Paroxysmal EEG Activity Research Articles

Effects of EEG of the osmotic opening of the blood-brain barrier in rats

EEG activity was recorded in rats submitted to osmotic opening of the BBB by intracarotid mannitol infusion. This procedure produced an immediate short-lasting depression of the EEG and a tardive paroxysmal EEG activity. Both these phenomena were more relevant on the ipsilateral hemisphere. In some instances a tonico-clonic seizure was recorded. Pre-treatment with diazepam abolished the occurrence of the tardive EEG and behavioral modifications. In accord with previous findings, focal seizure activity is likely to be responsible for the metabolic abnormalities associated with osmotic opening of the BBB. This preparation therefore produces in the brain unphysiological states in respect to local metabolism and electrical function.

Television epilepsy — The role of pattern

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.

Paroxysmal EEG Activity and Psychopathology During the Treatment with Clozapine

EEG effects and psychopathological changes during treatment with clozapine* and haloperidol* were compared. Thirty-nine acute schizophrenic patients (20 clozapine and 19 haloperidol) were treated with doses adjusted to the patients' needs. Data was collected on days 0, 3, 10, 20 and 30. Paroxysmal EEG patterns during a 20-minute recording were counted (blind evaluation) in 6 scalp areas. Twelve psycho-pathological syndromes were assessed using a standardized rating scale (AMP System).

Drug-induced paroxysmal EEG-activities.

Drug-induced paroxysmal EEG-activities.

Neurophysiological aspects of pattern-sensitive epilepsy.

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.

Evoked and spontaneous corticofugal multiple unit activity during different phases of metrazol infusion in cats

Multiple unit activity (MUA) was recorded from the cerebral peduncle during preictal, ictal and postictal phases of Metrazol infusion in cats. During preictal EEG paroxysmal activity MUA activity increased, sustained MUA discharge preceded the onset of tonic EEG seizure activity and bursts of MUA activity coincided with positive transients during late tonic and clonic periods. No MUA discharge was observed during postictal depression. During preictal periods, Metrazol increased the amplitude and duration of the initial MUA burst to stimulation of the ventralis posterolateralis nucleus. The duration and intensity of the MUA suppression following the response was also increased. The burst-suppression pattern of MUA activity during repetitive stimulation was replaced by a burst-sustained discharge pattern. The changes observed in EEG and MUA are correlated with previously described intracellular changes and provide a consistent picture of EEG, neuronal and axonal behaviour during Metrazol administration. Axonal activity provides a more relevant indication of effective corticofugal activity than does intracellular recording. The level of axonal discharge correlates better with the degree of soma-dendritic depolarization than it does to somatic spike generation.

Electroencephalogram and somatosensory evoked potential changes after administration of six convulsant drugs

Electrophysiological effects of convulsant drugs in mammalian brain have been reported, but it has not been clear whether the changes described were indicative of general increases in neuronal excitability or whether they varied as a function of the different modes of convulsant action. Cats with chronically implanted electrodes were administered intraperitoneal injections of six convulsant drugs: allylglycine, bemegride, bicuculline, picrotoxin, pentylenetetrazol, and strychnine. The electroencephalogram (EEG) was monitored continuously and somatosensory evoked potentials were elicited during the period to seizure onset. Enhancement of the primary response of the evoked potentials recorded at the cortex paralleled the increases in EEG paroxysmal activity. Both EEG and evoked potential changes were regarded as indicating general preseizure excitability rather than varying with the presumed mechanisms of the individual drugs.

