Search

Self-induction of epileptic seizures is generally regarded as a rarity, chiefly observed in patients of subnormal intelligence. During EEG recordings with open eyes in a consecutive series of 48 photosensitive patients, however, 13 subjects induced paroxysmal activity of seizures by eyeclosure with forced upward deviation of the eyes. Eyeclosure on command produced a different type of oculographic artefact and induced paroxysmal activity in only one subject. Two patients were of subnormal intelligence but all displayed psychiatric or psychosocial problems. The incidence of induced paroxysmal activity was reduced by reduction of ambient lighting. Eight patients admitted self-induction of seizures. We conclude that this phenomenon occurs more often than was previously supposed and can be recongnized by the recording in photosensitive patients of prolonged EEGs with eyes open and in a brightly lit environment. [ABSTRACT FROM AUTHOR]

A group of 15 volunteers with both photosensitive epilepsy and pattern sensitivity were shown patterns of stripes in the left and right visual hemifields. In the majority of patients the resulting paroxysmal epileptiform EEG activity was maximal in the posterior temporal and occipital regions contralateral to the stimulus. Patterns in the upper and lower hemifields were also presented and in two patients there was a difference in the vertical distribution of the response such as to suggest that in these patients the discharges were largely confined to the striate and prestriate cortex. The probability with which paroxysmal activity was evoked was usually different for the two lateral hemifields. This difference between the hemifields (which was dramatic in some patients) was mirrored in a lateralisation of the responses to diffuse intermittent photic stimulation. The association between the asymmetries in pattern sensitivity and in the responses to photic stimulation suggests that the two cerebral hemispheres often differed in hyperexcitability. It is therefore interesting that the putative differences in hyperexcitability were observed in patients with primary generalised epilepsy as well as those with other types.

A multivariate pattern recognition technique has been developed, to distinguish the EEGs of patients with cerebral pathology from those of normal controls and to localize any abnormalities detected. Two methods of feature extraction have been used, power spectral density and slope descriptor analysis, together with various types of feature compression. These techniques have been evaluated on EEGs from 63 patients with proven pathology. Spectral analysis proved more reliable than slope descriptor analysis and predicted the site of cerebral pathology more accurately than did visual assessment of the EEGs. This apparent improvement over the diagnostic reliability of visual analysis in considered to justify further development and evaluation of this technique.

Seven patients with pattern-sensitive epilepsy were examined repeatedly over a period of 4-12 months during which the dose of sodium valproate was adjusted. Patterns were presented in series in which the size of successive patterns was progressively increased until paroxysmal activity appeared, or until the largest pattern (radius 24 degrees visual angle) had been presented. As valproate dose increased, paroxysmal activity was less likely to occur. When it did occur it was less likely to include a spike; it had a lower voltage, involved fewer electrodes, and lasted a shorter time. The size of the pattern just sufficient to induce paroxysmal activity showed relatively little change with valproate dose. The degree to which the various electrodes were involved in the discharges showed considerable stability. The paroxysmal response to patterns presented in one visual half-field was almost invariably maximal over the contralateral posterior quadrant, usually at the posterior temporal electrode.

The capacity of striped patterns (square-wave gratings) to induce paroxysmal EEG activity in a group of pattern-sensitive epileptic patients is shown to depend on: 1. The spatial frequency of the pattern. The optimum spatial frequency lies between 1 and 4 cycles/degree in every patient tested. 2. The orientation of the pattern. Although, for the patient group as a whole, no one orientation is consistently more likely to induce paroxysmal activity than any other, the responses of individual patients can show marked orientation selectivity. 3. The brightness contrast of the pattern. The probability of paroxysmal EEG activity increases dramatically as contrast is increased from 0.2 to 0.4. Red/green gratings at isoluminance fail to induce paroxysmal activity. 4. The size of the pattern. There is considerable variation between patients in the subtense of a centrally-fixated circular pattern necessary to induce paroxysmal activity with a given probability. However, for every patient an increase in the probability of paroxysmal activity from near zero to near unity is effected by an increase in the angular subtense of the pattern by a factor of two. Patterns other than square-wave gratings are capable of inducing paroxysmal activity but, in general, patterns that stimulate more than one orientation system are less epileptogenic. The above findings are compatible with the hypothesis of a seizure trigger in the striate cortex and are incompatible with a trigger confined to the lateral geniculate nucleus of the thalamus. Further evidence against a geniculate trigger is obtained from an investigation of the response of a pattern-sensitive patient to a diffuse (unpatterned) flickering field in which it is shown that the effects of counter-phase interocular flicker implicate binocular mechanisms.

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.

Patients with photosensitive epilepsy were asked to view normally functioning 625-line televisions while the EEG was monitored. In the first of two studies paroxysmal EEG activity was reliably induced by television at a viewing distance related to a patient's sensitivity to intermittent photic stimulation (IPS); patients who were sensitive to diffuse IPS at 50 Hz were sensitive to the television at greater viewing distances than those who were not. No such relationship was obtained with patterned IPS. On the other hand, patterned IPS was generally more epileptogenic than diffuse IPS with the same luminance. In the second study, where the angular subtense of the television screen and the subtense of its lines were manipulated independently, the convulsive response was found to be a function of both factors, the relative contribution of each depending on the viewing distance at which the patient was sensitive. For patients sensitive at normal viewing distances, where 50 Hz diffuse flicker appeared to be responsible for the induction of paroxysmal activity, the probability with which paroxysmal activity was induced was closely related to the subtense of the screen. For patients sensitive only at closer viewing distances the probability was influenced not by the subtense of the screen but by the subtense of its lines, suggesting that the paroxysmal activity was induced by the 25 Hz pattern alternation produced by the scan. A television with a small screen was considerably less epileptogenic than one with a large screen for all patients, presumably due to the reduced contribution of both diffuse flicker and pattern alternation.