Central cord syndrome (CCS) is the most common sis of axoplasmic flow, causing edematous injury rather form of cervical spinal cord injury. It is characterized than destructive hematomyelia. More recently, autopsy by loss of motion and sensation in arms and hands. It studies have demonstrated that CCS may be caused by usually results from trauma which causes damage to the bleeding into the central part of the cord, portending less neck, leading to major injury to the central grey matter favorable prognosis. Studies also have shown from post- of the spinal cord. The syndrome is more common in mortem evaluation that CCS probably is associated with people over the age of 50 because osteoarthritis in the selective axonal disruption in the lateral columns at the neck region causes weakening of the vertebrae. CCS level of the injury to the spinal cord with relative preser- most frequently occurs among older persons with cervi- vation of the grey matter.[4] cal spondylosis, however, it also may occur in younger individuals.[1] CCS is the most common incomplete spinal cord injury syndrome. It accounts for approximately 9% of traumatic 3 Management SCIs.[2] After an incomplete injury, the brain still has the capacity to send and receive some signals below the site of injury. Sending and receiving of signals to and from 3.1 Nonsurgical parts of the body is reduced, not entirely blocked. CCS gives a greater motor loss in the upper limbs than in the In many cases, individuals with CCS can experience a re- lower limbs, with variable sensory loss. duction in their neurological symptoms with conservative It was first described by Schneider in 1954.[3] It is gen- management. The first steps of these intervention strate- erally associated with favorable prognosis for some de- gies include admission to an intensive care unit (ICU) af- gree of neurological and functional recovery. However, ter initial injury. After entering the ICU, early immo- factors such as age, preexisting conditions, and extent of bilization of the cervical spine with a neck collar would injury will affect the recovery process. be placed on the patient to limit the potential of further injury.[5] Cervical spine restriction is maintained for ap- proximately six weeks until the individual experiences a reduction in pain and neurological symptoms.[5] Inpatient 1 Presentation rehabilitation is initiated in the hospital setting, followed by outpatient physical therapy and occupational therapy CCS is characterized by disproportionately greater mo- to assist with recovery. tor impairment in upper compared to lower extremities, An individual with a spinal cord injury may have many and variable degree of sensory loss below the level of in- goals for outpatient occupational and physiotherapy. jury in combination with bladder dysfunction and urinary Their level of independence, self-care, and mobility are retention.[4] This syndrome differs from that of a com- dependent on their degree of neurological impairment. plete lesion, which is characterized by total loss of all sen- Rehabilitation organization and outcomes are also based sation and movement below the level of the injury. on these impairments.[6] The physiatrist, along with the rehabilitation team, work with the patient to develop specific, measurable, action-oriented, realistic, and time- 2 Causes centered goals. With respect to physical therapy interventions, it has been In older patients, CCS most often occurs after a determined that repetitive task-specific sensory input can hyperextension injury in an individual with long-standing improve motor output in patients with central cord syn- cervical spondylosis. However, this condition is not ex- drome. These activities enable the spinal cord to incorpo- clusive to older patients as younger individuals can also rate both supraspinal and afferent sensory information to sustain an injury leading to CCS. Typically, younger pa- help recover motor output.[7] This occurrence is known as tients are more likely to get CCS as a result of a high-force "activity dependent plasticity". Activity dependant plas- trauma or a bony instability in the cervical spine.[4][5] ticity is stimulated through such activities as: locomo- Historically, spinal cord damage was believed to origi- tor training, muscle strengthening, voluntary cycling, and nate from concussion or contusion of the cord with sta- functional electrical stimulation (FES) cycling[8]
1 2 6 EXTERNAL LINKS
3.2 Surgical [8] Yadla, S.; Klimo, J.; Harrop, J.S. (2010). “Traumatic Central Cord Syndrome: Etiology, Management, and Surgical intervention is usually given to those individu- Outcomes”. Topics in Spinal Cord Injury Rehabilitation. als who have increased instability of their cervical spine, 15 (3): 73–84. doi:10.1310/sci1503-73. which cannot be resolved by conservative management [9] Yadla, Sanjay; Paul Klimo; James S. Harrop (2010). alone. Further indications for surgery include a neuro- “Traumatic Central Cord Syndrome: Etiology, Manage- logical decline in spinal cord function in stable patients ment, and Outcomes”. Topics in Spinal Cord Injury Reha- as well as those who require cervical spinal decompres- bilitation. 15 (3): 73–84. doi:10.1310/sci1503-73. sion.[9]
6 External links 4 See also • NINDS Central Cord Syndrome Information Page • Spinal cord injury
• Anterior cord syndrome
• Brown-Sequard syndrome
5 References
[1] Rich V, McCaslin E (2006). “Central Cord Syndrome in a High School Wrestler: A Case Report”. J Athl Train. 41 (3): 341–4. PMC 1569555 . PMID 17043705.
[2] McKinley W, Santos K, Meade M, Brooke K (2007). “Incidence and Outcomes of Spinal Cord Injury Clinical Syndromes”. J Spinal Cord Med. 30 (3): 215–24. PMC 2031952 . PMID 17684887.
[3] Schneider RC, Cherry G, Pantek H (1954). “The syndrome of acute central cervical spinal cord injury; with special reference to the mechanisms involved in hyperextension injuries of cervical spine”. J. Neurosurg. 11 (6): 546–77. doi:10.3171/jns.1954.11.6.0546. PMID 13222164.
[4] Harrop, James S; Ashwini Sharan; Jonathon Ratliff (2006). “Central cord injury: pathophysiology, manage- ment, and outcomes”. The Spine Journal. 6 (6 Suppl. 1): 198S–206S. doi:10.1016/j.spinee.2006.04.006. PMID 17097539.
[5] Nowak, Douglas D.; Joseph K. Lee; Daniel E. Gelb; Ko- rnelis A. Poelstra; Steven C. Ludwig (December 2009). “Central Cord Syndrome”. Journal of the American Academy of Orthopaedic Surgeons. 17 (12): 756–765. PMID 19948700.
[6] Behrman, Andrea, L.; Harkema, Susan J. (2007). “Phys- ical Rehabilitation as an Agent for Recovery After Spinal Cord Injury”. Physical Medicine and Rehabil- itation Clinics of North America. 18 (2): 183–202. doi:10.1016/j.pmr.2007.02.002. PMID 17543768.
[7] Behram, A.L.; Harkema, S.J. (2007). “Physical Re- habilitation as an Agent for Recovery After Spinal Cord Injury”. Physical Medicine and Rehabilita- tion Clinics of North America. 18 (2): 183–202. doi:10.1016/j.pmr.2007.02.002. PMID 17543768. 3
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