Saeki N, Iwadate Y, Namba H, Odaki M
Department of Neurosurgery, Kawatetsu Chiba Hospital, Japan.
No To Shinkei. 1988 Apr;40(4):335-9.
A case of partial oculomotor palsy due to midbrain infarction is reported.
Fifty-one-year old man noted a sudden onset of double vision. He transiently presented right hemiparesis, right hemihyposthenia and cerebellar ataxia. The main symptom was the left oculomotor palsy selectively involving extraocular muscles (levator and pupil sparing), lasting for more than 6 months. The CT scan showed localized and well demarcated low-density areas at the left tegmentum of midbrain and left anteromedial thalamus, diagnosed as lacunar infarction due to occlusion of paramedian perforators at the basilar bifurcation. This midbrain infarct was supposed to be responsible for the partial oculomotor palsy. Extramedullary compressive and ischemic lesions have been well-known main causes of partial oculomotor palsy. This case, however, has emphasized the importance of recognition of midbrain lesion as a causative location of the partial oculomotor palsy. While the anatomical elucidation of this infrequent palsy is not sufficient, a topography of oculomotor nuclear complex in rhesus monkey proposed by Warwick, is worthwhile to correlate with midbrain oculomotor palsy in human cases. The pupil and levator sparing oculomotor palsy is most frequently caused by the laterally localized lesion at the fascicular portion which extends transversely at the midbrain tegmentum. This is the most likely lesion in this reported case. It is reported, on the other hand, that the levator sparing type oculomotor palsy is caused by a paramedian lesion of rostral midbrain and pupil sparing type by caudal midbrain. These may be explainable by rostro-caudal extension of the nuclear complex.
报告一例因中脑梗死导致的部分动眼神经麻痹病例。
一名51岁男性突然出现复视。他曾短暂出现右侧偏瘫、右侧半身轻瘫和小脑共济失调。主要症状为左侧动眼神经麻痹，选择性累及眼外肌（提上睑肌和瞳孔未受累），持续超过6个月。CT扫描显示中脑左侧被盖部和左侧丘脑前内侧有局限性且边界清晰的低密度区，诊断为基底动脉分叉处旁正中穿支闭塞所致的腔隙性梗死。该中脑梗死被认为是导致部分动眼神经麻痹的原因。髓外压迫性和缺血性病变是部分动眼神经麻痹的众所周知的主要原因。然而，该病例强调了认识到中脑病变作为部分动眼神经麻痹的致病部位的重要性。虽然对这种罕见麻痹的解剖学解释尚不充分，但沃里克提出的恒河猴动眼神经核复合体的地形图，值得与人类病例中的中脑动眼神经麻痹进行关联。瞳孔和提上睑肌未受累的动眼神经麻痹最常见的原因是在中脑被盖部横向延伸的束状部外侧局限性病变。这是本报告病例中最可能的病变。另一方面，据报道，提上睑肌未受累型动眼神经麻痹由中脑前部的旁正中病变引起，瞳孔未受累型由中脑后部病变引起。这些可能通过核复合体的头尾延伸来解释。
