Original articleAttention and executive functions profile in childhood absence epilepsy
Introduction
Childhood absence epilepsy (CAE) is the most common form of pediatric epilepsy [1] and accounts for 10–17% of all cases of childhood-onset epilepsy. The syndrome is characterized by daily, frequent but brief staring spells that typically beginning at 4–10 years of age in an otherwise apparently healthy child [2]. Absence seizures are short, generalized epileptic seizures clinically characterized by impairment of consciousness without major motor symptoms, and a typical EEG pattern of generalized, bilateral, synchronous, symmetrical spike–wave discharges of 3–4 Hz [1]. Children with epilepsy, particularly CAE, suffer from attention and executive function problems between seizures [3], [4], and these impairments often persist even when seizures are treated [5], as recently demonstrated by an important multicenter study [6]. The term “executive functions” (EFs) is used to define a set of mental control cognitive processes that permit the use of goal-directed behavior. EFs include different main domains, such as planning, cognitive flexibility/set shifting, working memory and verbal fluency. EFs have been highlighted as integral components of young children’s growing regulatory abilities and have been implicated in the development of both social-emotional and academic competence [7]. The term attention defines a set of processes that enhance cognitive, motor and sensory processing. Sustained attention is the ability to maintain attention during continuous activities that require vigilance and resistance to distraction. Divided attention is the ability to shift attention to different stimuli, using the same or different perceptive modalities. Studies in the literature report aberrant thalamocortical rhythms in absence seizures with preferential involvement of the frontal cortex rather than other cortical regions [8]. The most recent studies using simultaneous EEG and fMRI have provided evidence of the involvement and thus disruption of the dorsolateral, orbitofrontal, anterior cingulated and motor/premotor basal ganglia-thalamocortical (BGT) circuits in the pathogenesis of childhood absence epilepsy [8], [9]. Much neuroanatomic, neuropsychological and neuroimaging research suggests that the BGT circuits sub-serve a complex set of higher-order cognitive processes needed for adaptive, context-appropriate, goal-directed behavior [10]. These processes are collectively referred to as executive functions. Children with CAE or adults with a history of absence epilepsy may exhibit significant neuropsychological difficulty [8]. Nevertheless, the findings of available studies are difficult to interpret and the precise areas and extent of potential cognitive deficits in this population are still unknown [8] due to methodological discrepancies, the use of potentially mixed or atypical groups and limited test batteries. The aim of this study was to evaluate EF and attention dysfunction in a well-defined group of patients with typical CAE, under treatment with valproic acid (VPA), compared with healthy children.
Section snippets
Subjects
The study included 15 children with CAE (8 boys, 7 girls) and 15 controls (8 boys, 7 girls) matched for age, sex and IQ. Children who met the criteria for CAE were recruited in the Day Hospital of the Child Neuropsychiatry Unit of “Tor Vergata” Hospital. Selection criteria included: (1) age between 8 and 15 years; (2) IQ >80; (3) no physical impairment that prevented execution of the neuropsychological battery; (4) a history of CAE characterized by the following: several absence seizures per
Results
We found no significant differences between children with absence epilepsy and healthy children matched for IQ level and age.
Discussion
Patients with CAE often demonstrate attention and executive function problems, even when their seizures are controlled by medication. Moreover, the nature and extent of the neuropsychological difficulties associated with CAE are still unclear. The primary goal of this study was to compare the neuropsychological functioning of a well-defined group of children with CAE and a group of healthy children. In our sample, age at onset of CAE was between 6 and 11 years. This is an important inclusion
Conflict of interest statement
The authors disclose any commercial or other associations that might pose a conflict of interest in connection with the submitted article.
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