CHAPTER.

S The Spinal Cord 59

la neuron

lnterneuron - --

FIGURE 5-20 Schematlcll-

lustratlon of the neurons Involved
In the stretch reflex (right half)
showing innervation of extrafusal
(striated muscle) fibers by alpha
motor neurons, and ofintrafusal
fibers (within muscle spindle)
by gamma motor neurons. The
left half of the diagram shows Spindle (lntrafusal)
an Inhibitory reflex arc, which musdeftber
Includes an Intercalated Inhibitory Sensory
lnterneuron. ending

syndrome). while loss or reduction ofone particular deep tendon
reflex (eg. loss of the knee jerk on one side) suggests injury to the
afferent or efferent nerve fibers in the nerves or roots supplying
that reflex.
1he large extensor muscles that support the body are kept
constantly active by coactivation of alpha and gamma motor
neurons. Transection of the spinal cord acutely reduces mus-
cle tone below the level of the lesion, indicating that supraspi-
nal descending axons modulate the alpha and gamma motor
neurons. In the chronic phase after transedion of the spinal
cord, there is hyperactivity of stretch reflexes below the level
of the lesion, producing spaaticity. This condition is a result of
the loss ofdescending, modulatory infiuences. Spasticity can be
disabling and is often treated with baclofen, a gamma-amino-
butyric acid agonist. In some patients, however, the increased
extension tone in spastic lower extremities is useful, providing
at least a stiff-legged spastic gait after damage to the corti.co-
spinal system (eg. after a stroke).
H. Polysynaptlc Reftexes
In contrast to the extensor stretch reflex (eg. patellar, Achilles
tendon), polysynaptic;, crossed extensor reflexes are not lim-
ited to one muscle; they usually involve many muscles on the
same or opposite side of the body (Fig 5-21). These refiexes
have several physiologic characteristics:
f. Reciprocal action of antagonlsts-Flexors are excited
and extensors inhibited on one side of the body; the opposite
occurs on the opposite side of the body.
2. Divergence-Stimuli from a few receptors are distributed
to many motor neurons in the cord.
3. Summation-Consecutive or simultaneous subthreshold
stimuli may combine to initiate the reflex.
Propriosplnal u.ona, located on the periphery of the
spinal gray matter, are the axons oflocal circuit neurons that
convey impulses upward or downward, for several segments,
to coordinate reflexes involving several segments. Some re-
searchers refer to these axons as the propriospinal tract.
LESIONS IN THE MOTOR PATHWAYS
Lesions in the motor pathways, the muscle or its myoneural
junction, or the peripheral nerve all result in disturbances of mo-
tor function (see Fig 5-20; see also Otapter 13). Two main types
of lesions-of the upper and lower motor nemons-are distin-
guished in spinal cord disorders (Table 5-6). It can be crucially
important for the clinician to differentiate between an upper-
motor-neuron lesion versus a lower-motor-neuron lesion.
Lower-Motor-Neuron Lesions
A lower motor neuron, the motor cell concerned with striated
skeletal muscle activity, consists of a cell body (located in the
anterior gray column of the spinal cord or brain stem) and its
axon, which passes to the motor end-plates of the muscle by
way of the peripheral or cranial nerves (Fig 5-22). Lower mo-
tor neurons are considered the final common pathway because
many neural impulses funnel through them to the muscle; that
is, they are acted on by the corti.cospinal, rubrospinal, olivo-
spinal, vestibulospinal, reticulospinal, and tectospinal tracts as
well as by intersegmental and intrasegmental reflex neurons.
Lesions of the LMNs may be located in the cells of the
ventral gray column of the spinal cord or brain stem or in their
60 SECTION In Spinal Cord and Spine
FIGURE 5-21 Schematic Illustration oflpsllateral and crossed
polysynaptlc reflexes.
axons, which constitute the ventral roots of the spinal or cra-
nial nerves. Lesions can result from trauma, toxins, infections
(eg. poliomyelitis, which can affect purely lower motor neu-
rons). vascular disorders, degenerative processes, neoplasms,
or congenital malformations affecting LMNs in the brain stem
or spinal cord. Compression of ventral root axons (le, the ax-
ons of LMNs in the spinal cord) by herniated intervertebral
disks is a common cause of LMN dysfunction. Signs of LMN
