Photosensitive Epileptic Patients Research Articles

Flash-evoked high-frequency EEG oscillations in photosensitive epilepsies

ObjectiveTo determine the feasibility of measuring scalp-recorded, flash-evoked, high-frequency EEG oscillations (F-HFOs) using a relatively simple technique. Furthermore, to assess whether F-HFOs are enhanced in photosensitive epileptic patients and if they might be proposed as a putative non-provocative biomarker of photosensitivity. MethodsWe studied 19 photosensitive patients with idiopathic generalized epilepsy, and 22 controls matched for demographic features. We extracted F-HFOs from the broadband scalp flash-visual evoked potential (b F-VEP) through appropriate filtering. We measured F-HFO amplitude, number and latency. Also, we carried out a time-frequency domain spectral F-HFO analysis. Inter-group statistics was performed. Within-groups, F-HFO features were correlated to the b F-VEP. ResultsThe N3-N3I wave of the b F-VEP was significantly (p = 0.01) larger in patients compared to controls. The same was true for the inter-group F-HFO amplitude (p = 0.01). F-HFOs showed two main spectral peaks (∼88 and ∼125 Hz), whose power was greater (p = 0.001) in patients than in controls. The ∼88 Hz peak power exceeded the upper normal range in 15/19 patients. Patients showed a significant (p = 0.04) correlation between the ∼88 Hz peak power and the size of the N3-N3I wave. SignificanceA simplified F-HFO measurement proved feasible. In patients, F-HFOs were enhanced in terms of both size and spectral power, suggesting a role in the generation of the photoparoxysmal response. Some spectral features of the F-HFOs may be proposed as a putative non-provocative marker of epileptic photosensitivity.

Ocular defects in photosensitive epilepsy.

Patients with photosensitive epilepsy are susceptible to seizures due to photoparoxysmal response (PPR). This response adversely precipitates factors that modify the functional status of the visual system. Such factors may or may not be evident superficially, but may lead to ocular defects due to trauma, hormonal imbalance, abnormal intraocular pressure (IOP), or any other reflex-inducing stimuli. The extent to which photosensitive epileptic patients suffer from PPR-related ocular defects has not been documented fully. In this investigation, ocular defects in patients with photosensitive epilepsy are studied using visual-evoked response (VER). A total of 212 photosensitive epileptic patients were studied to ascertain the magnitude and distribution of ocular defects using the changes in EEG and visual-evoked potential (VEP); 51% of the patients were female, the age range was 1—46 years. The major ocular defects and complications found were visual field defects, optic nerve abnormalities, nystagmus, cataracts, amblyopia, and migraine. These findings were analyzed according to age and sex. The relationship between the ocular abnormalities and the interpretations of the changes in the characteristics of the VEP indicated that optic-related atrophies, visual defects, optic neuritis, chiasmal compression, nystagmus, migraine headache, cataracts, and amblyopia were prevalent in photosensitive epileptic patients at varying degrees. The results showed that although ocular defects in photosensitive epilepsy may not be obvious differentially, VEP can be used in their diagnosis, contrary to earlier studies reporting that VEP is not of much value in epilepsy diagnosis.

Optical Filters for TV-Induced Photosensitive Epilepsy

Two different types of optical filters were tested in 20 photosensitive epileptic patients for ability to inhibit photoparoxysmal response (PPR) and seizures, in a study at Gifu Prefectural Gifu Hospital, Japan.

Pupillary response to chromatic flicker.

There is significant evidence for higher-level cortical control of pupillary responses to visual stimuli, suggesting that factors other than luminance changes may induce a pupillary response. In the present study, the pupillary responses to equiluminant flickering stimuli in a range of 3-13 Hz were examined. Flicker stimuli included color-black (luminance-modulated) and color-color (hue-modulated) flicker. Equiluminance was determined both by objective luminance measures as well as by subjective, perceptual equiluminance for each subject. For both objectively and subjectively equiluminant flicker, significant, sustained pupillary constrictions were recorded. The magnitude of these responses was sensitive to both color and frequency parameters; red-blue color-paired flicker consistently produced the strongest constrictions. These responses occurred even when the flicker was of a lower luminance, both physically and perceptually, than a preceding nonflickering color, indicating that chromatic rather than luminance-sensitive mechanisms are involved in this response. Interestingly, the color- and frequency-sensitivity of constriction parallels those of flickers which maximally stimulate photosensitive epileptic patients, raising the possibility that chromatic response may be a factor in photosensitivity.

Mechanisms of Photosensitive Epilepsies

Intermittent photic stimulation was performed in 21 photosensitive epileptic patients and the relation of the photoparoxysmal response (PPR) to the epilepsy syndrome was determined in a study at the National Epilepsy Center, Shizuoka Higashi Hospital, Shizuoka, Japan.

Photosensitive epilepsies and pathophysiologic mechanisms of the photoparoxysmal response.

To identify the pathophysiologic mechanisms of the photoparoxysmal response (PPR) in various photosensitive epilepsy syndromes, and to discuss the relation between these pathophysiologic mechanisms and the classification of epilepsies and epileptic syndromes. The authors found two types of pathophysiologic mechanisms of PPRs (wavelength-dependent PPRs and quantity-of-light-dependent PPRs) in patients with idiopathic generalized epilepsy and hereditary dentatorubral-pallidoluysian atrophy. Intermittent photic stimulation with wavelength-specific optical filters was performed in photosensitive epileptic patients: six patients had severe myoclonic epilepsy in infancy (SMEI), eight had localization-related epilepsy (LRE), and seven had symptomatic generalized epilepsy (SGE). Four of the six photosensitive SMEI patients had quantity-of-light-dependent PPRs. Five of the eight photosensitive LRE patients had wavelength-dependent PPRs. Four of the seven photosensitive SGE patients had wavelength-dependent PPRs, and two had quantity-of-light-dependent PPRs. The type of pathophysiologic mechanism for eliciting PPRs by low-luminance photic stimulation was closely related to the classification of the epilepsy syndrome.

