Central cord syndrome (CCS)

Introduction

Central cord syndrome (CCS), an acute cervical spinal cord injury (SCI), was initially described by Schneider and colleagues in 1954. CCS most often occurs after a hyperextension injury in an individual with long-standing 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.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. 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. CCS-related motor impairment results from the pattern of lamination of the corticospinal and spinothalamic tracts in the spinal cord. Age

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.

• Symptoms occur following trauma (most commonly falls) and consist of upper and lower extremity weakness with varying degrees of sensory loss.

Physical

Physical findings are limited to the neurologic system and consist of upper motor neuron weakness in the upper and lower extremities. • Sensory loss is variable, although sacral sensation is usually present. • Muscle stretch reflexes may initially be absent but will eventually return along with variable degrees of spasticity in affected muscles.

Causes

• The most common cause of CCS is trauma.

• In older adults, premorbid cervical spondylosis is a significant risk factor.

• In younger age groups, CCS results from major trauma, such as that associated with cervical fracture/subluxations.

Treatment Rehabilitation Program Physical Therapy

Patients with CCS offer a unique challenge for the physical therapist with regard to ambulation and gait training. 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. Occupational Therapy

Given the predominance of upper extremity weakness that occurs in CCS, the restoration of the basic activities of daily living (ADLs), upper extremity strength, and ROM are the main goals of occupational therapy. 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 CCS who have dysphagia from the head position maintained by cervical orthoses or as a result of anterior cervical spine fusion. Recreational Therapy

The primary goal of recreational therapy is to help patients with CCS to return to preinjury areas of interest. Medical Issues/Complications

• Autonomic dysreflexia

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

o Proper medical management of the skin, bowel, and bladder should prevent most occurrences. • Neurogenic bladder

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

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

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

• Spasticity

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

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

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

• Neuropathic pain

o Patients with CCS occasionally experience allodynia below the level of injury.

• Pressure ulcers

o 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.

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

o 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.

• Neurogenic bowel

Surgical Intervention

Surgery is rarely indicated because of the inherently favorable prognosis for CCS patients. Consultations
Neurologic surgeon

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