Ishii K, Ohkoshi N, Tamaoka A, Mizusawa H, Shoji S
Department of Neurology, University of Tsukuba.
Rinsho Shinkeigaku. 1996 Aug;36(8):951-6.
Here we report two cases of pseudoradicular sensory impairment (PRSI) caused by cerebral infarctions. Case on was a 49-year-old male who presented with dysesthesia in the left ulnar nerve distribution, and case 2 was a 57-year-old male who developed dysesthesia and weakness in the left radial nerve distribution. In both cases, the symptoms began with dysesthesia, followed by disturbance of cortical sensation, and distal motor weakness of the left upper extremity. Although the temperature, superficial pain, tactile, and vibratory sensations were well preserved, position sense, and cortical sensations such as two-point discrimination, material discrimination and stereognostic sensations were severely disturbed. No abnormalities were found in nerve conduction studies or cervical magnetic resonance imaging (MRI). Findings of somatosensory evoked potential (SEP) indicated that cortical components (N20, P24, N35 and P55) were missing in the left ulnar nerve in case 1, and in the median nerve in case 2. MRI of the brain revealed cerebral infarctions in the right parietal lobe including the postcentral gyrus. From the above results sensory disturbances of these two cases are caused by infarctions of the right parietal lobe. The characteristics of sensory disturbances caused by parietal lesions in our cases are similar to the previous reports. In addition, we found that the impaired cortical and subcortical areas were larger than the predicted areas indicated by Penfield's somatosensory homunculus. From the thermography, we found that the dermal regions with sensory impairment were more or less hypothermal. This suggests that cortical and subcortical infarctions may lead to localized sympathetic dysfunctions of the skin.
在此,我们报告两例由脑梗死引起的假性神经根性感觉障碍(PRSI)病例。病例1是一名49岁男性,表现为左侧尺神经分布区感觉异常,病例2是一名57岁男性,出现左侧桡神经分布区感觉异常和无力。在这两个病例中,症状均始于感觉异常,随后出现皮质感觉障碍以及左上肢远端运动无力。尽管温度觉、浅痛觉、触觉和振动觉保存完好,但位置觉以及两点辨别觉、实体辨别觉和立体觉等皮质感觉严重受损。神经传导研究或颈椎磁共振成像(MRI)未发现异常。体感诱发电位(SEP)结果表明,病例1左侧尺神经以及病例2正中神经的皮质成分(N20、P24、N35和P55)缺失。脑部MRI显示右侧顶叶包括中央后回存在脑梗死。根据上述结果,这两例的感觉障碍是由右侧顶叶梗死所致。我们病例中由顶叶病变引起的感觉障碍特征与先前报道相似。此外,我们发现受损的皮质和皮质下区域大于彭菲尔德体感小人图所示的预测区域。通过热成像,我们发现感觉障碍的皮肤区域或多或少温度较低。这表明皮质和皮质下梗死可能导致皮肤局部交感神经功能障碍。