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  • Updated 01.23.2024
  • Released 02.12.2004
  • Expires For CME 01.23.2027

Visual-sensitive epilepsies



Visual-sensitive seizures elicited mainly by video games, television, and flickering lights in nightclubs are the more common reflex seizures, and most physicians can expect to encounter them. Children and teenagers are more vulnerable. However, in modern life with the increasing numbers of video game players and the spread of visual electronic media, the demographics of visual-induced seizures have expanded to nearly any age, and they sometimes get to epidemic proportions. This updated article reviews these seizures and their triggers and explains the basics of photosensitive epilepsy, pattern-sensitive epilepsy, fixation-off sensitivity, and seizures triggered by television screens, video games, computers, and cell phones. It details developments in their clinical manifestations, differential diagnosis, pathophysiology, and genetics as well as means of their detection and management. It emphasizes populations at risk, factors of misdiagnosis, treatment strategies, avoidance of various triggers, and certain antiepileptic drugs that may aggravate the seizures.

Key points

• Visual-sensitive seizures are provoked by photic, pattern, and other visual stimuli, alone or in combination.

• They are the commonest type of reflex seizures and are mainly triggered by video games, computers, cellphones, and flickering lights of nightclubs.

• Children and teenagers are more affected by visual-sensitive epilepsies, but people of all ages can be affected due to the widespread usage of visual media.

• Clinically, generalized seizures (absences, myoclonic jerks, generalized tonic-clonic seizures) are more common than focal seizures, which are usually visual.

• Certain epileptic syndromes (eg, juvenile myoclonic epilepsy, Dravet syndrome, Unverricht-Lundborg disease) commonly manifest with photosensitive seizures.

• The role of EEG is fundamental in identification of the offending stimuli with significant clinical and pathophysiological implications.

• Avoidance, prevention, or modification of the provocative triggers is the key point of management.

Historical note and terminology

Seizures triggered by visual stimuli were known in classical antiquity (123; 90; 57; 10; 71; 94; 63).

The first reference to photosensitive epilepsy is attributed to Apuleius Lucius (150 AD), a Roman philosopher in his “Apologia and Florida.” However, Apuleius does not refer to flickering lights:

Nay, even supposing I had thought it a great achievement to cast an epileptic into a fit, why should I use charms when, as I am told by writers on natural history, the burning of the stone named gagates is an equally sure and easy proof of the disease? For its scent is commonly used as a test of the soundness or infirmity of slaves even in the slave-market. Again, the spinning of a potter's wheel will easily infect a man suffering from this disease with its own giddiness. For the sight of its rotations weakens his already feeble mind, and the potter is far more effective than the magician for casting epileptics into convulsions (Apuleius Lucius, 150 AD).

The oldest clear reference to photosensitive epilepsy is by Soranus Of Ephesus (2nd century AD) a Greek gynecologist, obstetrician, and pediatrician, who in Acute and Chronic Diseases, which contains an excellent chapter on nervous disorders, wrote:

The use of flame, or very bright light obtained from flame, has an agitating effect. In fact when a case of epilepsy is in its quiescent stage, the ultimate use of light with its sharp penetrating action may cause the recurrence of an attack. (Soranus Of Ephesus, 2nd century AD).

Clementi was the first to describe experimental, light-induced epilepsy in studies of photic stimulation in dogs after strychnine application to the visual cortex (35). The effective triggering stimuli had to be repetitive. The following quote is from an English translation of Clementi’s report (71):

Under such experimental conditions, (continuous strychninisation of dog occipital cortex for 20’-30’), photic stimulation triggered an epileptic attack that began after a few minutes with nystagmus, mydriasis, and tonic eye deviation toward the side contralateral to the strychninised hemisphere, and continued with clonic movements involving first the periocular muscles and then the entire body. . . . Noteworthy extension of the strychninised occipital cortical area appears to be a necessary condition for onset of reflex epilepsy if strychninisation is limited to a single hemisphere. If, on the other hand, strychnine is applied over both hemispheres, strychninisation of a highly limited area may be sufficient (35).

