No to shinkei = Brain and nerve · 1988
[Partial oculomotor nerve palsy due to midbrain lesion--case report and discussion on its characteristics].
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Saeki N, Iwadate Y, Namba H, Odaki M
Аннотация
UNLABELLED: A case of partial oculomotor palsy due to midbrain infarction is reported.
CASE PRESENTATION: 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.
CASE PRESENTATION: 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.