1 280 Part 5 DISEASES OF SPI NAL CORD, PERIPHERAL NERVE, AND M USCLE
A. Spinal cord tumors (usually intramedul-
SYRI NGOMYELIC SYN DRO M E
OF SEGMENTAL SENSORY DISSOCIATION
WITH BRACH IAL AMYOTROPHY
This syndrome is most often attributable to develop
mental syringomyelia, i.e., a central cavitation of the
spinal cord of undetermined cause, but a similar clinical
syndrome may be observed in association with other
pathologic states such as intramedullary cord tumors, trau
matic myelopathy, postradiation myelopathy, infarction
(myelomalacia), bleeding (hematomyelia), and, rarely,
with extramedullary tumors, cervical spondylosis, spinal
arachnoiditis, and cervical necrotizing myelitis.
Syringomyelia (Syrinx) (See also Chap. 38)
Syringomyelia (from the Greek syrinx, "pipe" or "tube")
is defined as a chronic progressive degenerative or
developmental disorder of the spinal cord, characterized
clinically by painless weakness and wasting of the hands
and arms (brachial amyotrophy) and segmental sensory
loss of dissociated type (loss of thermal and painful sen
sation with sparing of tactile, joint position, and vibra
tory sense, as described later) . The cause is a cavitation of
the central parts of the spinal cord, usually in the cervical
region, but extending upward in some cases into the
medulla and pons (syringobulbia) or downward into the
thoracic and even into the lumbar segments. Frequently,
there are associated developmental abnormalities of the
vertebral column (thoracic scoliosis, fusion of vertebrae,
or Klippel-Feil anomaly), of the base of the skull (platy
basia and basilar invagination), and there is a special
relationship to developmental deformations of the cer
ebellum and brainstem (particularly type I Chiari mal
formation). A large proportion of cases of developmental
syringomyelia have type I Chiari malformation, consist
ing of a descent of cerebellar tonsils below the foramen
magnum as discussed in Chap. 38. There is also a group
of less frequent but well-described syringomyelias that
derives from the acquired processes mentioned earlier
such as intramedullary tumor (astrocytoma, hemangio
blastoma, ependymoma) and from preceding traumatic
or hemorrhagic necrosis of the spinal cord.
Wider experience with the pathology of developmen
tal syringomyelia has led to the following classification,
modified from Barnett and colleagues that unfortunately
creates some confusion because it simulates the Roman
numeral classification of the Chiari malformations, with
which it is sometimes allied:
Type I. Syringomyelia with obstruction of the foramen
magnum and dilatation of the central canal
(developmental type)
A. With type I Chiari malformation
B. With other obstructive lesions of the fora
men magnum, usually bony anomalies
Type II. Syringomyelia without obstruction of the fora
men magnum (idiopathic developmental type)
Type III. Syringomyelia with other diseases of the spinal
cord (acquired types)
lary, especially hemangioblastoma)
B. Traumatic myelopathy
C. Spinal arachnoiditis and pachymeningitis
D. Secondary myelomalacia from cord com
pression (tumor, spondylosis), infarction,
hematomyelia
Type IV. Pure hydromyelia (developmental dilatation
of the central canal), with or without hydro
cephalus
Historical Note Although pathologic cavitation
of the spinal cord was recognized as early as the six
teenth century, the term syringomyelia was first used
to describe this process in 1 827 by Ollivier d' Angers
(cited by Ballantine et al) . Later, following recogni
tion of the central canal as a normal structure, it was
assumed by Virchow (1 863) and by Leyden (1876)
that cavitation of the spinal cord had its origin in an
abnormal expansion of the central canal, and they
renamed the process hydromyelia . Cavities in the cen
tral portions of the spinal cord, unconnected with the
central canal, were recognized by Hallopeau ( 1 870);
Simon suggested in 1 875 that the term syringomyelia
be reserved for such cavities and that the term hydro
myelia be restricted to simple dilatation of the central
canal. Thus, a century ago, the stage was set for an
argument about pathogenesis that has not been settled
to the present day.
C l i n i c a l Featu res
The clinical picture varies in the four pathologic types
previously listed, the differences depending not only
on the extent of the syrinx but also on the associated
pathologic changes, particularly those related to the
Chiari malformation. In the type I developmental syr
inx (idiopathic, Chiari-associated developmental syrin
gomyelia), symptoms usually begin in early adult life
(20 to 40 years). Males and females are equally affected.
