vehicle accident.
49.5.6 Atlantoaxial Rotatory
Subluxation
Because of its unique anatomy, the C1–C2 joint is
prone to rotational injuries. Most atlantoaxial
rotatory subluxation (AARS) injuries are mild and
self-limited, but severe AARS injuries can occur,
causing significant signs and symptoms, including
neck pain and torticollis.
● A general rule of thumb is that if C1–C2
rotational angulation is greater than 30 degrees
on axial computed tomography (CT) scan, then
the C1–C2 joint capsule is likely incompetent
and surgical fixation may be required.
49.5.7 Lower Cervical and
Thoracolumbar Injuries
Fractures and dislocations of the lower cervical
spine are relatively rare in young patients because
of factors involving the maturing spine. Fractures
involving the thoracolumbar spine in young chil-
dren tend to involve the junction between the
thoracic and lumbar spine where the relatively
rigid thoracic segments join the more mobile lum-
bar segments. Again, the injuries of younger chil-
dren tend to involve the soft tissues and ligaments
resulting in cartilage or growth plate injuries. The
AO classification is generally used to describe frac-
ture types and determine stability.9
● In automobile accidents with frontal impact,
children restrained by standard rear seat lap
belts can sustain mid lumbar spine fractures.
Clues to an injury include lap belt abrasions
across the abdomen or lower thorax.
49.5.8 Adolescent Injuries
Adolescents and young adults in the 16- to 24-
year-old age group have the highest incidence of
spinal injury in many studies. Once the patient’s
age reaches 15 to 16 years, injury mechanisms and
patterns closely resemble those of adults. Typically,
fractures are seen more often than soft tissue inju-
ries. Combination fracture and dislocation injuries
are seen more often as well. In this age group, the
level of injury in the cervical spine is more evenly
distributed throughout the entire neck, with the
most common level of injury at the C5–C6 level.
Spinal column injuries to the thoracic and lumbar
levels assume greater importance in the adoles-
cent age group.
● Changes in lifestyle patterns among adolescents
account for a large part of the injury pattern
di erences. Drugs, alcohol, and motor vehicles
are all important causative factors in this age
group.
● Sports-related accidents also assume a higher
prominence in the adolescent age group. In the
United States, organized tackle football has the
highest incidence of spinal column and spinal
cord injury of any sport. In other countries,
hockey and rugby account for a significant
fraction of sports-related spinal column and
spinal cord injuries. Other “at-risk” sports
include wrestling and boxing. A more detailed
discussion of sports-related spinal column
injuries in adolescents is beyond the scope of
this discussion.
49.5.9 Spinal Cord Injury without
Radiographic Abnormality
SCIWORA is defined as a spinal cord injury that
cannot be observed on normal plain radiographic
studies and CT.10,11 There are wide di erences in
the reporting of SCIWORA and its incidence ranges
from 5 to 70% of all pediatric spinal cord injuries,
depending on the study examined. A true inci-
dence is probably close to 20% of all pediatric spi-
nal cord injuries. Cervical and thoracic spinal levels
are injured with almost equal frequency and lum-
bar levels are rarely involved. In all cases of
suspected SCIWORA injury, an MRI should be per-
formed. It is possible that compressive, treatable
Trauma
392

lesions may be identified that are not seen on
X-ray or CT. Examples of such lesions include hem-
atomas or ligamentous injury not shown on other
studies.
SCIWORA is ultimately due to the ligamentous
flexibility and elasticity of the immature spine. A
young child’s vertebral column can withstand
elongation without evidence of deformity while
the spinal cord is injured. The infant spine and
cadaver specimens can withstand up to 2 in of
stretch without disruption. In contrast, the spinal
cord ruptures after only 1/4 in of stretching. This
mismatch of elasticity response between the spinal
column and spinal cord is the major factor contri-
buting to the high incidence of SCIWORA injuries
in young children.
● SCIWORA occurs almost exclusively among
younger children. SCIWORA is very uncommon
in adolescents and rare among adults. There are
important di erences in SCIWORA injury
patterns between younger age groups (0–8
years) and older children (9–16 years). Younger
patients account for two-thirds of all SCIWORA
injuries and have a higher proportion of
complete neurological injuries.
● Strict guidelines regarding treatment of this
injury are lacking, and there is significant
variability between physicians regarding the
type of treatment necessary. In general, once a
diagnosis of SCIWORA is made, most
practitioners are very conservative in their
approach, and some type of external
immobilization is usually necessary for at least 1
to 2 months.
49.5.10 Birth Injuries
Spinal cord injury due to birth-related trauma is
probably underdiagnosed and underreported
because of the lack of radiographic findings in
most instances. Typically, the upper cervical spine
or cervicothoracic junction is a ected; however,
any level of the spinal cord can be involved and
involvement in multiple levels is not uncommon.
Two-thirds of all birth injuries accompany breech
presentation and one-third occur with cephalic
presentation or transverse lie. A wide variety of
factors have been implicated in birth-related spinal
cord trauma, including mechanical repositioning,
breech presentation, and forceps extraction.
● The mortality for birth-related spinal cord injury
is high, and survivors may have a poor
prognosis. Improved prenatal monitoring and
obstetrical techniques have helped reduce these
injuries over time.
49.6 Examination
The principles involved in treatment of pediatric
spinal cord injury are similar to those established
in adults. Spinal cord injury in the pediatric age
group is usually caused by a traumatic insult, and
the resulting neurological deficit ranges from an
incomplete spinal cord injury with partial loss of
function to complete spinal cord injuries where all
function below the level of injury is lost.
● Injuries in the high cervical spinal cord a ect
muscles required for respiration as well as
nerves responsible for motor strength and
sensation in the arms or legs. In addition, bowel
and bladder function is lost if the lesion is
complete.
● Injuries to the lower cervical cord have varying
degrees of sparing of arm strength depending on
the level of the lesion. In these instances, lower
extremity and bowel and bladder function are
also lost. Injuries in the thoracic spine or in the
upper lumbar areas have sparing of the upper
extremities, but loss of function in the lower
extremities and bowel and bladder.
● Injuries in the lower lumbar spine can show
incomplete and patchy loss of function in the
lower extremities as well as incomplete loss of
function in the bowel and bladder, consistent
with a cauda equina syndrome.
● Identifying the proper level and injury a ecting
the spinal column is important to determine the
appropriate treatment protocol. This includes
identification of the fracture type (if any),
recognition of dislocation and instability,
identification of any mass lesions that may be
compressing the spinal cord (such as hematomas
or ruptured disks), and identification of spinal
cord injury.
● This evaluation is firmly based on adequate
history and clinical examination as well as the
acquisition of proper radiographic studies.
Radiographic studies include plain films with or
without dynamic (flexion/extension) views and
CT and MRI scans.
49.7 Prehospital Management
The treatment of traumatic spinal cord injury
should begin in the field shortly after the accident.
Modern techniques of resuscitation and transport
Pediatric Spine Trauma
393

