Abstract
Impairments of the dialog between excitation and inhibition (E/I) is commonly associated to neuropsychiatric disorders like autism, bipolar disorders and epilepsy. Moderate levels of hyperexcitability can lead to mild alterations of the EEG and are often associated with cognitive deficits even in the absence of overt seizures. Indeed, various testing paradigms have shown degraded performances in presence of acute or chronic non-ictal epileptiform activity. Evidences from both animal models and the clinics suggest that anomalous activity can cause cognitive deficits by transiently disrupting cortical processing, independently from the underlying etiology of the disease. Here, we will review our understanding of the influence of an abnormal EEG activity on brain computation in the context of the available clinical data and in genetic or pharmacological animal models.
Highlights
Epilepsy is a heterogeneous disorder that includes a great variety of phenotypes and pathological manifestations, all characterized by enhanced neuronal excitability due to an impaired balance between excitation and inhibition (E/I)
It is fair to conclude that several clinical evidence and the acute animal models suggest that interictal epileptic discharges (IEDs) activity interfere with brain computation in the focus and in connected areas, contributing to the overall cognitive impairment
It is important to understand whether IEDs should receive pharmacological treatment even in absence of seizures
Summary
Epilepsy is a heterogeneous disorder that includes a great variety of phenotypes and pathological manifestations, all characterized by enhanced neuronal excitability due to an impaired balance between excitation and inhibition (E/I). These studies require to correlate the EEG recording with the outcome of the cognitive task, to verify whether the presence of interictal epileptic discharges (IEDs) causes a temporary deficit.
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