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PubMed2001

Identifying genetic influences on sleep: an approach to discovering the mechanisms of sleep regulation.

Comparisons of sleep patterns of various inbred strains of mice have revealed differences in daily amounts of slow-wave sleep and rapid-eye movement sleep, in circadian patterns of sleep, and in some parameters of the electroencephalograms both in healthy mice and in mice undergoing microbial infections. Technical considerations will probably be an important variable in achieving consensus between different independent studies that use a genetic approach to identify sleep-regulatory genes or mechanisms. However, despite such differences, current data suggest that both normal sleep and various sleep disorders either have a genetic basis or are influenced by genetically determined physiologic or environmental predispositions. Excessive sleepiness, abnormal sleep patterns, nonrestorative sleep, and fatigue are becoming increasingly pervasive in modern society. Identifying genes that influence vigilance may ultimately contribute to a better understanding of the processes that control normal sleep and contribute to sleep disorders and may eventually promote the development of interventions to prevent or alleviate these disabling medical conditions.

Animals↗
PubMed1992

Isolated sleep paralysis elicited by sleep interruption.

We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.

Adolescent↗
PubMed2001

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation.

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.

Adult↗
PubMed2005

Cold exposure and sleep in the rat: effects on sleep architecture and the electroencephalogram.

STUDY OBJECTIVES: Acute exposure to low ambient temperature modifies the wake-sleep cycle due to stage-dependent changes in the capacity to regulate body temperature. This study was carried out to make a systematic analysis of sleep parameters during the exposure to different low ambient temperatures and during the following recoveries at ambient temperature 24 degrees C. DESIGN: Electroencephalographic activity, hypothalamic temperature, and motor activity were studied during a 24-hour exposure to ambient temperatures ranging from 10 degrees C to -10 degrees C and for 4 days during the recovery. SETTING: Laboratory of Physiological Regulation during the Wake-Sleep Cycle, Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna. SUBJECTS: Twenty-four male albino rats. INTERVENTIONS: Animals were implanted with electrodes for electroencephalographic recording and a thermistor for measuring hypothalamic temperature. MEASUREMENTS AND RESULTS: Wake-sleep stage duration and the electroencephalographic spectral analysis performed by fast Fourier transform were compared among baseline, exposure, and recovery conditions. The amount of non-rapid eye movement sleep was slightly depressed by cold exposure, but no rebound was observed during the recovery period. Delta power during non-rapid eye movement sleep was decreased in animals exposed to the lowest ambient temperatures and increased during the first day of the recovery. In contrast, rapid eye movement sleep was greatly depressed by cold exposure and showed an increase during the recovery. Both of these effects were dependent on the ambient temperature of the exposure. Moreover, theta power was increased during rapid eye movement sleep in both the exposure and the first day of the recovery. CONCLUSION: These findings show that sleep-stage duration and electroencephalogram power are simultaneously affected by cold exposure. The effects on rapid eye movement sleep appear mainly as changes in the duration, whereas those on non-rapid eye movement sleep are shown by changes in delta power. These effects are temperature dependent, and the decrease of both parameters during the exposure is reciprocated by an increase in the subsequent recovery.

Animals↗
PubMed1985

Effect of sleep disruption on sleep, performance, and mood.

Eleven young adult subjects were briefly awakened after each minute of electroencephalographic-defined sleep for 2 consecutive nights after undisturbed laboratory adaptation and baseline nights. Two undisturbed recovery nights followed disruption nights. On disruption nights, subjects were awakened with an audiometer and signaled the awakening by subjective rating of sleep state or button push response. The disruption procedure resulted in severely fragmented sleep with only very small amounts of slow-wave and REM sleep. Total sleep time was reduced by approximately 1 h on each night. Arousal threshold increased 56 dB across the disruption nights. Following disruption, subjects performed more poorly and rated themselves sleepier than on baseline. The level of decline was similar to that seen after periods of total sleep loss of 40-64 h. Recovery sleep was also similar to that seen after total sleep loss. It was concluded that periodic disruption of sleep, perhaps by destroying sleep continuity, quickly results in impaired function. These data may help explain function loss in severe sleep apneics.

Achievement↗
PubMed1985

Recovery sleep at different times of the night following loss of the last four hours of sleep.