include complete spine immobilization, applica-
tion of a rigid cervical collar, and prevention of
hypotension. The high-dose methylprednisolone
protocol has shown little or no benefit to patients
with spinal cord injury,12 and most major Level 1
trauma centers no longer use it routinely. In the
intensive care unit, treatment should be directed
at maintaining adequate blood flow and oxygena-
tion to the spinal cord.
49.8 Nonsurgical Management
● There are certain instances in which spinal
column injuries may be managed conservatively,
often with a hard cervical orthosis. These
situations generally include stable fractures and/
or ligamentous injuries. Chip fracture, unilateral
facet fractures, linear vertebral body fractures,
and mild compression fractures are all examples
of injuries that might be managed in a hard
collar. The time required for hard collar
immobilization varies between fractures, but
typically is in the range of 1 to 2 months.
● The injury that most commonly requires an
external halo orthosis in the pediatric
population is a C2 synchondrosis fracture across
the base of the odontoid. These fractures most
often occur in young children, a population in
which direct surgical repair is challenging, and
the odds of successful healing across the fracture
are high with a halo orthosis.
● The final step in nonsurgical management is close
follow-up of the patient after treatment. For
example, a patient who has not been operated on
and is placed in an external cervical collar may
develop progressive kyphotic instability over time.
Serial follow-up X-rays are important to make
sure that proper treatment is given. In the case of
progressive cervical kyphosis, most patients go on
to require operative fusion.
49.9 Surgical Indications
The surgical indications for a spinal column injury
with or without spinal cord injury include spinal
instability (i.e., radiographic demonstration of
two-column injury of the cervical spine), the pres-
ence of a mass lesion such an epidural hematoma,
and/or a traumatic disc rupture with neurological
deficit. There are various published adult criteria13
for predicting instability of the cervical spine, but
these criteria have not been validated in children
(Table 49.1).
49.10 Surgical Technique
● Once the level and injury a ecting the spinal
column have been identified, the next step is
correction of any spinal column deformity that is
present. This may require the use of preoperative
traction in either Gardner–Wells tongs or a halo
ring. A general rule of thumb in children is to use
5 lb of traction per vertebral level.
● An anterior approach is commonly used for
treating unstable pediatric cervical spine
fractures. The approach is similar to those
performed in adults, with minor variations. In
children, with their long, slender necks, it is
typically very easy to get from C2 all the way
down to C7 with an anterior approach.
● The disc material in children is typically very
hydrated and fibrous, making for a tedious
resection. When preparing the vertebral bodies
for fusion, it is very important to remove all of
the cartilaginous end plate at each level to
ensure bone-to-bone contact for the graft.
Table 49.1 Checklist for the diagnosis of clinical
instability in the middle and lower cervical spine
Element

Point value
Anterior elements destroyed or unable to
function
2
Posterior elements destroyed or unable to
function
2
Positive stretch test

2
Radiographic criteria
● Flexion/extension X-rays
– Sagittal plane translation >3.5 mm or
20% (2 points)
– Sagittal plane rotation >20 degrees
(2 points)
OR
● Resting X-rays
– Sagittal plane displacement >3.5 mm
or 20% (2 points)
– Relative sagittal plane angulation >11
degrees (2 points)
4
Abnormal disc narrowing

1
Developmentally narrow spinal canal
● Sagittal diameter <13 mm
● 2. Pavlov’s ratio <0.8
1
Spinal cord damage

2
Nerve root damage

1
Dangerous loading anticipated

1
Total of 5 or more = unstable
Source: Reproduced with permission from White and
Panjabi.14
Trauma
394

● An interbody allograft is commonly used both
for discectomies and corpectomies in children.
● One of the most important surgical issues is
finding an anterior cervical plating system that
fits the patient. In young patients, an adult-sized
implant may not fit and another solution must
be found. Some device manufacturers make
anterior cervical plates with only one fixation
screw per level, which is a possible alternative in
selected cases.
● Posterior cervical approaches are preferred for
occipitocervical instability and atlantoaxial
instability, both out of the scope of this chapter.
Posterior approaches to subaxial instability in
children are commonly performed and are
similar to their adult counterparts. The biggest
caveat for most posterior lateral mass fixation in
children is the size of the lateral mass complex
in a given patient. In our experience, after the
age of 8 to 10 years, the lateral mass complex is
of su cient size to accept full adult-sized
instrumentation.
● For cases involving extreme instability, such as
traumatic spondyloptosis, a combined anterior
and posterior approach is necessary. The general
principles outlined above apply in these
situations as well.
49.11 Complications
● Fortunately, complications after cervical spine
surgery in children are rare. In general, the risk
of surgical site infection is low, but it may be
possibly higher for posterior approaches.
● Vascular injury, tracheoesophageal injury, spinal
cord injury, and postoperative hematoma are the
main complications of anterior cervical surgery.
● Posterior cervical surgery has a similar set of
complications as anterior approaches.
49.12 Outcomes
● The rate of successful arthrodesis in the
stabilization of traumatic cervical spine injuries
is quite high, probably approaching 100%.
● The outcomes for pediatric spinal cord injuries
depend primarily on the severity of the initial
insult to the spinal cord, followed by the timing
and quality of early management. In general,
however, children tend to recover better and
more quickly than their adult counterparts.
49.13 Postoperative Care and
Rehabilitation of Spinal Cord
Injury
Once a spinal cord and spinal column injury has
been diagnosed and treated, rehabilitation begins.
Some patients are lucky enough to have no neuro-
logical deficit and will just require close follow-up
by their physicians. Other patients have significant
neurological deficits and require intensive rehabi-
litation programs to maximize their potential for
recovery of function or learn to function with their
new neurological status. Many pediatric hospitals
have in-house rehabilitation units where this may
be done. Rehabilitation includes physical therapy,
occupational therapy, speech therapy, as well as
close follow-up by physiatrists and rehabilitation
medicine specialists. Rehabilitation doctors typi-
cally work closely with the treating surgeons.
Some rehabilitation centers are freestanding,
o ering many, if not all, of the same features of in-
hospital rehabilitation centers.
49.14 Surgical Pearls
● Most unstable pediatric spinal column injuries
can be managed with surgical instrumentation
and fusion. The choice of approach (anterior vs.
posterior) varies with surgeon training,
preference, and experience.
● Removal of all the cartilaginous end plate and
proper preparation of the vertebral body are
critical for the success of an anterior interbody
fusion.
● Preoperative traction should be used judiciously.
The pediatric spine is in general very flexible,
and even major deformities may be corrected
with intraoperative reduction.
49.15 Common Clinical
Questions
1. Is high-dose methylprednisolone indicated for
spinal cord injury in children?
2. Why does SCIWORA happen so frequently in
young children?
3. What age group has the highest incidence of
upper cervical spinal injury?
4. What is the CCI for measuring AOD?
Pediatric Spine Trauma
395