Re-evaluation of estrogen-induced cortical and thalamic paroxysmal EEG activity in the cat

Conjugated estrogens (Premarin), piperazine-esterone-sulfate (Ogen) and esterone-3-sulfate were applied bilaterally or unilaterally to sensory-motor cortex in locally anesthetized, paralyzed cats. All these agents (1–2% concentration) initiated paroxysmal activity characterized by 2–3 c/sec spike and wave discharge that was generalized bilaterally over cortex and in the nuclei ventralis anterior, medialis dorsalis and centrum medianum of thalamus. In contrast, unilateral micro-injection (2%, 0.01 cc) of conjugated estrogens into thalamic nuclei resulted in 7–20 c/sec poly-spike activity recorded bilaterally over cortex and in the contralateral thalamus. Spike and wave discharges were not observed following thalamic injection of estrogens. Ipsilateral electrolytic lesions of either ventralis anterior or centrum medianum failed to decrease spike and wave discharge originating from a cortical focus. In chronically-isolated slabs of suprasylvian cortex, topically applied conjugated estrogens induced 1–3 c/sec spike and wave activity restricted to the isolated tissue in the absence of spread of activity to surrounding intact cortex. In contrast to the estrogenic steroids, progesterone, testosterone and diethylstillbesterol failed to initiate paroxysmal activity after bilateral topical application in concentrations of 10% although the application of either testosterone or progesterone was associated with spindle formation in some animals. These findings demonstrate a capacity of cerebral cortex to generate spike and wave discharge in the absence of subcortical influences, a generalization of spike and wave discharge from a unilateral cortical focus and an epileptogenic specificity of estrogens. The experimental spike and wave complex produced by topically-applied estrogens is discussed in reference to the epileptiform EEG of clinical petit mal or petit mal variant.

Electroencephalographic correlates of myoclonus

In order to overcome various drawbacks of the conventional polygraphic study of a relationship between myoclonus and EEG, the EEG preceding and following the myoclonic jerk was simultaneously averaged by the CNV program. The subjects were 7 patients presenting with myoclonus of various kinds. The conventional polygraphs showed various paroxysmal EEG activities in 4 patients, but none of those paroxysmal activities was temporally related to myoclonus except for one case. As a result of the present averaging technique, 2 patients with cerebellar ataxia with intention myoclonus showed myoclonus-related EEG spikes or spike-and-slow-waves in the contralateral central or centroparietal region. These myoclonus-related spikes preceded the myoclonus by 10–17 msec, suggesting the presence of a discharging focus in the deep cerebral structures, rather than in the cerebral cortex, in these cases. Two other patients, one with resting myoclonus and the other with postural myoclonus, showed myoclonus-related slow waves on the contralateral hemisphere. This previously undescribed method of averaged polygraphic recording will be very useful in detecting an EEG correlate of spontaneously occurring myoclonus.

Drugs modifying dopaminergic activity and behaviour, the EEG and epilepsy in Papio papio

Acute changes in spontaneous motor activity, the EEG and photically induced epileptic responses have been observed in baboons ( Papio papio) following the i.v. injection of drugs acting on dopaminergic transmission. Apomorphine hydrochloride, 0.5–1.0 mg/kg, produced a phase of acute excitement with accentuated vigilance and abnormal buccal motor activity lasting 30–40 min; during this phase myoclonic responses to intermittent photic stimulation were absent. After piribedil (ET 495, 1,2″-pyrimidyl-4-piperonylpiperazine), 2–10 mg/kg, acute excitement was not seen. Intermittent δ activity was prominent in the EEG for 1–3 hr, and was associated with a slight reduction in photically induced epileptic responses. Haloperidol 0.6–1.2 mg/kg, produced a long-lasting reduction in spontaneous motor activity with an increased incidence of spontaneous EEG spikes and waves and a great enhancement of paroxysmal EEG activity during photic stimulation. Pimozide, 0.5–2.5 mg/kg, normally produced mild sedation and some EEG slowing. 2 animals responded idiosyncratically to both haloperidol and pimozide, displaying intermittent dystonic episodes with bucco-facial dyskinesia. These findings suggest that activation of dopaminergic receptors can lead to a reduction in myoclonic responses to photic stimulation.

A context analysis of psychological states prior to petit mal EEF paroxysms.

