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Seizure precipitants: do we have enough scientific data to impose lifestyle limitations?
Alcohol:
G. Brathen, Dept. of Clinical Neurosciences, Medical Faculty, Norwegian University of Science and Technology, Trondheim, Norway
Not all alcohol abusing individuals develop seizures, and not all epilepsy patients get seizures when they drink alcohol. Thus giving advice based on what alcohol amount might generally be needed to induce a seizure is impossible. Still, this is an important consideration in the daily life of many epilepsy patients, who have traditionally been advised to abstain totally from alcohol.
The effect of alcohol intake on seizure control in epilepsy has been poorly investigated. In an uncontrolled study from 1961, 25 epilepsy patients were intoxicated with 1.7 dl 50% alcohol on a single occasion. EEG slowing was observed but no epileptiform activity occurred, and none had subsequent seizures. From a survey of 112 epilepsy patients and exacerbation of seizures after moderate to high intakes of alcohol was reported, and out of those who drank a large amount of alcohol on infrequent occasions, 88% had increased seizure frequency. Only one controlled clinical trial exists, in which small amounts of alcohol were given to epilepsy patients. No seizure exacerbation was observed from a consumption of 1-3 drinks, twice a week. However, consecutive studies of patients hospitalized for acute seizures have shown increased alcohol intake prior to seizure in 26-49% of cases.
A small number of mainly methodologically weak papers indicate that epilepsy patients may safely consume low to moderate amounts of alcohol. The studies have generally not addressed important factors such as epilepsy syndromes, seizure types, or degree of seizure control. Studies on consecutive hospital admissions indicate an important role for alcohol as seizure precipitating factor. Thus, alcohol may be a more important seizure-precipitating factor than indicated from the few, methodologically weak papers that have addressed this topic.
Well designed, controlled clinical studies are needed. From the present knowledge, epilepsy patients with good seizure control may consume alcohol in low quantities. This may not be true for patients with generalized epilepsy syndromes. The role of sleep deprivation, which often accompanies alcohol use, is probably also important.
Sleep deprivation and stress:
A Gil-Nagel, Servicio Neuroadiologia. Hospital Ruber Internacional, Madrid Spain.
Sleep deprivation facilitates both epileptiform abnormalities and seizures. This has been documented extensively both in generalized as well as focal epilepsies.
EEG studies demonstrated an activating effect of sleep deprivation on interictal epileptiform activity. Activation can occur during drowsiness after awakening, or during wakefulness. EEGs obtained after sleep deprivation show increased epileptiform activity in 16-57% of patients; this activation is more pronounced on complex partial and generalized tonic clonic seizures than in simple partial seizures. Stress often causes insomnia and decreased sleep efficiency, mechanisms that can activate seizures. During stress disorders there is excessive release of norepinephrine at the locus coreleus, increasing noradrenergic activity at the hippocampus and amygdale. In addition, there are changes in the release of corticosteroids, hypothalamic and pituitary hormones. These biochemical changes can activate seizures as well. Sleep deprivation and stress are common during normal life, and are almost impossible to eliminate completely. Managing stress and sleep deprivation in patients with epilepsy remains a clinical challenge. The clinician often has to balance the avoidance of these seizures precipitants and the need to expose them in order to maintain a normal lifestyle.
From Epilepsia – the Journal of the International League Against Epilepsy.
Abstracts from the 5th European Conference of Epileptology.
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