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MINISTRY OF HEALTH OF UKRAINE
VINNYTSIA NATIONAL MEDICAL UNIVERSITY
NAMED AFTER M.I.PYROGOV
NEUROLOGY DEPARTMENT
MODULE -1
Lesson # 8
Spinal Cord.
Syndromes due to Lesions at Specific Sites
along the Spinal Cord.Plexus Syndromes
1. Goals:
1.1. To study the anatomical fundamentals of the Spinal Cord,
the main Spinal Cord syndromes and their anatomical
localization.
1.2. To acquire the technique of the examination of the spinal
cord in normal condition and in different pathological
conditions.
1.3. To study the anatomical fundamentals of the Cervical,
Brachial, Lumbsacral Plexus and Plexus Syndromes.
2. Basic questions:
2.1. Anatomical Fundamentals:
2.1.1. Topographical relations of the vertebral column and nerve
roots to the spinal cord.
2.1.2. Important fiber tracts of the spinal cord.
2.2. The Main Spinal Cord Syndromes and Their Anatomical
Localization:
2.3. Plexus Syndromes
2.4. Peripheral Nerve Syndromes
3. Literature:
Mathias Baehr, M.D., Michael Frotscher, M.D. Duus’ Topical
Diagnosis in Neurology. – P.70-91, 100-120
Mark Mumenthaler, M.D., Heinrich Mattle, M.D. Fundamentals
of Neurology. – P.141-145
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Spinal Cord Syndromes
Because the spinal cord contains motor, sensory, and autonomic
fibers and nuclei in a tight spatial relationship with one another, lesions
of the spinal cord can cause a wide variety of neurological deficits,
which can be combined with each other in many different ways.
General anatomical preliminaries.
The spinal cord, like the brain, is composed of gray matter and
white matter. The white matter contains ascending and descending fiber
tracts, while the gray matter contains neurons of different kinds: the
anterior horns contain mostly motor neurons, the lateral horns mostly
autonomic neurons, and the posterior horns mostly somatosensory
neurons participating in a number of different afferent pathways.
In the adult, the spinal cord is shorter than the vertebral column:
it extends from the craniocervical junction to about the level of the
intervertebral disk between the first and second lumbar vertebrae (L12)
(Fig. 2.4).
The segments of the neural tube (primitive spinal cord)
correspond to those of the vertebral column only up to the third month of
gestation, after which the growth of the spine progressively outstrips that
of the spinal cord. The nerve roots, however, still exit from the spinal
canal at the numerically corresponding levels, so that the lower thoracic
and lumbar roots must travel an increasingly long distance through the
subarachnoid space to reach the intervertebral foramina through which
they exit. The spinal cord ends as the conus medullaris (or conus
terminalis) at the L1 or L2 level (rarely at L3). Below this level, the
lumbar sac (theca) contains only nerve root filaments, the so-called
cauda equina (“horse’s tail”; Fig. 3.22).
The fanlike filaments of the nerve roots still display the original
metameric structure of the spinal cord, but the cord itself shows no
segmental division. At two sites, however, the spinal cord is somewhat
swollen, namely at the cervical andlumbar enlargements. The former
contains the segments corresponding to the upper limbs (C4-T1), which
form the brachial plexus; the latter contains the ones for the lower limbs
(L2-S3), which form the lumbosacral plexus (Fig. 2.4).
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Spinal cord lesions occasionally affect only the white matter (e.
g., posterior column lesions) or only the gray matter (e. g., acute
poliomyelitis), but more often affect both. In the following paragraphs,
the manifestations of typical spinal cord syndromes will be presented
from a topical point of view. For completeness, a number of syndromes
characterized primarily or exclusively by somatosensory deficits will
also be presented here.
Syndromes due to Lesions of Individual Spinal Tracts and
Nuclear Areas and the Associated Peripheral Nerves
Syndrome of the dorsal root ganglion (Fig. 3.8). Infection of
one or more spinal ganglia by a neurotropic virus occurs most commonly
in the thoracic region and causes painful erythema of the corresponding
dermatome(s), followed by the formation of a variable number of
cutaneous vesicles. This clinical picture, called herpes zoster, is
associated with very unpleasant, stabbing pain and paresthesiae in the
affected area. The infection may pass from the spinal ganglia into the
spinal cord itself, but, if it does, it usually remains confined to a small
area within the cord. Involvement of the anterior horns causing flaccid
paresis is rare, and hemiparesis or paraparesis is even rarer.
