Katsuhiko Ogawa1, Yutaka Suzuki2, Keiko Takahashi2, Satoshi Kamei2, Hiroshi Ishikawa3. 1. Division of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. Electronic address: ogawa.katsuhiko@nihon-u.ac.jp. 2. Division of Neurology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. 3. Division of Ophthalmology, Department of Visual Sciences, Nihon University School of Medicine, Tokyo, Japan.
Abstract
BACKGROUND: Midbrain lesion-induced oculomotor nerve palsy can be divided into the nuclear and infranuclear types. In the infranuclear type, the degree of each subtype of ocular muscle palsy usually varies. METHODS: The neuroradiological findings of 11 patients with midbrain infarction-induced oculomotor nerve palsy were analyzed. Their infarcts were grouped into rostral and caudal lesions. Each group was then divided into lesions that occurred in the paramedian and lateral regions before being subdivided further into lesions that occurred in the tegmental, central, and ventral areas. RESULTS: Unilateral and bilateral infarcts were seen in 9 and 2 patients, respectively. The ventrocentral area of the rostral paramedian region was the most commonly affected part. External ocular muscle palsy was observed in all 11 patients. Ten patients had infranuclear oculomotor nerve palsy. Of these 10 patients, 9 had adduction palsy. Internal ocular muscle palsy was detected in 4 patients. The patient with nuclear type had bilateral ptosis and bilateral elevation palsy and did not exhibit Bell's phenomenon; however, her lesion was unilateral. Vertical gaze palsy was detected in 3 patients who continued to exhibit Bell's phenomenon. CONCLUSIONS: In the 3 cases in which patients with vertical gaze palsy continued to exhibit Bell's phenomenon, it was considered that the palsy was caused by impairment of the rostral interstitial nucleus of the medial longitudinal fasciculus. Our study suggested that the intra-axial fascicular fibers innervating the medial rectus muscle are particularly susceptible to infarction, possibly because they are the most centrally located in the intra-axial oculomotor fascicular fibers.
BACKGROUND: Midbrain lesion-induced oculomotor nerve palsy can be divided into the nuclear and infranuclear types. In the infranuclear type, the degree of each subtype of ocular muscle palsy usually varies. METHODS: The neuroradiological findings of 11 patients with midbrain infarction-induced oculomotor nerve palsy were analyzed. Their infarcts were grouped into rostral and caudal lesions. Each group was then divided into lesions that occurred in the paramedian and lateral regions before being subdivided further into lesions that occurred in the tegmental, central, and ventral areas. RESULTS: Unilateral and bilateral infarcts were seen in 9 and 2 patients, respectively. The ventrocentral area of the rostral paramedian region was the most commonly affected part. External ocular muscle palsy was observed in all 11 patients. Ten patients had infranuclear oculomotor nerve palsy. Of these 10 patients, 9 had adduction palsy. Internal ocular muscle palsy was detected in 4 patients. The patient with nuclear type had bilateral ptosis and bilateral elevation palsy and did not exhibit Bell's phenomenon; however, her lesion was unilateral. Vertical gaze palsy was detected in 3 patients who continued to exhibit Bell's phenomenon. CONCLUSIONS: In the 3 cases in which patients with vertical gaze palsy continued to exhibit Bell's phenomenon, it was considered that the palsy was caused by impairment of the rostral interstitial nucleus of the medial longitudinal fasciculus. Our study suggested that the intra-axial fascicular fibers innervating the medial rectus muscle are particularly susceptible to infarction, possibly because they are the most centrally located in the intra-axial oculomotor fascicular fibers.