Preliminary Assessment of the Efficacy of Org 6370 in Photosensitive Epileptic Patients: Paradoxical Enhancement of Photosensitivity and Provocation of Myoclonic Seizures

Photosensitivity has proved to be a useful model to study the acute effects of experimental antiepileptic drugs (AEDs). The photosensitivity range is usually diminished or even abolished after administration of a known or experimental AED. An increase in photosensitivity, an unexpected reaction, was found in four photosensitive epileptic patients after oral ingestion of 500, 100, or 50 mg of Org 6370. Moreover, the three patients receiving doses of 100 and 500 mg reported nausea, dizziness, restlessness, and an increase in spontaneous epileptic seizures (myoclonus and in one patient a generalized tonic-clonic convulsion). The side effects coincided with peak Org 6370 serum levels. Our findings indicate that in the photosensitivity model experimental drugs with proven anticonvulsant properties in animals may increase rather than decrease the degree of patient photosensitivity. Photosensitive patients may represent a special subgroup of epileptic patients and therefore need to be classified as such.

Seasonal variations in the incidence of photoparoxysmal response to stimulation among photosensitive epileptic patients: evidence from repeated EEG recordings.

EEG records of photosensitive epileptic patients with repeated EEG recordings at different seasons of the year, were examined for the occurrence of photoparoxysmal response to photic stimulation (photoparoxysmal discharges (PPD]. Recordings in summer showed a lower incidence of PPD compared with recordings in other seasons. Recordings in winter showed a higher incidence of PPD compared with recordings in other seasons. Details of the 11 patients, each of whom had EEG recordings in summer and in winter confirmed the relative rarity of PPD in summer compared with winter. This reflects a lower cerebral neuronal excitability in summer compared with winter. Mechanisms for this, though not clear, may be related to an increased amount of environmental sunshine during summer and/or reduced temperature during winter.

Colour and photosensitive epilepsy

Red-coloured flicker is claimed to be more epileptogenic than white or that of other colours matched for subjective intensity. A feature of the colour opponent system is that the response of luminosity-sensitive cortical units to stimulation of ganglion cells of a particular spectral sensitivity is reduced when cells of other sensitivities are simultaneously stimulated. We hypothesized that the apparent effect of colour on photosensitivity was not a property of red light per se but arose simply from the fact that, with commercially available filters a light can be provided to stimulate only red sensitive cones, but owing to the overlap of the absorption spectra of the visual pigments it is difficult to stimulate only green or blue sensitive cones. Such stimulation of a single cone population can be achieved by the ‘silent substitution method’ which has been used for evoked response studies. In 12 photosensitive epileptic patients we find that, using stimulus intensities (less than 20 nits) at which white flicker is without effect, stimulation of either red or green cones by the silent substitution method may produce epileptiform discharges, there being a slight (and not significant) excess of patients showing a greater sensitivity for green than for red cone stimulation. The findings are considered to support the hypothesis set out above.

Interhemispheric differences in photosensitive epilepsy. II. intermittent photic stimulation

Of a consecutive series of 138 photosensitive epileptic patients 57 showed a unilateral preponderance of asymmetrical discharges on IPS, significant in each individual at the 5% level. There was no association between asymmetry of IPS-induced discharges and clinical evidence of cerebral pathology (partial or secondary generalized epilepsy, neurological deficit, left handedness, etc.). It is concluded that these results, together with our previous findings of asymmetrical pattern sensitivity suggest that the cortical hyperexcitability postulated in primary cortico-reticular epilepsy is not uniformly distributed.

EEG sensitivity to television: Effects of ambient lighting

The effect of ambient lighting on EEG sensitivity to television has been tested in 16 photosensitive epileptic patients. Those who were not sensitive to 50 Hz IPS responded to TV at a viewing distance of 1 m or less and showed a consistent increase of EEG activation by television when the room was brightly lit. Most of those who were sensitive to 50 Hz IPS were also TV-sensitive at viewing distances greater than 1 m and the effect was most marked with lights off. The results are discussed in the context of previous work showing that some patients with TV epilepsy respond to the raster pattern of the screen and some, at greater distance, to 50 Hz flicker.

Photomyoclonic response of epileltic and non-epileptic subjects during wakefulness, sleep and arousal

1. 1. The clinical photomyoclonic response (PMR) of eleven photosensitive epileptic patients and two non-epileptic subjects was studied by polygraphic EEG and ultraviolet apparatus recording of single responses and by computer summation. The responses spread after single light flashes over the deltoid, biceps, forearm flexors, quadriceps and gastrocnemius muscles with latencies of about: 61, 64, 65, 83 and 95 msec respectively. Agonists and antagonists contracted almost simultaneously. 2. 2. These latencies are virtually identical to those of the sub-clinical physiological reflex described by Bickford as the “photo-motor response”. The PMR is considered as an enhancement of it. 3. 3. In NREM sleep, following arousal from NREM sleep and during REM sleep, the PMR and the photoconvulsive response were diminished. Following arousal from REM sleep they were less diminished and quickly became those of wakefulness. 4. 4. In patients with petit mal absences and petit mal myoclonus, arousal from NREM sleep, unlike that from REM sleep, provoked prolonged myoclonus associated with EEG poly-spike and wave discharges while the PMR and PCR remained suppressed.