Epileptic aphasia: a consequence of regional hypometabolic encephalopathy?
A series of 25 children, 13 females and 12 males, who had an acquired communication disorder together with epilepsy, but did not fulfil the strict criteria of the Landau-Kleffner syndrome, was studied. All children had a clinical neurological evaluation, speech and language assessment, an awake and sleep EEG, cranial MRI, SPET scan, and audiometry. Clinical seizures were most often polymorphic in type (17 of 25). Atypical absences were the commonest individual seizure type occurring in 15 cases. All patients had an unequivocal epileptiform EEG. Normal sleep phenomena were only observed in 10 cases, enhancement of epileptiform activity in sleep was seen in 16. Cranial MRI was abnormal in six and normal in 19 cases. The SPET scans were abnormal in 22 of 25 children. The language deficits were classified neurologically as receptive aphasia, 24 of 25; expressive aphasia, 20 of 25; nominal aphasia, eight of 25; articulatory dyspraxia, 10 of 25; and auditory agnosia, nine of 25. It is hypothesized that the loss of communication skills is due to an encephalopathy secondary to the persistent epileptic discharge and manifests as a hypometabolic area on the SPET scan.[1]References
- Epileptic aphasia: a consequence of regional hypometabolic encephalopathy? O'Regan, M.E., Brown, J.K., Goodwin, G.M., Clarke, M. Developmental medicine and child neurology. (1998) [Pubmed]
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