Electromyography can demonstrate a segmental motor deficit in
up to 2/3 of all cases, but, because herpes zoster is usually found in the
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thoracic area, the deficit tends to be functionally insignificant, and may
escape the patient’s notice. In some cases, the cutaneous lesion is absent
(herpes sine herpete). Herpes zoster is relatively common, with an
incidence of 35 cases per 1000 persons per year; immunocompromised
individuals (e. g., with AIDS, malignancy, or immunosuppression) are at
elevated risk. Treatment with topical dermatological medication as well
as aciclovir, or another specific virustatic agent, is recommended. Even
with appropriate treatment, postherpetic neuralgia in the affected area is
a not uncommon complication. It can be treated symptomatically with
various medications, including carbamazepine and gabapentin.
Posterior root syndrome (Fig. 3.9). If two or more adjacent
posterior roots are completely divided, sensation in the corresponding
dermatomes is partially or totally lost. Incomplete posterior root lesions
affect different sensory modalities to variable extents, with pain
sensation usually being most strongly affected. Because the lesion
interrupts the peripheral reflex arc, the sensory deficit is accompanied by
hypotonia and hyporeflexia or areflexia in the muscles supplied by the
affected roots. These typical deficits are produced only if multiple
adjacent roots are affected.
Posterior column syndrome (Fig. 3.10). The posterior columns
can be secondarily involved by pathological processes affecting the
dorsal root ganglion cells and the posterior roots. Lesions of the posterior
columns typically impair position and vibration sense, discrimination,
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and stereognosis; they also produce a positive Romberg sign, as well as
gait ataxia that worsens significantly when the eyes are closed (unlike
cerebellar ataxia, which does not). Posterior column lesions also often
produce hypersensitivity to pain. Possible causes include vitamin B12
deficiency (e. g., in “funicular myelosis”; see below), AIDS-associated
vacuolar myelopathy, and spinal cord compression (e. g., in cervical
spinal stenosis).
Posterior horn syndrome (Fig. 3.11) can be a clinical
manifestation of syringomyelia, hematomyelia, and some intramedullary
spinal cord tumors, among other conditions. Like posterior root lesions,
posterior horn lesions produce a segmental somatosensory deficit; yet,
rather than impairing all sensory modalities like posterior root lesions,
posterior horn lesions spare the modalities subserved by the posterior
columns, i.e., epicritic and proprioceptive sense. “Only” pain and
temperature sensation are lost in the corresponding ipsilateral segments,
because these modalities are conducted centrally through a second
neuron in the posterior horn (whose axon ascends in the lateral
spinothalamic tract). Loss of pain and temperature sensation with sparing
of posterior column sense is called a dissociated somatosensory deficit.
There may be spontaneous pain (deafferentation pain) in the analgesic
area. Pain and temperature sensation are intact below the level of the
lesion, as the lateral spinothalamic tract, lying in the anterolateral
funiculus, is undamaged and continues to conduct these modalities
centrally.
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Graymatter syndrome (Fig. 3.12). Damage to the central gray
matter of the spinal cord by syringomyelia, hematomyelia,
intramedullary spinal cord tumors, or other processes interrupts all of the
fiber pathways passing through the gray matter. The most prominently
affected fibers are those that originate in posterior horn cells and conduct
coarse pressure, touch, pain, and temperature sensation; these fibers
decussate in the central gray matter and then ascend in the anterior and
lateral spinothalamic tracts. A lesion affecting them produces a bilateral
dissociated sensory deficit in the cutaneous area supplied by the
damaged fibers.
Syringomyelia is characterized by the formation of one or more
fluid-filled cavities in the spinal cord; the analogous disease in the
brainstem is called syringobulbia. The cavities, called syringes, can be
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formed by a number of different mechanisms and are distributed in
different characteristic patterns depending on their mechanism of
formation. Some syringes are an expansion of the central canal of the
spinal cord, which may or may not communicate with the fourth
ventricle; others are a hollowing-out of the parenchyma and are separate
from the central canal. Syringomyelia most commonly affects the
cervical spinal cord, typically producing loss of pain and temperature
sensation in the shoulders and upper limbs. A progressively expanding
syrinx can damage the long tracts of the spinal cord, producing spastic
(para)paresis and disturbances of bladder, bowel, and sexual function.