The sleep of 8 women was restricted to the first half of the night for 1 night on two separate occasions. On each occasion, heavy loss of REM (64%) and stage 2 (60%) with only a relatively light loss (20%) of slow wave sleep resulted. The purpose of the present study was to investigate whether or not the circadian timing of recovery sleep, particularly the second 4 h, would affect the response of the sleep system to the differential loss of the sleep stages. Recovery sleep commenced at 2000 h (i.e., after a normal daily span of 16 h of wakefulness) and was either continuous or interrupted after 4 h with 4 h of enforced wakefulness. Thus, the second 4 h of recovery sleep occurred between either 0000-0400 h or 0400-0800 h, two periods of the night normally associated with low and high levels of REM, respectively. The composition of recovery sleep, particularly the level of REM sleep, was found to be relatively unaffected by circadian factors. Instead, the response of the sleep system was mainly determined by stage 4 debt. It was suggested that obtaining a daily stage 4 quota acts as the primary drive mechanism of the sleep system.

Adolescent↗
PubMed1985

Sleep, sleep loss, and breathing.

Sleep and sleep loss have remarkable effects on breathing. Although sleep causes ventilatory disturbances of greater severity and variety than does sleep deprivation, the effects of sleep and sleep loss on respiration are similar. For example, both impair ventilatory drive and arousal responses to a variety of stimuli. Although the mechanism of impaired ventilation after sleep loss is not entirely understood, there is evidence to suggest that both respiratory muscle fatigue and central nervous system depression play a role. Patients who suffer from both disturbed sleep and lung disease are particularly vulnerable to the adverse effects of sleep disruption on breathing. Since sleep restoration returns many respiratory parameters to normal in sleep-deprived individuals, perhaps we should include rest in our treatment of certain patients with respiratory disease.

Humans↗
PubMed2002

Interhemispheric sleep EEG asymmetry in the rat is enhanced by sleep deprivation.

Vigilance state-related topographic variations of electroencephalographic (EEG) activity have been reported in humans and animals. To investigate their possible functional significance, the cortical EEG of the rat was recorded from frontal and parietal derivations in both hemispheres. Records were obtained for a 24-h baseline day, 6-h sleep deprivation (SD), and subsequent 18-h recovery. During the baseline 12-h light period, the main sleep period of the rat, low-frequency (<7.0 Hz) power in the non-rapid eye-movement (NREM) sleep EEG declined progressively. Left-hemispheric predominance of low-frequency power at the parietal derivations was observed at the beginning of the light period when sleep pressure is high due to preceding spontaneous waking. The left-hemispheric dominance changed to a right-hemispheric dominance in the course of the 12-h rest-phase when sleep pressure dissipated. During recovery from SD, both low-frequency power and parietal left-hemispheric predominance were enhanced. The increase in low-frequency power in NREM sleep observed after SD at the frontal site was larger than at the parietal site. However, frontally no interhemispheric differences were present. In REM sleep, power in the theta band (5.25-8.0 Hz) exhibited a right-hemispheric predominance. In contrast to NREM sleep, the hemispheric asymmetry showed no trend during baseline and was not affected by SD. Use-dependent local changes may underlie the regional differences in the low-frequency NREM sleep EEG within and between hemispheres. The different interhemispheric asymmetries in NREM and REM sleep suggest that the two sleep states may subserve different functions in the brain.

Animals↗
PubMed1991

Influence of antihypertensive drug therapy on sleep pattern and sleep apnea activity.

Sleep apnea, which affects 10% of men in the mean age group, is a common illness, and arterial hypertension one of its early symptoms. For the large group of, mainly young, patients with mild to moderate sleep apnea and arterial hypertension it is important to have a drug treatment available which will effectively control blood pressure without exacerbating symptoms of sleep apnea. We studied the effects of antihypertensive agents on blood pressure, sleep and sleep apnea in a randomized double-blind study of 24 patients with a sleep apnea activity of more than 10 apnea phases per hour of sleep and arterial hypertension with diastolic blood pressure values in the sitting position greater than or equal to 95 mm Hg. Mean age was 51 (range: 33-69) years, mean body mass index 31.4 (24.9-40.6) kg/m2. The study protocol envisaged two baseline measurements in the sleep laboratory, after which the medication was administered for 8 days. On the last 2 days of the treatment, polysomnographic leads were once again recorded in the sleep laboratory. The patients received either the beta-blocker metoprolol (1 x 100 mg/day) or the angiotensin-converting enzyme inhibitor cilazapril (1 x 2.5 mg/day). Systolic and diastolic blood pressure were decreased by both substances as expected. Total sleep time was 358 (233-425) min vs. 332 (255-383) min in the metoprolol group and 368 (295-424) min vs. 341 (265-434) min in the cilazapril group which is statistically not different between the two groups nor between the proportions of non-REM and REM sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Glucocorticoid replacement is permissive for rapid eye movement sleep and sleep consolidation in patients with adrenal insufficiency.

