APPLIED ANATOMY OF

SPINAL CORD
Lesions of the Anterior and Posterior
Nerve Roots
• Either or both spinal nerve roots may be involved in syphilitic spinal
meningitis or pyogenic meningitis
• The posterior roots may be involved in tabes dorsalis and herpes
zoster.
• A herniated intervertebral disc, a primary or secondary vertebral
tumor, vertebral destruction by tumor or infection, or a fracture
dislocation can press on the spinal nerve roots in the intervertebral
foramina.
• A lesion of one posterior spinal nerve root will produce pain in the
area of skin innervated by that root and in the muscles that receive
their sensory nerve supply from that root.
• Movements of the vertebral column in the region of the lesion will
heighten the pain, and coughing and sneezing will also make it worse
by raising the pressure within the vertebral canal.
• A lesion of an anterior root will result in paralysis of any muscle that is
supplied exclusively by that root and a partial paralysis of any muscle
that is supplied partially by that root. In both cases, fasciculation and
muscle atrophy occur.
Injury to the Ascending Tracts Within the
Spinal Cord
• Lateral Spinothalamic Tract
• Destruction of this tract produces contralateral loss of pain and thermal
sensibilities below the level of the lesion. The patient will not, therefore, respond
to pinprick or recognize hot and cold objects placed in contact with the skin.
• Anterior Spinothalamic Tract
• Destruction of this tract produces contralateral loss of light touch and pressure
sensibilities below the level of the lesion. Remember that discriminative touch
will still be present, because this information is conducted through the fasciculus
gracilis and fasciculus cuneatus. The patient will not feel the light touch of a piece
of cotton placed against the skin or feel pressure from a blunt object placed
against the skin.
• Fasciculus Gracilis and Fasciculus Cuneatus
• Destruction of these tracts cuts off the supply of information from the
muscles and joints to consciousness; thus, the individual does not
know about the position and movements of the ipsilateral limbs
below the level of the lesion.
• The patient also has loss of vibration sense below the level of the
lesion on the same side.
• There will also be a loss of tactile discrimination on the side of the
lesion.
Upper Motor Neuron Lesions
• Lesions of the Corticospinal Tracts (Pyramidal Tracts)
• The Babinski sign is present. Normally, the corticospinal tracts produce
plantar flexion of the toes in response to sensory stimulation of the skin of
the sole. When the corticospinal tracts are nonfunctional, the influence of
the other descending tracts on the toes becomes apparent, and a kind of
withdrawal reflex takes place in response to stimulation of the sole, with
the great toe being dorsally flexed and the other toes fanning out.
• superficial abdominal reflexes are absent. The abdominal muscles fail to
contract when the skin of the abdomen is scratched. This reflex is
dependent on the integrity of the corticospinal tracts, which exert a tonic
excitatory influence on the internuncial neurons.
• The cremasteric reflex is absent. The cremaster muscle fails to
contract when the skin on the medial side of the thigh is stroked. This
reflex arc passes through the first lumbar segment of the spinal cord.
This reflex is dependent on the integrity of the corticospinal tracts,
which exert a tonic excitatory influence on the internuncial neurons.
• There is loss of performance of fine-skilled voluntary movements.
This occurs especially at the distal end of the limbs.
• Lesions of the Descending Tracts Other Than the Corticospinal Tracts
(Extrapyramidal Tracts)
• Severe paralysis with little or no muscle atrophy (except secondary to
disuse).
• Spasticity or hypertonicity of the muscles. The lower limb is
maintained in extension, and the upper limb is maintained in flexion.
• Exaggerated deep muscle reflexes and clonus may be present in the
flexors of the fingers, the quadriceps femoris, and the calf muscles.
 Lower Motor Neuron Lesions
• Flaccid paralysis of muscles supplied.
• Atrophy of muscles supplied.
• Loss of reflexes of muscles supplied.
• Muscular fasciculation. This is twitching of muscles seen only when there is slow destruction
of the lower motor neuron cell.
