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Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice
Published on: July 16, 2015
Spinal cord infarction secondary to cocaine use
Adam L Schreiber1, Christopher S Formal
1Thomas Jefferson University Hospital, Department of Rehabilitation, Philadelphia, Pennsylvania 19107, USA.
Abstract:
A 27-yr-old woman recreationally inhaled cocaine. Several hours later, she noted chest tightness, back and neck pain, and later bilateral upper-extremity weakness. Physical examination revealed flaccid paresis of the upper extremities. Spasticity at 2 mos after injury, but no detectable weakness, developed in the lower extremities. Cocaine was detected in her urine. Magnetic resonance imaging showed hyperintensity in the anterior cervicothoracic spinal cord. Electrodiagnostic studies of the upper extremities were consistent with anterior horn cell death. Cocaine abuse is associated with cerebrovascular events; spinal cord effects are rarely reported. The patient seems to have an infarct in the anterior spinal artery distribution, with clinical, imaging, and electrodiagnostic findings of upper-extremity lower-motor neuron injury, accompanied by spasticity of the lower extremities. Gray matter has increased susceptibility to ischemia compared with white matter, producing flaccid weakness in the cervical region with isolated arm weakness. Although uncommon, cocaine abuse can cause spinal cord infarction.
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