KEY POINT:

SPINAL CORD ANATOMY, A notch in the

inferior aspect of

LOCALIZATION, AND the pedicle will

contribute to the
boundary of the

OVERVIEW OF SPINAL intervertebral

foramen when

CORD SYNDROMES adjacent

vertebrae are
articulated and
Gregory Gruener, Jose Biller through which
the spinal nerve
and
intervertebral
ABSTRACT vessels will pass.
Spinal cord syndromes are unique clinical presentations that localize lesions to
the spinal cord by their pattern of anatomic dysfunction while implying their underlying
etiology. Recognizing these patterns and their significance is best accomplished by
relearning and appreciating the relevant anatomy and relationships, which are the
major focus of this review. This clinical-anatomic background will provide the frame-
work for the clinical topics that follow in this issue.

ANATOMY OF THE SPINAL A notch in the inferior aspect of the

CORD
Relationship to the Vertebral
Levels and Spine
The typical vertebra consists of a co-
lumnar body with a larger transverse
than anterior-posterior diameter and
serving as the primary support for the
spine. The vertebral arch extends from
the body, forming a protective enclo-
sure, and consists of a pedicle on ei-
ther side that unites posteriorly
through the two laminae. Three pro-
cesses arise from the vertebral arch,
laterally the transverse and posteriorly
the spinous, serving as the attachment
site for muscles (Figure 1-1). Four
separate articular processes, a superior
pair extending cranially and an infe-
rior pair extending caudally, serve to
direct or limit movement to specific
directions by articulating with the ver-
tebra above and below (Figure 1-2).
pedicle will contribute to the boundary
of the intervertebral foramen when ad-
jacent vertebrae are articulated and
through which the spinal nerve and in-
tervertebral vessels will pass.
An intervertebral disc is interposed
between each vertebral body and con-
sists of alternating, crisscrossing bands
of fibrous connective tissue, the annu-
lus fibrosus, which surround a gelati-
nouslike core, nucleus pulposus. The
vertebral discs will contribute 25% of the
height of the vertebral column. Several 11
ligaments and fibrous attachments of
muscles help to bind together and en-
close the vertebral column. The most
prominent are the anterior longitudinal
(along the anterior aspect of the bodies),
the posterior longitudinal (along their
posterior aspect), the ligamentum fla-
vum (posterior wall of spinal canal), and
the interspinous ligament.
The fused periosteum of the cra-

Relationship Disclosure: Dr Gruener has received personal compensation for speaking engagements with
Medical Education Resources, Inc. Dr Biller has nothing to disclose.
Unlabeled Use of Products/Investigational Use Disclosure: Drs Gruener and Biller have nothing to
disclose.

Copyright 2008, American Academy of Neurology. All rights reserved.

 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

FIGURE 1-1 Functions of the constituent parts of a vertebra.

Reprinted with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams &
Wilkins, 1972.

nium and meningeal layer of the dura space, epidural space, which extends
matter will separate caudal to the fo- the length of the spinal column (Fig-
ramen magnum, forming an anatomic ure 1-3). Within this space reside fatty

12

FIGURE 1-2 Lateral view of a lumbar (second) vertebra.

Sup superior; Inf inferior.

Modified with permission from Grant JCB. An atlas of anatomy. 6th ed. Baltimore: Williams &
Wilkins, 1972.

Continuum: Lifelong Learning Neurol 2008;14(3)

 KEY POINT:
tissue and the vertebral venous plexus. tively numbered vertebrae (C2
At birth the
The separation of these fused layers of through C7), but C8 above the T1 ver- spinal cord
connective tissue allows the vertebral tebrae. The remaining spinal nerves typically extends
column to move separately relative to will exit below the vertebrae of the to the lower
the dural sac that surrounds the spinal corresponding number. The spinal border of L3. By
cord and roots. The dorsal and ventral nerves will have a dorsal root ganglion adulthood its tip
roots will enter a dural sleeve at the usually located within the interverte- is usually at the
level of their intervertebral foramina, bral foramen. C1 lacks a cutaneous L1-2 vertebral
lateral to the dorsal spinal ganglia, fus- sensory dermatome. Below the L1 ver- disk level but
ing to form the spinal nerves. A layer tebra, lumbar and sacral spinal nerve can end at T12
of pia mater surrounds the surface of roots need to descend in order to or descend to
the lower border
the spinal cord, and between it and the reach their point of exit; this collection
of the L2
inner layer of the arachnoid tissue is of spinal roots is called the cauda
vertebrae.
the subarachnoid space. Between suc- equina. The cord will terminate in a
cessive nerve roots, a bandlike exten- thin-walled sac covered by pia mater,
sion of the pia mater will arise from the filum terminale, which fuses with
the surface of the spinal cord, dentic- the periosteum of the dorsal surface of
ulate ligament, attaching to the dura the coccyx.
and serving to anchor the spinal cord The gray matter of the spinal cord
(Figure 1-4). The ventral nerve roots can be divided into a posterior column
lie anterior and the dorsal nerve roots
posterior to this ligament.
The spinal cord is cylindrical in
shape, but flattened dorsoventrally. It
is widest at the cervical enlargement,
and a second enlargement occurs in
the lumbosacral level of the cord, both
reflecting the innervation levels of the
limbs. At birth the spinal cord typically
extends to the lower border of L3. By
adulthood its tip is usually at the L1-2
vertebral disk level but can end at T12
or descend to the lower border of the
L2 vertebrae.
Each segment of the spinal cord
usually has a set of dorsal (sensory) 13
and ventral (motor) rootlets that
emerge and join together to form their
corresponding root; dorsal roots have
their corresponding ganglia (dorsal
root ganglia). The dorsal and ventral
roots will fuse to form the spinal nerve
as it exits from the spinal canal. The
spinal nerves then divide into individ-
ual branches. There are usually 31
pairs of spinal nerves: eight cervical,
12 thoracic, five lumbar, five sacral,
and usually one coccygeal (Figure FIGURE 1-3 Spaces associated with the spinal meninges.
1-5). The first pair of spinal nerves will Modified with permission from Fitzgerald MJ, Gruener G,
Mtui E. Clinical neuroanatomy and neuroscience. 5th ed.
exit between the skull and the atlas London: Saunders, 2007:49. Copyright 2007, Elsevier.
(C1), the next six above their respec-
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINT:
The first pair of
spinal nerve
roots will exit
between the
skull and the
atlas (C1), the
next six above
their respectively
numbered
vertebrae (C2
through C7), but
C8 above the T1
vertebrae. The
remaining spinal
nerves will exit
FIGURE 1-4 Relationships of the sixth cervical spinal nerve.
below the
vertebrae of the Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and
neuroscience. 5th ed. London: Saunders, 2007:171. Copyright 2007, Elsevier.
corresponding
number.