Rarely, some abnormality is noted at birth, but usually
the first symptom appears in late childhood or adoles
cence. The onset is usually insidious and the course
irregularly progressive. In many instances, the symp
toms or signs are discovered accidentally, for example,
as a result of painless burn or atrophy of the hand, and
the patient cannot say when the disease began. Rarely,
there is an almost apoplectic onset or worsening; there
are cases on record of an aggravation of old symptoms
or the appearance of new symptoms after a violent
strain or paroxysm of coughing. Trauma is a less cer
tain precipitant. Once the disease is recognized, some
patients remain much the same for years, even decades,
but more often there is intermittent progression to the
point of being chair-bound within 5 to 20 years. This
extremely variable course makes it difficult to evaluate
therapy.
The precise clinical picture at any given point in the
evolution of the disease depends on the cross-sectional
and longitudinal extent of the syrinx, but certain clinical
features are so common that the diagnosis can hardly be

made without them. These traditionally cited elements
are: (1) segmental weakness and atrophy of the hands and
arms, (2) loss of some or all tendon reflexes in the arms, and
(3) segmental anesthesia of a dissociated type (loss of pain
and thermal sense and preservation of the sense of touch)
over the neck, shoulders, and arms . The last of these leads
to one of the most characteristic features of syringomy
elia: painless injuries and burns of the hands. Finally,
there are in cases of extensive cavitation weakness and
ataxia of the legs from involvement of the corticospinal
tracts (possibly at their decussation) and posterior col
umns in the cervical region.
Kyphoscoliosis is added in many of the cases and in
nearly one-quarter of them there is an overt cervicooccip
ital malformation (short neck, low hairline, odd posture
of the head and neck, fused or missing cervical vertebrae,
i.e., Klippel-Feil abnormality).
The particular muscle groups that are affected on
the two sides may vary. Exceptionally, motor function
is spared, and the segmental dissociated sensory loss
and /or pain are the only marks of the disease. In a few
of the cases, especially those with the Chiari malfor
mation, the reflexes in the arms are preserved or even
hyperactive, as might be expected with upper rather
than lower motor neuron involvement. Or the shoulder
muscles may be atrophic and the hands spastic. In the
lower extremities the weakness, if present, is of a spastic
(corticospinal) type.
The characteristic segmental sensory dissociation is
usually bilateral but a unilateral pattern affecting only
one hand and arm is not unknown, and this is true of
the amyotrophy as well. The sensory loss is distributed
in a "cape" or hemicape pattern, often extending to back
of the head or the face and onto the trunk Although
.
tactile sensation is usually preserved, there are cases in
which it is impaired, usually in the region of the densest
analgesia over the trunk or hand. Exceptionally there is
no sensory loss in the presence of amyotrophy, and cases
have been recorded in which only a hydrocephalus and
hydromyelia were present with spastic paraparesis. If
tactile sensation is affected in the arms, joint position and
vibratory sense tend also to be impaired. In the lower
extremities and over the abdomen there may be some
loss of pain and thermal sensation proximally, but more
often there is a loss of vibratory and position sense, which
is indicative of a posterior column lesion and is the basis
of ataxia. A Horner syndrome may result from ipsilateral
involvement of the intermediolateral cell column at the
C8, Tl, and T2 levels.
Pain has been a symptom in about half of our
patients with developmental types of syringomyelia. The
pain is usually unilateral or more marked on one side
of the neck, shoulder, and arm; it is of a burning, aching
quality, mostly in or at the border of areas of sensory
impairment. In a few patients, it involves the face or
trunk An aching pain at the base of the skull or posterior
.
cervical region that is intensified by coughing, sneezing,
or stooping (brief exertional pain) is often present, but, as
Logue and Edwards point out, pain of this type may be
a feature of Chiari malformation without syringomyelia
CHAPTER 44 Diseases of the Spinal Cord 1 28 1
and in that case is probably attributable to compression
or stretching of cervical roots.
Syringobulbia is the lower brainstem equivalent of
syringomyelia. Usually the two coexist and the brainstem
cavity is simply an extension of one in the upper cord, but
occasionally the bulbar manifestations precede the spinal
ones or, rarely, occur independently. The glial cleft or cav
ity is located most often in the lateral tegmentum of the
medulla, but it may extend into the pons and, rarely, even
higher. The symptoms and signs are characteristically
unilateral and consist of nystagmus, analgesia, and ther
moanesthesia of the face (numbness); wasting and weak
ness of the tongue (dysarthria); and palatal and vocal
cord paralysis (dysphagia and hoarseness). Diplopia,
episodic vertigo, trigeminal pain or facial sensory loss,
and persistent hiccough are less common symptoms.
