Management of Acute Traumatic Central Cord Syndrome

Abstract

PATHOPHYSIOLOGY The mechanism of injury for ATCCS has been described as cervical hyperextension in the setting of cervical spinal stenosis (Figure 1).3 In older patients, who are most commonly affected, this is due to a spondylotic spinal canal with stenosis caused by a hypertrophied or buckled ligamentum flavum.2,4 Indeed patients with ATCCS have been shown to have a canal diameter (Figure 2) more than 14 mm narrower than in control patients.4 Compression of the cord in the stenotic canal results in damage to the deep regions of the lateral white matter tract, specifically the lateral corticospinal tracts, often because of cord edema secondary to local inflammation.4 The preferential loss of upper extremity motor function has been explained by various theories, including somatotopic organization of the corticospinal tracts, with more centrally located upper extremity fibers, and, more recently, an overall A cute traumatic central cord syndrome (ATCCS) is the most common form of incomplete cervical spinal cord injury (SCI), accounting for 70% of incomplete cervical spinal cord injuries and occurring in approximately 11,000 patients annually.1 ATCCS is distinguished from other spinal cord pathologies as the deficit is primarily related to the central regions of the cord and classically affects upper extremities more than lower extremities.