EEG in the diagnosis, classification, and management of patients with epilepsy

Abstract

T he human electroencephalogram (EEG) was discovered by the German psychiatrist, Hans Berger, in 1929. Its potential applications in epilepsy rapidly became clear, when Gibbs and colleagues in Boston demonstrated 3 per second spike wave discharge in what was then termed petit mal epilepsy. EEG continues to play a central role in diagnosis and management of patients with seizure disorders-in conjunction with the now remarkable variety of other diagnostic techniques developed over the last 30 or so years-because it is a convenient and relatively inexpensive way to demonstrate the physiological manifestations of abnormal cortical excitability that underlie epilepsy.However, the EEG has a number of limitations. Electrical activity recorded by electrodes placed on the scalp or surface of the brain mostly reflects summation of excitatory and inhibitory postsynaptic potentials in apical dendrites of pyramidal neurons in the more superficial layers of the cortex. Quite large areas of cortex-in the order of a few square centimetres-have to be activated synchronously to generate enough potential for changes to be registered at electrodes placed on the scalp. Propagation of electrical activity along physiological pathways or through volume conduction in extracellular spaces may give a misleading impression as to location of the source of the electrical activity. Cortical generators of the many normal and abnormal cortical activities recorded in the EEG are still largely unknown. Spatial sampling in routine scalp EEG is incomplete, as significant amounts of cortex, particularly in basal and mesial areas of the hemispheres, are not covered by standard electrode placement. Temporal sampling is also limited, and the relatively short duration of routine interictal EEG recording is one reason why patients with epilepsy may not show interictal epileptiform discharge (IED) in the first EEG study.If inappropriate questions are asked of the EEG, diagnostic errors will occur, and there will be poor yield of information that could be useful in the management of patients with seizure disorders. It is crucial to recognise that a normal EEG does not exclude epilepsy, as around 10% of patients with epilepsy never show epileptiform discharges. Secondly, an abnormal EEG demonstrating IED does not in itself indicate that an individual has a seizure disorder, as IED are seen in a small percentage of normal subjects who never develop epilepsy, and IED may also be found in patients with neurological disorders which are not complicated by epilepsy. Table 1 lists the areas in epilepsy diagnosis and management for which interictal and ictal EEG are useful, strongly so in some, but in a more limited way in others. SPECIFICITY AND SENSITIVITY OF ROUTINE EEG cEpileptiform activity is specific, but not sensitive, for diagnosis of epilepsy as the cause of a transient loss of consciousness or other paroxysmal event that is clinically likely to be epilepsy. EEG has relatively low sensitivity in epilepsy, ranging between 25-56%. Specificity is better, but...

Wearable Electroencephalography

“…Synchronous video monitoring is also used often. Interictal epileptic discharges (IEDs) are found in approximately 50% of individuals with epilepsy in this short test [16], and the yield can be increased to around 80% through the use of multiple tests, sleep deprivation, and photic stimulation.…”

“…It may also facilitate the recording of ictal (seizure) activity. Such monitoring is required in a significant number of cases that present diagnostic or management difficulty [16]. Additional recording noise less than 1.5 lV peak to peak or 0.5 lV RMS.…”

Clinical Significance of Epileptiform Activity in Electroencephalogram

“…Так, при проведении стандартной (рутинной) ЭЭГ в общей группе взрослых пациентов с эпилепси-ей частота обнаружения эпилептиформной активно-сти варьирует от 29 до 55 % [72]. Но повторные ЭЭГ (до 4 исследований) с депривацией сна увеличивают вероятность выявления эпилептиформных измене-ний у больных эпилепсией до 80 % [80]. Длительный ЭЭГ-мониторинг повышает выявляемость эпилепти-формной активности на ЭЭГ у больных эпилепсией на 20 % [80].…”

“…Но повторные ЭЭГ (до 4 исследований) с депривацией сна увеличивают вероятность выявления эпилептиформных измене-ний у больных эпилепсией до 80 % [80]. Длительный ЭЭГ-мониторинг повышает выявляемость эпилепти-формной активности на ЭЭГ у больных эпилепсией на 20 % [80]. Запись ЭЭГ во сне повышает выявляе-мость эпилептиформных изменений до 85-90 % [37].…”

“…При предъявлении РФС в целом 5-10 % всех больных эпилепсией имеют фотопароксизмальный ответ на ЭЭГ [80,91]. Показано, что фотопароксиз-мальная реакция имела место у 15,2 % пациентов с генерализованными формами эпилепсии и только у 2,7 % пациентов с фокальными формами эпилепсии [91].…”