• Muscular contracture. This is a shortening of the paralyzed muscles. It occurs more often in
the antagonist muscles whose action is no longer opposed by the paralyzed muscles.
• Reaction of degeneration. Normally innervated muscles respond to stimulation by the
application of faradic (interrupted) current, and the contraction continues as long as the
current is passing. Galvanic or direct current causes contraction only when the current is
turned on or turned off. When the lower motor neuron is cut, a muscle will no longer
respond to interrupted electrical stimulation 7 days after nerve section, although it still will
respond to direct current. After 10 days, the response to direct current also ceases. This
change in muscle response to electrical stimulation is known as the reaction of degeneration.
Spinal Cord Injuries
1. Acute Spinal Cord Injuries
2. Chronic Compression of the Spinal Cord
• The causes of compression may be divided into extradural and intradural.
• The intradural causes may be divided into those that arise outside the spinal
cord (extramedullary) and those that arise within the cord (intramedullary).
• The extradural causes include herniation of an intervertebral disc, infection of
the vertebrae with tuberculosis, and primary and secondary tumors of the
vertebra; leukemic deposits and extradural abscesses may also compress the
spinal cord.
• The two common extramedullary tumors are meningiomas and nerve
fibromas. Intramedullary causes include primary tumors of the spinal cord,
such as gliomas.
• One of the earliest signs is pain. This may be local pain in the vertebra involved or pain
radiating along the distribution of one or more spinal nerve roots. The pain is made worse
by coughing or sneezing and is usually worse at night, when the patient is recumbent.
• Interference with motor function occurs early.
• Involvement of the anterior gray column motor cells at the level of the lesion results in
partial or complete paralysis of muscles, with loss of tone and muscle wasting.
• The early involvement of the corticospinal and other descending tracts produces
muscular weakness, increased muscle tone (spasticity), increased tendon reflexes below
the level of the lesion, and an extensor plantar response.
• The degree of sensory loss will depend on the nerve tracts involved. A lesion of the
posterior white columns of the spinal cord will cause loss of muscle joint sense
(proprioception), vibration sense, and tactile discrimination below the level of the lesion
on the same side.
• Involvement of the lateral spinal thalamic tracts will cause loss of pain and heat and cold
sensations on the opposite side of the body below the level of the lesion.
Spinal Cord Syndromes
Complete Cord Transection Syndrome
• complete loss of all sensibility and voluntary movement below the
level of the lesion.
• can be caused by fracture dislocation of the vertebral column
1. Bilateral lower motor neuron paralysis and muscular atrophy in the
segment of the lesion. This results from damage to the neurons in the
anterior gray columns (i.e., lower motor neuron) and possibly from
damage to the nerve roots of the same segment.
2. Bilateral spastic paralysis below the level of the lesion. A bilateral
Babinski sign is present, and depending on the level of the segment of the
spinal cord damaged, bilateral loss of the superficial abdominal and
cremaster reflexes occurs. All these signs are caused by an interruption of
the corticospinal tracts on both sides of the cord.
3. Bilateral loss of all sensations below the level of the lesion. The loss of
tactile discrimination and vibratory and proprioceptive sensations is due
to bilateral destruction of the ascending tracts in the posterior white
columns. The loss of pain, temperature, and light touch sensations is
caused by section of the lateral and anterior spinothalamic tracts on both
sides. Because these tracts cross obliquely, the loss of thermal and light
touch sensations occurs two or three segments below the lesion distally.
4. Bladder and bowel functions are no longer under voluntary control,
since all the descending autonomic fibers have been destroyed.
• If there is a complete fracture dislocation at the L2-3 vertebral level
(i.e., a level below the lower end of the cord in the adult), no cord
injury occurs and neural damage is confined to the cauda equina, and
lower motor neuron, autonomic, and sensory fibers are involved.
 Anterior Cord Syndrome
• Anterior cord syndrome can be caused by cord contusion during vertebral fracture or
dislocation, from injury to the anterior spinal artery or its feeder arteries with resultant
ischemia of the cord, or by a herniated intervertebral disc.