lesions include fiacdd paralyaia of the involved muscles (see
Table 5-6); muscle atrophy with degeneration of muscle :fi-
bers after some time has elapsed; clim1nished or absent deep
tendon refia:a (hyporefiexia or arefiexia) of the involved
muscle; and absence of pathologic refleus (discussed next).
Fasciculations and :fibrillations may be present.
Upper-Motor-Neuron Lesions
Damage to the cerebral hemispheres or lateral white column
of the spinal cord can produce signs of upper-motor-neuron
lesions (Fig. 5-22). 1hese signs include spastic paral.,Us or pa-
resis (weakness) of the involved muscles (see Table 5-6), little
or no muscle atrophy (merely the atrophy ofdisuse), hyperac-
tive deep tendon reflaes, diminished or absent superficial re-
flexes, and pathologic reflexes and signs, especially the extensor
plantar re:flex (Babinski.'s sign) (Fig 5-23).
Upper-motor-neuron lesions are commonly seen as a
result of strokes, which can damage upper motor neurons in
the cortex, and infections or tumors, which injure upper mo-
tor neurons or their axons either in the brain or as they de-
scend in the spinal cord. 1he corticospinal, rubrospinal, and
reticulospinal tracts lie close together or overlap within the
lateral white column. Interruption of the corticospinal tract
is usually accompanied by spasticity and hypertlexia. Isolated
lesions of the corticospinal tract are rare; when these lesions
occur, they cause loss of fine motor control (eg, loss of dex-
terity of the individual fingers) but tend to spare axial muscle
groups (ie, those located proximally in the limbs) that control
gross trunk and limb movement.
Disorders of Muscle or Neuromuscular
Endings
Abnormal muscle may be unable to react normally to stimuli
conveyed to it by the LMNs. This may manifest as weakness, pa-
ralysis. or tetanic contraction caused by disturbances in the mus-
cle itself or at the neuromuscular junction. Myasthenia gravia
and the myasthenic syndrome (Lambert-Eaton myuthenic syn-
drome) are disorders of the neuromuscular junction that pres-
ent with weaknen. 1he musc:ular dyatrophies and in8amma-
tory m:yopathies (such as polym.yosi.tis) are typical disorders of
muscle, characterized by muscular dysfunction (weakness in the
presence of apparently normal nerve tissue). Sensory function is
normal in these disorders.
Localization of Spinal Cord Lesions
In localizing spinal cord lesions, it is important to ask the fol-
lowing questions:
(1) At what level does the clinical abnormality begin (ie, is
there a sensorylevd below which sensation is impaired)? Is
motor function impaired below a specific myotomal level?
(2) Which tracts are involved?
(3) On which side are they located?
(4) Which sensory modalities are involved (all modalities,
suggesting involvement of the lateral and dorsal columns;
vibration and position sense, suggesting dorsal column
dysfunction; or dissociated Jo55 of sensibility for pain and
temperature, suggesting a lesion involving the spinotha-
lamic fibers, possibly in the central part of the cord where
they cro55)?
A segmental lesion (a lesion involving only some seg-
ments of the spinal cord) injures motor neurons at the site of
injury (causing LMN dysfunction at that level) and also in-
jures descending tracts (producing upper-motor-neuron dys-
function and sensory loss below the site of injury).
Types of Spinal Cord Lesions
Several typical sites of pathologic lesions in the spinal cord
produce characteristic syndromes:
(1) A am.all central lesion can affect the decussating 6.bers of
the spinothalamic tract from both sides without affecting
other ascending or descending tracts. As a result, these
lesions can produce dissociated sensory abnormalities
with loss of pain and temperature sensibility in appropri-
ate dermatomes but with preserved vibration and position
sense. 1his occurs, for example, in syringomyelia (see the
following section) (Fig 5-24A).
(2) A large central le.ion involves, in addition to the pain and
temperature pathways, portions of adjacent tracts, adjacent
gray matter, or both. Thus, there can be I.MN weakness in
the segments involved, together with upper-motor-neuron
dysfunction and, in some cases, loss of vibratory and
position sense at levels below the lesion (Fig 5-248).
 CHAPTER 5 Tue Spinal Cord 61

Motor cortex,..{ .. r---......