For understandable reasons, the diagnosis of brainstem
MS is often raised. The clinical and pathologic features
of syringobulbia have been described in great detail by
J onesco-Sisesti.
When a Chiari malformation is associated with
syringomyelia and syringobulbia, it may be difficult to
separate the effects of the two disorders. A typical exam
ple is shown in Fig. 38-4. Clinical features that favor the
predominance of Chiari malformation are nystagmus,
cerebellar ataxia, exertional head and neck pain, promi
nent corticospinal and sensory tract involvement in the
lower extremities, hydrocephalus, and craniocervical
malformations. In syringomyelia without a Chiari mal
formation but with some other type of obstructive lesion
at the foramen magnum, the clinical picture is much the
same, and the nature of the foramen magnum lesion can
be determined only by MRI or surgical exploration.
The association of syringomyelia with an intramed
ullary tumor (type III) should be suspected when there
is a disassociated sensorimotor abnormality extending
over many segments of the body. With von Hippel
Lindau disease, the diagnosis hinges on the finding of
the characteristic hereditary hemangioblastoma in the
syrinx and retinal and cerebellar vascular malforma
tions. In the posttraumatic cases, necrosis of the spinal
cord that has been stable for months or years begins to
cause pain and spreading sensory or motor loss, rec
ognizable only in segments above the original lesion
(Schurch et al) . This occurred in approximately 3 per
cent of the traumatic myelopathy cases of Rossier and
coworkers, more often in quadriplegics than in paraple
gics. The posttraumatic syrinx is not as well defined
anatomically as the usual forms of syringomyelia but
consists instead of several contiguous areas of glia-lined
myelomalacia with differing degrees of cavitation. In
some instances of progressive spinal cord symptoms
occurring several years after spinal surgery, the lesion
has proved to be one of arachnoiditis and cord atrophy
and not a syrinx (Avraharni et al).
Hyd romye l i a
This refers to a dilatation of the central canal that i s dis
tinct from developmental syringomyelia. The relation
ship between hydromyelia and syringomyelia has been
1 282 Part 5 DISEASES OF SPI NAL CORD, PERIPHERAL NERVE, AND M USCLE
the source of endless debate, in part the result of the lack
of a coherent pathophysiologic explanation for either pro
cess. At least one hypothesis for the origin of syringomy
elia includes an initial dilatation of the central canal (see
later) . Our impression is that a relatively nonprogressive,
well-defined, cylindrical enlargement of the central canal
over a few thoracic segments is a frequent enough occur
rence in the absence of clinical changes that it represents
an independent entity. In the few cases of symptomatic
hydromyelia that have come to our attention, there had
usually been a long-standing congenital hydrocephalus
complicated years later by progressive weakness and
atrophy of the shoulders and the muscles of the arms
and hands. More often, there is no associated obstruc
tion at the upper cord and no hydrocephalus for which
reason it is our impression that most cases are benign
and relatively nonprogressive. Proof of the existence of
pure hydromyelia in the past has been based on necropsy
demonstration of an enormously widened central canal,
with or without hydrocephalus. Now, hydromyelia is
easily diagnosable by MRI and numerous asymptomatic
cases are being discovered, causing unnecessary concern
and neurologic consultation.
Pathogenesis
Experimental work i n animals has indicated that there
is a normal flow of CSF from the spinal subarachnoid
space through perivascular spaces to the parenchyma of
the cord and possibly into the central canal. It has been
suggested that impediments to flow might explain dila
tation of the central canal, or the creation of a parallel or
attached syrinx cavity.
One theory of the pathogenesis of developmental
syringomyelia, of which Gardner was the main advocate,
is that the normal flow of CSF from the central canal to
the fourth ventricle and its outlets is prevented by an
obstruction of the foramina of Luschka and Magendie. As
a result, a pulse wave of CSF pressure that is generated
by systolic pulsations of the choroid plexuses is transmit
ted into the cord from the fourth ventricle through the
central canal. According to this theory, the syrinx consists
essentially of a greatly dilated central canal with a diver
ticulum that ramifies from the central canal and dissects
along gray matter and adjacent fiber tracts. The frequency
with which syringomyelia is linked to malformations
at the craniocervical junction, i.e., to Chiari and other
lesions that could interfere with normal flow of CSF,
lends credence to this theory.
