Blood pressure and heart rate in the rabbit during animal hypnosis.
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Five patients with seizures poorly controlled by standard anticonvulsant medication, underwent EEG operant conditioning. The operant paradigm reinforced the production of low voltage fast activity while decreasing frequencies below 10 c/sec. Seizure frequency decreased in 2 patients, seizure severity was attenuated in 2 others, and one patient who was only given reinforecement for scalp EMG suppression whowed no change in seizure parameters. Pseudoconditioning and control periods ruled out placebo effects. A rationale for this phenomenon is proposed.
A new method which enables quantification of event-related desynchronization (ERD) by measuring changes in the power of rhythmic activity within the alpha band during sensory stimulation and during the interstimulus interval of a CNV paradigm is described. For the processing, EEG trials recorded under the same stimulus conditions and with eyes closed are used. For the power changes, the statistical significance is tested with a non-parametric test. With the proposed method it is possible to measure very brief power changes of the order of 21 percent (corresponding to amplitude changes of 11%). An ERD may thus be observed in a restricted cortical region.
Hippocampal RSA (theta), neocortical EEG, and heart rate were recorded during surface and underwater swimming in the rat. RSA was present with slightly reduced frequency during the apnea, bradycardia, and vibrissae arrest associated with under water swimming. Atropine sulfate (50 mg/kg) blocked bradycardia did not affect RSA. Contrary to previous suggestions, no causal relation was found between RSA and respiration, heart rate, or vibrissae movement. The study supports the view that RSA is related to the neural control of voluntary movement. It is suggested that the slight reduction in RSA frequency during underwater swimming may be part of an oxygen conservation process.
Changes in the background EEG activity occurring at the same time as visual and auditory evoked potentials, as well as during the interstimulus interval in a CNV paradigm were analysed in human subjects, using serial power measurements of overlapping EEG segments. The analysis was focused on the power of the rhythmic activity within the alpha band (RAAB power). A decrease in RAAB power occurring during these event-related phenomena was indicative of desynchronization. Phasic, i.e. short lasting, localised desynchronization was present during sensory stimulation, and also preceding the imperative signal and motor response (motor preactivation) in the CNV paradigm.
The relation of the hippocampal EEG to behavior and to the neocortical EEG is being studied in psychomotor epileptics. Hippocampal recordings displaying only rare epileptiform spikes and slow waves are found to follow grossly the simultaneously recorded neocortical EEG, becoming desynchronized during wakefulness and paradoxical sleep (PS), and displaying large irregular slow waves during slow-wave sleep. In the one patient reported in this clinical note, strong rhythmic 5--6 c/sec waves dominated the neocortical and hippocampal EEG during quiet wakefulness. These slow waves were replaced by desynchronized activity during PS and during difficult tasks, suggesting a further desynchronizing influence. The findings in all patients suggest that the rhythmic slow activity ('theta') found in rats and cats during specific behaviors is not observed in the human hippocampal formation during the homologous behaviors.
The variations in amplitude of visual evoked potentials (VEPs) and parallel changes in amount of event-related desynchronization (ERD) of the rhythmic activity within the alpha band were studied in central derivations of scalp EEG, in 10 normal subjects. Two methods were used to estimate the amplitude of VEPs in small groups of 10 responses: (1) inverse and matched filtering techniques; (2) two-way rank analysis of variance by the Friedman test. The two methods gave similar results and two groups, statistically different, emerged. The first, with large VEP amplitude, having at the same time large ERD, and the second, with small VEP amplitude and small ERD.
A method of accurate storage and on-line preprocessing of an EEG signal, preceding and following a trigger signal, elicited by button pressing, is described. The method was used to study the changes occurring in the power of the rhythmic activity within the alpha band in central areas, during voluntary, self-paced movement in 10 normal humans. A short-lasting decrease or phasic event-related desynchronization (ERD) of alpha power, representing mu activity, was observed in all 10 subjects. During the 2 sec period preceding movement the phasic ERD was mostly bilateral, but larger prior to right than to left thumb movement. At onset and during the first second of execution of movement, the phasic ERD was mostly bilateral but predominant in ipsilateral areas. Preceding or during movement, maximum ERD was observed in most cases in central-vertex regions.
Full-term newborns with seizures exhibit EEG patterns that appear reliable in predicting neurological outcome in almost 75% of the cases in a prospective investigation. These patterns are unreliable for over 25% of infants with seizures and even more so for term and pre-term babies with other complications. Observations that such newborns often show maturational delay in various physiological and/or behavioral parameters, raises the issue of whether indices other than specific EEG patterns might prove reliable in predicting prognosis. As a prerequisite for testing such an hypothesis in prospective investigations of term and pre-term babies with 'risk' factors other than seizures, it appears necessary to obtain quantification of these parameters in normals. Hence a longitudinal study was designed to obtain simultaneously 3 parameters in a control group of newborns born after 30-32 weeks of gestational age, followed with serial polygraphic recordings at weekly intervals until a conceptional age of 43 weeks. The selected parameters were purposefully restricted to three that can be obtained and measured easily in routine recordings without need for more complex instrumentation and analysis. These were: the percentage of interhemispheric synchrony between bursts of 'trace alternant'; the number of spindle-delta complexes ('brushes') during 5 min of REM and NREM sleep; and the concordance between various parameters during the same 5 min epochs. The range of these indices was thus established in a group of normal prematures followed prospectively. Establishing such normative data will allow greater inter-study reliability, and form the basis for other prospective studies of infants 'at risk' to investigate whether those that lag behind the norm in these indices when followed serially during the newborn period differ prognostically from those who recover and reach expected norms for conceptional age.