There is a well described temporal relation between hormonal secretion and sleep phase, with hormones of the hypothalamic-pituitary-adrenal (HPA) axis possibly playing a role in determining entry into and duration of different sleep stages. In this study sleep features were studied in primary Addison's patients with undetectable levels of cortisol treated in a double blind, randomized, cross-over fashion with either hydrocortisone or placebo supplementation. We found that REM latency was significantly decreased in Addison's patients when receiving hydrocortisone at bedtime, whereas REM sleep time was increased. There was a trend toward an increase in the percentage of time in REM sleep and the number of REM sleep episodes. Waking time after sleep onset was increased, whereas no differences were observed between the two conditions when total sleep time or specific non-REM sleep parameters were evaluated. Our results suggest that in Addison's patients, cortisol plays a positive, permissive role in REM sleep regulation and may help to consolidate sleep. These effects may be mediated either directly by the central effects of glucocorticoids and/or indirectly through CRH and/or ACTH.

Addison Disease↗
PubMed1998

[Breathing control of patients with obstructive sleep apnea syndrome (OSAS) during sleep].

OBJECTIVE: It is assumed that reduced ventilatory control function during sleep may be one of the mechanisms resulting in obstructive sleep apnea syndrome (OSAS), but the breathing drive has never been measured in patients with OSAS during sleep. METHOD: P0.1, delta P0.1/delta SaO2, delta VE/delta SaO2, delta P0.1/delta PaCO2 and delta VE/delta PaCO2 in sixteen patients with severe OSAS were measured via nasopharyngeal tubes connected with nasal mask to maintain upper airway patent, during wake and NREM I + II, NREM III + IV, REM sleep stages, and the same parameters in eleven normal subjects, non-snorers were also measured, by nasal mask as control. RESULT: (1) During wake: P0.1 in all the OSAS patients was remarkably higher than that of the normal subjects (P < 0.05), but there was no difference in delta VE/delta SaO2, delta P0.1/delta SaO2, delta VE/delta PaCO2 and delta P0.1/delta PaCO2 between the two groups (P > 0.05). (2) The above parameters measured during sleep compared with that measured during wake: In NREM I + II and NREM III + IV, normal subjects showed no significant decrease in P0.1, delta P0.1/delta SaO2, delta P0.1/delta PaCO2 (P > 0.05), but delta VE/delta SaO2 and delta VE/delta PaCO2 decreased significantly (P < 0.05). In REM1 P0.1 maintained the same level as that during wake, but both hypoxic and hypercapnic responses decreased remarkably (P < 0.05). In the OSAS patients, P0.1 decreased during NREM I + II and REM sleep (P < 0.5), but not during NREM III + IV (P > 0.05). delta VE/delta SaO2, delta P0.1/delta SaO2, delta P0.1/delta PaCO2 and delta VE/delta PaCO2 decreased markedly during all sleep stages (P < 0.01). (3) From wake to sleep, delta VE/delta SaO2 decreased by 51.6 +/- 30.4% (Mean +/- SD) in the OSAS patients vs 33.6 +/- 26.0% decreased in the normal subjects; delta VE/delta PaCO2 decreased by 56.9 +/- 25.5% in OSAS vs 40.8 +/- 17.5% in the normal subjects; The hypoxic and hypercapnic responses in OSAS patients decreased much more than those in the normal subjects during sleep (P < 0.05). CONCLUSION: This is the first study to measure the hypoxic and hypercapnic responses successfully in OSAS patients during sleep. It was found that the breathing drive was significantly reduced in sleeping OSAS patients, which may play an important role in the development of OSAS, possibly through the reduced action upon the dilators causing the upper airway in predilection for collapse.

