There is a bidirectional relationship between attention-deficit/hyperactivity disorder (ADHD) and epilepsy. ADHD increases seizure risk, while patients with epilepsy have an increased prevalence of ADHD. The reasons explaining this association are not fully understood. Proposed mechanisms include effects of antiepileptic medications, underlying neurodevelopmental vulnerability, the effects of chronic seizures and subclinical epileptiform activity on cognitive functions and adrenergic dysfunction. There may also be a common genetic defect underlying both disorders in some families. Antiepileptics associated with ADHD-like side effects include phenobarbital, gabapentin, vigabatrin and topiramate. Methylphenidate has been studied in a double-blind setting against placebo for treatment of ADHD comorbid with epilepsy, and has a good risk-benefit ratio. Amphetamine, atomoxetine, clonidine and guanfacine only have case series to support their use and bupropion should be avoided.
To retrospectively examine response to stimulant treatment in patients with epilepsy and ADHD symptoms as predicted by seizure freedom for six months, use of methylphenidate (MPH) versus amphetamine (AMP) preparations, and cognitive level, medical records were searched for patients under age 18 with epilepsy and ADHD symptoms treated with MPH or AMP (n = 36, age 10.4±3.5; 67% male). “Responders” had a CGI-Improvement score of ≤2 and did not stop medication due to adverse effects. “Worsened” patients discontinued medication due to agitation/emotional lability. Seizure freedom did not predict treatment response. Lower cognitive level was associated with increased rate of worsening (p=0.048). No patients who were seizure-free at start of the medication trial experienced an increase in seizures. Of the patients having seizures at the start of trial, one patient on MPH and two on AMP had increased seizures during the trial. Seizures returned to baseline frequency or less after stimulant discontinuation or anticonvulsant adjustment. MPH was associated with a higher response rate, with 12 of 19 given MPH 0.62±0.28mg/kg/day compared to 4 of 17 given AMP 0.37±0.26mg/kg/day responding (p=0.03). MPH treatment and higher cognitive level were associated with improved treatment outcome while seizure freedom had no clear effect. Confidence in these findings is limited by the study’s small, open label, and uncontrolled nature.
Background The N100 is a negative deflection in the surface EEG approximately 100ms after an auditory signal. It has been shown to be reduced in individuals with schizophrenia and those at clinical high risk (CHR). N100 blunting may index neural network dysfunction underlying psychotic symptoms. This phenomenon has received little attention in pediatric populations. Method This cross-sectional study compared the N100 response measured via the average EEG response at the left medial frontal position FC1 to 150 sinusoidal tones in participants ages 5 to 17 years with a CHR syndrome (n = 29), a psychotic disorder (n = 22), or healthy controls (n=17). Results Linear regression analyses that considered potential covariates (age, gender, handedness, family mental health history, medication usage) revealed decreasing N100 amplitude with increasing severity of psychotic symptomatology from healthy to CHR to psychotic level. Conclusions Longitudinal assessment of the N100 in CHR children who do and do not develop psychosis will inform whether it predicts transition to psychosis and if its response to treatment predicts symptom change.
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