Yoshii F, Shinohara Y, Tamura K, Iyori S
Department of Neurology, Tokai University School of Medicine, Isehara, Japan.
No To Shinkei. 1996 Oct;48(10):937-41.
We report a patient with medial medullary infarction who showed deep sensory impairment as his prominent neurological manifestation. A 54-year-old man with a history of hypertension was admitted to our hospital with numbness of the bilateral upper and lower extremities, followed by dysarthria and right hemiparesis. Physical examination revealed no abnormalities except for high blood pressure. He hiccuped continuously. On neurological examination, he exhibited dysarthria, mild dysphagia and right hemiparesis without facial or lingual paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and thromboxane synthetase inhibitor. His hiccups stopped within two weeks, and his right hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive lupus anticoagulant. MRI showed bilateral infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities. Neurological manifestations of our patient are not typical of medial medullary infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable hiccups to the bilateral medial medullary lesions, and emphasize the importance of lupus anticoagulant as one of the risk factors in brainstem infarction.
我们报告了一例延髓内侧梗死患者，其主要神经学表现为深度感觉障碍。一名54岁有高血压病史的男性因双侧上下肢麻木入院，随后出现构音障碍和右侧偏瘫。体格检查除高血压外无异常。他持续打嗝。神经学检查发现他有构音障碍、轻度吞咽困难和右侧偏瘫，无面部或舌肌麻痹。对轻触觉和针刺的感觉正常，但双侧上下肢对振动和关节位置的感觉严重减退，主要是下肢以及上肢右侧。他接受了抗水肿药物和血栓素合成酶抑制剂治疗。他的打嗝在两周内停止，右侧偏瘫在一个月内逐渐改善。然而，他的深度感觉障碍仍然很明显。血液检查显示狼疮抗凝物阳性。MRI显示双侧延髓上部内侧梗死，延伸至双侧锥体，尤其是左侧。正中神经刺激后的体感诱发电位（SEP）显示P14及后续成分潜伏期延长。胫后神经刺激后未记录到SEP。P14的潜伏期与上肢深度感觉障碍的严重程度密切相关。我们患者的神经学表现并非延髓内侧梗死的典型表现，对延髓深部感觉传导束的功能解剖具有参考价值。我们讨论了顽固性打嗝与双侧延髓病变的关系，并强调狼疮抗凝物作为脑干梗死危险因素之一的重要性。