1. Bilateral lower motor neuron paralysis in the segment of the lesion and muscular
atrophy. This is caused by damage to the neurons in the anterior gray columns (i.e., lower
motor neuron) and possibly by damage to the anterior nerve roots of the same segment.
2. Bilateral spastic paralysis below the level of the lesion, the extent of which depends on
the size of the injured area of the cord. The bilateral paralysis is caused by the interruption
of the anterior corticospinal tracts on both sides of the cord. The bilateral muscular
spasticity is produced by the interruption of tracts other than the corticospinal tracts.
3. Bilateral loss of pain, temperature, and light touch sensations below the level of the
lesion. These signs are caused by interruption of the anterior and lateral spinothalamic
tracts on both sides.
4. Tactile discrimination and vibratory and proprioceptive sensations are preserved
because the posterior white columns on both sides are undamaged.
 Central Cord Syndrome
• Central cord syndrome is most often caused by hyperextension of the cervical region of the
spine (Fig. 4-31). The cord is pressed on anteriorly by the vertebral bodies and posteriorly by
the bulging of the ligamentum flavum, causing damage to the central region of the spinal
cord.
1. Bilateral lower motor neuron paralysis in the segment of the lesion and muscular atrophy.
This is caused by damage to the neurons in the anterior gray columns (i.e., lower motor
neuron) and possibly by damage to the nerve roots of the same segment.
2. Bilateral spastic paralysis below the level of the lesion with characteristic sacral sparing.
The lower limb fibers are affected less than the upper limb fibers because the descending
fibers in the lateral corticospinal tracts are laminated, with the upper limb fibers located
medially and the lower limb fibers located laterally
3. Bilateral loss of pain, temperature, light touch, and pressure sensations below the level of
the lesion with characteristic sacral sparing. Because the ascending fibers in the lateral and
anterior spinothalamic tracts are also laminated, with the upper limb fibers located medially
and the lower limb fibers located laterally, the upper limb fibers are more susceptible to
damage than the lower limb fibers.
Brown-Secquard Syndrome or Hemi
section of the Cord
• Hemisection of the spinal cord can be caused by fracture dislocation of the
vertebral column, by a bullet or stab wound, or by an expanding
tumor.Incomplete hemisection is common; complete hemisection is rare.
1. Ipsilateral lower motor neuron paralysis in the segment of the lesion and
muscular atrophy. These signs are caused by damage to the neurons on the
anterior gray column and possibly by damage to the nerve roots of the same
segment.
2. Ipsilateral spastic paralysis below the level of the lesion. An ipsilateral Babinski
sign is present, and depending on the segment of the cord damaged, an
ipsilateral loss of the superficial abdominal reflexes and cremasteric reflex
occurs. All these signs are due to loss of the corticospinal tracts on the side of
the lesion. Spastic paralysis is produced by interruption of the descending
tracts other than the corticospinal tracts.
3. Ipsilateral band of cutaneous anesthesia in the segment of the lesion. This results
from the destruction of the posterior root and its entrance into the spinal cord at the
level of the lesion.
4. Ipsilateral loss of tactile discrimination and of vibratory and proprioceptive
sensations below the level of the lesion. These signs are caused by destruction of the
ascending tracts in the posterior white column on the same side of the lesion.
5. Contralateral loss of pain and temperature sensations below the level of the
lesion. This is due to destruction of the crossed lateral spinothalamic tracts on the
same side of the lesion. Because the tracts cross obliquely, the sensory loss occurs
two or three segments below the lesion distally.
6. Contralateral but not complete loss of tactile sensation below the level of the
lesion. This condition is brought about by destruction of the crossed anterior
spinothalamic tracts on the side of the lesion.
The contralateral loss of tactile sense is incomplete because discriminative touch
traveling in the ascending tracts in the contralateral posterior white column remains
intact.
Syringomyelia
• Syringomyelia, which is due to a developmental abnormality in the formation of
the central canal, most often affects the brainstem and cervical region of the
spinal cord. At the site of the lesion, there is cavitation and gliosis in the central
region of the neuroaxis.