., \
I '
t ____ ---
...,,.....- \
i
capsule ""- · __,
- >G
..
• - - \ J"'- -
-

Upper FIGURE 5-23 Testing fur extensor plantar reflexes also called
motor Babinski reflexes.
neuron

Spinal cord - \ \
\\ •, syphilis (see later discussion), which is rare at present
because of the availability of antibiotics (Fig 5-24C).
(4) An irregular peripheral lesion (eg, stab wound or com-
pression of the cord) involves long pathways and gray
matter; functions below the level of the lesion are abol-
ished. In practice, many penetrating wounds of the spinal
cord (stab wounds, gunshot wounds) cause in'egular
lesions (Fig 5-240).
(S) Complete hemiaection of the cord produces a Brown-
sequard ayndrome (see later discussion; Figs 5-24E and
5-25).
Lesions outside the cord (extramedullary lesions) may
Lower affect the function of the cord itself as a result of direct me-
motor
neuron chanical injury or secondary isc.hemic injury resulting from
nerve the compromise of the vascular structures or vasospasm.
Motor - - (6) A tumor of the dorsal root (such as a neurofi.broma or
end-plate schwannoma) involves the first-order sensory neurons of
a segment and can produce pain u well as sensory loss.
Deep tendon reflexes at the appropriate level may be lost
because of damage to la :fibers (Fig 5-24F).
FIGURE 5-22 Motor pathways dMded Into upper- and lower- (7) A tumor of the meninges or the bone (extramedullary
motor-neuron regions.
masses) may compress the spinal cord against a vertebra,
causing dysfunction of ascending and descending fiber
s}'5tems (Fig 5-24G). Tum.ors can metastasize to the epi-
(3) A clonal column lesion affects the dorsal columns, leav- dural space, causing spinal cord compression. Herniated
ing other parts of the spinal cord intact 1hus, proprio- intervertebral disks can also compress the spinal cord.
ceptive and vibratory sensation are involved, but other Spinal cord compression may be treatable if diagnosed
functions are nonnal. Isolated involvement of the dorsal early. Suspected spinal cord compression thus requires
columns occurs in tabes dorsalis, a form of tertiary aggressive diagnostic workup on an urgent basis.

TABLE 5-6 Lower- Versus Upper-Motor-Neuron Lesions.

V•rillble UpJMr-Motor-Neuron l.ellon

Weakness Flaccld paralysis Spastic paralysis

Deep tendon reflexes Decreased or absent Increased

Bablnskl's reflex Absent Present

Atrophy May be marted Absent or resulting from disuse
Fasciculations and librlllatlons May be present Absent
62 SECTION III Spinal Cord and Spine

EXAMPLES OF SPECIFIC SPINAL

CORD DISORDERS
Spinal Cord Compression
Spinal cord compresaion-due, for example, to an extramed- A. Small oentral lesion
ullary tumor such as meningioma, neurofibroma, or meta-
static cancer, an epidural abscess, or a ruptured intervertebral
disc-can injure the spinal cord and can rapidly progress to
irreversible paraplegia or quadriplegia if not promptly diag-
nosed and treated.
Spinal cord compression should be suspected in any
patient with weakness, numbness or sensory loss in the legs. B. Large central leslon
A "sensory level." that is, impaired sensation below a specific
dermatomal level, or the presence ofBabinski reflexes and hy-
perreftexia in the lower extremities supports the diagnosis (al-
though in the acute phase of spinal cord compression, spinal
shock can produce transient hyporeflexia below the lesion).
Bowel or bladder dysfunction may be present Pain over the C. Dorsal column lesion
spinal column, or tenderness on mild percussion, provides
further support for the diagnosis. If the lesion compresses
the conw medullaris or cauda equina, there may be sensory
loss in a "saddle· distribution and hyporeftexia. Spinal cord
compression is surgically treatable but can rapidly progress to
irreversible paraplegia if not treated. Imaging of the spine is
required on an urgent basis in any patient in whom spinal D. Irregular lesion
cord compression is suspected.

Syringomyelia
Syringomyelia presents a classical clinical picture, character-
ized by loss of pain and temperature sensation at several seg-
mental levels, although the patient usually retains touch and E. Complete hemiseclion
pressure sense as well as vibration and position sense (disso-
ciated anelthesla) (Fig 5-26). Because the lesion usually in-
volves the central part of the spinal cord and is confined to a
limited number of segments, it affects decussating spinotha-
lamic tracts only in these segments and results in a pattern
of segmental loss of pain and temperature sense. When this
type of injury occurs in the cervical region, there is a cape-like
F. Dorsal root tumor
pattern of sensory loss. If the lesion also involves the ventral
gray matter, there may be LMN lesions and atrophy of the
denervated muscles.