There are many instances, however, in which
Gardner 's hydrodynamic theory could not explain
syringomyelia. In some cases, for example, the foram
ina of Luschka and Magendie are found to be patent,
and other abnormalities of the posterior fossa or fora
men magnum that block CSF flow are not in evidence.
Furthermore, in many cases, including several we have
inspected, serial histologic sections have failed to dem
onstrate a connection between the fourth ventricle and
the syrinx in the spinal cord or of a widening of the cen
tral canal above the syrinx (see also Hughes). Gardner 's
theory has been questioned on other grounds. Ball and
Dayan calculated the pulse-pressure wave transmit
ted into the cord to be of such low amplitude as to be
unlikely to produce a syrinx. In their view, the CSF
around the cervical cord, under increased pressure dur
ing strain or physical effort because of subarachnoid
obstruction at the craniocervical junction, tracks into
the spinal cord along the Virchow-Robin spaces or other
subpial channels. Over a prolonged period, abetted per
haps by traumatic lesions, small pools of fluid coalesce
to form a syrinx. In their view, originally the syrinx
forms independently of the central canal, but eventually
the two may become connected, allowing secondary
enlargement of the canal (hydromyelia ex vacuo). The
findings of Heiss and colleagues lend support to this
theory. They found that progression of syringomyelia
is produced by the compressive effect of the cerebellar
tonsils, which partially occlude the subarachnoid space
at the foramen magnum and create pressure waves that
compress the spinal cord from without and not from
within; the pressure waves propagate syrinx fluid cau
dally with each heartbeat. This hardly exhausts the list
of hypotheses that have been offered over the years but
none of them has been confirmed.
The authors favor the type of hydrodynamic mech
anism as postulated originally by Gordon Holmes and
elaborated by Ball and Dayan. In this view, a relation
ship exists between basal cranial, cervical spine, the
cerebellospinal Chiari malformation, syringomyelia,
and disturbed hydrodynamics of perispinal CSF. Logue
and Edwards documented several cases of syringomy
elia in which the foramen magnum was obstructed by
a lesion other than a Chiari formation, e.g., by dural
cyst, localized arachnoiditis, atlantoaxial fusion, simple
cerebellar cyst, and basilar invagination (see Williams
for a review of the numerous hypotheses of causation) .
Irrespective of its mode of origin, the syrinx first
occupies the central gray matter of the cervical portion of
the spinal cord, usually independent of the central canal
but sometimes extending into it. It interrupts the crossing
pain and temperature fibers in the anterior commissure at
several successive cord segments. As the cavity enlarges,
it extends symmetrically or asymmetrically into the pos
terior and anterior horns and eventually into the lateral
and posterior funiculi of the cord. It may enlarge the
spinal cord. The cavity is lined with astrocytic glia and a
few thick-walled blood vessels, and the fluid in the cavity
is clear and in our patients, has had relatively low protein
content, like intracranial CSF.
The cavitation nearly always arises in the cervi
cal portion of the cord and can only reach the thoracic
and lumbar portions by its extension from the cervical
region, sometimes by a small, flat and thin, eccentrically
placed. Either a cavity or a glial septum may extend
asymmetrically into the medulla, usually in the vicinity
of the descending tract of the fifth cranial nerve to create
a syringobulbia.
Diag nosis
The clinical picture o f syringomyelia i s s o characteristic
that diagnosis is seldom in doubt. Now one can obtain

Figure 44- 1 3 . Sagittal T2-weighted MRI showing a developmental
syringomyelia without Otiari malformation. The cervical spinal
cord is greatly expanded but there were only signs of spinothalamic
sensory loss over the arms.
spectacular demonstrations of the syrinx, either trau
matic or developmental (Fig. 44-13), Chiari malforma
tions, and other foramen magnum lesions by MRI of the
sagittal planes of the brain and spinal cord (see Fig. 38-4) .
Also, hours after a CT myelogram, contrast material fills
the syrinx and the central canal directly, possibly by dif
fusion from the surface of the cord.