(or horn), a lateral column, and an laminae I through V, more clearly

anterior column (or horn) that respec-
tively divide the adjacent white mat-
ter into a posterior, lateral, and ante-
rior funiculus. At the junction
between white and gray matter are
short ascending and descending axons
that arise from small neurons within
the spinal cord gray matter and com-
prise the intrinsic or intersegmental re-
flex pathways, proprius bundles (or
system) or fasciculi proprii and are
named by their location. While the
posterior funiculi primarily consist of
ascending sensory fibers, they also
contain their descending collateral fi-
14 bers, which serve to further integrate
intrinsic spinal reflexes and form their
own distinct, but small, fasciculi.
Within the gray matter of the spi-
nal cord cell groups can be identified
(right portion of Figure 1-6), with
those in the posterior horn participat-
ing in sensory pathways and those in
the intermediate and anterior horns
serving motor functions. In addition,
layers of synaptic inputs within the
spinal cord have also been identified.
These are called Rexed laminae and
are labeled I to X (left side of Figure
1-6). Those within the posterior horn,
demonstrate a laminated appearance.
Major Ascending Tracts
The diagrammatic representation of
both ascending and descending tracts
within the spinal cord reflects a level
of certainty that, while useful for com-
prehension, oversimplifies a more
complex anatomic distribution and an-
atomic variations that likely exist
(Nathan et al, 1990; Nathan et al, 1996;
Nathan et al, 2001). Indeed, the con-
cept of a tract as a homogenous group
of fibers is also an oversimplification.
Despite their shortcomings, however,
such generalizations have proven to
be clinically useful.
The sensory pathways and tracts
we will first review are responsible for
transmitting sensory information that
is perceived (conscious) as well as
nonconscious sensation. The dorsal
root ganglia contribute nerve fibers
that at the dorsal root entry zone will
further segregate into a medial group
of large-diameter fibers, which will en-
ter the posterior funiculi of the spinal
cord, and a lateral group of small-di-
ameter myelinated and unmyelinated
fibers. This segregation is modality

Continuum: Lifelong Learning Neurol 2008;14(3)

specific and will give rise to the major
ascending tracts within the spinal cord
(Figure 1-7). This lateral group of fi-
bers will divide into short ascending
and descending branches within the
tract of Lissauer and predominantly
synapse on neurons within laminae I
and II of the posterior horn.
The posterior columnmedial lem-
niscal pathway receives its input from
the largest group of sensory receptors
(neuromuscular spindles and Golgi
tendon organs) entering through the
medial portion of the dorsal root entry
zone. These fibers form a lamination
within the posterior column, and most
medial are those originating from the
lower extremity and trunk, fasciculus
gracilis, carrying sensory information
from the lower extremity; and laterally
is the fasciculus cuneatus, carrying
similar sensory information from the
upper trunk and limb (Figure 1-8). As
these fibers enter the posterior column
they bifurcate and one branch ascends
to the medulla where it will synapse
onto its second-order neuron within
the nucleus gracilis or cuneatus.
Those neurons will then project across
the midline in the sensory decussation,
continuing their ascent to the thalamus FIGURE 1-5 Vertebral column, spinal cord, and nerve
relationships.
as the medial lemniscus. The third-
Modified with permission from Moore KL, Dalley AF.
order neurons of this pathway will Clinically oriented anatomy. Philadelphia: Lippincott
then arise from the thalamus and William & Wilkins, 1999:478.
project to the somatic sensory cortex.
The other branch of that initial bifur- 15
cation of entering fibers will synapse pathway is the anterolateral spinotha-
within the posterior gray horn laminae lamic tract (Figure 1-9). This tract
II, III, and IV at various levels (the arises from neurons in laminae I, II, IV,
ascending branch also gives off collat- and V that receive excitatory as well as
erals to the dorsal gray horn). The tra- inhibitory input from neurons within
ditional functions of this system are the substantia gelatinosa (lamina II).
believed to be relaying conscious pro- The axons that arise from those neu-
prioception as well as discriminative rons cross in the anterior commissure
touch. Yet, its role in supporting the of the spinal cord and arrange them-
motor cortex as it carries out its intri- selves in the anterolateral location
cate and precise digital movements within those spinal cord funiculi.
may better or more accurately charac- There are two divisions, and the most
terize its function and importance anterior is the anterior spinothalamic
(Davidoff, 1989). tract, which has a somatotopic organi-
The other major conscious sensory zation and mediates the sensory mo-
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES
FIGURE 1-6 Spinal cord laminae and cell groups
(midthoracic level).
Reprinted with permission from Fitzgerald MJ, Gruener
G, Mtui E. Clinical neuroanatomy and neuroscience. 5th
ed. London: Saunders, 2007:182. Copyright 2007,
Elsevier.
dality of touch and pressure. The lat-
eral spinothalamic tract is lateral and
posterior, somatotopically as well as
16
Primary afferent neuron targets in the
FIGURE 1-7
posterior horn.
Reprinted with permission from Fitzgerald MJ, Gruener
G, Mtui E. Clinical neuroanatomy and neuroscience. 5th
ed. London: Saunders, 2007:183. Copyright 2007,
Elsevier.
Continuum: Lifelong Learning Neurol 2008;14(3)
modality arranged with cervical repre-
sentation most medial and sacral most
lateral; pain, tickle, and itch sensory
modalities are more peripheral while
temperature is more medially repre-
sented within this tract. These tracts
ascend, merge within the brainstem as
the spinal lemniscus, are joined later
by the trigeminal lemniscus (afferents
from the head), and together terminate
within the thalamus. Their third-order
neurons will also project to the so-
matic sensory cortex. The spinoreticu-
lar tract arises from neurons within
laminae V to VII and accompanies the
spinothalamic pathway, both as a
crossed and uncrossed tract, terminat-
ing within the brainstem. It serves as
an arousal system for the cerebral cor-
tex (through the reticular activating
system), and it helps to interpret the
nature of a stimulus (pleasurable or
not).
The spinocerebellar tracts provide
nonconscious proprioception (Figure
1-8). Fasciculus gracilis collaterals pro-
vide information from lower limb pri-
mary afferents (especially muscle spin-
dle), synapse upon the posterior
thoracic nucleus in lamina VII (ex-
tends from T1 through L1 spinal cord
levels, previously called the dorsal nu-
cleus or Clarke column), and give rise
to the posterior spinocerebellar tract.
The tract ascends and reaches the cer-
ebellum through the inferior cerebel-
lar peduncle. A similar group of affer-
ents from the fasciculus cuneatus
provides information from the upper
limb and synapses on the accessory
cuneate nucleus, which gives rise to
the cuneocerebellar tract. It also
reaches the cerebellum through the in-
ferior cerebellar peduncle. The follow-
ing two spinocerebellar tracts will pro-
vide information about the state of
internuncial function in regard to spi-
nal cord reflexes and arise from the
intermediate gray matter of the spinal
cord. (1) The anterior spinocerebellar
tract arises from the lower spinal cord
and will initially cross, ascend to the
superior cerebellar peduncle, cross
again to its side of origin, and termi-
nate within the cerebellum. (2) From
the upper half of the spinal cord the
rostral spinocerebellar tract will as-
cend and, through the inferior cerebel-
lar peduncle, enter the cerebellum.
The remaining tracts to be consid-
ered include the spinotectal tract,
which ends in the superior colliculus,
runs with the spinothalamic tract, and
brings somatic sensory information to
the superior colliculus. The spinooli-
vary tract projects to the inferior oli-
vary nucleus and through its effects on
the contralateral cerebellar cortex will
modify motor activity.