Syringobulbia often causes unilateral atrophy of the tongue, hypalgesia
or analgesia of the face, and various types of nystagmus depending on
the site and configuration of the syrinx.
The syndrome of combined lesions of the posterior columns
and corticospinal tracts (funicular myelosis) (Fig. 3.13) is most
commonly produced by vitamin B12 deficiency due to a lack of gastric
intrinsic factor (e. g., in atrophic gastritis). Foci of demyelination are
found in the cervical and thoracic regions in the posterior columns (7080%), and somewhat less commonly in the pyramidal tracts (40-50%),
while the gray matter is usually spared. Posterior column damage causes
loss of position and vibration sense in the lower limbs, resulting in spinal
ataxia and a positive Romberg sign (unstable stance with eyes closed).
The accompanying pyramidal tract damage causes spastic paraparesis
with hyperreflexia and bilateral Babinski signs.
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Anterior horn syndrome (Fig. 3.14). Both acute poliomyelitis
and spinal muscle atrophy of various types specifically affect the anterior
horn cells, particularly in the cervical and lumbar enlargements of the
spinal cord. In poliomyelitis (a viral infection), a variable number of
anterior horn cells are acutely and irreversibly lost, mainly in the lumbar
region, causing flaccid paresis of the muscles in the corresponding
segments. Proximal muscles tend to be more strongly affected than distal
ones. The muscles become atrophic and, in severe cases, may be
completely replaced by connective tissue and fat. It is rare for all of the
muscles of a limb to be affected, because the anterior horn cells are
arranged in long vertical columns within the spinal cord.
Combined anterior horn and pyramidal tract syndrome (Fig.
3.15) is seen in amyotrophic lateral sclerosis as the result of degeneration
of both cortical and spinal motor neurons. The clinical picture is a
combination of flaccid and spastic paresis. Muscle atrophy, appearing
early in the course of the disease, is generally so severe that the deep
tendon reflexeswould ordinarily be absent, if only the lower motor
neurons were affected. Accompanying degeneration of the motor cranial
nerve nuclei can cause dysarthria and dysphagia (progressive bulbar
palsy).
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Syndrome of the corticospinal tracts (Fig. 3.16). Loss of
cortical motor neurons is followed by degeneration of the corticospinal
tracts in a number of different diseases, including primary lateral
sclerosis (a variant of amyotrophic lateral sclerosis) and the rarer form of
hereditary spastic spinal paralysis. The disease appears in childhood and
progresses slowly thereafter. Patients complain initially of a feeling of
heaviness, then ofweakness in the lower limbs. Spastic paraparesis with a
spastic gait disturbance gradually develops and worsens. The reflexes are
brisker than normal. Spastic paresis of the upper limbs does not develop
until much later.
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Syndrome of combined involvement of the posterior columns,
spinocerebellar tracts, and (possibly) pyramidal tracts (Fig. 3.17).
When the pathological process affects all of these systems, the
differential diagnosis should include spinocerebellar ataxia of Friedreich
type, the axonal form of a hereditary neuropathy (HSMN II), and other
ataxias. Characteristic clinical manifestations are produced by the lesions
in each of the involved systems.
The spinal cord hemisection syndrome (Brown-Sequard
syndrome, Fig. 3.18) is rare and usually incomplete; its most common
causes are spinal trauma and cervical disk herniation. Interruption of the
descending motor pathways on one side of the spinal cord causes an
initially flaccid, ipsilateral paresis below the level of the lesion (spinal
shock), which later becomes spastic and is accompanied by
hyperreflexia, Babinski signs, and vasomotor disturbances. At the same
time, the interruption of the posterior columns on one side of the spinal
cord causes ipsilateral loss of position sense, vibration sense, and tactile
discrimination below the level of the lesion. The ataxia that would
normally be caused by the posterior column lesion cannot be
demonstrated because of the coexisting ipsilateral paresis. Pain and
temperature sensation are spared on the side of the lesion, because the
fibers subserving these modalities have already crossed to the other side
to ascend in the lateral spinothalamic tract, but pain and temperature
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sensation are lost contralaterally below the level of the lesion, because
the ipsilateral (crossed) spinothalamic tracts are interrupted. Simple
tactile sensation is not impaired, as this modality is subserved by two
different fiber pathways: the posterior columns (uncrossed) and the
anterior spinothalamic tract (crossed). Hemisection of the cord leaves
one of these two pathways intact for tactile sensation on either side of the
body—the contralateral posterior columns for the side contralateral to the
lesion, and the contralateral anterior spinothalamic tract for the side
ipsilateral to it.
