eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Central Cord Syndrome

Michelle J Alpert, MD, Clinical Instructor, Department of Physical Medicine and Rehabilitation, Harvard Medical School

Updated: Jul 29, 2009

Introduction

Background

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 level of injury.^1,2

Although CCS has been reported to occur more frequently 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 is the most common incomplete SCI syndrome. (See image below and Image 1.)

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

Pathophysiology

Central cord syndrome (CCS) most often occurs after a hyperextension injury in an individual with long-standing cervical spondylosis. (See also the eMedicine 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.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.⁴ 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.

Frequency

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.^1,5,6

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.⁵

Clinical

History

• 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

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.

Causes

• 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.

Differential Diagnoses

Other Problems to Be Considered

Cruciate paralysis of Bell
Bilateral brachial plexus injury or avulsion of cervical roots

Workup

Laboratory Studies

• 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.⁷
  • MRI demonstrates direct evidence of spinal cord impingement from bone, a disc, or a hematoma.⁸
  • CT scanning of the cervical spine shows spinal canal compromise and allows the indirect approximation of the degree of spinal cord impingement.
  • 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.

Treatment

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.⁹ 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.¹⁰ 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

• 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.^4,11

Consultations

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

Medication

Since 1990, intravenous methylprednisolone has been given within the first 8 hours following injury to all patients with acute SCI. A multicenter, randomized, double-blind, placebo-controlled trial showed that patients who were treated with steroids within 8 hours of injury had significant neurologic recovery compared with those who received a placebo.¹²

Corticosteroids

Steroids may suppress membrane breakdown by inhibiting lipid peroxidation and hydrolysis at the injury site. Vasoactive byproducts of arachidonic acid also may be reduced, improving local blood flow to the injured spinal cord.

Methylprednisolone (Medrol, Solu-Medrol)

Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and by reversing increased capillary permeability.

Dosing

Adult

30 mg/kg IV over 15 min initial, followed in 45 min by IV infusion of 5.4 mg/kg/h for 23h

Pediatric

Not established

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Follow-up

Further Inpatient Care

• 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).

Further Outpatient Care

• 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.

Inpatient & Outpatient Medications

• Lioresal is often indicated to treat spasticity that interferes with function.
• Anticonvulsants (eg, carbamazepine, gabapentin) may be prescribed to treat recalcitrant neuropathic pain.¹³

Complications

• Pain/hyperpathia
• Bladder retention
• Spasticity

Prognosis

• 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.
• Favorable long-term prognostic factors include good hand function, evidence of early motor recovery, documented increases in upper and lower extremity strength during initial rehabilitation, young age, and an absence of lower extremity neurologic impairment at admission to rehabilitation.⁶
• 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.¹⁴ The authors determined, therefore, that for patients with CCS, length of spinal cord edema may provide a significant indication of prognosis.

Patient Education

• 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.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize cervical spine instability

Multimedia

Media file 1: Illustration of the pathophysiology of central cord syndrome. Note the "pincer" effect on the central cord by anterior and posterior compression.

References

1. Massaro F, Lanotte M, Faccani G. Acute traumatic central cord syndrome. Acta Neurol (Napoli). Apr 1993;15(2):97-105. [Medline].

2. Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord injury; with special reference to the mechanisms involved in hyperextension injuries of cervical spine. J Neurosurg. Nov 1954;11(6):546-77. [Medline].

3. Quencer RM, Bunge RP, Egnor M, et al. Acute traumatic central cord syndrome: MRI-pathological correlations. Neuroradiology. 1992;34(2):85-94. [Medline].

4. Aarabi B, Koltz M, Ibrahimi D. Hyperextension cervical spine injuries and traumatic central cord syndrome. Neurosurg Focus. 2008;25(5):E9. [Medline].

5. McKinley W, Santos K, Meade M, et al. Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord Med. 2007;30(3):215-24. [Medline]. [Full Text].

6. Aito S, D'Andrea M, Werhagen L, et al. Neurological and functional outcome in traumatic central cord syndrome. Spinal Cord. Apr 2007;45(4):292-7. [Medline].

7. Song J, Mizuno J, Inoue T, et al. Clinical evaluation of traumatic central cord syndrome: emphasis on clinical significance of prevertebral hyperintensity, cord compression, and intramedullary high-signal intensity on magnetic resonance imaging. Surg Neurol. Feb 2006;65(2):117-23. [Medline].