49.16 Answers to Common
Clinical Questions
1. No, it is not.
2. The soft tissues and ligaments of the neck are
more distensible than the spinal cord at that
level.
3. 0 to 4 years old.
4. The CCI measures the distance between the
occipital condyle and superior articular capsule
of C1.
References
[1] Brown RL, Brunn MA, Garcia VF. Cervical spine injuries in
children: a review of 103 patients treated consecutively at a
level 1 pediatric trauma center. J Pediatr Surg. 2001; 36(8):
1107–1114
[2] Polk-Williams A, Carr BG, Blinman TA, Masiakos PT, Wiebe
DJ, Nance ML. Cervical spine injury in young children: a
National Trauma Data Bank review. J Pediatr Surg. 2008; 43
(9):1718–1721
[3] Eleraky MA, Theodore N, Adams M, Rekate HL, Sonntag VK.
Pediatric cervical spine injuries: report of 102 cases and
review of the literature. J Neurosurg. 2000; 92 suppl 1:12–17
[4] Cervical spine injuries—Orthopaedic Trauma Association (OTA)
classification. OrthopaedicsOne Articles. OrthopaedicsOne—
The Orthopaedic Knowledge Network.
orthopaedicsone.com/x/TYEXBQ. Accessed April 1, 2014
[5] Klimo P, Jr, Kan P, Rao G, Apfelbaum R, Brockmeyer D. Os
odontoideum: presentation, diagnosis, and treatment in a
series of 78 patients. J Neurosurg Spine. 2008; 9(4):332–342
[6] Fassett DR, McCall T, Brockmeyer DL. Odontoid
synchondrosis fractures in children. Neurosurg Focus. 2006;
20(2):E7
[7] Brockmeyer DL, Ragel BT, Kestle JR. The pediatric cervical
spine instability study. A pilot study assessing the prognostic
value of four imaging modalities in clearing the cervical
spine for children with severe traumatic injuries. Childs Nerv
Syst. 2012; 28(5):699–705
[8] Pang D, Nemzek WR, Zovickian J. Atlanto-occipital
dislocation—part 2: the clinical use of (occipital) condyle-C1
interval, comparison with other diagnostic methods, and the
manifestation, management, and outcome of atlanto-
occipital dislocation in children. Neurosurgery. 2007; 61(5):
995–1015, discussion 1015
[9] Reinhold M, Audigé L, Schnake KJ, Bellabarba C, Dai LY, Oner
FC. AO spine injury classification system: a revision proposal
for the thoracic and lumbar spine. Eur Spine J. 2013; 22(10):
2184–2201
[10] Pang D. Spinal cord injury without radiographic abnormality
in children, 2 decades later. Neurosurgery. 2004; 55(6):
1325–1342, discussion 1342–1343
[11] Pang D, Pollack IF. Spinal cord injury without radiographic
abnormality in children—the SCIWORA syndrome. J Trauma.
1989; 29(5):654–664
[12] Walters BC, Hadley MN, Hurlbert RJ, et al. American
Association of Neurological Surgeons, Congress of Neurological
Surgeons. Guidelines for the management of acute cervical
spine and spinal cord injuries: 2013 update. Neurosurgery.
2013; 60 suppl 1:82–91
[13] White AA, III, Johnson RM, Panjabi MM, Southwick WO.
Biomechanical analysis of clinical stability in the cervical
spine. Clin Orthop Relat Res. 1975(109):85–96
[14] White AA III, Panjabi MM. The problem of clinical instability
in the human spine: a systematic approach. In: White AA
3rd, Panjabi MM, eds. Clinical Biomechanics of the Spine.
2nd ed. Philadelphia, PA: J.B. Lippincott; 1990:277–378
Trauma
396

50 Pediatric Peripheral Nervous System Trauma
Kambiz Kamian, Andrew T. Healy
50.1 Introduction
The peripheral nervous system (PNS) has the capa-
bility to regenerate itself at a rate of 1 mm/day,
a orded by the unique di erences in contrast to the
central nervous system (CNS), including a basal lam-
ina provided by Schwann’s cells and central inhibi-
tory signals not present in the periphery.1 Despite a
rich blood supply and regenerative capacity, severe
injury often yields poor recovery without interven-
tion. In children, speed and extent of functional
recovery is felt to exceed that of adults2 given the
lower likelihood of negative systemic factors, neuro-
plasticity, higher metabolic rates, and shorter dis-
tances to target organs.3 Schwann’s cells provide a
sca olding and a hospitable milieu to guide and
support daughter axons emerging from endbulbs of
the proximal stump of injured nerves, powered by a
new regenerative neuronal phenotype, which
become “regeneration units.”4
Proceeding with operative intervention, inter-
rupting this slow regenerative process is often the
crucial decision point in treating PNS injury.
Proximal injuries that are required to regrow long
distances (hand intrinsic muscles) have poorer
functional outcomes and target muscles will atro-
phy up to 80 to 90% in 3 months, undergoing fatty
replacement5,6 that is likely permanent beyond 1
year7 and completely replaced by fibrosis in 2
years.1 Proximal sciatic or brachial plexus lesions
rarely restore distal limb function.4 When opera-
tive intervention is decided upon, the most impor-
tant factor is a tension-free approximation. Surgi-
cal strategies range from neurolysis in the setting
of a spontaneously regenerating nerve, resection
and reapproximation in a short segment of
dysfunction, resection with donor grafting for
long-segment dysfunction, and neurotization (sac-
rificing less important donor nerve function to
transplant to more desired targets) in the setting
of nerve root avulsion.
50.2 Peripheral Nerve Anatomy
The functional unit of the nerve, the neuron, is
ensheathed by Schwann’s cells (+ /- myelin).
Each axon w ith its Schwann’s cells is enveloped
by the endoneurium , w hich provides the loose
connective tissue sca olding and itself provides
an endoneurial tube. Altogether the axon,
Schwann’s cells, and endoneurium are consid-
ered a single “nerve.”8 The perineurium is a
thicker collagenous connective tissue sheath
around a group of axons creating the fascicle,
which includes tight junctions—form ing the
blood–nerve barrier.1 Multiple fascicles travel
within the epineurium , along with arteries and
veins. The epineurium is dense and m ore fibrous
connective tissue with both collagen and elastin
and is contiguous with the dura m atter proxi-
m ally. Epineurial vessels provide collateral flow,
which m ost often can be safely sacrificed without
disrupting perineural/endoneurial blood supply.1
50.3 Mechanism of Neuronal
Injury
Peripheral nerve injury occurs in 5% of multitrauma
patients.9 This underestimates the peripheral nerve
injuries in patients who are not multiple trauma
patients or who have other neural injuries that pre-
clude the diagnosis of distal nerve injury.4 After
peripheral nerve axotomy, there is a period of ante-
rograde and retrograde change.
● Anterograde: “Wallerian” degeneration
detectable beyond 48 hours from injury:
– Target organ denervation.
– Schwann’s cell sca old remains.
● Retrograde:
– Cell body change10 or “chromatolysis”.
○ Cell body swelling.
○ Upregulation of genes involved with
regeneration.
○ Dissolution of the Nissl bodies.
○ Prominent migration of the nucleus toward
the periphery.
○ Increase in the size of nucleolus and nucleus.
– Proximal stump sprouts endbulbs (distal
swellings of axoplasmic material), which yield
daughter axons.4
Directed regrowth is guided by distal stump
Schwann’ cells, whereas misdirected regrow th can
result in neuroma formation, or neuroma in con-
tinuity in partial injury.4 Regrow th is limited by
the rate of anterograde slow axonal transport
(1–2 mm/day).1 Mechanism of injury is one major
397