Major Descending Tracts

The motor cell types within the ante-
rior gray horns are of two types: (1)
Alpha motor neurons (physiologically
defined as tonic or phasic in regard to
the physiologic/functional type of
muscle fibers they innervate) supply
the extrafusal skeletal muscle fibers,
and (2) gamma motor neurons supply
the intrafusal muscle fibers of neuro-
muscular spindles. The motor unit
comprises an individual alpha motor
neuron, its axon, and all the muscle
fibers (varying from a few to hun-
dreds, dependent on the precision of
the movement) it will subsequently in-
nervate. Recurrent axons of alpha mo-
tor neurons excite inhibitory internun-
cial neurons, Renshaw cells, which
serve to inhibit their own firing (recur-
rent inhibition). At each segmental
level of the spinal cord, however, al-
pha motor neurons also receive nu-
merous inhibitory (usually on their
soma) as well as excitatory (through
synapses on their dendritic trees) in-
puts. These inputs arrive from both
supraspinal pathways as well as
through the propriospinal neurons (lo-
cal) and their pathways. Most of these
fibers and inputs will exert an inhibi-
tory effect on alpha motor neurons. If
FIGURE 1-8 Ascending pathways (upper cervical level).
GF gracile fasciculus; CF cuneate
fasciculus; PLT posterolateral tract;
PSCT posterior spinocerebellar tract; RSCT rostral
spinocerebellar tract; LSTT lateral spinothalamic tract;
ASCT anterior spinothalamic tract; SOT spinoolivary
tract; ASTT anterior spinothalamic tract; ST
spinotectal tract; SRT spinoreticular tract.
Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical
neuroanatomy and neuroscience. 5th ed. London: Saunders, 2007:187.
Copyright 2007, Elsevier.
those effects are abolished by a cord 17
lesion, the disproportionately strong
influence of the spinal intrinsic circuits
will lead to the clinical phenomenon
of spasticity.
Figure 1-10 demonstrates the co-
lumnar organization of motor neurons
into groups that then innervate mus-
cles with similar function. Those most
medial innervate the axial muscula-
ture, and moving traversely through
those groups of neurons, they also
move from the innervation of proximal
to distal limb muscles and finally to the
intrinsic muscles of the hand or foot.
Another result of this neuronal organi-
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:
The dorsal root
ganglia
contribute nerve
fibers that will
further
segregate at the
dorsal root entry
zone into a
medial group of
large-diameter
fibers that will
enter the
posterior funiculi
of the spinal
cord and a
lateral group of
small-diameter
myelinated and
unmyelinated
fibers.

The traditional
functions of the
posterior FIGURE 1-9 Spinothalamic pathways (sensory modalities, upper cervical level).
columnmedial Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and
lemniscal system neuroscience. 5th ed. London: Saunders, 2007:187. Copyright 2007, Elsevier.
are believed to
relay conscious
proprioception zation is alpha neurons innervating ex- The majority of fibers that give rise
and to mediate tensor muscles lying ventral or anterior to the corticospinal tract have their or-
discriminative to those that innervate flexor muscles. igin in primary motor cortex (perhaps
touch. Yet, its
Dysfunction of these neurons results in 50%), but supplementary motor cortex
role in
the clinical features of weakness, atro- and premotor cortex, as well as so-
supporting the
motor cortex as
phy, and fasciculations, as well as matic sensory cortex, also contribute.
it carries out its areflexia when their loss is marked. Some of these projections will end on
intricate and The long descending tracts (corti- brainstem nuclei (corticobulbar or
precise digital cospinal, reticulospinal, tectospinal, corticonuclear), while those from sen-
18 movements may vestibulospinal, raphespinal) and sory cortex project onto sensory nuclei
better or more aminergic and autonomic pathways in the brainstem and spinal cord that
accurately will terminate on interneurons, which modulate their transmission of sensory
characterize its influence alpha and gamma motor information. Those fibers that reach
function and neuron function. The rubrospinal tract the medulla form the pyramids, visible
importance. is small and lies anterior to the lateral on its ventral surface. Seventy percent
corticospinal; in humans its role is un- to 90% of these fibers cross the ventral
clear. Similar to sensory pathways, the midline in the pyramidal decussation,
discrete locations indicated within the giving rise to the lateral corticospinal
accompanying diagrams are used as tract within the spinal cord. A soma-
simplifications and conceal a more totopic organization results with fibers
complex and variable distribution of destined for the sacral area most lateral
these pathways that explains the dis- and those to the cervical, medial (Fig-
crepancy at times encountered be- ure 1-11). The remaining fibers de-
tween clinical findings and visualized scend uncrossed either within the lat-
anatomic lesions. eral corticospinal tract (uncrossed