The first clinical evidence of photosensitive epilepsy by Gowers and later by Holmes refers to occipital seizures induced by light (67; 83).

In very rare instances the influence of light seems to excite a fit. I have met with two examples of this. One was a girl of seventeen whose first attack occurred on going into bright sunshine for the first time, after an attack of typhoid fever. The immediate warning of an attack was giddiness and rotation to the left. At any time an attack could be produced by going out suddenly into bright sunshine. If there was no sunshine an attack did not occur.

The other case was that of a man, the warning of whose fits was the appearance before the eyes of “bright blue lights, like stars--always the same.” The warning, and a fit, could be brought on at any time by looking at a bright light, even a bright fire. The relation is, in this case, intelligible, since the discharge apparently commenced in the visual centre (67).

Holmes attributed this “reflex epilepsy” to an enhanced excitability of the visual cortex:

Some men subject to epileptiform attacks commencing with visual phenomena owing to gunshot wounds of the occipital region, have told me that bright lights, cinema exhibitions and other strong retinal stimuli tend to bring on attacks (83).

Radovici and associates in 1932 reported the first case of eyelid myoclonia (often erroneously cited as self-induced epilepsy) with experimental provocation of seizures documented with cine film (150).

AA...age de 20 ans, presente des troubles moteurs sous forme de mouvements involontaires de la tete et des yeux sous l' influence des rayons solaires.

Goodkind in 1936 also detailed various methods used to experimentally induce “myoclonic and epileptic attacks precipitated by bright light” in a photosensitive woman:

The patient was placed on a bed in a darkened room in such a position that when the black window shade was raised, her face only was directed towards the early afternoon sunlight, which came through an ordinary wire window screen. On such exposure of the eyes to the sun, she responded within a few seconds with marked, diffuse, and apparently uncontrollable clonic jactitatory movements. The movements ceased the moment a blindfold was applied or the black window shade was lowered. She reacted definitely also when either eye was uncovered separately. . . . The patient was also exposed to ultra violet radiation from a quartz mercury vapour lamp and to bright pocket flash light, to little or no effect. A small beam from a carbon arc lamp produced several rapid myoclonic jerks (66).

With the advent of EEG by Berger in 1929, a new era started for the study of photosensitive epilepsies. Adrian and Matthews in 1934 were the first to introduce intermittent photic stimulation in the use of EEG (01). The subject was looking at an opal glass bowl that was illuminated from behind by a lamp, in front of which a disc with cut-out sectors was rotated.

Strauss in 1940 was the first scientist to record epileptic seizures induced experimentally by photic stimulation (168). His patient, a woman aged 33 years, had suffered right hemiparalysis and right Jacksonian fits from childhood. The epileptic attacks could be provoked by various sensory stimuli (tactile, auditory, visual etc.). He recommended that these stimuli should be noted not only by purely clinical observation but also, if possible, by EEG studies on the patient.

Flashing light into the right eye was associated with changes in the electroencephalogram. Three-per-second waves at high potential appeared, associated with twitching around the right corner of the mouth. The slow waves did not appear when the same stimulus was applied after cocainization of the right eye. The potentials, without a doubt, were true brain potentials because they could not be reproduced by having the patient imitate the twitching activity. Moreover, their appearance in the record from the left side makes it improbable that they represent muscle potentials from the muscles on the right side of the face (168).

The real interest and detailed study of epilepsy by means of intermittent photic stimulation (IPS) activation was established by Walter and his associates in Bristol, England who started using a high intensity lamp of strobotron light to produce IPS (190; 191; 189). They found that IPS at a “magic frequency,” mostly 12 to 18 Hz, could induce subjective and objective symptoms, which correlated with specific EEG patterns. The most dramatic EEG abnormalities occurred in patients, mostly children, with a history of seizures but also to a lesser extent in subjects with only a family history of epilepsy. Clinically, these could be associated with bilateral or asymmetrical myoclonic jerks and “petit mal” attacks, rarely in combination.

Henri Gastaut and his associates in Marseilles, France have made numerous contributions to what we know about photosensitive epilepsies (60; 59; 58; 191; 61).