8. Dai L. Magnetic resonance imaging of acute central cord syndrome: correlation with prognosis. Chin Med Sci J. Jun 2001;16(2):107-10. [Medline].

9. Noonan VK, Kopec JA, Zhang H, et al. Impact of associated conditions resulting from spinal cord injury on health status and quality of life in people with traumatic central cord syndrome. Arch Phys Med Rehabil. Jun 2008;89(6):1074-82. [Medline].

10. Gil-Agudo A, Perez-Rizo E, Del Ama-Espinosa A, et al. Comparative biomechanical gait analysis of patients with central cord syndrome walking with one crutch and two crutches. Clin Biomech (Bristol, Avon). Aug 2009;24(7):551-7. [Medline].

11. Chen L, Yang H, Yang T, et al. Effectiveness of surgical treatment for traumatic central cord syndrome. J Neurosurg Spine. Jan 2009;10(1):3-8. [Medline].

12. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. May 17 1990;322(20):1405-11. [Medline].

13. Haller H, Leblhuber F, Trenkler J, et al. Treatment of chronic neuropathic pain after traumatic central cervical cord lesion with gabapentin. J Neural Transm. Sep 2003;110(9):977-81. [Medline].

14. Miranda P, Gomez P, Alday R. Acute traumatic central cord syndrome: analysis of clinical and radiological correlations. J Neurosurg Sci. Dec 2008;52(4):107-12; discussion 112. [Medline].

15. Chen TY, Lee ST, Lui TN, et al. Efficacy of surgical treatment in traumatic central cord syndrome. Surg Neurol. Nov 1997;48(5):435-40; discussion 441. [Medline].

16. Maroon JC, Abla AA, Wilberger JI, et al. Central cord syndrome. Clin Neurosurg. 1991;37:612-21. [Medline].

17. Nath M, Wheeler JS Jr, Walter JS. Urologic aspects of traumatic central cord syndrome. J Am Paraplegia Soc. Jul 1993;16(3):160-4. [Medline].

18. Roth EJ, Lawler MH, Yarkony GM. Traumatic central cord syndrome: clinical features and functional outcomes. Arch Phys Med Rehabil. Jan 1990;71(1):18-23. [Medline].

19. Siddall PJ, Taylor DA, McClelland JM, et al. Pain report and the relationship of pain to physical factors in the first 6 months following spinal cord injury. Pain. May 1999;81(1-2):187-97. [Medline].

20. Tow AM, Kong KH. Central cord syndrome: functional outcome after rehabilitation. Spinal Cord. Mar 1998;36(3):156-60. [Medline].

21. Waters RL, Adkins RH, Sie IH, et al. Motor recovery following spinal cord injury associated with cervical spondylosis: a collaborative study. Spinal Cord. Dec 1996;34(12):711-5. [Medline].

22. Yamazaki T, Yanaka K, Fujita K, et al. Traumatic central cord syndrome: analysis of factors affecting the outcome. Surg Neurol. Feb 2005;63(2):95-9; discussion 99-100. [Medline].

Keywords

central cord syndrome, SCI, spinal cord injury, spinal cord injuries, spinal compression, spinal cord compression, spine compression, cervical spinal cord injury, cord trauma, spinal cord trauma, hyperextension injury

Contributor Information and Disclosures

Author

Michelle J Alpert, MD, Clinical Instructor, Department of Physical Medicine and Rehabilitation, Harvard Medical School
Michelle J Alpert, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Congress of Rehabilitation Medicine, American Spinal Injury Association, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

Medical Editor

J Michael Wieting, DO, MEd, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Sports Medicine, Associate Director of Physician Assistant Training Program, Department of Osteopathic Principles and Practice, Lincoln Memorial University-DeBusk College of Osteopathic Medicine
J Michael Wieting, DO, MEd is a member of the following medical societies: American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Sports Medicine, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds Novaritis; Novaritis  Novaritis; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

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Cervical Spondylosis
Cervical Spondylosis, Diagnosis and Management
Fracture, Cervical Spine
Functional Outcomes per Level of Spinal Cord Injury
Spinal Cord Hemorrhage
Spinal Cord Injuries
Spinal Cord Injury and Aging
Spinal Cord Injury - Definition, Epidemiology, Pathophysiology
Spinal Cord, Topographical and Functional Anatomy
Spinal Cord Trauma and Related Diseases

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