1. Loss of pain and temperature sensations in dermatomes on both sides of the
body related to the affected segments of the cord. This loss commonly has a
shawl like distribution caused by the interruption of the lateral spinothalamic
tracts as they cross the midline in the anterior gray and white commissures.
The patient commonly complains of accidental burning injuries to the fingers.
2. Tactile discrimination, vibratory sense, and proprioceptive sense are normal.
The reason is that the ascending tracts in the posterior white column are
unaffected.
3. Lower motor neuron weakness is present in the small muscles of the hand. It may
be bilateral, or one hand may suffer before the other. As the lesion expands in the
lower cervical and upper thoracic region, it destroys the anterior horn cells of these
segments. Later, the other muscles of the arm and shoulder girdles undergo atrophy.
4. Bilateral spastic paralysis of both legs may occur, with exaggerated deep tendon
reflexes and the presence of a positive Babinski response. These signs are produced
by the further expansion of the lesion laterally into the white column to involve the
descending tracts.
5. Horner syndrome may be present. This is caused by the interruption of the
descending autonomic fibers in the reticulospinal tracts in the lateral white column
by the expanding lesion.
Poliomyelitis
• Poliomyelitis is an acute viral infection of the neurons of the anterior gray
columns of the spinal cord and the motor nuclei of the cranial nerves.
• Following death of the motor nerve cells, there is paralysis and wasting of
the muscles. The muscles of the lower limb are more often affected than
the muscles of the upper limb.
• In severe poliomyelitis, respiration may be threatened due to the paralysis
spreading to the intercostal muscles and diaphragm.
• The muscles of the face, pharynx, larynx, and tongue may also be
paralyzed.
Multiple Sclerosis
• Multiple sclerosis is a common disease confined to the central nervous
system, causing demyelination of the ascending and descending tracts.
• It is a disease of young adults, and the cause is unknown.
• Autoimmunity, infection, and heredity, alone or in combination, may play a
role in its etiology.
• It has been suggested that a breach in the integrity of the blood-brain barrier
in an individual who is genetically predisposed to the disease may be
responsible.
• This could result in the invasion of the brain and spinal cord by some infection
allowing leukocytes to enter the normally immunologically protected central
nervous system.
• The inflammation and demyelination with loss of the myelin sheath results in the
breakdown of the insulation around the axons, and the velocity of the action
potentials is reduced and ultimately becomes blocked.
• The course of multiple sclerosis is chronic with exacerbations and remissions.
Because of the widespread involvement of different tracts at different levels of the
neuroaxis, the signs and symptoms are multiple, but remissions do occur.
Weakness of the limbs is the most common sign of the disease. Ataxia due to
involvement of the tracts of the cerebellum may occur, but spastic paralysis may
also be present
• In patients who have the progressive form of the disease without remissions, it is
has been shown that they have a substantial damage to the axons as well as the
myelin. This would suggest that multiple sclerosis is not just a demyelinating
disease but one in which there is axonal pathology.
Amyotrophic Lateral Sclerosis
• Amyotrophic lateral sclerosis (Lou Gehrig disease) is a disease confined to
the corticospinal tracts and the motor neurons of the anterior gray
columns of the spinal cord.
• It is rarely familial and inherited in about 10% of patients.
• Typically, it occurs in late middle age and is inevitably fatal in 2 to 6 years.
• The lower motor neuron signs of progressive muscular atrophy, paresis,
and fasciculations are superimposed on the signs and symptoms of upper
motor neuron disease with paresis, spasticity, and Babinski response.
• The motor nuclei of some cranial nerves may also be involved
Pernicious Anemia
• Pernicious anemia, a form of megaloblastic anemia, is caused by
vitamin B12 deficiency.
• The disease may produce extensive damage to the tracts in the
posterior and lateral white columns of the spinal cord as well as
peripheral nerve degeneration.
• Widespread sensory and motor losses may be present due to
involvement of the ascending and descending tracts of the spinal
cord.
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