TABLE 5-7 Common Symptoms and Signs 1n Spinal

G. Compression of cord within lhe
Cord Compression. wrtebra by axtramedullary mass
Weakness or sensory lms In the legs
FIGURE 5-24 Schematic Illustrations (A-G) of various types of
Babinski reflexes
spinal cord lesions.
Hyper reflexla ln the lower extremities (although, ln the acute phase
of compression or ln lesions of the con us medullarls or cauda equine,
there c;m be hyporeflexia)
A •sensory level•

Pain or tenderness on percussion ever the vertebral column

 CHAPTER. S The Spinal Cord 63

}. y
Tabes Dorsalis .J
Tabes dorsalis, a form of tertiary neurosyphilis, is now rare, I

but was common in the pre-antibiotic era. and is characterized Loss of pain and
..,- temparature
by damage to the dorsal roots and dorsal columns. As a result ,/ , sensation
of this damage, there is impairment of proprioception and vi-
bratory sensation, together with loss of deep tendon reflexes,
which cannot be elicited because the la afferent pathway has
been damaged. Patients exhibit "sensory ataxia." Romberg's
}ll [
I
I (
.' •
)" .('l 1l
1
1
J '1 \
I \ \
I

sign (inability to maintain a steady posture with the feet close •' I I I \ 1,

I'
together, after the eyes are closed, because ofloss of proprio-
ceptive input) is usually present Charc:ot's joint.a (destruction /'IJI I \'
of articular surfaces as a result of repeated injury ofinsensitive rI
joints) are sometimes present. Subjective sensory disturbances I ,'
I I l
known as tabetic c:riles consist ofsevere cramping pains in the
'1 ,1 ,, 1'
stomach, larynx. or other viscera. 1I

Brown-54iquard Syndrome I\ l'I 1 /

,1

ll1'
This syndrome is caused by hemisection of the spinal cord as
a result of, for example, bullet or stab wounds, syringomy-
elia. spinal cord tum.or, or hematomyelia. Signs and symp-
toms include ipsilateral LMN paralysis in the segment of FIGURE 5-26
'# . )l I \

Syringomyelia involving the cervicothoracic por-

the lesion (resulting from damage to LMNs) (see Fig 5-25); tion of the spinal cord.
ipsilateral upper-motor-neuron paralysis below the level of
the lesion (resulting from damage to the lateral corticospinal
tract); an ipsilateral zone of cutaneous anesthesia in the seg- ipsilateral loss of proprioceptive, vibratory, and two-point
ment of the lesion (resulting from damage to afferent fibers discrimination sense below the level of the lesion (resulting
that have entered the cord and have not yet crossed); and from damage to the dorsal columns). There is also a contra-
lateral loss of pain and temperature sense below the lesion
(resulting from damage to the spinothalamic tracts, which
have already de<:Ussated below the lesion). Hyperesthesia
may be present in the segment of the lesion or below the
r.
r- ""'·1 level of the lesion, ipsilaterally, or on both sides. In practice,
r "pure" syndromes are rare because most
lesions of the spinal cord are irregular.
/ -..
/ \ Subacute Combined Degeneration
r ..
I I
,.j II
I /' ro '1 (Posterolateral Sclerosis)
} 1• \ 11\,..,..-...... Lo$$ of. all
i" ,1
\
,,.. " , sensation
Deficiency in intake (or metabolism) of vitamin B12 (cyanoco-

l •,
balamin) may result in degeneration in the dorsal and lateral
I;•
•' ...
·'
1' •,\
\ •,
'1
I
white colwnns. There is a loss of position sense, two-point
4 .. ,. discrimination, and vibratory sensation. Ataxic gait, muscle
4.,:l weakness, hyperactive deep muscle reflexes, spasticity of the
extremities, and a positive Babinski sign are seen.
Impaired pain- i "
and I - + - - Impaired
proprioception,
vibration, 2-polnt Spinal Shock
sensation \
discrimination,
and Joint and This syndrome results from acute transection of, o.r severe in-
position sensation jury to, the spinal cord from sudden loss of stimulation from

G.u
\ high.er levels or from an overdose of spinal anesthetic. All
body segments below the level of the injury become pa.ralyzed
and have no sensation; all reflexes below the lesion, includ-
ing autonomic reftexes, are suppressed. Spinal shock is usually
FIGURE 5-25 syndrome with lesion at left transient; it may disappear in 3 to 6 weeks and is followed by a
tenth thoracic level (motor deficits not shown}. period of increased reflex response.