determinant of recovery and also surgical manage-
ment.
● Sharp laceration: Clean, sharp laceration (with
predictable degree of neural damage) should be
reapproximated within 72 hours.11
● Blunt division: Proximal and distal stumps
appearing contused (with unpredictable length
of neural injury) should be tagged and
reapproximation planned in 3 to 4 weeks.11
● Blunt injury/contusion/stretch: Common, with
a greater tendency to be nonfocal with
multilevel plexal involvement,11 more
commonly, supraclavicular (72 vs. 28%)12 with
injury expected over longer segments. About
85% of gunshot wounds (GSWs) do not directly
transect the nerve and result in this injury.1
Managed expectantly for 3 to 4 months, if
surgical repair is indicated, outcome is less
favorable.11,12
● Avulsion: Often seen in perinatal and traction
brachial plexus injuries. Recovery is not
expected, however, with other functional plexal
elements in children, some advocate longer
expectant management11 prior to neurotization
procedures.
50.4 Sunderland’s Classification
● First degree (aka neurapraxia13): Disturbance
of axonal conduction (+/– demyelination)
without significant damage to or degeneration of
the nerve. Transient alteration of function
usually lasts seconds to minutes, but more
severe cases can last up to a few weeks.
Electrophysiological evidence of denervation is
absent when tested 18 to 21 days after the
injury. Prognosis for full recovery is excellent.
● Second degree (aka axonotm esis13): Axonal
injury (with wallerian degeneration) within an
intact endoneurial tube. Electromyography
(EMG) will show denervation and it may remain
abnormal up to 1 year. Full recovery is
expected.7
● Third degree (aka axonotm esis13 with
endoneurial dam age): More severe axonal
injury, which includes disruption of the
endoneurium, conveying variability in the
expected spontaneous regeneration.8 EMG after
2 weeks will show fibrillation potentials
reflecting wallerian degeneration. This injury is
often managed expectantly but degree of
recovery is unpredictable.8
● Fourth degree (neurotm esis13): Complete
disruption of the nerve with degeneration.
Clinical picture is consistent with “complete
interruption of the nerve.” Scarring is more
severe with epineurial damage, some motor
units may attempt to regenerate, but rarely of
good quality.8 EMG will be similar to
axonotmesis; however, spontaneous recovery is
unexpected.1
● Fifth degree (avulsion): Involves discontinuity
of the nerve trunk yielding complete loss of its
motor, sensory, and autonomic function. Dorsal
horn injury predisposes to pain.
50.5 Examination
Physical examination of children is di cult to
assess isolated motor function. In the older child,
the preferred method is the British Council system
used in adults (Medical Research Council) or the
Louisiana State University (LSU) medical center
system.1 Gilbert described a more global system
M0–M3 describing limb position to determine
flexor, extensor, or total plexus involvement in
perinatal neuronal injury.14
Other important
examination findings include phrenic nerve
involvement (diaphragm paralysis), long thoracic
nerve (serratus paralysis), or sympathetic involve-
ment (Horner’s syndrome), which likely indicate
root avulsion.7 Sensory preservation in motor-
a ected distribution is a good prognostic sign indi-
cating neurapraxia.15
See Appendix A.1 and
Appendix A.2 for motor and sensory examination
scales and peripheral nerve examination pearls.
Examining children is di cult. Other signs of
neuronal injury other than volitional movement
must be utilized: (1) skin changes: smooth, dry
skin in the denervated digit; (2) fingerprints made
on ninhydrin paper revealing anhydrosis; and (3)
muscular atrophy. Anhydrosis may be the only
indication of denervation in a child.5 Under magni-
fication, perspiration on the palmar surface can be
detected by visual inspection alone. Another crude
test is the O’Riain’s wrinkle test, where digits are
submerged in tepid water for 5 minutes and para-
sympathetic-injured digits will not wrinkle.1 On
sensory examination, 2-point discrimination
should be 2 to 5 mm at fingertips and 7 to 12 mm
at palmar base.1 This can be tested with paper clips
if calipers are not available. During the regenera-
tion phase, a progressive Tinnel’s sign can be seen
with grade 2 or above as axon regenerates.7
Trauma
398

Note: Rapidly advancing Tinnel’s sign may be a
positive prognostic factor for recovery, but is felt
to have a less valuable positive predictive value.
On the other hand, the lack of a Tinnel sign at 4 to
6 weeks is much more specific for poor regenera-
tive potential.1
50.6 Neurophysiology
Neurophysiological tests are useful in determining
whether the lesion is pre- or postganglionic,
although not to replace computed tomography
(CT) myelography (gold standard) for this purpose.
EMG can be utilized in children with 80% sensitiv-
ity for root avulsion and can document subclinical
recovery.
50.6.1 Electromyography
A normal muscle will generate the following:
● Insertional activity.
● Followed by absence of signal during rest.
● Electrical activity with voluntary/proximal
neuronal activation.
A denervated muscle with axonal loss will gener-
ate the following:
● Spontaneous electrical activity at rest after 2
weeks from the injury that include the
following:
– Fibrillation potentials.
– Positive sharp waves.
EMG is most useful 2 to 3 weeks after injury to
permit denervation changes to occur in target
muscles. Note: EMG will falsely show distal activa-
tion over the first 1 to 2 days prior to the onset of
wallerian degeneration. Therefore, in the acute
setting, an absent response to proximal stimulus
and an intact response to distal stimulus cannot dif-
ferentiate conduction block from axonal disruption.
An important sign of recovery at 6 weeks is dener-
vation potential or nerve action potential (NAP)
from neural stimulation.1
50.6.2 Nerve Action Potentials
Denote direct stimulation of the nerve proximal to
a lesion and recording distal to that lesion. This
test is more sensitive and will reveal neuronal
regeneration prior to actual muscular activation,
or EMG detection. NAPs may be conducted across
lesions that do not permit voluntary signaling of
muscle contraction. Intraoperative NAPs can
determent if axonal regeneration has occurred
across the site of injury. If not, grafting has been
shown to improve outcomes (Table 50.1).1
50.6.3 Somatosensory-evoked
Potentials and Muscular-evoked
Potentials (SSEPs/MEPs)
Useful to determine complete avulsions (absent
motor but intact sensory nerve action potentials),
however, clinically complete avulsions may have
sparse sensory fiber connections resulting in false-
negative results of SSEP. MEPs are useful in testing
the ventral fibers. Electrodiagnostic is an impor-
tant tool especially with function loss.5 It is recom-
mended that a baseline study be taken 1 week to
10 days and repeating at 3 to 4 weeks and 10 to 12
weeks.5 A common protocol is as follows:
● Baseline (0–7 days).
● Initial Follow-up (10–21 days): Distinguish
demyelination (preserved distal responses) from
axonal loss.
Table 50.1 Brachial plexus outcomes (in-continuity lesions)
Plexus elements with (+) NAP,
neurolysis alone
Plexus elements with (−) NAP,
nerve repair
Injury type

