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1
Introduction
The corticospinal tract controls primary motor activity for the somatic
motor system from the neck to the feet. It is the major spinal pathway
involved in voluntary movements. The tract begins in the primary motor
cortex, where the soma of pyramidal neurons are located within cortical
layer V. Axons for these neurons travel in bundles through the internal
capsule, cerebral peduncles, and ventral pons. They stay in the ventral
position within the medulla as the pyramids. A majority of the axons
cross the midline at the pyramidal decussation between the brainstem and
spinal cord to form the lateral corticospinal tract (Figure 1A). This
crossover causes the left side of the brain to control the right side of the
spinal cord and the right side of the brain to control the left side of the
spinal cord. A small number of axons remain on the ipsilateral side to
form the anterior corticospinal tract. Axons of both anterior and lateral
corticospinal tracts move into the gray matter of the ventral horn to
synapse onto lower motor neurons. These lower motor neurons exit the
spinal cord to contract muscle.[1] While the anterior corticospinal tract
assists with axial muscle motor control, the lateral corticospinal tract is
the primary pathway for motor information to the body. Injuries to the
lateral corticospinal tract results in ipsilateral paralysis (inability to
move), paresis (decreased motor strength), and hypertonia (increased
tone) for muscles innervated caudal to the level of injury.[2] The lateral
corticospinal tract can suffer damage in a variety of ways. The most
common types of injury are central cord syndrome, Brown-Sequard
syndrome, and anterior spinal cord syndrome.
Etiology
There are numerous causes for spinal cord injuries: trauma, ischemic
events, and disease are the most common methods of damage. Central
cord syndrome (Figure 1B) affects the central portion of the spinal cord.
It results from hyperextension of the cord, typically within the cervical
region. This type of injury is common in shaken baby syndrome. Another
cause can be motor vehicle accidents where the head hyper-extends due
to contact with the vehicle or air-bag or high impact contact sports such
as football.[3]
Anterior spinal cord syndrome is the result of damage or obstruction of
the anterior spinal artery (Figure 1C). The spinal cord has one anterior
spinal artery and two posterior spinal arteries. The anterior spinal artery
supplies the anterior 2/3 of the spinal cord.[4] Thrombosis or an
embolism can lead to damage. One of the more common sites of anterior
spinal injury is at the artery of Adamkiewcz. This radicular artery
branches from the aorta at the level of the 9 to 12 intercostal spaces in
most individuals. In a small percentage of people, it originates between
L1-L2 or T5-T8.[5] The artery of Adamkiewcz terminates at an acute
angle that makes it more prone to damage. Because the artery of
Adamkiewcz is prone to damage from surgical procedures that involve
the retroperitoneal space, identification and preservation of the artery is
important for numerous surgical procedures (e.g., thoracoabdominal
aortic aneurysm repair, thoracic or lumbar spine surgery, removal of
intramedullary tumors, and retroperitoneal procedures).[6] Other forms
of damage that cause anterior spinal cord syndrome include
atherosclerotic disease, spinal muscular atrophy, multiple sclerosis, or
infections (e.g., West Nile virus, poliomyelitis).[7]
Brown-Sequard syndrome is a condition in which the left or right half of
the spinal cord is damaged (Figure 1D). Its typical cause is traumatic
injuries such as gunshot and stabbing wounds, motor vehicle accidents,
or fractured vertebra due to falls.[7] Other causes for this disorder
include vertebral disc herniation, cervical spondylosis, tumors, multiple
sclerosis, decompression sickness, cystic disease, as well as infections
(e.g., meningitis, tuberculosis, transverse myelitis, and herpes zoster).[8]
Epidemiology
Central cord syndrome (Figure 1B) has a bimodal distribution (young
and old age groups), mostly affecting males, and accounts for 9.0% of
adult spinal cord injuries and 6.6% of pediatric spinal cord injuries.
