Central Cord Syndrome 

  • Author: Michelle J Alpert, MD; Chief Editor: Denise I Campagnolo, MD, MS   more...
 
Updated: Apr 6, 2010
 

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, 3]

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

Recent studies

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.[4]

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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.[5] 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.[6] 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.

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Epidemiology

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, 7, 8]

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.[7]

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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.

Specialty Editor Board

J Michael Wieting, DO, MEd  Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Program Development, Director of Sports Medicine, Associate Director of Physician Assistant 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 Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Osteopathic Academy 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.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Patrick M Foye, MD  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 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.

Kelly L Allen, MD  Medical Director, Medevals

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

References

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  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. Nowak DD, Lee JK, Gelb DE, et al. Central cord syndrome. J Am Acad Orthop Surg. Dec 2009;17(12):756-65. [Medline].

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  8. 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].

  9. 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].

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

  11. 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].

  12. 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].

  13. 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].

  14. 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].

  15. 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].

  16. Wirz M, Zorner B, Rupp R, et al. Outcome after incomplete spinal cord injury: central cord versus Brown-Sequard syndrome. Spinal Cord. Nov 10 2009;[Medline].

  17. Hohl JB, Lee JY, Horton JA, et al. A Novel Classification System for Traumatic Central Cord Syndrome: The Central Cord Injury Scale (CCIS). Spine (Phila Pa 1976). Mar 11 2010;[Medline].

  18. 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].

  19. 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].

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

  21. 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].

  22. 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].

  23. 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].

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

  25. 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].

  26. 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].

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