EEG FEATURES OF FOCAL MALFORMATIONS OF CORTICAL DEVELOPMENT

Citation
Aa. Raymond et Dr. Fish, EEG FEATURES OF FOCAL MALFORMATIONS OF CORTICAL DEVELOPMENT, Journal of clinical neurophysiology, 13(6), 1996, pp. 495-506
Citations number
50
Categorie Soggetti
Neurosciences,"Clinical Neurology
ISSN journal
07360258
Volume
13
Issue
6
Year of publication
1996
Pages
495 - 506
Database
ISI
SICI code
0736-0258(1996)13:6<495:EFOFMO>2.0.ZU;2-6
Abstract
Recent advances in neuroimaging have allowed the detection and charact erization of focal malformations of cortical developmental in a signif icant proportion of patients with epilepsy, many of whom were previous ly labelled as cryptogenic, allowing a better description of the assoc iated electroencephalogram (EEG) features. Alpha activity is usually p reserved, although superficial gyral abnormalities are often associate d with overlying localized polymorphic delta activity, and occasionall y abnormal fast activity. Most affected patients with epilepsy show in terictal spikes. These are often broadly concordant with the structura l abnormality but may show a wider anatomic distribution and be multif ocal, or occasionally appear only in anatomically distant sites. In ma ny patients the spikes are frequent and sometimes they occur continuou sly or in long trains. EEG findings are often stable over time, but so me patients only show the development of slow wave changes or interict al spikes when followed serially for several years. A small proportion of patients with focal malformations of cortical development have EEG features mimicking idiopathic generalized epilepsy, and occasionally patients exhibit continuous generalized spike and slow wave activity i n sleep. Electrocorticography studies confirm the often widespread nat ure of interictal spiking, but may also show highly epileptogenic patt erns recorded directly from dysplastic cortex. The intrinsic epileptog enicity of areas of cortical developmental abnormalities has also been demonstrated by chronic intracranial studies and in vitro recordings of slices obtained from resected human dysplastic cortex. In this rega rd such developmental abnormalities are fundamentally different from a cquired lesions such as tumors/vascular anomalies that usually exert t heir effects through changes in adjacent cortex.