Previous studies had suggested that the epileptic bursts of feline generalized penicillin epilepsy represent the response of hyperexcitable cortex to thalamocortical volleys normally evoking spindles. If this were the case, it should be possible to convert the epileptic bursts of generalized penicillin epilepsy into spindles by decreasing the excitability of cortical neurons. In cats exhibiting the EEG signs of feline generalized penicillin epilepsy cortical excitability was decreased by hypoxia, by the topical application to the cortex of KCl (inducing spreading depression), barbiturates, GABA, AMP or noradrenaline. During generalized penicillin epilepsy, hypoxia and KCl-induced spreading depression abolished epileptic bursts which were replaced by spindles. When spindles and epileptic complexes occurring in the same animal were compared, a direct correlation between the frequencies of these two rhythms could be demonstrated, that of the epileptic complexes being about half that of the spindle waves. These observations support the hypothesis that the epileptic bursts of feline generalized penicillin epilepsy are induced by thalamocortical volleys normally involved in spindle genesis. Topical cortical applications of barbiturates, GABA, AMP and noradrenaline reduced or inverted the negative spikes of the spike and wave complexes, while augmenting the negative slow waves, or revealing them clearly in instances in which they had been poorly developed. This effect is interpreted as being due to a selective inactivation of the superficial cortical layers. That topical cortical application of barbiturates, GABA, AMP and noradrenaline was capable of transforming into typical spike and wave complex epileptic bursts, which had not previously conformed to this pattern, indicates that the intracortical electrophysiological events of typical and atypical epileptic bursts in feline generalized penicillin epilepsy are fundamentally the same and reflect an alternation between excitatory and inhibitory sequences.
In cats prepared in a 'semi-chronic' manner (spinal cord transected, brachial plexus sectioned bilaterally) all states of alertness are present; their quantitative evolution is characterized by an immediate postoperative period with continuous wakefulness and a secondary period of recovery of the states of sleep, which are then maintained. In such a preparation, localized moderate cooling (+10 degrees C) of the nucleus raphe dorsalis induces slow wave sleep and paradoxical sleep; the same type of cooling of the nucleus raphe magnus induces wakefulness; however, the electrical stimulation of these two nuclei always induces wakefulness. Cooling of the nuclei raphe centralis or pontis suppresses only the 'ponto-geniculo-occipital' (PGO) waves. Colling of the nuclei raphe obscurus and pallidus induces wakedfulness, but stage I of slow wave sleep may occur. Treatment with p-chlorophenylalanine (PCPA) before making the semi-chronic preparation produces the classical syndrome characterized by cortical activation and continuous discharge of PGO waves; in this case cooling of the nucleus raphe dorsalis no longer induces slow wave sleep but only paradoxical sleep; after injection of DL-5-HTP, slow wave sleep is obtained again through cooling; this effect diminishes progressively.
A quantitative analysis of desynchronized sleep (DS) deprivation (exposure to low ambient temperature) and recovery was carried out in unrestrained cats. The results show that: (1) the circadian obligate quota of DS is precisely regulated by a control mechanism paying by the 24th h the DS debt induced by up to 14 h of total DS deprivation, if recovery occurs during the rest phase of circadian photoperiodicity (CP); (2) during static rebound DS hourly duration is increased by 40 +/- 4 sec/h of total deprivation (mean and S.E.) and there is a statistically significant increase in the hourly frequency and in the duration of DS episodes, with respect to control values; (3) the hourly obligate and facultative quotas of DS amount to 409 +/- 82 and 229 +/- 140 sec/h (mean and S.D.), respectively. (4) preoptic heating during deprivation at low ambient temperature decreases the DS static rebound during recovery at control ambient temperature by an amount corresponding to the cumulative duration of DS episodes elicited by the preoptic treatment; (5) preoptic temperature decreases the more markedly the shorter the duration of exposure to low ambient temperature and regains control values the sooner the smaller the DS debt incurred during deprivation; (6) DS debt cumulation is a continuous process which develops at a steady rate during day and night, whereas DS debt payment is a discontinuous process (ultradian rhythm of DS) which develops at a variable rate depending on the DS debt and on the phase of CP.
(1) Administration of methadone in rats elicited high voltage, slow activity in the cerebral cortex and low voltage irregular waves in the hippocampus. Intravenous administration of methadone (0.2-0.5 mg/kg) markedly increased the threshold for cortical desynchronization by stimulation of the MRF. This increase by methadone was dose dependent. (2) Cortical desynchronization following mechanical stimulation of the tail or foot was blocked by methadone at a dose level of 0.5 mg/kg. At this dose level, the cortical desynchronizing threshold for MRF stimulation increased more than 8-fold whereas the threshold for MT and DH stimulations showed only small but measurable increases. A minimum dose of 0.5 mg/kg was needed to raise the threshold of these structures significantly (3) The increased threshold following injection of methadone was completely blocked by prior injection of the antagonist naloxone, indicating this response to be specific. Naloxone alone had no effect on electrical activity at any site. (4) The incidence of dissociation of the cortical response from the limbic system response after stimulation of the dorsal hypothalamus was approximately 4 times greater in methadone-treated than in untreated animals.