Central Cord Syndrome 

Updated: May 07, 2018
Author: Michelle J Alpert, MD; Chief Editor: Stephen Kishner, MD, MHA 



Central cord syndrome (CCS), an acute cervical spinal cord injury (SCI), was initially described by Schneider and colleagues in 1954. 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 injury level.[1, 2, 3, 4, 5]

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.[2] CCS, the pathophysiology of which appears in the image below, is the most common incomplete SCI syndrome.

Illustration of the pathophysiology of central cor Illustration of the pathophysiology of central cord syndrome. Note the "pincer" effect on the central cord by anterior and posterior compression.


Central cord syndrome (CCS) most often occurs after a hyperextension injury in an individual with long-standing cervical spondylosis. (See also the Medscape Reference article Cervical Spondylosis.) Injury may result from posterior pinching of the cord by a buckled ligamentum flavum or from anterior compression of the cord by osteophytes.[6] 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.[7] 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.



United States

The prevalence rate of central cord syndrome is 15.7-25%.


In a retrospective French study, by Ronzi et al, of 63 patients hospitalized for traumatic SCI associated with cervical spinal canal stenosis (without spinal instability), 78.6% of subjects were found to have a clinical syndrome, with central cord syndrome being the second most common, after Brown-Séquard–plus syndrome.[8]


Central cord syndrome is generally associated with a favorable prognosis for the achievement of some degree of neurologic and functional recovery.[1, 9, 10, 11]


Similar to all other SCIs, central cord syndrome predominantly affects males.[11]


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.[9, 12]




See the list below:

  • 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.


See the list below:

  • 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.[13, 14]



Diagnostic Considerations

These include the following:

  • Cruciate paralysis of Bell

  • Bilateral brachial plexus injury or avulsion of cervical roots



Laboratory Studies

See the list below:

  • No specific laboratory blood tests are required to support the diagnosis of central cord syndrome.

Imaging Studies

Magnetic resonance imaging (MRI), computed tomography (CT) scanning, and the production of plain radiographs of the cervical spine can facilitate the diagnosis of central cord syndrome.[15] If vertebral fracture is seen with the central cord syndrome, then neurologic recovery can be different. With vertebral fracture, neurologic deficits are generally more severe, but more early recovery can be seen.[16]

Radiographic films of the cervical spine delineate fractures and dislocations, as well as the degree and extent of spondylotic changes. Flexion/extension views assist in the evaluation of ligamentous stability.

CT scanning of the cervical spine shows spinal canal compromise and allows the indirect approximation of the degree of spinal cord impingement.

MRI demonstrates direct evidence of spinal cord impingement from bone, a disc, or a hematoma.[17]  MRI T2-signal intensity can be helpful in evaluating patients for future neurologic deficits. If there is increased T2-signal intensity, then more severe initial neurologic deficits generally exist; however, the patient is less likely to experience neurologic deterioration. If there is no increased T2-signal intensity, then the initial injury is less severe but is more likely to undergo early neurologic deterioration.[18]



Rehabilitation Program

Physical Therapy

The focus of physical therapy in central cord syndrome (CCS) is the preservation of range of motion (ROM) and the enhancement of mobility skills.[19] The strengthening of any preserved lower extremity musculature is essential, as are trunk balance and stabilization. Safe transfer and wheelchair mobility are other goals to be accomplished prior to the initiation of gait training. Patients with CCS offer a unique challenge for the physical therapist with regard to ambulation and gait training.[20] Despite the usual preservation of some lower extremity strength, upper extremity deficits can limit the use of possible assistive devices and, ultimately, the functional quality of ambulation. For example, platform walkers are often used to compensate for deficient hand strength, although walking with this assistive device is frequently of limited functional value.

Occupational Therapy

Given the predominance of upper extremity weakness that occurs in central cord syndrome, the restoration of the basic activities of daily living (ADLs), upper extremity strength, and ROM are the main goals of occupational therapy. Splinting is often used to maintain the functional position of the hand and to prevent the formation of contractures in the fingers. Surface electromyelogram (EMG) biofeedback can often be beneficial to patients in the isolation of specific weak muscles in the upper extremities. Facilitating self-care skills by selecting appropriate assistive devices and training patients in their usage is another priority.

Speech Therapy

A speech therapist should be involved in the treatment of patients with central cord syndrome who have dysphagia from the head position maintained by cervical orthoses or as a result of anterior cervical spine fusion. Various compensatory strategies need to be taught to these patients to make swallowing safer and to prevent aspiration.