Complete LOF
preoperatively
Incomplete LOF
preoperatively
Complete LOF
preoperatively
Incomplete LOF
preoperatively
Stretch/contusion

90.3

94.1

44.6

62.2
GSW

97.6

93.6

55.2

87.5
Iatrogenic

94.4

100

71.9

66.7
Laceration I/C

90.0

94.4

66.7

75.0
Totals

92.6

94.6

49.5

66.7
Abbreviations: GSW, gunshot wound; I/C, in-continuity, LOF, loss of function; NAP, nerve action potential.
Source: Adapted from Kline and Hudson.1
Note: Values represent percent of plexal elements gaining grade 3 function or better.
Pediatric Peripheral Nervous System Trauma
399

● Follow-up (3–6 months): Determine the extent
of reinnervation +/– operative intervention.
● Follow-up (6–12 months): Documents extent of
distal muscle reinnervation. Note: EMG recovery
may take more than 12 months, however,
waiting beyond this time frame may result in
poorer outcomes due to target muscle loss and
fibrosis.6
50.7 Imaging
50.7.1 X-Ray
In brachial plexus injury may be suggested by frac-
ture. Transverse apophysis clavicular fracture or
fracture of the first rib may suggest proximal
lesions. Chest X-ray (CXR) may also reveal an ele-
vated hemidiaphragm indicating phrenic nerve
injury. Extremity fractures are also associated with
peripheral nerve injury.
50.7.2 MRI
Noninvasive and more sensitive for BP injury,
therefore examination of choice for children ahead
of CT myelography.16 T1 provides useful anatomi-
cal information outlining the neuronal adiposity
with hyperintensity. Note: Coronal views for con-
tralateral plexus comparison are important.16
Short T1-inversion recovery (STIR) sequences to
see pathological neuropraxic/inflammatory plex-
opathy and T2 is most useful for pseudomeningo-
celes with axial gradient recalled echo (GRE) for
nerve root avulsions. In traumatic injury, imaging
may reveal associated fractures.
50.7.3 CT Myelography
It may be more sensitive than MRI for detecting
avulsions and is considered gold standard in this
regard.17,18
Sensitivity in perinatal Behavioral
Problems Index (BPI) is 63%, whereas the specific-
ity is about 85%. Nerve root integrity may be
present in up to 18% of pseudomeningoceles and
therefore CT is most sensitive when pseudomenin-
gocele is combined with the absence of the respec-
tive nerve root.16,18
50.8 Nonsurgical Management
● Bracing: Prevents contracture, however, stresses
the importance of range-of-motion (ROM)
exercises multiple times/day. Immobilized joints
sti en rapidly.
● Physical therapy: Full ROM exercises, prevents
joint contracture.
● Painkillers: For the acute stage, avoid long-term
use.
● Neuropathic pain: Neurontin, Lyrica, tricyclic
antidepressants (TCAs), transcutaneous
electrical nerve stimulation (TENS).
● Frequent follow-up.
50.9 Surgical Repair
50.9.1 Repair Types
● Exploration: If operation is required for another
pathology (i.e., pseudoaneurysm, open fracture
reduction, hematoma) or ongoing neuronal
compression, the peripheral nerve surgeon may
be needed for exploration alone.
● Neurolysis: Consists of decompressing neural
elements. It is best served for injuries in
continuity which reveal preexisting neuronal
regeneration (intraoperative NAPs present).1
Note: Neurolysis includes epineurial scar
resection (external neurolysis) and even
splitting fascicles to determine the need for a
split repair (internal neurolysis).
● Direct repair.
Epineurial: Epineurial repair using neural vessels
to help alignment19 after injured nerve is sec-
tioned back to healthy functioning nerve.
Grouped fascicular or fascicular: Group fascic-
ular repair or fascicular repair should be carried
out when these groupings can be clearly identi-
fied.20 Note that fascicular orientation can change
along the length of a nerve every few centimeters.1
● Grafting:
– Minimize number of sutures (4–10) with 8 to
11.0 monofilament nylon to limit scar
formation.21
– Harvested nerve should be 25% longer than
what is needed due to nerve shortening and
end preparation.21
– Alternatives for repair (defects <3 cm):
Autologous vein grafts, perineurial tubes,
silicone alloplastic tubes, and resorbable
conduits (polyglycolic acid, collagen).
– Graft should be as close to proximal nerve
diameter as possible.
– Graft should match the size and number of
injured nerve fascicles as closely as possible.21
Trauma
400

– Note: With distinct fascicles, cable grafting is
an option to either match up clearly
di erentiated polyfascicular nerves or to
better match the cross-sectional area of the
injured nerve with a small nerve graft.21
● Neurontization: See brachial plexus section.
50.9.2 Repair Timing
● “Rule of 3s”:
– Sharp laceration: 3 days (72 hours, immediate
repair)22—Rule out associated vascular injury
(computed tomography angiography [CTA],
angiogram); pseudoaneurysm, hematoma, or
fistula, rule out and other organ damage
(esophagus, trachea). Ask for help from other
specialties, need immediate repair.23
– Blunt laceration: 3 to 4 weeks (delayed)22: If
during the primary repair for sharp laceration,
any contusion or long-segment damage was
noticed, tag the nerve with silk and wait 3 to 4
weeks.
– Blunt injury/stretch/avulsion: 3 to 6 months
with electrodiagnostic studies to distinguish
neuropraxia from axonal loss +/– spontaneous
recovery.22
50.10 Pearls
● Proximal injuries convey poorer prognosis.24,25
● Upper extremity injury recovers better than
lower.24,25
● About 10% of an injured nerve’s axons after
simple transaction will reach a target after
surgical approximation.26
● Tension-free approximation is best, avoid
interposed graft as much as possible with long
dissection and neurolysis especially when
damage is proximal, but if not possible,
interposed graft is acceptable.
● Primary approximation if the ends are within
2 cm.5
● Intraoperative NAPs: If present, leave them as
is, if absent then reapproximation is best,
nerve graft is second best and neural tubes are
third.1,27
● Nerve growth occurs at 1 mm/day or 1 in/month,
two more delays; (a) 3 to 4 weeks crossing any
suture line, (b) 3 to 4 weeks for reaching the end
plate and end plate maturation.1,28
● Proximal function has better chance of
restoration of function, in follow-up, test the
muscles proximal to distal.
● EMG recovery can be detected 3 to 4 weeks prior
to clinical recovery.
● Grouped fascicular repair is favorable if
components can be distinguished, if not,
epineural repair with alignment based on
epineural vessels and gross fascicular
approximation.
● Sural nerve: 2.1 mm in diameter mark the
direction of axoplasmic flow when harvesting
(mark or tag it) and use it along the flow. Locate
it lateral to gastrocnemius tendon.1,21
● Other grafts available: Lateral cutaneous nerve
of the forearm.
● Open injury—explore. If the nerve cut is blunt,
then tag it for delayed exploration.
● No long-acting paralytics from anesthesia!
● Use motor nerve graft for critical motor
restoration.29
● Protecting the nerve from surrounding tissues
during peripheral nerve surgery can improve
outcomes by providing a protective barrier,
reducing fibrosis, decreasing adhesions to
surrounding tissues, and providing a
vascularized wound bed.30
50.11 Postoperative Care/
Follow-up
● Ensure dressings are not too tight, check distal
vascular examination.
● CXR postoperative for brachial plexus.
● Immobilization temporarily after surgery for
short period of time, 1 to 2 weeks.
● Start physical therapy 3 to 4 weeks after the
surgery; full ROM exercises, prevent contracture
and development of capsular contractures and
muscular contraction.
● Painkillers; short period.
● Neuropathic pain; Neurontin, TCA, Lyrica, TENS
● Electrotherapy.
● Bracing; splints to encourage finger flexion.
● Treating contractures: Botox.
● As the patient ages, add physical activity such as
swimming.
● Ancillary surgeries
– Tendon transfer.
– Free muscle transfer.
– Joint fusion, open joint (glenohumeral)
reduction.
– Subscapular muscle release for fixed shoulder
adduction.
– Biceps tendon transfer brachioradialis tendon
transfer for wrist extension.
Pediatric Peripheral Nervous System Trauma
401

