Attention deficit hyperactivity disorder is a syndrome of unknown etiology that affects 3% to 7% of the population. Although no objective test exists to support the diagnosis, EEG discharges related to the neuropsychiatric abnormalities have a high incidence in attention deficit hyperactivity disorder. The aim of this study was to elucidate the quantitative and qualitative characteristics of EEG abnormality in attention deficit hyperactivity disorder. Nonrapid eye movement sleep EEGs were evaluated in 134 patients with attention deficit hyperactivity disorder in terms of age, EEG timing, spike and wave index, foci, and seizures. All patients had spike and wave paroxysms that changed with age at and time to first EEG. Only half of the patients had seizures and 46 patients had neither seizures nor foci. Thirty-eight patients had the EEG findings of benign focal epilepsy of childhood. Our data support the view that spike and wave activity evolves in time and that EEG discharges are related to neuropsychiatric symptoms even when a diagnosable seizure disorder is absent.
Objectives: Among patients with West Syndrome (WS), the underlying brain dysfunction is considered to be the major determinant of cognitive outcome. However, regardless of whether the WS type is symptomatic or cryptogenic, patients with infantile spasms may have a favourable or grim prognosis. The purpose of this study was to utilize electroencephalography (EEG) to guide treatment, and to assess cognitive outcome. Methods: We retrospectively reviewed the clinical and sleep EEG data in 16 patients who received adrenocorticotropic hormonal therapy between 2002 and 2014. The hypsarrhythmia paroxysm index (HPI), the frequency or duration of hypsarrhythmia paroxysms in non-rapid eye movement (NREM) sleep, and sleep spindles were evaluated in groups constituted according to etiology. Results: Cryptogenic patients whose onset of spasms began after 3 months of age and who experienced a shorter treatment delay had preserved spindles and favourable cognitive outcomes. Sleep spindles disappeared in cryptogenic patients with an early onset of spasms, long treatment delay, and high HPI at referral; their neurodevelopmental prognosis was unfavourable. In symptomatic cases in which the age of onset of spasms was earlier than 3 months and there had been a short treatment delay, sleep spindles never fully evolved, and the prognosis was poor. Patients with corpus callosum hypogenesis, a relatively mild malformation, had high HPI values at referral. While two of these patients did not display spindles during the follow-up, three had reappearing spindles as HPI values diminished, and the outcome was less severe in these patients. Conclusion: This study highlights the significance of EEG in studies of the prognosis of infantile spasms and demonstrates an objective approach that utilizes concurrent evaluation of sleep spindles and HPI.
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