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lateral corticospinal tract) or the ma-
jority adjacent to the anterior median
fissure as the anterior corticospinal
tract to innervate paraspinal and axial
muscles. At the appropriate level fi-
bers will cross through the anterior
white commissure to provide their
contralateral innervation.
All corticospinal neurons appear ex-
citatory with glutamate as their neuro-
transmitter. The corticospinal tract inner-
vates not only alpha and gamma motor
neurons, but also Renshaw cells, excita-
tory and inhibitory internuncials, and,
through presynaptic inhibition, sup-
presses some sensory transmission
within the spinothalamic tract in volun-
tary movement. The proximity of the
lateral corticospinal tract to the motor
neurons that innervate distal limb mus-
cles supports its role in facilitating the
performance of skilled movements and
the belief that an isolated pyramidal le-
sion only results in flaccid paralysis
and loss of skilled motor function of the
distal limb muscles.
FIGURE 1-10 Anterior gray horn cell column and somatotopic organization.
Reprinted with permission from Fitzgerald MJ, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. 5th ed. London:
Saunders, 2007:192. Copyright 2007, Elsevier.
KEY POINT:
The reticulospinal tracts, through
The lateral
shared internuncials with the cortico- spinothalamic
spinal tract, act upon motor neurons of tract is
axial as well as proximal limb muscles. somatotopically,
They are considered part of the extra- as well as
pyramidal system of motor control modality,
(with the lateral vestibulospinal and arranged with
tectospinal tracts) and are involved in cervical
locomotion as well as posture. The representation
medullary reticulospinal tract is be- most anterior
lieved to act on flexor motor neurons and sacral most
posterior. Pain,
and the pontine reticulospinal tract on
tickle, and itch
extensor motor neurons.
sensory
The tectospinal tract arises from modalities are
brainstem tectum and orients the head more peripheral
to visual or auditory stimulation. The while
lateral vestibulospinal tract originates temperature is
in the lateral vestibular nucleus (of more medially
Deiters) and helps in maintaining the represented
center of gravity for the body. The within this tract.
raphespinal tract originates from its
nucleus in the medulla and modulates
sensory transmission from its position
within the Lissauer tract. The aminer-
gic pathways arise from their cell
groups within the pons and medulla
19
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES
KEY POINT:
and have inhibitory effects on sensory
The long
descending
neurons and facilitatory effects on mo-
tracts tor neurons through a widespread dis-
(corticospinal, tribution in the spinal cord gray mat-
reticulospinal, ter. The central autonomic pathways
tectospinal, arise from the hypothalamus as well as
vestibulospinal, associated brainstem nuclei, terminat-
raphespinal), ing on neurons within the intermedio-
and aminergic lateral cell columns.
and autonomic
pathways will Vascular Supply of the Spinal
terminate on Cord
interneurons,
The arterial blood supply to the spinal
which then
cord comprises three longitudinally
influence alpha
and gamma
oriented vessels as well as contribu-
motor neuron tions from numerous radicular vessels
function. (Bowen and Pattany, 1999). A rich vas-
cular plexus (arterial or pia vasoco-
rona or plexus) arises from anastomo-
ses between these vessels along the
surface of the spinal cord and from
which medullary vessels penetrate
into both the white and gray matter.
These penetrating vessels are end ar-
teries and do not anastomose further.
20
FIGURE 1-11 Descending pathways (upper cervical level).
Reprinted with permission from Fitzgerald MJ, Gruener
G, Mtui E. Clinical neuroanatomy and neuroscience. 5th
ed. London: Saunders, 2007:198. Copyright 2007,
Elsevier.
Continuum: Lifelong Learning Neurol 2008;14(3)
The anterior spinal artery arises
from the union of the anterior spinal
branches of the vertebral artery and
descends within the anterior median
fissure of the spinal cord down to the
conus medullaris. Its largest caliber is
at the lumbosacral area, and smallest
at the thoracic area, which is also con-
sidered its watershed area. The two
posterior spinal arteries also originate
from the vertebral arteries but descend
along the line of attachment of the
dorsal nerve roots, posterolateral sul-
cus, on either side. At the conus med-
ullaris, the anterior and posterior spi-
nal arteries communicate though
anastomotic branches (Figure 1-12).
Thirty-one pairs of small radicular
arteries enter every intervertebral fora-
men supplying their corresponding
nerve roots. Some of these are larger
and also supply the spinal cord, ra-
diculomedullary branches. There may
be six to 10 such arteries, and through
their anterior radicular branch they
contribute to the anterior spinal artery.
The cervical and first two thoracic seg-
ments receive these arteries from
branches of the vertebral and thyro-
cervical trunk, T3 to T7 spinal cord
usually from an intercostal artery, and
the remainder of the spinal cord re-
ceives the largest and most constant
artery of Adamkiewicz (arises from a
left-sided intercostal or lumbar artery,
usually at the T9 through L2 spine
level), which supplies the lumbar en-
largement and conus medullaris. The
posterior spinal arteries receive contri-
butions from 12 to 16 posterior radicular
arteries, including a radicular branch
from the artery of Adamkiewicz.
The intrinsic arterial supply of the
spinal cord consists of a centripetal
(posterior spinal arteries and the an-
terolateral plexuses) and a centrifugal
(anterior sulcal arteries) system (Fig-
ure 1-13). The centripetal system is
formed from radial arteries directed in-
ward and supplying the posterior
white columns, and through shorter
 KEY POINTS:
The majority of
fibers that give
rise to the
corticospinal tract
have their origin
in primary motor
cortex, but
supplementary
motor cortex and
premotor cortex,
as well as
somatic sensory
cortex, also
contribute.
Within the
pyramidal
decussation,
70% to 90% of
fibers will
decussate and
give rise to the
lateral
corticospinal
tract. A
somatotopic
organization
develops with
fibers to the
sacral area most
lateral and those
to the cervical,
medial.
Thirty-one pairs
of small
radicular arteries
enter every
intervertebral
foramen
supplying their 21
corresponding
FIGURE 1-12 Arterial supply of the spinal cord.
nerve roots.
Reprinted with permission from Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Some of these
Lippincott William & Wilkins, 1999:487.
are larger and
also supply the
spinal cord,
radial penetrating vessels the periph- also contribute to the arterial vasoco- (radiculomedullary
eral rim of perhaps one-third to one- rona that envelops the spinal cord and branches). There
half of the spinal cord. The centrifugal through their short penetrating arteries may be six to 10
such arteries,
system arises from sulcal arteries of the supply the anterior rim of the spinal
and through
anterior spinal artery that pass back cord. In general, the centrifugal system
their anterior
into the anterior medial sulcus and (anterior spinal artery) supplies the an- radicular branch
then turn right or left to supply the terior two-thirds of the spinal cord. they contribute
adjacent gray and white matter. Smaller Analogous to the arterial blood to the anterior
branches from the anterior spinal artery supply, venous drainage of the spinal spinal artery.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

FIGURE 1-13 Arterial supply of a spinal cord segment.

Reprinted with permission from Haerer AF. DeJongs: the neurologic examination. 5th ed. Philadelphia: Lippincott Company,
1992:582.

cord also involves a longitudinal sys-

tem of veins, the larger posterior spinal
vein and the anterior. Through a cir-
22 cumferentially arranged venous anas-
tomosis, coronal venous plexus, within
the pia mater on the spinal cords sur-
face, they are connected (Figure
1-14). The anterior spinal vein will
communicate superiorly with the ve-
nous system of the brainstem and in-
feriorly end at the dural sac in the
sacrum. The posterior spinal vein
communicates with radicular veins at
the cervical level and extends down to
FIGURE 1-14 Venous drainage of a spinal cord segment.
the conus medullaris. At each spinal
Krauss WE. Vascular anatomy of the spinal
cord. Neurosurg Clin N Am 1999;10(1):915.
cord segment small radicular veins
drain the nerve roots, but at some lev-
Reprinted with permission from Mayo Foundation for Medical Education
and Research. All rights reserved. els larger veins, medullary veins, will
arise from the anterior median spinal
Continuum: Lifelong Learning Neurol 2008;14(3)
vein. There are approximately 10 to 20
anterior veins and a similar number of
posterior medullary veins, asymmetric
in location and not concomitant with
the medullary arteries. The largest are
in the lumbar region: the great ante-
rior medullary vein (usually accompa-
nying the nerve roots between T11
and L3) and the great posterior medul-
lary vein usually at L1 or 2. The pos-
terior half of the spinal cord will drain
into the posterior and the anterior half
into the anterior medullary veins.
These medullary veins follow and FIGURE 1-15 Vertebral venous plexus.
penetrate the dura with the nerve root Modified with permission from Moore KL, Dalley AF.
Clinically oriented anatomy. Philadelphia: Lippincott
and in the intervertebral foramen will William & Wilkins, 1999:466.
unite with the radicular veins, internal
and external vertebral plexus to form
the intervertebral vein that drains blood with the intercostal veins and then via
from the spine and spinal cord. Prior to the azygos and hemiazygous veins will
their exit from the dura matter, these enter the superior vena cava. The re-
veins are valveless (Gillilan, 1970; mainder of the venous drainage from
Krauss, 1999). the spinal cord can follow a similar
The cervical intervertebral veins pathway or, through the azygous and
will drain into the deep cervical and hemiazygous veins, enter the common
vertebral veins and will empty into the iliac veins and then the inferior vena
superior vena cava through the bra- cava.
chiocephalic and subclavian vein. At Within the spinal canals epidural
the thoracic cord they will connect space is also a longitudinally and cir-

23

FIGURE 1-16 Cord transection (modalities involved).

