Literature DB >> 18717714

Periictal diffusion abnormalities of the thalamus in partial status epilepticus.

Angelos M Katramados1, David Burdette, Suresh C Patel, Lonni R Schultz, Shailaja Gaddam, Panayiotis D Mitsias.   

Abstract

PURPOSE: To identify and describe thalamic dysfunction in patients with temporal as well as extratemporal status epilepticus (SE) and to also analyze the specific clinical, radiological, and electroencephalography (EEG) characteristics of patients with acute thalamic involvement.
METHODS: We retrospectively identified patients who presented with clinical and electrographic evidence of partial SE and had thalamic abnormalities on diffusion-weighted imaging (DWI) within 5 days of documentation of lateralized epileptiform discharges (group 1). The spatial and temporal characteristics of the periodic lateralized epileptiform discharges (PLEDs) and the recorded electrographic seizures were analyzed and correlated with magnetic resonance imaging (MRI)-DWI hyperintense lesions. The findings of group 1 patients were compared with those of patients with partial SE without thalamic abnormalities on DWI (group 2).
RESULTS: The two groups were similar with regard to clinical presentation and morphology of epileptiform discharges. Group 1 patients had thalamic hyperintense lesions on DWI that appeared in the region of the pulvinar nucleus, ipsilateral to the epileptiform activity. Statistically significant relationship was noted between the presence of thalamic lesions and ipsilateral cortical laminar involvement (p = 0.039) as well as seizure origin in the posterior quadrants (p = 0.038). A trend towards PLEDs originating in the posterior quadrants was also noted (p = 0.077). DISCUSSION: Thalamic DWI hyperintense lesions may be observed after prolonged partial SE and are likely the result of excessive activity in thalamic nuclei having reciprocal connections with the involved cortex. The thalamus likely participates in the evolution and propagation of partial seizures in SE.

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Year:  2009        PMID: 18717714      PMCID: PMC2879152          DOI: 10.1111/j.1528-1167.2008.01736.x

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


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