The neurologist · 2016
Ischemic Cervical Myelopathy Caused by Vertebral Artery Dissection: The Clinical Utility of a Motor-evoked Potential Study.
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Lee Woo Hyung, Lee Shi-Uk, Jung Se Hee
Аннотация
INTRODUCTION: Vertebral artery dissection (VAD) has been increasingly recognized as one of the important causes of ischemic stroke especially in young and middle-aged population. Rarely, VAD can involve the spinal cord, causing ischemic cervical myelopathy.
CASE REPORT: A 51-year-old man presented with sudden onset of weakness and hypesthesia involving right upper extremity, accompanied by posterior neck pain and headache. He also complained nonwhirling type of dizziness and nausea and he exhibited ataxic gait. Brain magnetic resonance imaging showed acute infarction at the right cerebellar hemisphere and temporo-occipital lobe. Right VAD was identified by MR angiography and confirmed by transfemoral cerebral angiography. Because the selective proximal weakness of the right upper extremity and hypesthesia at C5 and C6 dermatomes was not be fully explained by the brain lesion, electrophysiological studies were performed. The motor-evoked potential studies revealed that the latency and central motor conduction time was prolonged in the right cervical and lumbosacral roots. These studies implied cervical myelopathy involving the right anterior column. Magnetic resonance imaging of the cervical spine demonstrated high signal intensity of the right anterior column at C3-C4 level, which confirmed cervical ischemic myelopathy.
CONCLUSIONS: When there is diagnostic ambiguity between the upper and lower motor neuron lesions in VAD, motor-evoked potential study can be helpful to diagnose peripheral neurological complication of VAD.
CASE REPORT: A 51-year-old man presented with sudden onset of weakness and hypesthesia involving right upper extremity, accompanied by posterior neck pain and headache. He also complained nonwhirling type of dizziness and nausea and he exhibited ataxic gait. Brain magnetic resonance imaging showed acute infarction at the right cerebellar hemisphere and temporo-occipital lobe. Right VAD was identified by MR angiography and confirmed by transfemoral cerebral angiography. Because the selective proximal weakness of the right upper extremity and hypesthesia at C5 and C6 dermatomes was not be fully explained by the brain lesion, electrophysiological studies were performed. The motor-evoked potential studies revealed that the latency and central motor conduction time was prolonged in the right cervical and lumbosacral roots. These studies implied cervical myelopathy involving the right anterior column. Magnetic resonance imaging of the cervical spine demonstrated high signal intensity of the right anterior column at C3-C4 level, which confirmed cervical ischemic myelopathy.
CONCLUSIONS: When there is diagnostic ambiguity between the upper and lower motor neuron lesions in VAD, motor-evoked potential study can be helpful to diagnose peripheral neurological complication of VAD.