Epilepsia · 1996
Paroxysmal staring and masticatory automatisms during postural hypotension in a patient with multiple system atrophy.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Iani C, Attanasio A, Manfredi M
Аннотация
PURPOSE: We studied a 51-year-old man with multiple system atrophy and autonomic insufficiency. He had repeated episodes of loss of contact, staring, and masticatory automatisms.
METHODS: Blood pressure during these events documented a systolic pressure of 60 mm Hg. Cardiovascular reflex tests provided evidence of autonomic failure. Head computed tomography (CT) revealed moderate, diffuse cortical and cerebellar atrophy.
RESULTS: These events were strictly related to blood pressure decreases and could be reproduced consistently by having the patient sit up after a meal. Ictal polygraphic recordings showed EEG changes consistent with anoxia, preceded by sudden hypotension with fixed heart rate.
CONCLUSIONS: Cerebral anoxia during a syncopal attack may therefore precipitate transient, sudden neurologic dysfunction that closely mimics complex partial seizures. Masticatory automatisms may represent a release phenomenon resulting from inactivation of neocortical structures by cerebral anoxia or reticular disconnection.
METHODS: Blood pressure during these events documented a systolic pressure of 60 mm Hg. Cardiovascular reflex tests provided evidence of autonomic failure. Head computed tomography (CT) revealed moderate, diffuse cortical and cerebellar atrophy.
RESULTS: These events were strictly related to blood pressure decreases and could be reproduced consistently by having the patient sit up after a meal. Ictal polygraphic recordings showed EEG changes consistent with anoxia, preceded by sudden hypotension with fixed heart rate.
CONCLUSIONS: Cerebral anoxia during a syncopal attack may therefore precipitate transient, sudden neurologic dysfunction that closely mimics complex partial seizures. Masticatory automatisms may represent a release phenomenon resulting from inactivation of neocortical structures by cerebral anoxia or reticular disconnection.