Adult↗
PubMed2000

Nighttime sleep and daytime functioning (sleepiness and fatigue) in less well-defined chronic rheumatic diseases with particular reference to the 'alpha-delta NREM sleep anomaly'

For the past 25 years, the 'alpha-delta NREM sleep abnormality' has been used by some as a defining or legitimizing marker for poorly defined rheumatic diseases such as fibromyalgia and chronic fatigue syndrome. Comprehensive review of the literature reveals no support for such a conclusion. Most studies involve small numbers of patients. The lack of control subjects, non-standardized recording techniques, and confusion between tonic and phasic alpha frequency activity patterns make comparison difficult. There is much evidence that this sleep EEG pattern is not only non-specific, but may actually reflect a sleep maintaining process. The 'sleep fragmentation' theory of the complaint of non-restorative sleep in this patient population is invalidated by the fact that conditions characterized by severe sleep fragmentation, such as obstructive sleep apnea, are not associated with musculoskeletal symtoms. It is difficult to attribute musculoskeletal symptoms to disorders of sleep in view of the fact that the only organ of the body known to benefit from sleep, or to be adversely affected by lack of sleep, is the brain. It is concluded that fibromyalgia and chronic fatigue syndrome are associated with subjective sleep complaints, but do not represent sleep disorders.

Journal Article↗
PubMed1993

Naltrexone improves blood gas patterns in obstructive sleep apnoea syndrome through its influence on sleep.

Endogenous opiates have been shown to depress ventilation, and could therefore play a role in sleep apnoea syndrome (SAS). Hence, opiate antagonists have been used to treat SAS. The improvement they seem to give in blood-gas monitoring could derive either from a direct blocking of endorphins that inhibit respiration or else, indirectly, through an influence on sleep patterns. The present study used a double blind cross-over protocol to investigate the relationships between the effects on blood-gas and on sleep patterns of the oral opiate antagonist naltrexone in obstructive SAS. Sleep patterns and transcutaneous blood gas (tcPO2 and tcPCO2) were recorded in parallel. Control recordings, without treatment, were carried out over two nights, followed by two nights of recording after administration either of naltrexone followed by a placebo or of a placebo followed by naltrexone. The number of obstructive apnoea and hypopnoea events per hour of sleep (Apnoea-Hypopnoea Index: AHI), of hypoxic events (defined as a tcPO2 fall of at least 10, 15 or 20 mm Hg) and of hypercapnic events (defined as a tcPCO2 increase of at least 5 mm Hg) were counted. A Metabolic Suffering Index (MSI) was calculated, defined as the product of the number, duration and magnitude of hypoxic and hypercapnic events. Compared to placebo, naltrexone resulted in significant improvements in blood-gas patterns for the duration and MSI of hypoxic events and for the number, duration and MSI of hypercapnic events. Likewise, compared to placebo, naltrexone induced significant decreases in total sleep time, slow-wave sleep and rapid eye movement (REM) sleep, and, on the other hand, significant increases in total wake time and in the number of wakenings per hour of sleep (Nw h-1). Certain naltrexone-linked blood-gas improvements were closely correlated with certain of the sleep pattern changes: the decrease in number and duration of hypoxic events correlated with REM-time decrease and the decrease in number and duration of hypercapnic events correlated with the increase in Nwh-1. These findings suggest that the improvement in blood-gas patterns induced by naltrexone in SAS may be mediated by sleep pattern effects: i.e. a decrease in REM-time and an increase in intra-sleep wakening.

Journal Article↗
PubMed1995

Effects of flumazenil on recovery sleep and hormonal secretion after sleep deprivation in male controls.

The effects of flumazenil, a benzodiazepine antagonist, on the sleep electroencephalogram (EEG) and neuroendocrine secretion in early morning recovery sleep (0500-0800 hours) following sleep deprivation (SD; 2300-0500 hours) were studied in seven healthy men. SD induced an increase in slow wave sleep (SWS), a decrease in sleep onset latency (SOL), an enhancement of EEG delta and theta power in non-rapid-eye-movement sleep, an increase in plasma human growth hormone (GH) concentration, and a decrease in plasma cortisol levels in recovery sleep (0500-0800 hours). Plasma GH, but neither plasma cortisol nor adrenocorticotrophic hormone (ACTH) concentration was attenuated during SD as compared to sleep (2300-0445 hours). The administration of flumazenil (3 x 1 mg intravenously) during recovery sleep resulted in an inhibition in SWS, an increase in stage 2 sleep, a selective reduction in delta and theta power, and a tendency to prolongation of SOL. Plasma GH concentration was decreased but plasma cortisol and ACTH remained unaffected. Since the SD-induced changes in sleep EEG and plasma GH secretion were antagonized by flumazenil, it is suggested that electrophysiological and hormonal effects of SD are mediated at least in part through GABAergic mechanisms.