Aside from the interruption of the long tracts, the anterior horn
cells may be damaged to a variable extent at the level of the lesion,
possibly causing flaccid paresis. Irritation of the posterior roots may also
cause paresthesiae or radicular pain in the corresponding dermatomes at
the upper border of the sensory disturbance.
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Spinal Cord Transection Syndromes
General Symptomatology and Clinical Course of
Transection Syndromes
Acute spinal cord transection syndrome (Fig. 3.19). The
complete spinal cord transection syndrome is most commonly caused by
trauma, less commonly by inflammation or infection (transverse
myelitis). Acute spinal cord trauma initially produces so-called spinal
shock, a clinical picture whose pathophysiology is incompletely
understood. Below the level of the lesion there is complete, flaccid
paralysis, and all modalities of sensation are lost. Bladder, bowel, and
sexual function are lost as well. Only the bulbocavernosus reflex is
preserved—an important point for the diagnostic differentiation of this
condition from polyradiculitis, in which it is typically absent. There are
also trophic changes below the level of the lesion, in particular,
diminished sweating and disturbed thermoregulation. There is a marked
tendency to develop decubitus ulcers. The upper border of the sensory
deficit (the “sensory level”) is often demarcated by a zone of
hyperalgesia.
In the days and weeks after the causative event, the spinal
neurons gradually regain their function, at least in part, but remain cut
off from most of the centrally derived neural impulses that normally
regulate them. They thus become “autonomous,” and so-called spinal
automatisms appear. In many cases, a stimulus below the level of the
lesion induces sudden flexion of the hip, knee, and ankle (flexor reflex);
if the spinal cord transection syndrome is complete, the limbs retain the
flexed position for a long time after the stimulus because of a spastic
elevation of muscle tone. (In incomplete spinal cord transaction
syndrome, on the other hand, the legs are initially flexed upon
stimulation, but then return to their original position.) Defecation and
urination gradually function again, but are no longer under voluntary
control; instead, the bladder and bowel are emptied reflexively once they
are filled to a certain point. Detrusors phincter dyssynergia causes
urinary retention and frequent, reflexive micturition. The deep tendon
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reflexes and muscle tone gradually return and can become pathologically
elevated. Sexual potency, however, does not return
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Progressive spinal cord transection syndrome. When spinal
cord transaction syndrome arises gradually rather than suddenly, e. g.,
because of a slowly growing tumor, spinal shock does not arise. The
transection syndrome in such cases is usually partial, rather than
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complete. Progressively severe spastic paraparesis develops below the
level of the lesion, accompanied by a sensory deficit, bowel, bladder, and
sexual dysfunction, and autonomic manifestations (abnormal vasomotor
regulation and sweating, tendency to decubitus ulcers).
Spinal Cord Transection Syndromes at Different Levels
Cervical spinal cord transection syndrome. Spinal cord
transection above the level of the third cervical vertebra is fatal, as it
abolishes breathing (total loss of function of the phrenic and intercostal
nerves). Such patients can survive only if they can be artificially
ventilated within a few minutes of the causative injury, which is very
rarely the case. Transection at lower cervical levels produces
quadriparesis with involvement of the intercostal muscles; breathing may
be dangerously impaired. The upper limbs are affected to a variable
extent depending on the level of the lesion. The level can be determined
fairly precisely from the sensory deficit found on clinical examination.
Thoracic spinal cord transection syndrome. Transection of the
upper thoracic cord spares the upper limbs but impairs breathing and
may also cause paralytic ileus through involvement of the splanchnic
nerves. Transection of the lower thoracic cord spares the abdominal
muscles and does not impair breathing. Lumbar spinal cord transection
syndrome. Traumatic transection of the spinal cord at lumbar levels often
causes especially severe disturbances because of concomitant damage of
the major supplying artery of the lower spinal cord, the great radicular
artery (of Adamkiewicz). The result is infarction of the entire lumbar and
sacral spinal cord.