Reprinted with permission from Souayah N, Khella S. Neurology examination & board review.
New York: McGraw Hill, 2005:44.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

cumferentially arranged anastomosis SPINAL CORD SYNDROMES

of valveless veins, the internal venous
plexus (anterior and posterior) (Figure
1-15). It communicates with the spinal
cord through the medullary and radicu-
lar veins, and vertebral body through a
basivertebral vein, but it also drains to a
separate plexus that surrounds the ver-
tebra, the external vertebral plexus (an-
terior and posterior divisions). Through
the previously mentioned routes, it will
eventually empty into the superior or
inferior vena cava.
A syndrome (symptom complex) rep-
resents a complex of signs and symp-
toms that appear in combination and
present as a clinical picture. It may
have a specific cause, disease, or in-
herited abnormality, but this is not a
requirement and at times has resulted
in some confusion in the use and di-
agnostic significance of the term. Some
of the reported etiologies for the respec-
tive syndromes are listed in Table 1-1.

TABLE 1-1 Spinal Cord Syndromes and Their Etiologies (Representative Examples)

Etiology Complete Cord Brown- Anterior Spinal Artery

Transection Sequard Syndrome
Syndrome

Vascular *Aortic dissection,

*vasculitis, *atherosclerosis
of the aorta

Inflammatory or *Postinfectious,
infectious *multiple sclerosis,
*postvaccinal
Traumatic Traumatic spine *Traumatic
injury, herniated disc spine injury
Iatrogenic or Epidural hematoma Postoperative spine, aorta
toxin (anticoagulants) or thoracic surgery,
postoperative spinal
24 arteriovenous
malformation surgery,
decompression injury
Metabolic

Endocrine
Neoplastic Tumor, paraneoplastic Intramedullary
tumors
Degenerative or Cervical spondylosis
Hereditary
HTLV-I human T-cell leukemia virus I; HAM human T-cell lymphotropic virusassociated myelopathy.

*Classic or most common associated etiologies.

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 KEY POINT:
Complete Cord Transection the level of the lesion, the actual spinal
In cord
A complete cord transection disrupts cord level involved may be higher and transection, the
the sensory tracts ascending from be- the presence of radicular pain or seg- most valuable
low the level of the lesion and the mental paresthesias may serve as a finding that
descending tracts from above (Figure more accurate localizer. Radiation of identifies the
1-16). However, as many such lesions pain may also occur, and with cervical spinal cord as the
are incomplete, the clinical deficit will spinal cord lesions pain can radiate into site of the lesion is
reflect the extent of the injury. On the arms, thoracic into the chest or ab- pinprick sensation.
The actual spinal
physical examination a sensory level domen, and lumbar or sacral spinal cord
cord level involved
will be detected, using pinprick loss, into the legs. Careful examination for may be higher;
and is the most valuable finding that overlying vertebral spine tenderness the presence of
identifies the spinal cord as the site of may suggest an underlying destructive radicular pain or
the lesion. While sensory loss is ex- process such as a neoplasm or infection segmental
pected to involve all modalities below as the etiology, and pain that lessens paresthesias may
serve as a more
accurate localizer.

Posterolateral Central Lesion Posterior Anterior Horn Combined

Column Syndrome Column Cell Syndrome Anterior
Syndrome Horn Cell
Pyramidal
Syndrome
HIV HTLV-1 (HTLV *Neurosyphilis Poliomyelitis, HTLV-1
associated myelopathy, West Nile virus
HAM, or tropical
spastic paraplegia)
Late sequelae of Epidural spinal
spinal cord injury cord compression

Nitrous oxide Postradiation

myeloneuropathy

25

*Vitamin B12 deficiency Hexosaminidase

*Copper deficiency deficiency
myeloneuropathy

Intramedullary spinal
cord tumors
Cervical spondylosis *Syringomyelia *Spinal muscular *Amyotrophic
atrophies lateral sclerosis
(hereditary motor
neuropathies)

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES
FIGURE 1-17 Hemisection of the cord (Brown-Sequard
syndrome).
Reprinted with permission from Souayah N, Khella S.
Neurology examination & board review. New York:
McGraw Hill, 2005:46.
with sitting or standing is suggestive of a
malignancy. While further historical de-
tails may be helpful, laboratory and ra-
diologic studies are necessary to more
definitively identify an etiology.
Weakness, either paraplegia or tet-
raplegia, occurs below the level of the
lesion, owing to the interruption of the
descending corticospinal tracts. Ini-
tially, the paralysis may be flaccid and
areflexive because of spinal shock, but
eventually, hypertonic, hyperreflexive
paraplegia or tetraplegia occurs with
bilateral extensor toe signs, loss of su-
26 perficial abdominal and cremasteric
reflexes, and extensor and flexor
spasms (Adams and Hicks, 2005). At
the level of the lesion lower motor
neuron signs (paresis, atrophy, fas-
ciculations, and areflexia) in a seg-
mental distribution and reflecting
damage to the local anterior horn cells
or their ventral roots may be demon-
strated. These lower motor neuron
signs may be quite subtle in thoracic
lesions but can localize a lesion to a
specific spinal cord level. Urinary and
rectal sphincter dysfunction with in-
continence, sexual dysfunction, and
signs of autonomic dysfunction such
Continuum: Lifelong Learning Neurol 2008;14(3)
as anhidrosis, trophic skin changes,
impaired temperature control, and va-
somotor instability below the level of
lesion can also be demonstrated
(Cases 1-1 and 1-2).
Brown-Sequard Syndrome
A hemisection of the spinal cord re-
sults in this characteristic syndrome
(Tattersall and Turner, 2000) (Figure
1-17). Loss of pain and temperature
sensation occurs contralateral to the
side of injury due to interruption of the
crossed spinothalamic tract, but usu-
ally a clinical sensory level is one or
two segments below the level of the
lesion, reflecting the ascending nature
of this crossing tract (Nathan et al,
2001). Below the site of the lesion
there is ipsilateral loss of propriocep-
tive function due to interruption of the
ascending fibers of the posterior col-
umns, but such modalities of sensation
may also arise from within the spino-
cerebellar tracts as well (Davidoff,
1989). Ipsilateral weakness below the
lesion reflects the interruption of the
descending corticospinal tract. In a
slowly progressing lesion hyperre-
flexia and an extensor toe sign will be
elicitable, while in an acute lesion
those findings may initially be absent.
Damage to the ventral roots or anterior
horn cells results in segmental lower
motor neuron findings at the level of
the lesion, but these are clinically dif-
ficult to identify in thoracic spinal cord
lesions. Finally, if spinal root irritation
occurs, radicular pain, again at the site
and side of the lesion, may be experi-
enced and more clearly define the spi-
nal cord level.
Anterior Spinal Artery
Syndrome
The vascular nature of this syndrome
is manifested in its abrupt onset with
the deficit occurring within minutes or
hours from its initiation (Novy et al,
2006). Clinically the syndrome pre-
sents with back or neck pain and at
times in a radicular pattern, usually
followed by a flaccid paraplegia and
less commonly tetraplegia. Urinary
and bowel incontinence are usually
present. A sensory level to tempera-
ture and pinprick is found that reflects
the involvement of the spinothalamic
tracts bilaterally, but posterior column
modalities of sensation remain rela-
tively intact (Figure 1-18). Although FIGURE 1-18 Arterial spinal artery syndrome.
the thoracic spinal cord may be an Reprinted with permission from Souayah N, Khella S.
anatomic watershed zone with respect Neurology examination & board review. New York:
McGraw Hill, 2005:46.
to regional blood supply (Figure
1-19), the lumbosacral cord neurons
appear to be more susceptible to isch-
emia (Duggal and Lach, 2002). The
initial motor presentation progresses
from a flaccid paraplegia to one of
spasticity with hyperreflexia and Bab-
inski signs (Case 1-3).