Recreational Therapy

The primary goal of recreational therapy is to help patients with central cord syndrome to return to preinjury areas of interest. Potential sources of recreational activities are explored with the patient, and the adaptive devices (for instance, an adapted fishing rod) that will allow the individual to enjoy previous activities are explored and provided.

Medical Issues/Complications

See the list below:

  • Autonomic dysreflexia

    • Autonomic dysreflexia (AD) is a disorder of autonomic homeostasis.

    • Sensory input from bladder distension or other noxious stimuli induce generalized sympathetic activity, resulting in vasoconstriction and hypertension.

    • Proper medical management of the skin, bowel, and bladder should prevent most occurrences. A thorough search should be made for the nociceptive source, and when found, it should be removed/treated immediately.

    • If mechanical means do not resolve the syndrome, medical management should be directed toward the reduction of blood pressure.

    • Nifedipine and transdermal nitroglycerin are often used.

  • Neurogenic bladder

    • Acutely injured patients often experience bladder retention that requires the placement of a Foley catheter for drainage.

    • Once fluid status has been stabilized, the indwelling catheter should be discontinued and bladder training, as well as intermittent catheterization, should begin.

    • Bladder function usually returns in the first 6 months.

    • Studies show that 52-84% of patients eventually have normal, spontaneous voids.

    • Patients who do not return to normal bladder function should be taught to do intermittent catheterization if manual dexterity permits.

  • Spasticity

    • Initially, reflexes are depressed, but once the period of spinal shock resolves, patients may experience increased spasticity in the upper and lower extremities.

    • Skillful nursing care can reduce the nociceptive and exteroceptive stimuli that exacerbate hypertonia.

    • Proper bed positioning and a regular stretching program are essential to spasticity reduction and contracture prevention.

    • Consider a trial of medication if spasms begin to cause discomfort, interfere with sleep, or cause functional impairment.

    • Lioresal (baclofen) is the initial drug of choice for spasticity.

  • Neuropathic pain

    • Patients with central cord syndrome occasionally experience allodynia below the level of injury.

    • The first line of treatment is evaluation and removal of possible exacerbating factors (eg, infections, new pressure ulcers).

    • After that, the possible introduction of anticonvulsant medications should be considered.

  • Pressure ulcers

    • Sensory loss, resulting in a patient's decreased awareness of continued pressure and shear forces on the skin, contributes to the formation of pressure ulcers.

    • Prevention involves decreasing the amount of pressure and the length of time that it is applied, as well as eliminating shear. Special mattresses and wheelchair cushions protect bony prominences.

    • Frequent changes in position (ie, turning while in bed, pressure relief when the patient is in a wheelchair) are paramount.

    • The initial treatment of a pressure ulcer is the elimination of pressure, followed by local dressing changes. If the wound progresses, plastic surgery consultation, if indicated, should be considered.

    • Physiatric management should also include patient and/or family education regarding skin care and surveillance.

  • Neurogenic bowel

    • Given the lack of bowel control that often results from SCI, patients should be started on a regular bowel program to avoid incontinence. In addition, the patient should have adequate fluid intake to avoid constipation/fecal impaction.

    • The use of evacuants and/or manual removal by way of digital stimulation or other methods should be instituted.

Surgical Intervention

Surgery is rarely indicated, because of the inherently favorable prognosis for patients with central cord syndrome. However, surgical intervention should be considered when progress becomes inconsistent after an initial period of improvement, when compression of the spinal cord persists, when gross spinal instability is present, and when neurologic deficits progress.[7, 21, 22, 23]

Using data from the US Nationwide Inpatient Sample, Yoshihara and Yoneoka found that in patients in the United States with traumatic central cord syndrome whose condition did not involve bone injury, the percentage of those treated surgically increased between 2000 (14.8%) and 2009 (30.5%). The investigators also determined that although the overall in-hospital complication rate was higher in the surgical patients (18.6%) than in those treated conservatively (14.5%), the pulmonary embolism rate (0.5% vs 1.2%, respectively) and in-hospital mortality rate (2% vs 2.7%, respectively) were lower.[24]

Another study, by Brodell et al, examining US trends in the treatment of CCS found that nearly 40% of the 16,134 patients in the report underwent surgery for the condition, with anterior cervical decompression and fusion being the most commonly performed procedure.[25]