Epiconus syndrome, caused by a spinal cord lesion at the L4 to
S2 level, is relatively rare (Fig. 3.22a and b). Unlike conus syndrome
(see below), it is associated with spastic or flaccid paresis of the lower
limbs, depending on the precise level of the lesion. There is weakness or
total paralysis of hip external rotation (L4-S1) and extension (L4-L5),
and possibly also of knee flexion (L4-S2) and flexion and extension of
the ankles and toes (L4-S2). The Achilles reflex is absent, while the
knee-jerk reflex is preserved. The sensory deficit extends from L4 to S5.
The bladder and bowel empty only reflexively; sexual potency is lost,
and male patients often have priapism. There is transient vasomotor
paralysis, as well as a transient loss of sweating.
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Conus syndrome, due to a spinal cord lesion at or below S3 (Fig.
3.22), is also rare. It can be caused by spinal tumors, ischemia, or a
massive lumbar disk herniation.
An isolated lesion of the conus medullaris produces the following
neurological deficits:
- Detrusor areflexia with urinary retention and overflow incontinence
(continual dripping)
- Fecal incontinence
- Impotence
- Saddle anesthesia (S3-S5)
- Loss of the anal reflex
The lower limbs are not paretic, and the Achilles reflex is
preserved (L5-S2). If conus syndrome is produced by a tumor, the
lumbar and sacral roots descending alongside the conus will be affected
sooner or later (Fig. 3.22). In such cases, the manifestations of conus
syndrome are accompanied by deficits due to involvement of the cauda
equina:weakness of the lower limbs, and more extensive sensory deficits
than are seen in pure conus syndrome. Cauda equina syndrome involves
the lumbar and sacral nerve roots, which descend alongside and below
the conus medullaris, and through the lumbosacral subarachnoid space,
to their exit foramina; a tumor (e. g., ependymoma or lipoma) is the
usual cause. Patients initially complain of radicular pain in a sciatic
distribution, and of severe bladder pain that worsens with coughing or
sneezing. Later, variably severe radicular sensory deficits, affecting all
sensory modalities, arise at L4 or lower levels. Lesions affecting the
upper portion of the cauda equina produce a sensory deficit in the legs
and in the saddle area. There may be flaccid paresis of the lower limbs
with areflexia; urinary and fecal incontinence also develop, along with
impaired sexual function. With lesion of the lower portion of the cauda
equina, the sensory deficit is exclusively in the saddle area (S3-S5), and
there is no lower limb weakness, but urination, defecation, and sexual
function are impaired. Tumors affecting the cauda equina, unlike conus
tumors, produce slowly and irregularly progressive clinical
manifestations, as the individual nerve roots are affected with variable
rapidity, and some of them may be spared until late in the course of the
illness.
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Plexus Syndromes
The cervical plexus is formed by nerve roots C2-C4, the brachial
plexus by nerve roots C5T1, and the lumbosacral plexus by nerve roots
L1-S3.
Lesions of the Cervical Plexus
The cervical plexus (Fig. 3.31) occupies a relatively sheltered position
and is thus rarely injured. Unilateral or bilateral phrenic nerve
dysfunction (C3, C4, and C5) is more commonly caused by a mediastinal
process than by a cervical plexus lesion.
Lesions of the Brachial Plexus
Brachial plexus lesions are classified into two types, upper and
lower, on clinical and pragmatic grounds. The anatomy of the brachial
plexus is shown in Fig. 3.32.
In upper brachial plexus palsy (Duchenne-Erb palsy), due to a
lesion of the C5 and C6 nerve roots, the deltoid, biceps, brachialis, and
brachioradialis muscles are paretic. There is a sensory deficit overlying
the deltoid muscle and on the radial side of the arm and hand.
In lower brachial plexus palsy (Klumpke palsy), due to a lesion
of the C8 and T1 nerve roots, the wrist and finger flexors and the
intrinsic muscles of the hand are paretic. Occasionally, Horner syndrome
is present in addition. There are prominent trophic abnormalities of the
hand and fingers.
Causes of Brachial Plexus Lesions
Trauma, usually due to road accidents or sporting injuries, is by
far the most common cause of damage to the brachial plexus. Brachial
plexus damage also has many etiologies other than trauma: compression
syndromes in the area of the shoulder (scalene syndrome; compression
by safety belts, rucksack straps, etc.; costoclavicular syndrome;
hyperabduction syndrome); tumors (e. g., apical lung tumor with
Pancoast syndrome); inflammatory-allergic lesions (neuralgic shoulder
amyotrophy); and birth injuries
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.
