Traumatic central cord syndrome (TCCS) is an incomplete spinal cord injury defined by greater weakness in upper versus lower extremities, variable sensory loss, and variable bladder dysfunction, bowel, and sexual dysfunction.
Acute cervical spinal cord injury (SCI), was initially described by Schneider and colleagues in 1954 1). It is marked by a disproportionately greater impairment of motor function in the upper extremities than in the lower ones, as well as by bladder dysfunction and a variable amount of sensory loss below the level of injury 2).
Although CCS has been reported to occur with particular frequency among older persons with cervical spondylosis who sustain hyperextension injury, it can be found in persons of any age and can be associated with various etiologies, injury mechanisms, and predisposing factors.
It is the most common incomplete spinal cord injury.
United States The prevalence rate of central cord syndrome is 15.7-25%.
Mortality/Morbidity Central cord syndrome is generally associated with a favorable prognosis for the achievement of some degree of neurologic and functional recovery.
Sex Similar to all other SCIs, central cord syndrome predominantly affects males.
Age Central cord syndrome (CCS) has a bimodal distribution; in young persons, CCS tends to result from trauma, while in older individuals, it is typically caused by falls sustained by persons with preexisting spondylosis.
The most common cause of central cord syndrome (CCS) is trauma. In older adults, premorbid cervical spondylosis is a significant risk factor. Accordingly, even minor falls may result in tetraplegia in populations with a narrowed spinal canal. In younger age groups, CCS results from major trauma, such as that associated with cervical fracture/subluxations.
Central cord syndrome (CCS) most often occurs after a hyperextension injury in an individual with long-standing cervical spondylosis.
The most common mechanism of injury may be direct compression of the cervical spinal cord by buckling of the ligamenta flava into an already narrowed cervical spinal canal; this would explain the predominance of axonal injury in the white matter of the lateral columns 3).
Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. Autopsy studies subsequently demonstrated that CCS may be caused by bleeding into the central part of the cord, portending a less favorable prognosis. Studies have also shown that CCS probably is associated with axonal disruption in the lateral columns at the level of the injury to the spinal cord, with relative preservation of the grey matter.
The syndrome also may be associated with fracture dislocation injury and compression fracture, especially in a congenitally narrowed spinal canal.
These anteroposterior compressive forces also distribute the greatest damaging effect on the central mass of the cord substance.
CCS-related motor impairment results from the pattern of lamination of the corticospinal and spinothalamic tracts in the spinal cord. Sacral segments are the most lateral, with lumbar, thoracic, and cervical components arranged somatotopically, proceeding medially toward the central canal.
Symptoms of central cord syndrome occur following trauma (most commonly falls) and consist of upper and lower extremity weakness, with varying degrees of sensory loss. Pain and temperature sensations, as well as the sensation of light touch and of position sense, may be impaired below the level of injury. Neck pain and urinary retention are common.
Physical findings related to central cord syndrome are limited to the neurologic system and consist of upper motor neuron weakness in the upper and lower extremities. This impairment can be described as follows:
Impairment in the upper extremities is usually greater than in the lower extremities and is especially prevalent in the muscles of the hand. Sensory loss is variable, although sacral sensation is usually present. Anal wink, anal sphincter tone, and Babinski reflexes should be tested. Muscle stretch reflexes may initially be absent but will eventually return along with variable degrees of spasticity in affected muscles.
The signal abnormality is often diffuse, spans several levels, and correlates with severe deficits.
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