Treatment of interictal epileptiform discharges in cerebral palsy patients without clinical epilepsy: hope for a better outcome in prognosis.
Cerebral palsy (CP) is a motor disorder due to cerebral damage. It is commonly associated with neuro-psychological retardation and also with epilepsy; hence, its management warrants a multi-dimensional approach. In a significant number of CP patients, interictal epileptiform discharges (IEDs) are obtained in their EEG even in absence of clinical epilepsy. Epileptiform discharge-firing cortical neurons are found to be associated with elevated intracellular Ca(2+) levels and exhibition of abnormal response on exposure to excitotoxic glutamate; both these features have been found to lead to subsequent death of these neurons. This further damage is likely to aggravate the already existing cortical damage in CP patients thereby worsening their prognosis. IEDs are also known to be associated with other neuro-psychological disorders like cognitive impairment and behavioral problems even in absence of clinical epilepsy. Thus, the IEDs cannot be viewed as benign events and their occurrence even in absence of clinical epilepsy cannot be ignored. A few trials aimed at treating IEDs in autistic patients without epilepsy and in children with behavior problems have yielded favorable results. Based on these studies, the author proposes inclusion of EEG investigation in the management protocol of CP patients and treatment of IEDs (when detected even in absence of clinical epilepsy) for a better outcome in their prognosis.
Jaseja
Harinder
H
Physiology Department, G.R. Medical College, Gwalior 474001, Madhya Pradesh, India. dr_jaseja@yahoo.com
D015220:Calcium Channels / Q000378:metabolism; D002547:Cerebral Palsy / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology; D004569:Electroencephalography; D004827:Epilepsy / Q000188:drug therapy* / Q000453:epidemiology* / Q000378:metabolism; D018698:Glutamic Acid / Q000009:adverse effects; D006801:Humans; D042541:Intracellular Space / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins / Q000009:adverse effects; D011379:Prognosis; D014635:Valproic Acid / Q000627:therapeutic use*
D015220:Calcium Channels; D009498:Neurotoxins; D018698:Glutamic Acid; D014635:Valproic Acid