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Factors That Can Exacerbate Seizures
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
David E. Burdette, Robert G. Feldman
The term photosensitive epilepsy designates those reflex epilepsies in which seizures are the direct result of characteristic retinal stimulation. The electroencephalo-graphic correlate of photosensitive epilepsy is the photoconvulsive response (36). In everyday life photosensitive epilepsy manifests itself as seizures which occur upon exposure to flickering lights in the environment or upon viewing of characteristic visual patterns such as checks on a tablecloth (36). The most common of these is television epilepsy (36). Unlike other forms of epilepsy, the number of reported female cases far outnumber the male in photosensitive epilepsy (36,37). The seizures most often described in association with environmental stimuli have been generalized tonic-clonic, with absence, myoclonic, and partial seizures being significandy less common (36,37). Much information concerning the epileptogenic characteristics of visual stimuli in photosensitive epilepsy has been obtained through induction of the photoconvulsive response in the EEG laboratory with intermittent photic stimulation and pattern viewing.
Pharmacokinetic/Pharmacodynamic Correlations of Anticonvulsants
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Meindert Danhof, Rob A. Voskuyl
A minority of all epileptic patients suffers from what is often referred to as “photosensitive epilepsy”. In these patients, exposure to photic stimulations using flash frequencies between 2 and 60 Hz will generally result in paroxysmal EEG responses. Antiepileptic drugs diminish the frequency range to which a patient is sensitive. This provides, therefore, a potentially useful measure of anticonvulsant effect intensity.31–33 It has been demonstrated that representatives of all the major groups of antiepileptic drugs can reduce the photosensitivity range. Also it has been demonstrated that the time course of this effect can be determined in individual patients (Figure 9). Thus far, however, this type of data has not been subjected to simultaneous pharmacokinetic/pharmacodynamic modeling.
Pharmacological treatment of focal epilepsy in adults: an evidence based approach
Published in Expert Opinion on Pharmacotherapy, 2021
Efficacy of CNB is based on Phase II and III studies. A Phase II RCT of 222 patients (age 18–65) with focal epilepsy compared CNB 200 mg against placebo [59]. CNB was started at 50 mg and increased by 50 mg increments every 2 weeks to a target dose of 200 mg, reached by 67% subjects. Responder rate (at least 50% seizure reduction) was 50.4% and seizure free rate 28.3% [59]. A Phase III RCT on 437 patients (age 18–70) with focal epilepsy compared placebo with CNB 100 mg, 200 mg, and 400 mg showing responder rates of 25%, 40%, 56%, 64%, and seizure free rates of 1%, 4%, 11%, and 21% for placebo, CNB 100 mg, 200 mg, and 400 mg, respectively [60]. Data on seizure freedom have been considered particularly promising given that a systematic review of RCTs of ASMs reported seizure freedom rates up to 6.5% for previous ASMs [49]. A proof-of-concept study in a small sample of six patients showed also promising therapeutic effect in photosensitive epilepsy for doses higher than 200 mg [61]. However, this would be relevant for generalized rather focal syndromes.
Adjunctive cenobamate for the treatment of focal onset seizures in adults with epilepsy: a critical review
Published in Expert Review of Neurotherapeutics, 2020
Patients with genetic generalized epilepsies may have a characteristic response to intermittent photic stimulation (IPS) consisting of an abnormal spike-and-wave discharge (photoparoxysmal response [PPR]) on electroencephalogram (EEG) [28]. A phase 2a, single-blind, single-dose multicenter study was conducted as a proof of principle of efficacy in patients (N=7) with photosensitive epilepsy who were stable on 0-2 concomitant ASMs [29]. Patients underwent IPS after a single dose of placebo or cenobamate 100 mg, 250 mg, or 400 mg. Compared with placebo, PPR was reduced at 1 hour with cenobamate 250 mg and 400 mg. Partial and complete suppression of the PPR was observed in 4/4 and 1/4 patients, respectively, on cenobamate 250 mg, and in 2/4 and 1/4 patients on cenobamate 400 mg. Overall, cenobamate suppressed the IPS-PPR response in these epilepsy patients and demonstrated an efficacy signal that supported further evaluation of treatment with cenobamate in patients with uncontrolled generalized epilepsy.
Cortical excitability in epilepsy and the impact of antiepileptic drugs: transcranial magnetic stimulation applications
Published in Expert Review of Neurotherapeutics, 2020
Photosensitive epilepsy is a form of epilepsy in which generalized seizures are triggered by visual stimuli that form patterns in time or space, such as flashing lights; bold, regular patterns; or regular moving patterns. TMS findings include: (1) a high prevalence of phosphene [46], (2) a reduction in phosphene threshold, indicating a regional hyperexcitability in the primary visual cortex [46], (3) a normal SICI at ISI of 3 and 4 ms and ICF at ISIs of 12 and 14 ms [42], and (4) a lack of shortening of CSP duration to intermittent photic stimulation at 20 Hz in patients with photosensitive epilepsy and also have photoparoxysmal responses but not in those without photoparoxysmal response. It has to be remembered that photoparosysmal response and photosensitive generalized epilepsy are different entities but share a common feature which is the abnormal tendency to develop hypersynchronized neuronal activity throughout the brain. In normal individuals, there is a shortening of CSP duration to intermittent photic stimulation at 20 Hz which may have a possible protective nature [42]. The failure to shorten the CSP with intermittent photic stimulation in both conditions indicates an altered control of cortical excitability by visual input that may be linked to the abnormal tendency toward hypersynchronization and the weak influence of intermittent photic stimulation on the motor cortical output in such patients [47].