[3] Central cord syndrome is prevalent among patients with cervical
stenosis and the elderly with spinal diseases. However, it is more
common in younger patients with cervical spine fractures, disk
herniation, or shaken baby syndrome.[9]
Anterior spinal cord syndrome is most common in adults as a result of
postoperative complications.[10] It is most prevalent after either
retroperitoneal surgeries or spinal surgeries.
Brown-Sequard syndrome is rare, estimated to account for 2 to 4% of
spinal cord injuries.[2] Eleven thousand new cases are reported yearly
within the United States.[8] Some form of penetrating trauma is the most
common cause.
Pathophysiology
Patients with central cord syndrome have compression of the dorsal
column tracts, lateral corticospinal tracts, and spinothalamic tracts. The
compression of the dorsal column tracts causes bilateral sensory
impairments below the level of injury. Sensory impairment is typically
experienced in a “cape-like’ distribution across the upper back and down
the posterior side of the upper limbs.[11] Damage to the lateral
corticospinal tracts causes bilateral weakness of the upper body, but
patients retain strength in the lower limbs.[3] Compression of the
spinothalamic tracts results in the bilateral loss of pain/temperature for
the upper body more than the lower body. Deficits affecting upper body
functions more than the lower body result from compression of the
central aspect of the cord. Both corticospinal and spinothalamic tracts
have homunculi in which the upper body is located centrally while the
lower body is located more peripherally within the spinal cord.[11]
Patients with anterior spinal cord syndrome have bilateral deficits to the
corticospinal tracts and spinothalamic tracts. They experience bilateral
paralysis and paresis below the site of the lesion.[10] They also
experience bilateral pain/temperature and light touch deficits due to the
injury of the spinothalamic tract.[12] Sacral sparing of the spinothalamic
tract occurs due to a dual blood supply by the posterior spinal arteries.
The posterior spinal arteries wrap around the peripheral aspect of the
cord. This secondary supply enables the full functionality of the
peripheral spinothalamic tract, which transmits pain, temperature, and
light touch for the feet.
Patients with Brown-Sequard syndrome have a unilateral deficit of the
lateral cord.[8] Deficits associated with this syndrome include ipsilateral
paralysis, paresis, and hypertonia; ipsilateral proprioception loss; and
contralateral loss of pain and temperature sensation.[2][8]
In any of these syndromes, the locus of the injury can cause additional
symptoms. If the injury is at or above T1-L2, a compression will disrupt
sympathetic neurons within the intermediolateral nucleus in the lateral
horn of the spinal cord and cause an ipsilateral Horner syndrome.
Similarly, injuries within the lower lumbar region can cause autonomic
dysfunction that induces bladder, bowel, or sexual dysfunction.[8][10]
Evaluation
Examination of spinal cord injury caused by trauma should include
radiographs to reveal fractures and dislocations of the spine. In addition,
computed tomography (CT) or magnetic resonance imaging (MRI) can
be performed to identify impingement in these cases.[10]
[11] Impingement in Brown-Sequard syndrome will appear as an “owl’s
eye” configuration in the anterior horns.[4] If the anterior spinal
syndrome is suspected, a spinal cord angiogram may also be a
consideration.[10]
If there is no observable evidence of trauma in the physical exam, a
purified protein derivative and sputum for acid-fast bacilli along with a
chest X-ray should be performed to ensure that an infectious etiology is
not the cause of the symptoms.[8]
Treatment / Management
Treatment of corticospinal lesions involves steroid (methylprednisolone
or corticosteroids) administration within the first 8 hours to reduce
swelling and pressure on the cord.[11] However, steroids are not
recommended for Brown-Sequard syndrome patients because they may
make the patient more prone to subsequent infections.[8] If the injury is
in the high thoracic or cervical regions, respiratory support may be
required, with recommendations for respiratory therapy treatment.[8]
Decompression surgery can be a consideration for patients with a
traumatic injury or with a tumor or abscess that causes cord compression.
