The corticospinal tract controls primary motor activity for the somatic motor system from the neck to the feet.[1] 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.[1] 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.

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 in 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]

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.[3][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.

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 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]