– Biceps tendon transfer to remove it as a
supinator, need to restore wrist extension.
– Osteotomies.
– Pain from sclerotic DREZ may be treated with
ablation.15
50.12 Brachial Plexus
50.12.1 Epidemiology
Brachial plexus injuries are commonly associated
with head trauma causing loss of consciousness
(LOC) (72%) and coma (19%), upper extremity frac-
ture dislocation (20%), and rib fracture in 41% of
adult trauma populations. Subclavian artery
(15–30%) and spinal cord injury (5%) are also associ-
ated with these high-velocity accidents.15 Brachial
plexus injuries in the pediatric population, com-
pared to adults, are more often associated with ske-
letal injuries31 and nerve root avulsion (63–80%),32
as compared to the adult population (40 and 20%,
respectively).33
Children less frequently report
denervation pain (0–5%).32 Isolated infraclavicular
injury (Klumpke’s) is uncommon.12,17
Traumatic peripheral nerve injury in pediatrics
is predominantly as follows:
1. Perinatal (obstetric brachial plexus palsy) with
0.8 to 2.5 in 1,000 live births15,17 (covered
separately).
2. Traum a. Pediatric brachial plexus injury outside
of obstetrics is most often related to the
following:
● Motor vehicle collisions for only 1% of all
brachial plexus injury.33
● Pedestrian accidents predominate (67%).
● Road tra c injury.
● Falls from height, shoulder dislocation
(4.5%).17
● Gunshot wounds/stabbing injuries.15
Note: Contact sports. Less severe injuries to the
plexus occur frequently, given the term “Burner,”
transient dysesthesias and even motor weakness
can be the result of stretch injury or direct blunt
trauma to Erb’s point, a neuropraxia, which often
resolves within minutes but rarely can persist.
50.12.2 Anatomy
Covered separately (see perinatal brachial plexus
injury).
50.12.3 Distribution of Injury
● Upper (Erb’s): C5–C6 +/– C7: Often exceeds
lower BP injury 3:1 and is more often severe in
trauma populations,12,33 C5–7 results in the
classic “waiters tip” position.
● Interm ediate: C7 +/– C8, T1: Often the lower
roots are more mildly a ected in perinatal injury
and may result in distal improvement greater
than shoulder, however, recovery is variable.
● Lower (Klum pke’s): C8, T1: Most commonly
caused by stretch, GSW, and laceration.
Exceedingly rare in neonatal Traumatic Brain
Injury (nTBI) and less common than its
supraclavicular counterpart in adult trauma
populations and more often transient
neuropraxia (50%).33 Cord injuries at this level
are associated with other injuries to greater
extent than supraclavicular.12 IE: shoulder
dislocation, fracture, axillary artery injury. They
are surgically more demanding given
vasculature around the neural elements.
● Total plexus palsy: (C5–C8 +/– T1): Often
associated with multiple avulsions to variable
degree, often lower plexus avulsions. Poor
recovery expected for distal extremity function,
goal of surgery is proximal functional
restoration.
50.12.4 Examination
There are reliable methods of quantifying upper
extremity function in patients with brachial plexus
palsy and may be used clinically and to assess
functional outcomes. (Perinatal examination is
covered separately.)
● The Modified Mallet Classification.17
● The Toronto Test Score.34
● The Active Movement Scale.35
The physical examination for brachial plexus
injury must include the following:
● Musculoskeletal palpation: Trapezius, scapula,
clavicle, shoulder, etc. may elicit tenderness or
evidence of fracture/muscle spasm.
● Cervical spine palpation and neck clearance
must be done to rule out cervical fracture.
● Passive and active range of m otion testing.
● Detailed derm atom e and m yotom e-specific
neurological exam ination .
● Im aging: Evaluate for fracture.
Trauma
402