Central Lesions
In this and in the syndromes discussed
below, the underlying pathologic pro-
cess is usually an insidious one, and the
features of the disease develop over an
extended period of time. When fully de-
veloped, the specific syndrome is more
clearly recognized, but early during the
process features may be incomplete,
leading to difficulty and a delay in rec-
ognizing the syndrome.
This syndrome results from a patho-
logic process in and around the central
canal, initially involving those tracts that
cross through the gray matter (anterior 27
and lateral spinothalamic tracts) (Figure
1-22). The resulting sensory impairment is
termed a dissociated sensory loss (loss of
pain and temperature sensation with pres-
ervation of position, vibration, and touch).
The typical site of involvement in the cer-
vical spinal cord and the particular sensory
modalities initially involved result in a clin-
ical presentation in which sensory loss oc-
curs in a vest- or shawl-like pattern over
FIGURE 1-19 Arterial supply of the spinal cord and
the upper extremities and shoulders. As watershed areas.
the size of the lesion increases, other fiber Reprinted with permission from Bradley WG, Daroff RB,
tracts will be involved, dependent on the Fenichel GM, Marsden CD, editors. Neurology in clinical
practice. Volume II. 3rd ed. Boston: Butterworth
direction and extent of the pathologic pro- Heinemann, 1999:1226.
cess. With extension anteriorly, a flaccid

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

Case 1-1
A 64-year-old right-handed man was brought to the emergency department after having fallen
down a flight of steps. He was not able to move his limbs. His medical history included coronary
artery disease, status post coronary artery bypass graft, diabetes mellitus, and schizophrenia,
but no clear motor difficulties prior to this incident. He remembers that during the fall he hit his
shoulders as he slid down the steps, but he experienced no loss of consciousness. Afterward he
was aware of pain all over, but most of his discomfort was in both upper extremities and
electrical in quality. Before being brought to the emergency department he noted that
passive movements of his head
intensified his upper extremity pain, but
no associated worsening of his sensory
symptoms occurred.
On examination his vital signs were
normal and he was in a rigid cervical
collar. He had abrasions over both upper
extremities. He was awake, alert, and
followed all commands. His cranial nerve
examination showed no clear
abnormalities. He was able to shrug his
shoulders but unable to lift his arms
from the bed; proximal strength in the
upper extremities was 2-3/5 and distal
was 0/5. Lower extremity motor
examination demonstrated weakness of
hip flexion at 4-/5, and the other motor
groups were 4/5. His tone appeared to
be normal. Reflexes were depressed, but
there appeared to be a right and
perhaps a left extensor toe sign. Sensory
examination demonstrated a decrease in
pinprick up to the C4 level on the right
and a patchy decrease in pinprick over
the distal part of his left lower
extremity; sacral sensation to pin was
intact. Position sense appeared to be
intact in his extremities. Rectal tone was
normal; a urinary drainage catheter was
in place.
28 Routine cervical spine x-rays
FIGURE 1-20 Cervical spine MRI (sagittal view, T2
weighted).
demonstrated no clear fractures or
prevertebral soft tissue swelling. Extensive degenerative changes were noted at multiple levels.
An MRI of the cervical spine demonstrated spinal stenosis, worse at C3-4, and neuroforaminal
stenosis from C3 to C5. There was an increase in spinal cord T2 signal intensity from C3 to C5
without enhancement, which was interpreted as edema (Figure 1-20). Over the next 12 hours his
lower extremity strength improved and his sensory deficits appeared to retract, but upper
extremity strength remained significantly impaired. No improvement with steroids was noted.
His persistent deficit and underlying cervical spine stenosis led to the recommendation for
cervical spine surgery.
Comment. Spinal cord trauma presents with different anatomic syndromes that include
transection, cervicomedullary syndromes with high cervical spine lesions, anterior or posterior
cord syndromes, Brown-Sequard syndrome, conus/cauda equina syndrome, or, as in this case, a
central cord syndrome. Recovery and manifestations are related to the site and extent of the
trauma and underlying mechanisms, eg, presence of preexisting spinal stenosis. These influence
eventual outcome and dictate immediate management.

Continuum: Lifelong Learning Neurol 2008;14(3)

