K Chu1, D W Kang, J Y Kim, K H Chang, S K Lee. 1. Department of Neurology, Seoul National University Hospital, Clinical Research Institute, Neuroscience Research Institute, Seoul National University Medical Research Institute, 28, Yongon-dong, Seoul 110-744, South Korea.
Abstract
BACKGROUND: In human and experimental models, diffusion-weighted magnetic resonance imaging (DWI) findings in status epilepticus (SE) have been reported to show that apparent diffusion coefficients are reduced during the initial phase and normalized or increased in the later phase of prolonged SE. This effect is caused by cytotoxic edema induced by excitotoxicity. In humans, only focal DWI abnormalities have been reported in partial SE. OBJECTIVES: To report and discuss the DWI findings suggesting diffuse neuronal injury in a patient with nonconvulsive SE. DESIGN AND METHODS: A 56-year-old man was admitted because of changing levels of consciousness over 3 days. On admission he was comatose. He had nystagmoid eye movement, forced eye blinking, and oroalimentary automatism. The results of a search for possible infectious and metabolic etiologies were negative, and electroencephalographic findings showed continuous, semirhythmic, bifrontal sharp waves of 2 Hz. Phenytoin and midazolam hydrochloride were infused to alleviate the seizure activities. He underwent DWI initially (3 days after the onset of seizure) and at the 5-month follow-up. SETTING: The neurology department of a tertiary referral center. RESULTS: During SE, DWI findings showed marked, diffuse gyriform cortical hyperintensity throughout the brain. The apparent diffusion coefficient decreased in the corresponding areas, especially in the occipital lobes. Findings from T2-weighted magnetic resonance imaging showed the intense cortical hyperintensity with gyral swelling and no involvement of brainstem, basal ganglia, thalamus, and white matter. The follow-up DWI findings showed marked atrophy and hypointensity in the corresponding regions. The apparent diffusion coefficient increased in the corresponding regions. CONCLUSIONS: Diffusion-weighted imaging in our patient indicated that the magnetic resonance imaging abnormalities of the affected cortex were due to cytotoxic edema caused by neuronal excitotoxicity during prolonged SE. Diffusion-weighted imaging can be used in the localization of seizure focus for predicting the prognosis of the affected tissue and for researching the basic pathophysiology of SE.
BACKGROUND: In human and experimental models, diffusion-weighted magnetic resonance imaging (DWI) findings in status epilepticus (SE) have been reported to show that apparent diffusion coefficients are reduced during the initial phase and normalized or increased in the later phase of prolonged SE. This effect is caused by cytotoxic edema induced by excitotoxicity. In humans, only focal DWI abnormalities have been reported in partial SE. OBJECTIVES: To report and discuss the DWI findings suggesting diffuse neuronal injury in a patient with nonconvulsive SE. DESIGN AND METHODS: A 56-year-old man was admitted because of changing levels of consciousness over 3 days. On admission he was comatose. He had nystagmoid eye movement, forced eye blinking, and oroalimentary automatism. The results of a search for possible infectious and metabolic etiologies were negative, and electroencephalographic findings showed continuous, semirhythmic, bifrontal sharp waves of 2 Hz. Phenytoin and midazolam hydrochloride were infused to alleviate the seizure activities. He underwent DWI initially (3 days after the onset of seizure) and at the 5-month follow-up. SETTING: The neurology department of a tertiary referral center. RESULTS: During SE, DWI findings showed marked, diffuse gyriform cortical hyperintensity throughout the brain. The apparent diffusion coefficient decreased in the corresponding areas, especially in the occipital lobes. Findings from T2-weighted magnetic resonance imaging showed the intense cortical hyperintensity with gyral swelling and no involvement of brainstem, basal ganglia, thalamus, and white matter. The follow-up DWI findings showed marked atrophy and hypointensity in the corresponding regions. The apparent diffusion coefficient increased in the corresponding regions. CONCLUSIONS: Diffusion-weighted imaging in our patient indicated that the magnetic resonance imaging abnormalities of the affected cortex were due to cytotoxic edema caused by neuronal excitotoxicity during prolonged SE. Diffusion-weighted imaging can be used in the localization of seizure focus for predicting the prognosis of the affected tissue and for researching the basic pathophysiology of SE.
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