Literature DB >> 26341869

Claustrum damage and refractory status epilepticus following febrile illness.

Stefano Meletti1, Jana Slonkova2, Iva Mareckova2, Giulia Monti2, Nicola Specchio2, Petr Hon2, Giada Giovannini2, Vaclav Marcian2, Annalisa Chiari2, Petr Krupa2, Nicola Pietrafusa2, Dagmar Berankova2, Michal Bar2.   

Abstract

OBJECTIVE: To characterize the clinical, EEG, and brain imaging findings in an adult case series of patients with de novo refractory status epilepticus (SE) occurring after a febrile illness.
METHODS: A retrospective study (2010-2013) was undertaken with the following inclusion criteria: (1) previously healthy adults with refractory SE; (2) seizure onset 0-21 days after a febrile illness; (3) lacking evidence of infectious agents in CSF; (4) no history of seizures (febrile or afebrile) or previous or concomitant neurologic disorder.
RESULTS: Among 155 refractory SE cases observed in the study period, 6 patients (17-35 years old) fulfilled the inclusion criteria. Confusion and stupor were the most common symptoms at disease onset, followed after a few days by acute repeated seizures that were uncountable in all but one. Seizures consisted of focal motor/myoclonic phenomena with subsequent generalization. Antiepileptic drugs failed in every patient to control seizures, with all participants requiring intensive care unit admission. Barbiturate coma with burst-suppression pattern was applied in 4 out of 6 patients for 5-14 days. One participant died in the acute phase. In each patient, we observed a reversible bilateral claustrum MRI hyperintensity on T2-weighted sequences, without restricted diffusion, time-related with SE. All patients had negative multiple neural antibodies testing. Four out of 5 surviving patients developed chronic epilepsy.
CONCLUSIONS: This is a hypothesis-generating study of a preliminary nature supporting the role of the claustrum in postfebrile de novo SE; future prospective studies are needed to delineate the specificity of this condition, its pathogenesis, and the etiology.
© 2015 American Academy of Neurology.

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Year:  2015        PMID: 26341869      PMCID: PMC4607596          DOI: 10.1212/WNL.0000000000001996

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


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