This is the first report in the literature of an application of the rigorous symptom-context method for determining the nature of the psychological antecedents of petit mal EEG paroxysmal activity. The activity is defined by the presence of a 3 cycle/second spike and wave on the EEG which is recorded concurrently while the patient is speaking his thoughts freely during interviews. The content of the patient's speech before each petit mal episode is compared with the content of speech during nonparoxysmal periods. Three petit mal patients were examined in this way for four sessions each. (Total petit mal EEG paroxysms for patient no. 1 were 19, patient no. 2 were 25, and patient no. 3 were 55.) For the first patient, strong psychological antecedents were found before petit mal EEG paroxysms as compared with comparison periods from the same patient. These consisted of such usual negative affects as feeling depressed and blocked. For the two other patients, only a few psychological antecedents discriminated significantly and these were not of the same type across the three patients. We conclude that the patients differ in amount and type of psychological antecedents. The differences may be attributed to differences in the type of petit mal and/or differences in the psychological component to the petit mal. The differences among the patients are probably not related to the average length of the paroxysms since we have shown that the relationships with the duration were generally silences than during the patient's speech (for two of the three patients)--talking probably requires more focused attention than silence; more focused attention or activity tends to reduce these episodes.

Influence of chlordiazepoxide on paroxysmal EEG activity induced by hippocampal and-or thalamic cobalt foci.

The influence of chlordiazepoxide (Librium) on the paroxysmal 7–9/sec spike and wave and polyspike EEG discharges induced by chronic cobaltgelatine implantation into the dorsal hippocampus and/or nonspecific thalamus has been studied in rats with electrodes in the frontal cortices, dorsal hippocampi and the mesencephalic reticular formation. Both low (1.5–9 mg/kg i.p.) and high (9–15 mg/kg i.p.) doses of chlordiazepoxide reduced the incidence of paroxysmal EEG manifestations and shortened their duration (when present). Both effects were more pronounced after higher doses. The frequency of spike-wave complexes or spikes within the paroxysmal EEG discharges did not change systematically after chlordiazepoxide. The influence of the drug on the paroxysmal discharges is independent of whether the EEG after chlordiazepoxide is desynchronized or synchronized. In the latter case desynchronization of the EEG by reticular stimulation does not facilitate the occurrence of paroxysmal EEG dischartes.

La panencéphalite sclérosante su baigue : (Leucoencéphalite sclérosante subaiguë de van Bogaert) Historique de nos connaissances et perspectives

After a short historical introduction, the author presents the actual state of our biological knowledge with special reference to the increase of gamma-globulines and measle anti-bodies in the serum as well as in the CSF. He insists upon the works which identified and isolated the measle anti-gene but which nevertheless cannot define a special form of measle encephalities. Two hypothesis (a) immunologic (b) viral, could give an explanation of the observed facts. The neuro-pathological modifications are then related to the EEG abnormalities, but htese relations do not give an entire explanation of the genesis of periodic paroxysmal eeg activities, which are so unusual. The reproduction of encephalitis in the hamster and the ferret, from cerebral biopsies and cell cultures give hopes of further progress in the understanding of the etiopathology and perhaps the therapy of the subacute sclerosing panencephalitis.

The influence of barbiturates on paroxysmal EEG activity induced by hippocampal and-or thalamic cobalt foci.

Epileptiform 7–9/sec spike and wave and polyspike EEG discharges were induced in male albino rats by chronic cobalt-gelatine implantation into the dorsal hippocampus and/or non-specific thalamus.

Electrographic effects of diacetylmorphine (heroin) and naloxone in man

Sixty-three addicts were given heroin intravenously at a rate of 20–40 mg/2 cc/ 2 min, and 8–32 min later received 1–2 mg naloxone. The EEG was recorded in the preheroin, post-heroin and post-naloxone periods. The early response to heroin (first 4 min after the start of the injection) was an increase in alpha amplitudes, decrease of alpha frequency and an occasional increase in alpha spindling. The late response (5–32 min after the start of the injection) was a decrease in alpha abundance, an increase in theta and sometimes delta activities, and paroxysmal EEG activity. Two clinical seizures were seen. The tracings returned to the pre-heroin pattern after the administration of naloxone. These observations of heroin and naloxone are consistent with established theories of association of EEG and behavior in man after psychoactive drugs.