Case 1-2
A 43-year-old woman with no prior medical history began to develop episodic vertigo and
jumpiness in her eyes when she was in her late 30s. Attributed to vertigo, the symptom
persisted but did not result in a disability. It was not until several years later that she began to
notice numbness over both of her hands, unaccompanied by neck or radicular pain. She
attributed this to carpal tunnel syndrome precipitated by her administrative and secretarial
work. It was the gradual involvement of ambulatory difficulties and an acute worsening over
the last several months that led her to seek further evaluation.
Her general physical examination
and vital signs were normal. Cervical
spine examination and hairline were
normal; there was no spinal scoliosis.
Her cranial nerve examination
demonstrated a left Horner syndrome,
and rotary nystagmus was evident on
horizontal as well as downward gaze.
She had weakness predominantly in
the distal lower extremities, more so
on the left side and to a 4/5 degree,
but her tone appeared to be increased
in all extremities. Sensory examination
showed a decrease in pinprick over the
right extremity that extended onto
the upper thorax; similar, but less-
marked, findings were found on the
left, suggesting a shawl-like pattern.
Her reflexes were generally increased,
and she demonstrated bilateral
Babinski signs.
An MRI scan of her brain and
cervical spinal cord demonstrated a
Chiari type-one malformation
associated with syringomyelia. She
underwent foramen magnum
decompressive surgery, upper cervical
spine laminectomy, and fusion and
shunt placement (fourth ventricle to
upper cervical spine). The
postoperative cervical spine MRI scan FIGURE 1-21 Cervical spine MRI (sagittal view, T1 29
weighted).
is shown in Figure 1-21. Since surgery
her neurologic deficit has remained
relatively stable, but recently she has begun to experience lower extremity radicular pain
secondary to lumbar degenerative disc and neural foraminal stenosis.
Comment. The insidious nature of this patients deficit initially delayed her seeking further
clinical evaluation. However, the presence and pattern of her nystagmus, bilateral upper
extremity sensory impairment, and cortical spinal tract involvement suggest an intramedullary
spinal cord lesion that may extend into the brainstem. The onset of syringomyelia is often
insidious, and symptom onset occurs between the ages of 25 and 40. A presentation with
isolated findings may delay identification while the combination of brainstem dysfunction (eg,
vertigo, oscillopsia, dysphonia, and facial sensory loss), dissociated sensory loss in the extremities,
and later involvement of upper and lower motor neurons usually suggest the diagnosis.
Radiologic confirmation is necessary for definitive diagnosis. Surgical interventions and extent
are dependent on the assumed etiology and preexisting neurologic deficit. Decompression
surgery or shunting procedures may be required in selected cases.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:
The sensory
impairment in
Case 1-3
central cord A 67-year-old right-handed woman was brought to the emergency
lesions is termed department by her husband. Without any clear precipitants, she had
a dissociated awakened with severe low back pain, accompanied by radicular pain
sensory loss (loss down both lower extremities, and abdominal discomfort. She had gone to
of pain and her toilet but was unable to raise herself. While being transported to the
temperature emergency department she developed urinary incontinence and later
sensation with bowel incontinence.
preservation of On evaluation, her vital signs and cardiac and vascular examinations
position, were normal. Her examination was significant for lower extremity
vibration, and paraplegia and hyporeflexia. Plantar stimulation elicited no response; a
touch). Beevor sign was present. She demonstrated a sensory level to pinprick up
to T10, decreased temperature to L1, and normal position sense. Sacral
The lamination sensation to pinprick was absent; rectal tone was absent, and a urinary
of the lateral drainage catheter was in place (initially 1000 cc of urine had been
spinothalamic drained). There was no tenderness to percussion over the spine, and
tract results in straight-leg raise was negative. Her pain resolved over 2 days.
fibers conveying Steroids were initially administered because of the possibility of spinal
sensation from cord compression, and an emergent MRI of the entire spine was
the sacrum to be performed as well as imaging of the aorta. Both were normal. Over the
more laterally/ ensuing weeks her lower extremity strength improved, and hyperreflexia,
superficially as well as bilateral Babinski signs, appeared. However, her ambulation
placed within remained impaired. Her sensory deficits lessened, and although her bowel
the spinal cord. incontinence improved she required periodic urinary catheterization.
These are often Comment. While this initial clinical presentation suggested a spinal cord
preserved for an infarction and an anterior spinal artery syndrome, a compressive spinal
extended period cord or conus/cauda equina lesion required exclusion. Aortic dissection can
of time with also cause spinal cord ischemia/infarction, and such an evaluation is
central spinal required as soon as possible. Usually (67%) of the time MRI demonstrates
cord lesions a T2-weighted abnormality, but a normal study does not exclude a spinal
(sacral sensory cord infarction, which then becomes a diagnosis of exclusion. Back or neck
sparing). pain and radicular pain can occur at symptom onset (59%), resolving in
several days, but later neurogenic pain can develop. In the majority of
spontaneous cases (70%) an etiology is not discovered, but the possibility
of mechanical stress-induced vascular compromise has been suggested in
some cases. Prognosis is related to the extent of the injury, but
ambulation usually remains impaired (Novy et al, 2006).
30

paralysis with fasciculations and atrophy
occurs as the anterior horns and their mo-
tor neurons are affected. Lateral extension
involves the corticospinal tracts, resulting
in spastic paralysis of muscles below the
lesion, while posterior extension involves
the posterior columns with disruption of
their sensory modalities. The lamination of
the lateral spinothalamic tract results in fi-
bers conveying sensation from the sacrum
to be more laterally/superficially placed
within the spinal cord and are often pre-
served for an extended period of time
with central spinal cord lesions, represent-
ing a form of sacral sensory sparing.
At times an acute cervical spinal
cord injury, especially after hyperex-
tension injuries of the neck, results in a
unique neurologic presentation that
signifies an injury to the central por-
tion of the spinal cord (distinguished
from the man-in-the-barrel syndrome
reported after ischemic cerebral le-
sions within the border zone between
anterior and middle cerebral arteries
and cruciate paralysis, a syndrome of

Continuum: Lifelong Learning Neurol 2008;14(3)

brachial diplegia after medullary lesions).
Such individuals at first may be quadri-
plegic, but recovery of lower extremity
strength often occurs early, and the
prognosis may be better because of a
predominantly white matter injury (Col-
lignon et al, 2002). However, a unique
pattern of weakness that is more pro-
nounced in the arms, worse distally than
proximally, characterizes the syndrome
and the unique site of injury. Urinary
dysfunction, as well as patchy sensory
loss below the level of the injury or up-
per and lower levels of sensory loss (sus-
pended sensory level), can be demon-
strated (Cases 1-1 and 1-2). FIGURE 1-22 Syringomyelia (modalities involved).
Reprinted with permission from Souayah N, Khella S.
Neurology examination & board review. New York:
McGraw Hill, 2005:45.

Posterolateral Column
Syndrome
Involvement of the posterior and lateral
columns of the spinal cord will lead to a
pattern of sensory loss that predominantly
involves the modalities of position and vi-
bratory sense and a motor syndrome of
spastic paralysis that reflects involvement
of the corticospinal tract (Figure 1-23).
This pattern of dysfunction leads to a sen-
sory ataxia with a positive Romberg sign,
while pain and temperature sensation re-
main intact because of preservation of the
spinothalamic tracts. A spastic-ataxic gait
reflects this constellation of fiber tract dys-
function.
This pattern of involvement usu-
ally develops insidiously, reflecting
the underlying pathologic processes.
In the syndrome known as subacute
combined degeneration, related to a
deficiency of vitamin B12 or copper,
the initial neurologic manifestations
may be those of limb paresthesia, pre-
dominantly involving the feet, fol-
lowed later by the development of the
more distinctive posterior column and
corticospinal tract deficits. The complete
features of this syndrome usually de-
velop over an extended period of time.
Posterior Column Syndrome
A process involving the posterior columns
is characterized by loss of position sense,
vibration sense, and two-point discrimina-
tion. These deficits occur distal to the le-
sion. The lack of proprioceptive informa-
tion and feedback to the motor system
affects those muscle groups required for
discriminative movements, resulting in a
sensory ataxia. While vision can partially
compensate for this loss of proprioceptive
information when the eyes are open,
ataxia worsens when they are closed, re-
sulting in the presence of a Romberg sign.
The gait is described as ataxic (or stomp-
31
FIGURE 1-23 Posterolateral column syndrome.
Reprinted with permission from Souayah N, Khella S.
Neurology examination & board review. New York:
McGraw Hill, 2005:44.
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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