See “examination” above for imaging and neuro-
physiological testing. See Appendix A.1 and
Appendix A.2 for examination scoring and pearls.
50.12.5 Surgical Indications
Common indications include the following:
● Clear-cut upper trunk lesions (biceps function)
with no recovery at 2 to 3 months.
● Com plete plexus injury should be operated
sooner.
● No functional recovery in the first 3 weeks
should be further investigated with
electrodiagnostic studies for consideration of
exploration.15
In the presence of partial or minimal functional
recovery, reexploration may mean an initial loss of
function. This is especially challenging since most
commonly the surgeon will find neuroma in con-
tinuity and must decide to leave it or perform
resection.
● Repair after 9 m onths has success,15 however,
in perinatal injury some feel longer observation
is warranted given dramatically improved rates
of spontaneous recovery.22
50.12.6 Surgical Technique
● Supraclavicular incision It is most often used
given the preponderance of upper injury.
● Infraclavicular injury will often need clavicle
osteotomy and inferior clavicular incision (try to
avoid cutting the clavicle because of the high risk
of nonunion extending beyond deltopectoral
triangle toward axilla. Division of pectoralis near
the deltoid, often pectoralis minor will need
division as well. Musculocutaneous and median
nerve dissection are required, which lead to the
deeper axillary artery, which may be gently
retracted for exposure of the posterior cord.
Sural nerve grafting is needed almost invariably
with neuroma resection. Grafting procedure is
often sutured but some authors utilize solely
fibrin glue in neonatal injury.17
● If one functional root is found, goal is
renervation of the lateral cord or anterior
upper trunk for proximal restoration. A second
target is the posterior cord for axillary/radial
function.15
● In the setting of root avulsion, neurontization is
necessary.36
Common Donor Nerves
● Intraplexal:
– Medial pectoral nerve to axillary for upper
trunk lesion C5 to musculocutaneous.32
– Suprascapular nerve.37
– Partial ulnar.38
● Extraplexal:
– Accessory nerve.
– Phrenic nerve.37
– Intercostals.
– Partial contralateral plexus23,32: Used for C5–
C6 avulsions.
– Contralateral C7.23
Note: The more distal the recipient nerve the bet-
ter, no useful recovery from anastomosing to
donors proximal to the cords.
Complications include the following:
1. Damage to surrounding: Veins, arteries, trachea,
esophagus, thoracic duct
2. Infection: Wound dehiscence, deep infection,
abscess
3. Suture line disruption
50.12.7 Outcomes
In-continuity Brachial Plexus
Outcomes
See Table 50.1.
Infraclavicular Stretch Outcomes
LSU medical center reports on surgical interven-
tion of 1,019 traumatic BP lesions, 143 of which
(28%) were infraclavicular stretch injuries. Outcomes
were divided by division-cord and cord-nerve lesions
(which are the majority of infraclavicular stretch
injuries at 76%).12
Bottom line:
● Favorable: Lateral and posterior cords.
● Unfavorable: Medial cord and medial cord–
ulnar nerve injuries were poor especially if
excision and graft were needed.
Avulsion Outcomes
Avulsions treated with neurontization reveals up to
65 to 86% antigravity motor restoration at the level of
the biceps and up to 20 to 43% at the level of finger
flexion.37,39,40 C7 hemicontralateral transfer has not
shown adequate results when used independently.23
Pediatric Peripheral Nervous System Trauma
403

50.13 Extremities
50.13.1 Epidemiology
Upper extremity injury presenting the emergency
department is associated with peripheral nerve
injury about 1.7 to 2.5 of the time in children.41
Radial nerve is the most commonly injured
peripheral nerve of the extremities.9,42
● Nerve injury associated with fractures:
Especially predominant in the upper extremities
(80–90%).41
● Direct pen etrating or crush injury can injure
any regional peripheral nerve.
● Com partm ent syndrom e, untreated for 12.
hours, will likely yield permanent neurological
dysfunction.43
● Iatrogenic/injection injury.
In adult polytrauma populations:
● Hum eral fractures are associated with radial,
ulnar, and median nerve injury (9.5, 3.8, 1.4%).10
Although radial nerve injury is the most
common peripheral nerve injured and is
associated with humeral fracture,42
supracondylar fractures may be more often
associated with anterior interosseous nerve
(AIN)/median nerve injury (from 10 to 15% of the
time)44 and a higher preponderance of ulnar
injury depending on mechanism and fragment
displacement (anterior).45 Humeral neck
fracture or shoulder dislocation has a greater
correlation to axillary (16%), suprascapular (13%)
over radial (10%).46
● Forearm fractures also results in greater ulnar
nerve injury (2.4 %) versus median nerve (1.3%)
injury.
● Wrist fracture most commonly associated with
median nerve injury.9
● Pelvic fractu re sciatic nerve injury rates (1.2–
1.7%)9 less commonly femoral nerve injury
(0.16%).9
● Fem oral fracture neck fracture associated
w ith sciatic nerve injury (16%) m idshaft
associated with fem oral nerve injury
(0.16%).9
● Elbow fractures in children can be associated
with nerve injury 5 to 19%.45
● Distal lower extrem ity fractures Peroneal
nerve injury is the m ost com mon nerve injury
associated with lower extrem ity traum a (2.2%)
w ith fem oral and tibial nerves being the
least.9
50.13.2 Anatomy and Fractures
Associated Nerve Injury
See Appendix A.3 for nerve fracture association
table.
50.14 Upper Extremity
50.14.1 Surgical Indications/
Outcomes
The majority of peripheral nerve injuries with
closed fracture will improve spontaneously. About
82% of shoulder dislocation and humeral neck
fractures had complete recovery at 4 months,46 up
to 96% of radial nerve recovered with humeral
midshaft fractures.47 About 90 to 100% of supra-
condylar fractures will exhibit complete spontane-
ous recovery, but may take up to 4 to 9 months.48
Overall recovery rate for peripheral nerves of 85%,
the extent of which is established by 18 months.48
Most nerves need repair within 3 to 6 months48;
however, radial nerve has a longer recovery time
(6–9 months).49 Distal denervation or no improve-
ment on 3 to 4 month EMG (as compared with
6-week baseline) may support surgical exploration,
functioning neuromas in continuity will likely
improve from neurolysis alone, this sometimes will
include clearance of boney callous formation from
around the nerve.47,50 Initial conservative manage-
ment is considered to have more favorable out-
comes when nerve injury is a “primary injury” (i.e.,
associated with the initial fracture),50,51 whereas rec-
ommendations for iatrogenic injuries (“secondary
injuries”) associated with fracture reduction are less
clear and often early exploration is indicated.5,45
Children often are observed over longer periods
given their even greater chance of recovery (95%).52
At this time, it is the fracture type that dictates
exploration or not (complex or open fractures), and
there is no clear consensus on early versus late
exploration. Exploration of the nerve is recom-
mended when open reduction is pursued.5,42,45
More distal injury has better outcomes although
outcomes can be nerve specific49:
● High nerve regeneration potential: Radial,
musculocutaneous, and femoral.
● Moderate nerve regeneration potential:
Median, ulnar, and tibial.
● Poor nerve regeneration potential: Peroneal.
See Table 50.2 for upper extremity outcomes.
Trauma
404