Based on a literature search of material published between January 1966 and February 2013, Dahdaleh et al concluded that neither class I nor class II evidence exists regarding the efficacy of surgery for traumatic central cord syndrome. They state, however, that class III evidence suggests that surgery is superior to conservative treatment for this condition.[26]

A study by Jin et al of 17 patients with acute traumatic CCS who, following conservative therapy, experienced recurrent neurologic deterioration, found, on subsequent surgical treatment, obvious rupture of the anterior longitudinal ligaments (eight patients), posterior longitudinal ligaments (seven patients), and disks (three patients). These injuries caused cervical instability and secondary spinal cord compression. Moreover, 12 patients displayed serious adhesion between the posterior longitudinal ligaments and cervical disks, and five patients were found to have partial ossification of the posterior longitudinal ligaments. Good neurologic outcome was achieved in all patients via an anterior approach to cervical decompression, as well as internal fixation.[27]

A study by Kepler et al indicated that early surgical treatment of CCS (within 1 day or presentation) does not result in earlier neurologic improvement. The investigators evaluated results from early and delayed surgery and found that there was no significant difference in the American Spinal Injury Association motor score at 7 days between the two groups. Moreover, the percentage of patients who achieved early improvement did not significantly differ between the early and delayed groups, while time in the intensive care unit (ICU) and length of hospital stay also were not significantly different.[28]

A literature review by Park et al indicated that at follow-up of longer than 1 year, patients with CCS with underlying cervical stenosis who undergo early surgical decompression show similar improvement (in motor ability, functional independence, and walking ability) to those who undergo delayed surgery for the condition, but at follow-up of less than 1 year, patients who undergo early surgery show greater improvement than delayed-surgery patients. Complication rates did not differ between the two groups.[29]

A study by Samuel et al indicated that delaying surgery in acute traumatic CCS may be beneficial. The study, which included 1060 patients with the condition, found that the odds of mortality decreased by 19% with each 24-hour delay in time to surgery. Increased time to surgery may offer an advantage by allowing optimization of the patient’s general health and permitting some recovery of the spinal cord.[30]

On the other hand, guidelines published in 2016 by Wilson et al for the optimal timing of decompression surgery in CCS and traumatic SCI recommend “that early surgery be considered as a treatment option in adult patients with traumatic central cord syndrome.” A literature review by the investigators concluded that significantly greater neurologic and functional improvement is experienced by CCS patients who undergo early decompression (within 24 h) than by those who are decompressed after 24 hours.[31]


See the list below:

  • Neurologic surgeon

  • Orthopedic surgeon

  • Vocational rehabilitation specialist - These experts also should be consulted to facilitate a return to work or school.



Medication Summary

Despite initial enthusiasm for the use of methylprednisolone in the treatment of acute SCI, based on the results of the National Acute Spinal Cord Injury Study (NASCIS) II and III, further analysis of these studies’ results failed to adequately support the use of high-dose steroids to improve neurologic function.[32, 33]  In 2002, an expert panel from the American Association of Neurological Surgeons (AANS)/Congress of Neurological Surgeons (CNS) agreed that evidence supporting treatment standards and guidelines for methylprednisolone therapy in acute SCI was not sufficient. Even so, at that time the use of methylprednisolone for either 24 or 48 hours was a recommended option in cases of acute SCI. In 2013, however, the AANS/CNS came out with a level I recommendation against this treatment, since the US Food and Drug Administration (FDA) had not approved methylprednisolone for this application and because there was no class I or II evidence to support a clinical benefit. Furthermore, class I, II, and III evidence exists that high-dose steroids may be harmful to the patient.[34, 35, 36, 37] Needless to say, there remains an ongoing debate within the clinical community regarding the use of high-dose methylprednisolone in the treatment of acute SCI, but high-dose infusions within the first 8 hours postinjury are no longer the standard of care.



Further Outpatient Care

See the list below:

  • Carefully monitor neurologic recovery and the possible development of complications.

  • Spasticity, pressure ulcers, and neuropathic pain are commonly noted.

  • Provide whatever durable medical equipment (DME) the patient may need to facilitate safe ambulation or other mobility, as well as transfers, ADLs, or a return to vocational, avocational, educational, or social pursuits.

Further Inpatient Care

See the list below:

  • Admit to neurosurgical intensive care unit for neurologic monitoring.

  • Blood pressure monitoring is essential because mild hypertension is often recommended to ensure adequate blood flow to the spinal cord in the first 12-24 hours.

  • Perform prophylaxis for deep venous thrombosis (DVT), preferably with low molecular weight heparin.