KEY POINTS:
Dysfunction in
the posterior
column
syndrome is
characterized by
a sensory ataxia
with a positive
Romberg sign
while pain and
temperature
FIGURE 1-24 Combined anterior horn cellpyramidal
sensation remain syndrome.
intact because
Reprinted with permission from Souayah N, Khella S.
of preservation Neurology examination & board review. New York:
of the McGraw Hill, 2005:44.

spinothalamic
tracts.
ing) in character, and the deficit can be
With
more prominent in darkness or with eye
dysfunction of
closure as visual cues no longer can assist
the posterior
columns in the
in maintaining balance. The affected limbs
may become hypotonic but usually are
cervical region,
not weak. At times other spinal cord le-
neck flexion may
sions can produce a truncal ataxia but
elicit an electric-
like sensation without the associated proprioceptive dif-
that radiates ficulties. In such cases, spinocerebellar
down the back tract dysfunction, as a manifestation of spi-
or into the arms nal cord compression, appears to be re-
(Lhermitte sign). sponsible for this clinical syndrome.
With dysfunction of the posterior col-
umns in the cervical region, neck flexion
may elicit an electric-like sensation that
radiates down the back or into the arms
(Lhermitte sign). It is thought to represent
increased mechanosensitivity of the dorsal
columns with neck flexion further activat-
ing those sensory pathways. The symp-
32 tom is most frequently associated with spi-
nal cord involvement in multiple sclerosis.
Anterior Horn Cell Syndrome
Damage to the motor anterior horn cells
leads to an ipsilateral flaccid paralysis ac-
companied by atrophy and fasciculations.
Because larger muscles are supplied by
motor neurons from more than one seg-
ment, damage to a single spinal cord seg-
ment may lead only to muscular weak-
ness rather than complete paralysis of the
affected motor group (Figure 1-10).
When the lateral horns are involved, a
decrease in sweating and vasomotor func-
tions may also be demonstrated, as the
cell bodies of the sympathetic neurons are
involved.
Combined Anterior Horn Cell
Pyramidal Syndrome
This syndrome is perhaps best exempli-
fied by ALS. These lesions produce a com-
bination of flaccid and spastic paralysis.
Damage to the anterior horns or lower
motor neurons will result in a flaccid pa-
ralysis with atrophy and fasciculations,
while a lesion of the lateral corticospinal
tract or upper motor neurons results in a
spastic paralysis with associated hyperre-
flexia and Babinski sign (Figure 1-24).
The degree of injury to either site can be
highly variable and reflected in the clinical
presentation. If one site is more or pre-
dominantly affected, an additional lesion
in the other at the same level may not
produce noticeable effects.
INTRAMEDULLARY VERSUS
EXTRAMEDULLARY CORD
LESIONS
Neoplasms arising within the spinal
canal tend to produce their symptoms
and signs in a slow and progressive
manner, although an acute presenta-
tion can occasionally be encountered.
When arising from lesions within the
spinal cord (intramedullary), symp-
toms often begin within the vicinity of
the central canal. Sensory symptoms
are initially less localizing and dissoci-
ation of sensory loss can occur. Early

Continuum: Lifelong Learning Neurol 2008;14(3)

 KEY POINT:
A more
TABLE 1-2 Clinical Features of Intramedullary Versus
Extramedullary Spinal Cord Lesions symmetric
pattern of
sensory loss and
Symptoms and Extramedullary Intramedullary motor
Signs dysfunction is
Spontaneous pain Radicular in type and Burning in type and more consistent
distribution; an early poorly localized with a conus
and important than a cauda
symptom equina lesion.
Sensory deficit Contralateral loss of Dissociation of
pain and temperature; sensation; patchy
ipsilateral loss of distribution
proprioception
Changes in pain and More marked than at Less marked than at
temperature level of lesion level of lesion
sensations over
perineum (saddle area)
Lower motor neuron Segmental Widespread with
involvement atrophy and
fasciculations
Upper motor neuron Prominent, early Late, minimal
involvement
Muscle stretch reflexes Increased early, Late, minimal changes
markedly
Corticospinal tract Early Late
signs
Trophic changes Usually not marked Marked
Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: Lippincott
Williams & Wilkins, 2007:111.
Data from Haerer AF. DeJongs the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins,
1992:588.

evidence of lower motor neuron find- Brown-Sequard pattern may appear.

ings, later accompanied by corticospi-
nal tract findings, characterizes these
lesions, and their clinical presentation
can mimic a syrinx. Extramedullary
lesions can arise from the dura and
adjacent structures (extramedullary
intradural) or can have an extradural
site of origin such as the vertebral bod-
ies or extradural space (extramedul-
lary extradural). Spontaneous pain,
especially in a radicular pattern, can
be a presenting feature and suggests
the level of involvement. Subsequent
motor and sensory changes are usually
slow to develop, and because of the
asymmetric nature of such lesions a
The features of either type of clinical
syndrome are described and con-
33
trasted in Table 1-2.
CONUS MEDULLARIS VERSUS
CAUDA EQUINA LESIONS
The close anatomic localization of the co-
nus medullaris and overlying cauda
equina makes distinction of either syn-
drome difficult, and at times involvement
of both structures occurs. A symmetric
pattern of sensory loss and motor dysfunc-
tion is more consistent with a conus than a
cauda equina lesion. The clinical features
of both conditions are further described
and contrasted in Table 1-3.

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 SPINAL CORD ANATOMY, LOCALIZATION, SYNDROMES

TABLE 1-3 Clinical Features of Conus Medullaris and Cauda

Equina Lesions

Symptoms and Conus Medullaris Cauda Equina

Signs
Spontaneous pain Not common or May be most
severe; bilateral and prominent symptom;
symmetric; over severe and radicular in
perineum and thighs type; unilateral or
asymmetric; over
perineum, thighs, legs,
and back
Sensory deficit Saddle distribution; Saddle distribution;
bilateral, usually may be unilateral and
symmetric; dissociation asymmetric; all
of sensation modalities affected; no
dissociation of
sensation
Motor loss Symmetric; not Asymmetric; more
marked; fasciculations marked; atrophy may
may be present occur; usually no
fasciculations
Reflex loss Only Achilles reflex Patellar and Achilles
absent reflexes may be absent
Bladder and rectal Early and marked Late and less marked
symptoms
Trophic changes Decubitus common Decubitus less marked
Sexual function Erection and Less marked
ejaculation impaired impairment
Onset Sudden and bilateral Gradual and unilateral
Data from Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 5th ed. Philadelphia: Lippincott
Williams & Wilkins, 2007.
Data from Haerer AF. DeJongs the neurologic examination. 5th ed. Philadelphia: Lippincott Williams & Wilkins,
1992:591.

34

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Note: There are many general textbooks of neuroscience, neuroanatomy as well
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mendations represent our bias and are driven by familiarity with and the
usefulness we have found in the following general resources for teaching and
review.

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Moore KL, Dalley AF. Clinically oriented anatomy. Philadelphia: Lippincott Williams &
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Nathan PW, Smith M, Deacon P. The crossing of the spinothalamic tract. Brain
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