[A case of transient bilateral primary oculomotor nerve paresis associated with head injury].
A 13-year-old boy, with no past medical history, was admitted after a car accident on October 29, 1989. On admission, he was alert. Physical examination revealed a bruise on the left frontal region, a fracture of right clavicula and right hemopneumothorax. He was treated with respirator due to dyspnea. On November 1, 1989, he was removed from respirator and expressed diplopia. Neurological examination showed bilateral ptosis, mild anisocoria, normal light reflex and horizontal gaze nystagmus in lateral gaze. Both eyes were deviated outward slightly in the primary position and showed inability to converge. The external ocular movements of both eyes were mildly limited in elevation and adduction. Ataxia was observed in bilateral upper extremities. Deep reflexes were normal and no pathological reflexes were observed. Brain CT scans showed no abnormality. On November 6, 1989, his ptosis and diplopia improved. On November 8, he was completely recovered. A magnetic resonance imaging on November 10 revealed no abnormality. We suggested that transient dysfunction of midbrain associated with head injury might cause transient bilateral primary oculomotor nerve paresis, nystagmus and ataxia.
Yamamoto
K
K
Department of Neurology, Yamaguchi University School of Medicine.
Sasabe
F
F
Fukusako
T
T
Takase
Y
Y
Morimatsu
M
M
D000293:Adolescent; D006259:Craniocerebral Trauma / Q000150:complications*; D006801:Humans; D008297:Male; D008636:Mesencephalon / Q000503:physiopathology; D015840:Oculomotor Nerve Diseases / Q000209:etiology* / Q000503:physiopathology