Abstract

Objectives 5% of patients with epilepsy and migraines are photosensitive and liable to visually induces seizures. The similarity between intermittent photic stimulation (IPS) that provokes seizures and those provokes minimal discomfort and a headache suggests that the precipitants share a common neural mechanism. Material and methods With 10–20 system of electrode placement and Stellate-Harmonie EEG recording system for at least 20 min in bipolar montage with inclusion of ear reference and often sub temporal electrodes. Activation procedures include, eye opening–closing and hyperventilation, for 3–5 min; in early part of recording and IPS near end of recording at a stroboscope distance is 0.5 m from eyes and frequency runs from 1 Hz to 30 Hz every 10 s in incremental fashion. Results Photoparoxysmal responses (PPR) are abnormal electrographic response to photic stimulation marked by diffuse paroxysmal discharge occasional minor twitching of fingers or eye balls or clonic movements of the part of body. If it presents with generalized tonic clonic discharge, it is called photoconvulsive response. IPS induces spikes, spike-waves or sometimes intermittent slow waves, bilaterally synchronous, outlasting the end of IPS. It is hypothesized that membrane depolarization of some of the neurons to light stimuli, especially over the posterior head region contribute to photosensitivity. EEG lab, at NYGH, prevalence of migraine in epileptic population has been assessed at 8.3%, and EEG findings of PPR occurs in 1% of individuals aged 6–18 with seizures where as less than 1% in epileptic patients aged >18. The prevalence figure for migraine is assumed to be 5–10%, where as epilepsy is considered to be 0.5–1%. Prevalence of migraine in epileptic population has been assessed at 8–15%, and prevalence of epilepsy in migrainous population at 1–17%. Lifetime prevalence of 1 in 10,000 in the general population, as low as 2%, of the epilepsy population. PPR is present in 1.3–1.4% of healthy individuals aged 6–18. Discussion It’s been reported by Ernst and Quesnay that apomorphine, a dopamine receptor agonist, stops clinical and EEG findings of PPR without significantly reduction of spontaneous spike and wave activity. These signify different pathogenic mechanism in origin of spontaneous and evoked generalized epilepsy. It has been shown in cats that decreased endogenous release of dopamine and noradrenaline enhance pre-existing state of cortical excitability. Paroxysmal abnormalities including PPR found increased frequency with migraine and homozygous autosomal recessive inheritance. PPR sometimes outlasted the stimulus, and self-limited PPR probably have greater significance and are highly correlated with epilepsy. The PPR extending beyond the stimulus carries no increased risk of seizures.Photosensitive epilepsy has a good prognosis for seizure control that is independent of the persistence or disappearance of Photosensitivity. Encephalography has been much dispute in the study of migraine and epilepsy especially when both present as vice-versa triggers. An apparent increase in abnormalities, most of the times nonspecific and used as lateral relationship between migraine and epilepsy in presence of PPR, particularly in children.

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