The use of automated low frequency wave analysers in quantitative electroencephalography.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to G F Harding.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Visual evoked potentials (VEPs) to pattern reversal stimulation have been obtained in 10 premature babies. The babies were born between 32 and 35 weeks gestational age and had pattern reversal VEPs recorded on at least 2 separate occasions. The responses were obtained from 33 weeks gestational age, and all babies had their initial recording at or before 37 weeks gestational age. The pattern reversal stimulation was produced on a small hand-held television monitor. The black and white checks subtended a visual angle of 2 degrees. Flash VEPs were also recorded on each occasion for comparison. The pattern reversal response consisted of a major positive (P1) component around 280 msec. The latency of the P1 component correlated negatively with gestational age. Although the flash VEP in the same babies was often dominated by the initial negative component no similar negative components were seen in the pattern reversal response.
A patient presented with a right rolandic space occupying lesion resulting in a decrease of position sense, touch and stereognosis in the left upper limb. SEPs revealed an augmentation of the right hemisphere P22 component co-existing with relative attenuation of all other right hemisphere components. The augmented P22-N31 complex represented a 'giant' potential in relation to a control group (> 2.5 S.D.). The data provide further evidence that the P22-N31 complex has separate generators from those responsible for the N20-P27-N33 components parietally and P20-N30 components frontally. The focal nature of the lesion and symptomatology are of interest.
Vigabatrin is an antiepileptic drug for the treatment of partial seizures. The anticonvulsant effect is achieved by irreversible inhibition of the enzyme GABA-transaminase which catalyses the inactivation of GABA. Vigabatrin has been associated with visual field loss and electrophysiological abnormalities. The purpose of the study was to determine any alterations in normal volunteers of the visual field and the visual electrophysiology resulting from a short exposure to vigabatrin. A three-way, double-blind study of placebo, carbamazepine and vigabatrin was undertaken at baseline and on days two, four and nine. Seven subjects completed all three cycles and 14 subjects (six females and eight males; mean age 27.3 years SD 6.7) completed at least one cycle. Static threshold automated perimetry comprised Humphrey Visual Field Analyzer Programs 30-2 and 30/60-2. Electro-oculography and electroretinograms were performed with undilated pupils using the Medelec Ganzfeld stimulator GS2000. The visual field was unaffected by placebo, carbamazepine or vigabatrin. The group mean amplitudes and latencies for the scotopic ERG, 30 Hz flicker ERG and the oscillatory potentials remained unchanged for any cycle. The group mean photopic ERG b-wave latency increased from baseline (p<0.05); no significant change occurred with carbamazepine or placebo. The group mean Arden Index for vigabatrin decreased from baseline to day 9 (p<0.01); no significant differences were present for carbamazepine or placebo. Vigabatrin has a rapid effect on both the photopic ERG and the EOG; however, the changes merely reflect alterations in retinal GABA levels secondary to concomitant blocking of GABA transaminase by existing vigabatrin therapy.
The effect of enteric-coated sodium valproate on 10 normal volunteer subjects was evaluated using simple reaction times, the visual evoked potential (VEP), and EEG sleep recording. Placebo, low-drug (500 mg), high-drug (1,000 mg), and withdrawal conditions were investigated. No significant treatment effect was found for simple reaction time nor was there any significant effect on either the latency or the amplitude of the VEP. Sleep recordings were analysed visually and also using an automated technique consisting of simple period analysis. The automated sleep results suggested that there was a decrease in rapid eye movement activity and an increase in delta activity under the high-drug condition. The visually analysed data did not reach significance, although they followed the same trends as those analysed automatically. It is possible that the automated results reflect an EEG frequency change rather than a change in the sleep cycle itself caused by treatment with sodium valproate.
