原发性运动皮质梗死模拟C7运动神经根病

S. Sasaki
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摘要

一位87岁的高血压患者,早晨起床后立即出现左臂无力。医学研究委员会(MRC)量表显示肌肉无力仅发生在左三头肌(3/5级)和前臂旋前肌(3/5级)。没有发现感觉障碍。左肱二头肌和肱桡肌反射明显增强。左三头肌反射倒置,这是以前没有发现的。其他的反射都是正常的。这些临床表现令人联想到C7运动神经根病。左侧Hoffmann符号为正,Babinski符号为负。超声示双颈内动脉中度狭窄(右侧,56.1%;左侧,55.9%),符合北美症状性颈动脉内膜切除术试验(NASCET)标准[1]。左肘运动神经传导检查(点动试验)正常。颈椎MRI显示C5/C6和C6/C7水平有中度脊柱炎改变。弥散加权MRI显示对侧初级运动皮质中央前旋钮[2]内侧附近有一个小梗死(图1)。表观扩散系数图显示梗死区有低信号灶。磁共振血管造影模糊显示右侧远端大脑前动脉。在这种情况下,影响初级运动皮层的缺血性梗死可能是由于颈动脉的动脉粥样硬化改变,提示动脉-动脉血栓栓塞性卒中机制。有一些报道称,局限于运动前皮质[3]和桥脑[4]的病变可能导致对侧手臂无力。因此,当具有卒中危险因素的患者出现类似急性发作颈椎运动神经根病的临床特征时,应将原发性运动皮质梗死作为临床鉴别诊断。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Primary motor cortex infarction mimicking C7 motor radiculopathy
An 87-year-old man with hypertension presented with left arm weakness immediately after getting out of bed in the morning. Medical Research Council (MRC) scale demonstrated muscle weakness solely in the left triceps (grade 3/5) and forearm pronator (grade 3/5). No sensory impairment was recognized. The left biceps and brachioradialis reflexes were brisker. The left triceps reflex was inverted, which had not been recognized before. The other reflexes were normal. These clinical manifestations were reminiscent of C7 motor radiculopathy. The left Hoffmann sign was positive, while the Babinski sign was negative. Ultrasonography revealed moderate stenosis of both internal carotid arteries (right side, 56.1%; left side, 55.9%) according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria [1]. Motor nerve conduction study (inching test) at the left elbow was normal. The cervical MRI revealed moderate spondylotic changes at the levels of C5/C6 and C6/C7. Diffusion-weighted MRI showed a small infarction (Figure 1) next to the medial part of the precentral knob [2] of the contralateral primary motor cortex. An apparent diffusion coefficient map demonstrated a hypointense lesion in the infarcted region. MR angiography vaguely exhibited the right distal anterior cerebral artery. In this case, the ischemic infarct affecting the primary motor cortex may be due to atherosclerotic changes of the carotid artery, suggesting an arterio-arterial thromboembolic stroke mechanism. There have been several reports that lesions restricted to the premotor cortex [3] and the pons [4] could cause a contralateral arm weakness. Thus, when patients with risk factors for stroke develop clinical features mimicking acute-onset cervical motor radiculopathy, primary motor cortex infarction should be considered as a differential diagnosis in the clinical setting.
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