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Impact of severe epilepsy on development: Recovery potential after successful early epilepsy surgery
Author(s) -
RouletPerez Eliane,
Davidoff Véronique,
MayorDubois Claire,
MaederIngvar Malin,
Seeck Margitta,
Ruffieux Christiane,
Villemure JeanGuy,
Deonna Thierry
Publication year - 2010
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2009.02487.x
Subject(s) - epilepsy , electroencephalography , epilepsy surgery , neuropsychology , cognition , psychology , cognitive decline , neuroplasticity , pediatrics , neurology , audiology , medicine , neuroscience , anesthesia , dementia , disease
Summary Purpose: Epilepsy surgery in young children with focal lesions offers a unique opportunity to study the impact of severe seizures on cognitive development during a period of maximal brain plasticity, if immediate control can be obtained. We studied 11 children with early refractory epilepsy (median onset, 7.5 months) due to focal lesion who were rendered seizure‐free after surgery performed before the age of 6 years. Methods: The children were followed prospectively for a median of 5 years with serial neuropsychological assessments correlated with electroencephalography (EEG) and surgery‐related variables. Results: Short‐term follow‐up revealed rapid cognitive gains corresponding to cessation of intense and propagated epileptic activity [two with early catastrophic epilepsy; two with regression and continuous spike‐waves during sleep (CSWS) or frontal seizures]; unchanged or slowed velocity of progress in six children (five with complex partial seizures and frontal or temporal cortical malformations). Longer‐term follow‐up showed stabilization of cognitive levels in the impaired range in most children and slow progress up to borderline level in two with initial gains. Discussion: Cessation of epileptic activity after early surgery can be followed by substantial cognitive gains, but not in all children. In the short term, lack of catch‐up may be explained by loss of retained function in the removed epileptogenic area; in the longer term, by decreased intellectual potential of genetic origin, irreversible epileptic damage to neural networks supporting cognitive functions, or reorganization plasticity after early focal lesions. Cognitive recovery has to be considered as a “bonus,” which can be predicted in some specific circumstances.