Lesions of the Lumbosacral Plexus
Here, too, lesions may be classified into two types: lumbar plexus
lesions andnsacral plexus lesions. The anatomy of the lumbosacral
plexus is shown in Fig. 3.34.
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Lumbar plexus lesions (L1, L2, and L3) are less common than
brachial plexus lesions,nbecause of the sheltered location of the lumbar
plexus. The causes ofbdamage to both plexuses are largely the same.
There are, however, practically no cases of inflammatory-allergic
dysfunction of the lumbar plexus (which would be analogous to
neuralgic shoulder amyotrophy). On the other hand, metabolic
disturbances such as diabetes mellitus are more likely to affect the
lumbar plexus than the brachial plexus.
Sacral plexus lesions.
The sacral plexus is formed by nerve roots L4, L5, and S1
through S3. The most important nerves emerging from the sacral plexus
are the common peroneal and tibial nerves, which are joined together as
the sciatic nerve in its course down the posterior thigh. The two nerves
separate from one another just above the knee and then follow their
individual paths further down the leg (Fig. 3.35). The common peroneal
nerve mainly innervates the extensors of the foot and toe, while the tibial
nerve innervates the plantar flexors and most of the intrinsic muscles of
the foot. A lesion of the common peroneal nerve, or of the common
peroneal portion of the sciatic nerve, weakens the extensors, causing a
foot drop (steppage gait); a lesion of the tibial nerve weakens the plantar
flexors, making toe-walking impossible. Peroneal nerve palsy is more
frequent than tibial nerve palsy, because the course of the tibial nerve is
relatively sheltered. Peroneal nerve palsy impairs sensation on the lateral
surface of the leg and the dorsum of the foot, while tibial nerve palsy
impairs sensation on the sole.
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Peripheral Nerve Syndromes
Transection of a mixed peripheral nerve causes flaccid paresis of
the muscle(s) supplied by the nerve, a sensory deficit in the distribution
of the interrupted afferent fibers of the nerve, and autonomic deficits.
When the continuity of an axon is disrupted, degeneration of the axon as
well as of itsmyelin sheath begins within hours or days at the site of the
injury, travels distally down the axon, and is usually complete within 1520 days (socalled secondary or wallerian degeneration).
Damaged axons in the central nervous system lack the ability to
regenerate, but damaged axons in peripheral nerves can do so, as long as
their myelin sheaths remain intact to serve as a template for the
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regrowing axons. Even when a nerve is completely transected, resuturing
of the sundered ends can be followed by near-complete regeneration of
axons and restoration of functional activity. Electromyography (EMG)
and nerve conduction studies are often very helpful in assessing the
severity of a peripheral nerve injury and the chances for a good recovery.
Figure 3.35 illustrates the anatomical course of a number of important
peripheral nerves that are commonly injured. Figure 3.36 shows typical
clinical pictures of radial, median, and ulnar nerve palsies.
The more common causes of isolated peripheral nerve palsies are:
compression of a nerve at an anatomically vulnerable point or bottleneck
(scalene syndrome, cubital tunnel syndrome, carpal tunnel syndrome,
peroneal nerve injury at the fibular head, tarsal tunnel syndrome);
traumatic injury (including iatrogenic lesions, e. g., puncture and
injection injuries); and ischemia (e. g., in compartment syndrome and,
less commonly, in infectious/inflammatory processes).
Carpal Tunnel Syndrome
Carpal tunnel syndrome (Fig. 3.37a) is caused by median nerve
damage in the carpal tunnel, which can be narrowed at the site where the
nerve passes under the transverse carpal ligament (flexor retinaculum).
Patients typically complain of pain and paresthesiae in the affected hand,
which are especially severe at night and may be felt in the entire upper
limb (brachialgia paresthetica nocturna), aswell as of a feeling of
swelling in the wrist or the entire hand. Trophic abnormalities and
atrophy of the lateral thenar muscles (abductor pollicis brevis and
opponens pollicis) are common in advanced cases. The median nerve
contains an unusually large proportion of autonomic fibers; thus, median
nerve lesions are a frequent cause of complex regional pain syndrome.
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