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It is characterized by a disproportionately greater loss of motor power in the upper extremities than in the lower extremities spasms colon symptoms cheap 50mg sumatriptan with mastercard, bladder dysfunction usually in the form of urinary retention muscle relaxant 500 mg cheap sumatriptan 50mg fast delivery, and a varying degree of sensory loss below the lesion knee spasms pain purchase sumatriptan line. Pathological reports of patients presenting with this condition who succumbed after the initial injury revealed that the spinal column and ligaments were intact and that the cord often had a central area of hemorrhage spasms perineum purchase sumatriptan on line. Taylor has shown that it is possible to have compression of the spinal cord without damage to the vertebral column. He performed cervical myelography on cadavers with their necks in different positions and demonstrated that in the forced extension position, there were a series of indentations on the posterior surface of the spinal column at the level of the interlaminar spaces. These indentations appeared to be caused by inward bulging of the ligamentum flavum, resulting in a narrowing of the spinal canal by as much as 30%. The narrowing was even more marked when osteophytic protrusion in the posterior vertebral bodies were present. It is thus believed that the major mechanism of injury involved in central cord syndrome consists of hyperextension of the cervical spine resulting in acute anteroposterior compression of the spinal cord. In his analysis of spinal cord segments of patients with central cord syndrome, Holmes found a significant amount of edema in the tissue located at the level of the injury. Schneider postulated that the syndrome is caused by hematomyelia and surrounding edema in the central cord and suggested that the discrepancies in arm and leg weakness is due to the lamination of fibers in the corticospinal tracts. He also postulated that the involvement of anterior horn cells in the cervical cord could account for the more pronounced weakness of the arms. As explained earlier, modern studies have failed to show a somatotopic organization of the corticospinal tracts in the spinal cord. An alternative explanation may be that the function of the corticospinal tract kat. Several studies examined the effect of discrete lesioning of the corticospinal tracts. There were relatively few motor deficits and the animals showed significant recovery with time. The most consistent and specific motor deficit was the production of substantial hand dysfunction, which was more prominent than arm and leg dysfunction. The motor recovery was similar to what is seen in humans with central cord syndrome. Three post-mortem specimens were available for histological study, ranging from 3 days to 7 weeks after the injury. Again, there was no evidence of blood or blood products within the parenchyma of the spinal cord. The primary finding was diffuse disruption of axons, especially within the lateral columns of the cervical cord in the region occupied by the corticospinal tract. Moreover, 10 out of the 11 patients showed evidence of a prior underlying bone or disc abnormality leading to narrowing of the cervical spinal canal. The syndrome of central cord syndrome is important to recognize because its prognosis is usually good compared with other syndromes. Motor power returns in the lower extremities first, bladder function recovers next, and finally movement in the upper extremities returns. Hand and finger motion are the very last to return, and may not recover completely, while sensory recovery occurs in a non-specific pattern. Because of the spontaneous recovery, treatment is usually conservative but cases have to be examined individually. If instability or persisting compression are present, early surgical management may be indicated in order to optimize recovery. Anterior Cord Syndrome-This syndrome, also described initially by Schneider, consists of paralysis and hypalgia below the level of the lesion with sparing of discriminative touch, proprioception and vibration sense. The cases he described had either ruptured cervical discs, fracture dislocations, or both causing anterior compression of the spinal cord. Initial theories on the mechanism of tissue damage in these injuries suggested that they resulted from anterior spinal artery compression and insufficiency. Kahn originally postulated a mechanism for chronic myelopathy from anterior cord compression secondary to calcified disc protrusion. He proposed that chronic traction on a cord fixed in place by the dentate ligaments was responsible for the clinical presentation of affected patients consisting in hyperreflexia, spasticity, gait disturbance, weakness more severe in the lower extremities and subjective sensory disturbances. He believed that the corticospinal tracts were more susceptible to this stress compared with the spinothalamic tracts because of their larger fibers.
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