EEGs from the majority of patients with photosensitivity showed generalized discharges, and the view that photosensitivity was a generalized “centrencephalic” epilepsy dominated the relevant literature (60; 58; 15; 16).

Panayiotopoulos was the first to document that photosensitive epilepsy originates from the occipital regions (123).

Occipital spikes in photosensitive patients with generalized PPR
(Left) Patterned intermittent photic stimulation (2 mm × 2 mm graticule superimposed on the grass of the stroboscope) evoked occipital spikes, which are time-locked to flash at 6 flashes/second of a patient with spontaneous and ph...

Since then, different visual stimuli have been added to the list of visual-induced seizure possibilities. The problem of color was evident in 1997 when the Pokemon phenomenon occurred and was studied extensively (86; 174).

Numerous research groups, from basic science to the clinic, have been working on photosensitivity. They found that the physical characteristics of visual stimuli that can induce seizures include factors such as light intermittent frequency, intensity, contrast, type of color, and distance from the incentive. These characteristics are clues to trigger seizures, prevent them, and evaluate treatments (171).

The significance of reflex visual seizures lies in their connection to the external world and the brain, providing valuable insights into various aspects of epilepsy, including neural network mechanisms and treatment efficacy.

It is important to note that although visual sensitivity refers to an individual susceptibility to visual stimuli to trigger seizures, photosensitivity is a specific type of sensitivity that can trigger epileptiform activity on EEG in some individuals. Photoparoxysmal responses (PPR) were considered to be primarily generalized (58; 61; 12; 79), although the initial occipital onset of the generalized EEG discharge has been reported (137; 123; 123). Both visual sensitivity and photosensitivity are closely connected as they involve processing visual stimuli in the brain, and they have been extensively studied.

In 2012, a European group of experts led by Kasteleijn-Nolst Trenite emphasized the importance of testing photosensitivity on EEG with a correct and standardized activation protocol, promoting a European algorithm for visual stimulation in the EEG laboratory. This method is internationally recognized and is recommended as the appropriated method to test photosensitivity.

Modern functional image techniques, like EEG-MRI and PET, have increased the comprehension of the dysfunctional networks involved in the abnormal response to visual stimuli.

Nomenclature and classification. For a long time, the value of reflex seizures, like visually induced seizures, in epilepsy diagnosis was debated. In 2014, the International League Against Epilepsy’s (ILAE) practical clinical definition of epilepsy assumed that reflex seizure has the same value as an unprovoked seizure in defining epilepsy. (52).

The ILAE defines reflex seizures as seizures regularly induced by specific stimuli, such as sensory, sensory-motor, or cognitive, which cannot be avoided daily. Visual sensitivity is the most common form of stimulus-evoked seizure. Visual-sensitive epilepsies are enduring conditions predisposed to seizures induced by different physical characteristics of visual stimuli (153).

In 2022, the ILAE recognized two types of visually sensitive epilepsy syndromes: (1) photosensitive occipital lobe epilepsy (POLE) and (2) epilepsy with eyelid myoclonia. Although other visual epilepsies are not considered independent syndromes, seizures induced by visual stimuli can occur in syndromes such as juvenile myoclonic epilepsy, other generalized genetic epilepsies (GGE), developmental and epileptic encephalopathies (DEE), and other syndromes, such as Dravet syndrome.

Photosensitivity is the abnormal response to intermittent photic stimulation on EEG termed “photoparoxysmal response” (PPR). It consists of epileptiform discharges (spikes, polyspikes, or spike-and-wave complex) that are more frequently bilateral and more or less extended. Bilateral epileptiform discharges are the most frequent responses (58; 61; 12; 79), but they can occur with initial occipital onset (137; 123; 123).

Intermittent photic stimulation (IPS) responses were initially classified by Waltz and colleagues (192). Kasteleijn-Nolst Trenite and colleagues proposed an ILAE classification system for IPS responses in 2001. A simplified version by Meritam Larsen has been proposed to improve clinical utility and interobserver agreement (115).

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