[8][11] After stabilizing the spine, physical rehabilitation is needed to
preserve motor activity, muscle strength and to maintain coordination.
[10] Wheelchairs, limb supports, and splints can assist the patient with
ambulation.[8] Occupational therapy may also be needed to improve and
maintain the activity of the upper limbs, specifically in performing daily
actions.[10]
Differential Diagnosis
The differential diagnosis for spinal cord syndromes:[8][11]
Bilateral brachial plexus injuries
Cysts
Dislocations
Epidural abscesses or hematomas
Fractures
Infection
Other spine pathologies and traumas
Strokes
The trauma of peripheral nerve roots leading to avulsion in a
bilateral distribution
Tumors
Vascular injuries
Prognosis
Most patients with central cord syndrome have some recovery of
function. Patients who receive treatment soon after the injury have better
outcomes. A typical patient will recover in stages. Improvement usually
originates in the legs, followed by bladder/bowel, and finally, the arms
and hands. Patients with central cord syndrome have a good prognosis
but, some factors can put the patient at risk for a lower likelihood of
recovery (e.g., advanced age and severity of injury).[3]
The prognosis of patients with Brown-Sequard syndrome depends on the
cause and severity of the spinal cord injury. More than half of patients
recover and regain motor function.[8] Motor recovery is faster on the
contralateral side versus the ipsilateral side.[8] In 90% of cases where
bowel and bladder function were affected, patients regain these
functions.[8] Recovery typically occurs within 3 to 6 months to two
years.[8]
Of the spinal cord syndromes, anterior spinal cord syndrome cases have
the worst prognosis. Only 39% of patients recover motor function.
[2] Fifty percent of individuals diagnosed with this disorder show no
improvement of symptoms over time.[14]
Complications
Complications associated with spinal cord injuries include autonomic
dysregulation, neurogenic bladder, and chronic pain.[11] If left
untreated, additional symptoms such as hypotension, spinal shock,
pulmonary embolism, and infections of the lung or urinary tract can
occur.[8]
Review Questions
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References
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development, and human disorders. Dev Neurobiol. 2017
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2.
Diaz E, Morales H. Spinal Cord Anatomy and Clinical
Syndromes. Semin Ultrasound CT MR. 2016 Oct;37(5):360-
71. [PubMed: 27616310]
3.
Brooks NP. Central Cord Syndrome. Neurosurg Clin N Am. 2017
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4.
Harada K, Chiko Y, Toyokawa T. Anterior spinal cord
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Milen MT, Bloom DA, Culligan J, Murasko K. Albert
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Klakeel M, Thompson J, Srinivasan R, McDonald F. Anterior
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[PubMed: 25552812]
11.
Ameer MA, Tessler J, Gillis CC. StatPearls [Internet]. StatPearls
Publishing; Treasure Island (FL): Aug 13, 2021. Central Cord
Syndrome. [PubMed: 28722961]
12.
Imbert B, Brion JP, Janbon B, Gonzales M, Micoud M. [Erythema
nodosum associated with parvovirus B19 infection]. Presse
Med. 1989 Oct 28;18(35):1753-4. [PubMed: 2555812]
13.
Davenport D, Colaco HB, Kavarthapu V. Examination of the adult
spine. Br J Hosp Med (Lond). 2015 Dec;76(12):C182-5. [PubMed:
26646344]
14.
Schneider GS. Anterior spinal cord syndrome after initiation of
treatment with atenolol. J Emerg Med. 2010 Jun;38(5):e49-
52. [PubMed: 18597977]
Figures
Corticospinal tract lesion locations (A) Normal spinal cord cross section.
(B) Area affected by central cord syndrome (C) Area affected by anterior
cord syndrome (D) area affected by Brown-Sequard syndrome.
Contributed by Diana Peterson, Ph.D.
Comparison of spinal cord lesions and syndromes with corresponding
sensory/motor deficits. Contributed by Rian Kabir, MD
Copyright © 2021, StatPearls Publishing LLC.
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