Effects of convulsive doses of 1,1-dimethylhydrazine on somatic evoked responses in the cat

The effects of convulsive doses of 1,1-dimethylhydrazine (UDMH) on somatosensory evoked responses were studied in cats with chronically implanted electrodes in n. ventralis posterolateralis (VPL), in primary somatic cortex (SI), and cerebellar cortex. Stimulation was either to ulnar nerve or to thalamocortical afferent fibers. EEG recordings were made from cerebral cortex and hippocampus. Intraperitoneal administration of UDMH in doses sufficient to produce generalized seizures resulted in a small, inconstant increase of the primary positive evoked response and a large, consistent increase in the primary negative response in SI. The enhancement of cortical evoked responses prior to a seizure is due to increased excitability of superficial cortical layers rather than increased afferent inflow from VPL. The first two waves of the cerebellar evoked response were unaffected by UDMH, while the third wave was depressed prior to seizures. These results are consistent with previous suggestions that UDMH and other hydrazines block production of gamma-aminobutyric acid. Paroxysmal EEG activity sometimes began in the limbic system and then spread to cerebral cortex. The large and consistent increase of SI negative response amplitude prior to seizures is a good predictor of seirure onset. Some possible applications of such a predictor for neurochemical studies of convulsive agents and in epileptic patients are discussed.

Alterations of micromotoric tonus regulation during paroxysmal EEG activity : H. D. Weigeldt (Bremen, W. Germany)

Alterations of micromotoric tonus regulation during paroxysmal EEG activity : H. D. Weigeldt (Bremen, W. Germany)

Autonomic changes during paroxysmal EEG activity

1. 1. Changes in skin resistance, heart rate, skin temperature, respiration and finger vasomotor activity during paroxysmal EEG discharges were evaluated in 54 epileptic patients and five non-epileptic photo-sensitive subjects. Simultaneous recording of autonomic variables and EEG enabled an evaluation to be made of the association of autonomic changes with seizure discharges. 2. 2. All discharges recorded were generalized, bilaterally synchronous, and symmetrical. They were evaluated as to type of wave form and organization, length of burst, whether spontaneous or photically induced, and whether they were accompanied by clinical phenomena. 3. 3. Analysis indicated that no autonomic responses were associated with slow wave bursts and few autonomic responses were present during “subclinical” spike and slow wave discharges. “Clinical” spike and slow wave bursts ( i.e. bursts associated with objective or subjective signs) were usually accompanied by autonomic involvement, the degree of which correlated with the extent of clinical phenomena. Changes in skin resistance and HR were most frequently associated with paroxysmal activity. A GSR and change in heart rate were present during nearly all petit mal discharges, but respiration and temperature responses were variable. 4. 4. The latency of the GSR differed significantly for spike and slow wave complexes and petit mal discharges. Regardless of duration of the burst the GSR usually occurred within 2 sec following the first spike of the atypical spike and wave bursts, whereas it occurred several seconds after onset, or more frequently, following the cessation of the petit mal discharge. These observations of the GSR suggest that awareness of the manifestations of the discharge may be an important determinant of autonomic response.

Paroxysmal EEG activity and cognitive-motor performance

1. 1. Performance on four cognitive-motor tasks was investigated in 36 epileptic subjects. Simultaneous recording of the EEG enabled an evaluation to be made of the effect of seizure discharges on functioning. 2. 2. All discharges recorded were generalized, bilaterally synchronous, and symmetrical. They were evaluated as to type (on basis of appearance), duration, whether spontaneous or photically induced, and whether clinical or subclinical. 3. 3. Analysis indicated that duration of the burst and whether clinical ( i.e. associated with observable movement or subjective awareness) or subclinical were major factors in predicting performance. Long discharges and clinical discharges were significantly more likely to be associated with a break in functioning than short discharges or subclinical bursts. These two variables were found to be related in that the duration of the clinical discharges was significantly longer than that of the subclinical discharges. 4. 4. When duration was similar, there were no observable differences between photically induced and spontaneous discharges. 5. 5. From these results it would appear that other mechanisms besides the disruption of normal cortical electrical activity during discharges must be involved in explaining performance alterations in epileptic patients.