PubMed · 16602065
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J García-Fidalgo, M Arteche-Prior, A Sánchez-Lozano, A Goicoechea-Astencio, R Andrade. [Tooth-brushing-induced epilepsy].. https://pubmed.ncbi.nlm.nih.gov/16602065/
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PURPOSE OF REVIEW: Interest in visually induced seizures has increased in recent years as a result of the increasing number of precipitants in our modern environment. This review addresses new developments in this field with special attention given to the emergence of new diagnostic, therapeutic and preventive approaches; it also emphasizes the importance of this condition as a public health issue. RECENT FINDINGS: Current evidence indicates the presence of two different mechanisms of photosensitivity, one dependent on luminance changes and the other on wavelength. Both mechanisms may be active in the same patient, although one may be dominant. Magnetoencephalography studies revealed an enhancement in gamma frequency preceding the development of a paroxysmal response as well as underlying uncomfortable visual illusions, suggesting that a loss of control over high-frequency oscillatory processes may be involved in the genesis of both types of phenomenon. The genetics underlying this trait remain to be determined. More precise definition of different phenotypes should help in this search. Recognition of the risks posed by the audiovisual environment for induction of seizures in photosensitive individuals, who may not even be aware of their condition, will prompt further development of guidelines and devices designed to prevent the occurrence of seizures triggered by dangerous video sequences. SUMMARY: Photosensitive epilepsy constitutes a unique benchmark model in which to address important issues in human epileptogenesis. The scope of the health risks posed by the modern audiovisual environment is increasingly being recognized, and further development of guidelines and regulations to control exposure to provocative materials are warranted.
Human epileptic photosensitivity has been studied in several ways. (a) Visual stimulation that resembles the stimulation normally responsible for seizures, such as that from televisions or videogames, both of which typically use cathode ray tubes in which the display is created in a flickering pattern. Such stimulation is often rendered yet more epileptogenic by programmes with content that also involves flashing or patterned material. (b) Elementary visual stimuli that enable inferences to be drawn concerning the physiological trigger mechanisms. The topographic distribution of epileptiform EEG activity in response to such stimuli has complemented this approach, leading to the inference that the trigger is cortical and requires sychronised mass action of neurons. (c) Stimuli that avoid paroxysmal EEG activity and permit an investigation of the subepileptic response to visual stimuli, using the evoked potential. This has revealed abnormalities in the cortical mechanisms that control the response to strong visual stimulation.
Very few studies of photosensitivity or visual sensitive epilepsy could be called epidemiologic in the strict sense, that is, giving well-based incidence and prevalence rates of a well-defined clinical and electroencephalographic syndrome or group of syndromes. The available data suggest that photosensitivity is rare in the population as a whole, with an annual incidence rate around one case per 100,000 population. The incidence goes up to almost six per 100,000 in the late adolescent period, the age group at the highest risk. Well-established concepts, such as statements that one in 4,000 of the general population or that 10% of all epilepsy patients would be photosensitive, should be reevaluated. The more likely figures are a lifetime prevalence of one in 10,000 in the general population, perhaps as low as 2%, of the epilepsy population. Further epidemiologic studies, sensu strictu, are warranted to settle the basic question of the real incidence and prevalence of photoparoxysmal responses (PPRs) and epilepsy with seizures provoked by visual stimuli in the community.