Certain rare polyneuropathies (amyloid, Tangier dis
ease, and Fabry disease) that preferentially affect small
fibers in the nerves of the upper extremities can repro
duce the dissociated sensory loss that is characteristic
of a syrinx ("pseudosyringomyelic" deficit), but motor
abnormalities are not prominent in these neuropathic
cases. These diseases are discussed in Chap. 46.
Treatme nt
The only therapy of lasting value for type I syringomy
elia (related to Chiari malformation) is surgical decom
pression of the foramen magnum and upper cervical
canal. Headache and neck pain are helped most; ataxia
and nystagmus tend to persist, but these are related to
the Chiari process. The cavity tends to cease enlarging.
Radiation therapy, which was formerly recommended, is
of no benefit. The operation advised by Gardner, of plug
ging the connection between the fourth ventricle and the
central canal of the cervical cord, has been abandoned.
CHAPTER 44 Diseases of the Spinal Cord 1 283
There were complications of this operative procedure,
and the results were no better than those obtained from
simple decompression. The decompression operation
also carries some risk, especially if there is an attempt
to excise the tonsillar projections of the cerebellum. In
the series of Logue and Edwards, comprising 56 cases
of type I syringomyelia, the occipitocervical pain was
relieved by decompression in most patients, but the
shoulder-arm pain usually persisted. Upper motor neu
ron weakness of the legs and sensory ataxia were
often improved, whereas the segmental sensory and
motor manifestations of the syringomyelia were not.
Hankinson, in the past, had reported good results from
decompression in 75 percent of type I cases of syringo
myelia. In the retrospective review of 141 adult patients
by Stevens and colleagues, good surgical outcome was
achieved in 50 percent of those with minor degrees of
descent of the cerebellar tonsils, but in only 12 percent
of those with major cerebellar ectopia. A distended syr
inx also led to a more favorable outcome. Whether the
long-term course of these diseases is altered has not been
determined. Other surgical series of Chiari-syrinx are
discussed and cited in Chap. 38.
Syringotomy or shunting of the cavity has been
performed in type I and some of the type II (idiopathic)
cases, but the results have been unpredictable. Love and
Olafson, who performed this procedure in 40 patients of
both types (mainly type II), stated that 30 percent had
an excellent outcome. Schurch and coworkers obtained
improvement of pain and motor weakness in five of their
seven cases by stabilization of the spine and syringotomy
with placement of a T-tube within the syrinx. In a more
recent and comprehensive study of 73 patients with a
developmental syrinx operated by Sgouros and Williams
(1995), one-half remained clinically stable for a 10-year
period; 15 percent had serious complications from the
surgery, however. Our experience with this procedure
has not persuaded us of its lasting value; most of these
patients, even those who reported some improvement
originally, soon relapsed to their preoperative state,
and the disease then progressed in the usual way. An
enlarged cervical cord with progressive clinical worsen
ing may nonetheless justify an attempt to shunt the cav
ity. Other comments are found in Chap . 38.
Surgery for the posttraumatic cases has given only
slightly more favorable results. With incomplete myelop
athy, syringotomy relieved the pain in all 10 patients
of Shannon and associates. Where they found the
myelopathy to be complete, the cord was transected and
the upper stump excised. Sgouros and Williams (1996)
studied 57 such patients and recommend decompres
sive laminectomy and reconstruction of the subarach
noid space as the most effective of the several proce
dures used in the management of traumatic cavities. An
extensive review of surgical approaches to syringomy
elia can be found in the article by Brodbelt and Stoodley,
who tentatively recommend lysis of arachnoidal adhe
sions as preferable to shunting or filleting of the cord,
but acknowledge that the current state of treatment is
unsatisfactory.
1 284 Part 5 DISEASES OF SPI NAL CORD, PERIPHERAL NERVE, AND M USCLE
In the cases of syringomyelia with tumor, in which
the cyst fluid may be high in protein and viscid (unlike
the low-protein fluid of the usual syrinx), the tumor
should be excised if possible. This has been done success
fully with hemangioblastomas of the posterior columns
and occasionally with ependymomas.
The infrequent case of symptomatic purely hydro
myelic may benefit from ventriculoperitoneal shunts of
hydrocephalus, and a few excellent results are reported.
This procedure has also been attempted in type I devel
opmental cases, with unimpressive results unless there
is an associated hydrocephalus. Draining the central
canal by amputation of the tip of the sacral cord has been
unsuccessful and can be harmful. Most patients with
hydromyelia do not require treatment.
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