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Central cord syndrome (CCS)

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 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.


In the setting of severe spinal cord injuries, such as central cord syndrome, T2 hyperintensity in MRI correlates with acute intramedullary hemorrhage 4).

The signal abnormality is often diffuse, spans several levels, and correlates with severe deficits.


The optimal timing of surgery remains controversial.

Nine studies (3 prognostic, 5 therapeutic, 1 both) satisfied inclusion criteria. Low level evidence suggests that patients operated on <24 hours after injury exhibit significantly greater improvements in postoperative American Spinal Injury Association motor scores and the functional independence measure at 1 year than those operated on >24 hours after injury. Moderate evidence suggests that patients operated on <2 weeks after injury have a higher postoperative Japanese Orthopaedic Association score and recovery rate than those operated on >2 weeks after injury. There is insufficient evidence that lengths of hospital or intensive care unit stay differ between patients who undergo early versus delayed surgery. Furthermore, there is insufficient evidence that timing between injury and surgery predicts mortality rates or serious or minor adverse events.

Surgery for TCCS <24 hours after injury appears safe and effective. Although there is insufficient evidence to provide a clear recommendation for early surgery (<24 hours), it is preferable to operate during the first hospital admission and <2 weeks after injury 5)


In many cases, individuals with CCS can experience a reduction in their neurological symptoms with conservative management. The first steps of these intervention strategies include admission to an intensive care unit (ICU) after initial injury. After entering the ICU, early immobilization of the cervical spine with a neck collar would be placed on the patient to limit the potential of further injury.

Cervical spine restriction is maintained for approximately six weeks until the individual experiences a reduction in pain and neurological symptoms.

Inpatient rehabilitation is initiated in the hospital setting, followed by outpatient physical therapy and occupational therapy to assist with .

An individual with a spinal cord injury may have many goals for outpatient occupational and physiotherapy. Their level of independence, self-care, and mobility are dependent on their degree of neurological impairment. Rehabilitation organization and outcomes are also based on these impairments.

The physiatrist, along with the rehabilitation team, work with the patient to develop specific, measurable, action-oriented, realistic, and time-centered goals.

With respect to physical therapy interventions, it has been determined that repetitive task-specific sensory input can improve motor output in patients with central cord syndrome. These activities enable the spinal cord to incorporate both supraspinal and afferent sensory information to help recover motor output.

This occurrence is known as “activity dependent plasticity”. Activity dependant plasticity is stimulated through such activities as: locomotor training, muscle strengthening, voluntary cycling, and functional electrical stimulation (FES) cycling.

Vasopressor usage

Vasopressor usage is associated with complication rates that are similar to the reported literature for spinal cord injury (SCI). Dopamine was associated with a higher risk of complications in patients > 55 years. Given the increased incidence of central cord syndrome in older populations, determination of mean arterial pressure (MAP) goals and vasopressor administration should be carefully considered in these patients. While a randomized control trial on this topic may not be practical, a multiinstitutional prospective study for SCI that includes (CCS) patients as a subpopulation would be useful for examining MAP goals in this population 6).


Recent studies have shown benefits, particularly of early surgery to decompress the spinal cord in patients with pathologic conditions revealed by radiography or MRI 7).

Surgical intervention is usually given to those individuals who have increased instability of their cervical spine, which cannot be resolved by conservative management alone. Further indications for surgery include a neurological decline in spinal cord function in stable patients as well as those who require cervical spinal decompression.


In a sample of 16,134 patients, a total of 39.7% of patients (6,351) underwent surgery. ACDF was most common (19.4%), followed by PCDF (7.4%) and PCD (6.8%). From 2003-10, surgical management increased by an average of 40% each year. The overall inpatient mortality rate was 2.6% Increasing age and comorbidities were associated with higher rates of patient mortality and a decreasing surgical rate (p < 0.01). Hospitals greater than 249 beds (p < 0.01) and the south (p < 0.01) were associated with a higher surgical rate. Rural hospitals (p < 0.01) and persons in the second income quartile (p < 0.01) were associated with higher inpatient mortality 8).


The ASIA motor score and cervical spine canal diameter proved to be useful predictors of outcome. In the patient group of the Division of Neurosurgery, Groote Schuur Hospital, Cape Town,South Africa, timing of surgery did not appear to influence the outcome 9).

Case series

In a retrospective cohort analysis of 34 patients who received any vasopressor to maintain blood pressure above predetermined mean arterial pressure (MAP) goals at a single Level 1 trauma center. The collected variables were American Spinal Injury Association (ASIA) grades at admission and discharge, administered vasopressor and associated complications, other interventions and complications, and timing of surgery. The relationship between the 2 most common vasopressors-dopamine and phenylephrine-and complications within the cohort as a whole were explored, and again after stratification by age.

The mean age of the ATCCS patients was 62 years. Dopamine was the most commonly used primary vasopressor (91% of patients), followed by phenylephrine (65%). Vasopressors were administered to maintain MAP goals fora mean of 101 hours. Neurological status improved by a median of 1 ASIA grade in all patients, regardless of the choice of vasopressor. Sixty-four percent of surgical patients underwent decompression within 24 hours. There was no observed relationship between the timing of surgical intervention and the complication rate. Cardiogenic complications associated with vasopressor usage were notable in 68% of patients who received dopamine and 46% of patients who received phenylephrine. These differences were not statistically significant (OR with dopamine 2.50 [95% CI 0.82-7.78], p = 0.105). However, in the subgroup of patients > 55 years, dopamine produced statistically significant increases in the complication rates when compared with phenylephrine (83% vs 50% for dopamine and phenylephrine, respectively; OR with dopamine 5.0 [95% CI 0.99-25.34], p = 0.044).

Vasopressor usage in ATCCS patients is associated with complication rates that are similar to the reported literature for spinal cord injury (SCI). Dopamine was associated with a higher risk of complications in patients > 55 years. Given the increased incidence of ATCCS in older populations, determination of MAP goals and vasopressor administration should be carefully considered in these patients. While a randomized control trial on this topic may not be practical, a multiinstitutional prospective study for SCI that includes ATCCS patients as a subpopulation would be useful for examining MAP goals in this population 10).

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central_cord_syndrome.txt · Last modified: 2016/05/05 19:10 (external edit)