50.15 Lower Extremity
Peripheral nerve injury in the lower extremity is
more often associated with injection (for the prox-
imal sciatic nerve), followed by fracture disloca-
tion, contusion, compression (from motor vehicle
collisions [MVC] most frequently gunshot wounds
and in a delayed fashion with compartment syn-
drome or iatrogenic after fracture traction or
reduction.1,9,53 Sciatic nerve injury is associated
with pelvic fracture approximately 1.2 to 1.7% of
cases,9,54 whereas femoral nerve is injured in less
than 0.5% of the time with pelvic fractures9 and
possibly more proximally with iliopsoas hema-
toma.55 The lumbosacral plexus courses over the
posterior pelvic ring toward the sciatic notch. At
this junction, the sciatic nerve can be injured in
displaced pelvic fractures and crush injuries.56
More often the sciatic nerve is injured beyond this
point, where it lies adjacent to the ischial tuberos-
ity. Here, posterior hip dislocations can injure the
sciatic nerve 16% of the time.57 The sciatic nerve is
well protected in the thigh between the adductor
magnus and biceps, and sciatic nerve laceration
from femoral fracture here is rare.56,58
Distally, the peroneal nerve is much more sus-
ceptible to injury not only with fibular neck frac-
ture, but also adduction knee injuries, and distal
fibular or even tibial spiral fractures.9 The peroneal
nerve is the most common place where the sciatic
component is injured and is found to be injured
2.2% of the time with fibular or tibial fractures.59
The tibial nerve is more rarely injured as it courses
protected between muscles for the majority of its
course, found to be injured 0.5% of tibial or fibular
fractures, and is more often injured in the lower
extremity or ankle.9
50.15.1 Anatomical
Considerations
Lumbar plexus: Involves nerve fibers from L2 to
L5.
Mnemonic: “I Get Loud On Fridays”: Iliohypo-
gastric, Ilioinguinal, Genitofemoral, Lateral femoral
cutaneous, Obturator, Femoral.
● Fem oral nerve, exiting the pelvis deep to the
inguinal ligament and is responsible for hip
flexion and leg extension. Injury at this
location is m ost com mon. Trauma is the
m ost comm on cause of fem oral nerve
pathology.
● Obturator nerve exits via the obturator
foramen, innervating the thigh adductors.
● Sciatic nerve, from both lumbar and sacral
plexuses, passing through the greater sciatic
foramen (inferior to the piriformis) innervating
knee flexors and all muscles below the knee
after dividing near popliteal fossa into the tibial
and peroneal nerves.
Sacral plexus: other than its contribution to the
sciatic nerve, the sacral plexus gives rise to
● Gluteal nerves (greater sciatic foramen)
responsible for hip extension and abduction.
● Pudendal nerves (lesser sciatic foramen) to the
pelvic floor.
50.15.2 Surgical Indications/
Outcomes
It is the fracture type that dictates open or closed
reduction, no indication for immediate exploration
with primary nerve palsy.
Table 50.2 Upper extremity outcomes
Median

Radial

Ulnar
Level of
injury
NTM 1
repair
NTM
graft
ICL+NAP
neurolysis
NTM 1
repair
NTM
graft
ICL+ NAP
neurolysis
NTM 1
repair
NTM
graft
ICL+ NAP
neurolysis
High

67%

67%

100%

80%

60%

93%

60%

100% 88%
Inter.

100%

67%

100%

100%

67%

100%

82%

57%
95%
Low

100%

71%

100%

(PIN)
100%
(PIN)
100%
(PIN)
100%

67%

100% 100%
Other

(AIN)
N/A
(AIN)
N/A
(AIN)
100%
(DF)
100%
(DF)
50%
(DF)
100%

N/A

N/A

N/A
Abbreviations: AIN, anterior interosseous nerve; DF, nerve to dorsal forearm; ICL, in-continuity lesion; NAP, nerve action
potential; NTM, neurotmesis; PIN, posterior interosseus nerve.
Note: Values represent percentage of patients achieving recovery of strength grade 3 or better in a series of upper
extremity injuries.27
Pediatric Peripheral Nervous System Trauma
405

Best lower extrem ity prognosis: Tibial nerve.
Worst lower extrem ity prognosis: Proximal
peroneal division of sciatic nerve.
Table 50.3 represents lower extremity outcomes.
50.16 Common Clinical
Questions
1. How long after injury can wallerian
degeneration be detected on neurophysiological
testing?
2. How do second- and third-degree neuronal
injury, using the Sunderland’s classification,
di er from each other?
3. A 13-year-old adolescent boy is evaluated in the
emergency department after a high-speed
motor vehicle collision and is found to have a
fractured first rib on CXR and shoulder
examination is limited. What is the most
appropriate imaging modality to evaluate the
neural elements?
4. What is the most commonly injured peripheral
nerve and approximately what percentage will
recover function with observation alone?
5. A 12-year-old boy has a type 1 Monteggia
fracture and will be taken to the operating room
for open reduction and internal fixation. He has
no sensory deficit on examination, but gives
poor e ort with motor. What nerve(s) should
be evaluated by neurosurgery intraoperatively?
50.17 Answers to Common
Clinical Questions
1. 48 hours. Prior to this point, an absent response
to proximal stimulus and an intact response to
distal stimulus cannot di erentiate conduction
block from axonal disruption.
2. Both considered “axonotmesis” by Seddon, the
important di erentiating factor is disruption of
the endoneurium in third-degree injury,
conveying a more unpredictable neuronal
recovery.
3. Bilateral brachial plexus MRI with axial cervical
GRE sequences. CT myelography may more
sensitive in detecting nerve root avulsion,
however, MRI can delineate injury to the plexus
and soft tissue as well as root avulsion and is
the less invasive method.
4. The radial nerve is the most commonly injured
nerve, especially with humeral shaft fracture
and spontaneously recovers from 85 to 96% of
the time. However, site of fracture is key with
proximal humeral neck fractures more often
disrupting axillary nerve and supracondylar
fractures most commonly disrupting median
nerve (or AIN).
5. Posterior interosseous nerve (PIN) is the most
commonly injured nerve in Monteggia fracture
(especially type 1) and would most often
present without sensory deficit.
References
[1] Kline DG, Hudson AR. Nerve injuries. Operative Results for
Major Nerve Injuries, Entrapments and Tumors. Philadelphia,
PA: W.B. Saunders Company; 1995
[2] Tajima T, Imai H. Results of median nerve repair in children.
Microsurgery. 1989; 10(2):145–146
[3] Frykman GK. Peripheral nerve injuries in children. Orthop
Clin North Am. 1976; 7(3):701–716
[4] Zochodne DW. The challenges and beauty of peripheral
nerve regrowth. J Peripher Nerv Syst. 2012; 17(1):1–18
[5] Hosalkar HS, Matzon JL, Chang B. Nerve palsies related to
pediatric upper extremity fractures. Hand Clin. 2006; 22(1):
87–98
[6] Sulaiman W, Gordon T. Neurobiology of peripheral nerve
injury, regeneration, and functional recovery: from bench
top research to bedside application. Ochsner J. 2013; 13(1):
100–108
[7] Fox IK, Mackinnon SE. Adult peripheral nerve disorders:
nerve entrapment, repair, transfer, and brachial plexus
disorders. Plast Reconstr Surg. 2011; 127(5):105–118
[8] Sunderland S. A classification of peripheral nerve injuries
producing loss of function. Brain. 1951; 74(4):491–516
Table 50.3 Lower extremity outcomes
Sciatic

Tibial

Common peroneal
Level of
injury
NTM 1
repair
ICL+ NAP
neurolysis
NTM 1
repair
NTM
graft
ICL+ NAP
neurolysis
NTM 1
repair
NTM
graft
ICL+ NAP
neurolysis
High

30–73%
69–95%

100%

55–94%
95%

84%

11–41% 82–93%
Intermediate N/A

N/A

100%

64%

95%

N/A

15–31% N/A
Low

78–95%
78–100%
N/A

64–100% 73%

N/A

57–76% N/A
Abbreviations: ICL, in-continuity lesion; NAP, nerve action potential; NTM, neurotmesis.
Note: Values represent percentages of patients achieving recovery of strength grade 3 or better in a series of lower
extremity injuries.26,58,59
Trauma
406