Since 1968, annual EEG recordings during photic stimulation using a standardised technique have been made on photosensitive patients and siblings. In 1983, 72 were aged greater than or equal to 20 years and 14 were aged 16-19 years. Mean duration of follow-up was 9.8 +/- 4.8 years. Seventy-five patients were treated with sodium valproate (VPA), which was withdrawn in 15 but restarted in eight because of return of photosensitivity. Eighty-two patients had seizures at some time; at follow-up 58 were receiving monotherapy with VPA, seven were receiving comedication, and three were taking other drugs. Fifty-four of them were seizure free, as were 10 of the 15 who were not being treated with drugs. Photosensitivity disappeared in 44 of 65 patients at a mean dosage of VPA at 21.5 +/- 6 mg/kg day. In 55 of 86 patients photosensitivity was no longer present at follow-up; in 18, slight abnormality was evoked by intermittent photic stimulation, and in 13, photoconvulsive responses were still present. Eighteen patients were not receiving drugs, 10 of them being no longer photosensitive at the mean age of 24.5 +/- 4.9 years. Thirty-one treated and untreated patients were still photosensitive at age 21.5 +/- 3.4 years. Photosensitivity disappeared earlier in those treated with VPA than in the untreated. Spontaneous remission in the treated cases may have occurred at 22.9 +/- 2.5 years of age. Photosensitivity appears around puberty and may disappear around 24 years of age. Photosensitive epilepsy is easily and rapidly controlled by VPA.
Nine patients who had epileptic attacks while playing computer games were studied in the laboratory. Patients had an EEG recorded as well as their response to intermittent photic stimulation (IPS) at flash rates of 1-60 fps. In addition, pattern sensitivity was assessed in all patients by a gratings pattern. Only 2 patients had no previous history of convulsions, and only 2 had a normal basic EEG. All but 1 were sensitive to IPS, and all but 1 were pattern sensitive. Most patients were male, but although this appears to conflict with previously published literature results regarding the sex ratio in photosensitivity, it was due to the male predominance of video game usage. We compared our results with those reported in the literature. Diagnosing video game epilepsy requires performing an EEG with IPS and pattern stimulation. We propose a standard method of testing.
Over the last decade, vigorous efforts have been made by neuroscientists to unravel the cellular and molecular basis of photosensitive Epileptogenic activities in the central nervous system (CNS). Many neurotransmitters are implicated in brain activities but the extent to which they participate in these activities needs to be clarified. This review discusses the involvement of serotonin (5-hydroxytryptamine, 5-HT) in photosensitive epilepsy. The biosynthesis, metabolism, and structural and functional distribution of serotonin in the brain, and the role of 5-HT, its precursors, metabolites, receptors, agonists, antagonists, and the enzymes of reaction in photosensitive epileptogenic activity with reference to 5-HT cortical density, are discussed. The effects of biosynthetic and metabolic impairments in the serotonergic system, and the extent to which they contribute to the elicitation of myoclonic phenomena, hallucination, impulsivity, and migraine (HIMM) in photosensitive epilepsy are critically reviewed, and supported by evidence from animal models of photosensitive epilepsy. This evidence is correlated with the clinical findings in human photosensitive epilepsy.
Since 1975 four-channel ambulatory monitoring has been available as a technique for prolonged EEG recording in an unrestricted environment. This increases EEG sampling time so that attacks can be recorded and enables the differentiation of epileptic and non-epileptic attacks. In recent years an eight-channel system has become available which provides greater scalp coverage and allows better localization of attacks and EEG abnormalities. Four-channel recording has been widely used to assess the efficacy of anticonvulsant medication in patients with absence seizures. It has also been used to investigate the effect of the environment on discharges, as well as any circadian variations in discharges. Ambulatory monitoring provides a useful alternative to sleep recording in the laboratory, both for the detection of abnormalities during sleep and for experimental sleep studies. Automated analysis techniques have so far been confined to the analysis of spike and wave activity and to the scoring of sleep stages.
Visual evoked cortical and sub-cortical potentials are complementary to the electroretinogram in neuro-ophthalmology. By combining monocular stimulation with recordings from over the visual cortex of each cerebral hemisphere it is possible to accurately locate lesions which are both pre and post chiasmal. Chiasmal lesions can also be correctly identified using these techniques. The visual evoked sub-cortical potential, probably arising from a lateral geniculate or tectal site allows further post chiasmal variation. Flash and pattern reversal stimulation provide different information about the functioning of the visual system including the primary visual cortex and the association areas.