  • Parenteral feeding is often necessary because of an adynamic ileus.

  • Insert a Foley catheter for bladder retention problems.

  • Initiate a regular bowel program.

  • Pay special attention to skin care (eg, regular turning schedule, specialized mattress).

Inpatient & Outpatient Medications

See the list below:

  • Lioresal is often indicated to treat spasticity that interferes with function.

  • Anticonvulsants (eg, carbamazepine, gabapentin) may be prescribed to treat recalcitrant neuropathic pain.[38]


See the list below:

  • Pain/hyperpathia

  • Bladder retention

  • Spasticity


The prognosis for patients with central cord syndrome (CCS) who are aged less than 50 years is good. Within a short time, 97% of these individuals recover, regaining the ability to ambulate and complete self-care tasks. Only 17% of patients aged more than 50 years recover.

Lenehan et al investigated the effects of age on clinical outcome in 50 patients with acute traumatic CCS. Patient ages at the time of injury were as follows: under 50 years, 13 patients; 50-70 years, 24 patients; and over 70 years, 13 patients. The incidence of sphincter disturbance among all patients was 42% on admission. Over a mean 42.2-month follow-up period, improvements in upper and lower limb motor scores, as well as in total sensory scores, occurred in patients in all age groups. However, the greatest improvements, absolute and relative, were found in patients under age 50 years. At follow-up, residual sphincter disturbance was found in 60% of patients over age 70 years but in no patients below age 70. The authors concluded that patients aged 70 years or above with acute traumatic CCS tend to have significantly poorer clinical outcomes than do younger patients with this syndrome.[39]

In addition to younger age, favorable long-term prognostic factors in CCS also include good hand function, evidence of early motor recovery, documented increases in upper and lower extremity strength during initial rehabilitation, and an absence of lower extremity neurologic impairment at admission to rehabilitation.[10, 40, 41, 42]

In a retrospective review of 15 individuals with CCS, using plain radiographs, cervical CT scans, and MRI scans from each patient, Miranda et al concluded that the length of spinal cord edema in a patient correlates with his/her initial degree of neurologic impairment.[43] The authors determined, therefore, that for patients with CCS, length of spinal cord edema may provide a significant indication of prognosis.

Patient Education

See the list below:

  • If necessary, patients and family members should be taught passive ROM and stretching exercises to maintain joint mobility. They should also be instructed in appropriate strengthening exercises.


Questions & Answers


What is central cord syndrome (CCS)?

What is the pathophysiology of central cord syndrome (CCS)?

What is the prevalence of central cord syndrome (CCS) in the US?

What is the global prevalence of central cord syndrome (CCS)?

What is the prognosis of central cord syndrome (CCS)?

What are the sexual predilections of central cord syndrome (CCS)?

Which age groups have the highest prevalence of central cord syndrome (CCS)?


What are the signs and symptoms of central cord syndrome (CCS)?

Which physical findings are characteristic of central cord syndrome (CCS)?

What causes central cord syndrome (CCS)?


Which conditions should be included in the differential diagnoses of central cord syndrome (CCS)?


What is the role of lab testing in the diagnosis of central cord syndrome (CCS)?

What is the role of imaging studies in the diagnosis of central cord syndrome (CCS)?


What is the role of physical therapy in the treatment of central cord syndrome (CCS)?

What is the role of occupational therapy in the treatment of central cord syndrome (CCS)?

What is the role of speech therapy in the treatment of central cord syndrome (CCS)?

What is the role of recreational therapy in the treatment of central cord syndrome (CCS)?

How is autonomic dysreflexia managed in central cord syndrome (CCS)?

How is neurogenic bladder managed in central cord syndrome (CCS)?

How is spasticity managed in central cord syndrome (CCS)?

How is neuropathic pain managed in central cord syndrome (CCS)?

How are pressure ulcers managed in central cord syndrome (CCS)?

How is neurogenic bowel managed in central cord syndrome (CCS)?

What is the role of surgery in the treatment of central cord syndrome (CCS)?

Which specialist consultations are beneficial to patients with central cord syndrome (CCS)?


Which medications are used in the treatment of central cord syndrome (CCS)?


What is included in outpatient care for central cord syndrome (CCS)?

What is included in inpatient care for central cord syndrome (CCS)?

Which medications are used in the treatment of central cord syndrome (CCS)?

What are the possible complications of central cord syndrome (CCS)?

What is the prognosis of central cord syndrome (CCS)?

What is included in patient education about central cord syndrome (CCS)?