Adrenocorticotropic Hormone↗
PubMed1994

Should sleep EEG record always be performed after sleep deprivation?

Sleep deprivation (SD) is a known activator of epileptiform EEG activity in patients with epilepsy. In the workup of these patients, EEG recordings are performed following SD both in the awake state and during sleep. The latter significantly increases the duration and the cost of the examination; the specific yield of sleep tracing in single-session wake-sleep record after SD has not been evaluated in adult patients. Our study tried to answer this question, analyzing consecutive recordings of 76 adult patients who had an epileptiform abnormality in the SD record. Thirty-five of the patients were treated with antiepileptic drugs at the time of the study. After SD of 24-26 h, 1000-1500 mg of chloral hydrate were administered; an 18-channel standard awake EEG was performed, followed by 30 min sleep recording. Epileptiform activity was recorded in the wake part only in 7 (9%, 3 focal, 4 generalized); in 39 (51%) the activity was seen in both awake and sleep parts (21 focal, 5 focal with secondary generalization and 13 generalized); and in 30 (40%) it was found in the sleep part only (23 focal, 1 focal with secondary generalization and 6 generalized). Whenever epileptiform activity was apparent in both parts of the recording, its configuration and localization were identical in the sleep and the wake EEGs. This phenomenon was observed in both treated and untreated patients. In combined wake-sleep recording following SD in adults, sleep tracing may reveal epileptiform activity not demonstrated during the preceding wake EEG. However, if epileptiform activity appears already in the wake recording, subsequent sleep tracing may be redundant.

Adolescent↗
PubMed1989

Effects of repeated sleep deprivation in the dark- or light-period on sleep in rats.

This study was designed to examine the differences between sleep duration and EEG when sleep was restricted to the rest- or activity-phase for 5 successive days, achieved by repeated sleep deprivation in the dark (DSD) or light-period (LSD). In the DSD-experiment the percentages of the vigilance states were comparable to the level of the baseline light period. In LSD, the amounts of all sleep states increased substantially relative to baseline dark. The sleep episodes were lengthened in DSD and LSD. The duration of NREM-sleep and the sleep episodes remained longer in the light than in the dark, indicating circadian influences. In the first hours after sleep deprivation the delta activity during NREM-sleep was enhanced in LSD and to a lesser extent in DSD. This effect diminished over the consecutive days in both experiments. The EEG energy gained during sleep and its accumulation pattern on each day in DSD and LSD were strikingly similar, thereby reflecting a homeostatic process. After the sleep deprivation days, small changes were observed in the distribution of the vigilance states, the delta activity and EEG energy over the light- and dark-period.

Animals↗
PubMed1988

Relationship between sleep inertia and sleepiness: cumulative effects of four nights of sleep disruption/restriction on performance following abrupt nocturnal awakenings.

Performance deficits are usually evident following both extended wakefulness (sleep deprivation effects) and immediately upon awakening from sleep (sleep inertia effects). In order to determine whether sleep inertia effects are qualitatively different from sleep deprivation effects, performance on addition tests, Stanford Sleepiness Scale (SSS) ratings, and return-to-sleep latencies (RSLs) were assessed during four nights of sleep disruption/restriction. Eight subjects were polygraphically monitored in the sleep laboratory for five consecutive nights, from 2400 to 0700. On the last four nights (after an adaptation night) subjects were awakened at 0040, 0140, 0240, 0340, 0440, and 0540 for a 20-min test session. Sleepiness ratings and performance on 5-min addition tests were measured at 1.5, 7.5, and 13.5 min post-awakening, and RSL was measured at the end of each test session. Analysis of addition test performance across nights revealed that both speed and accuracy of calculations were adversely affected by the sleep disruption/restriction procedure, indicating that increasing sleepiness exacerbates sleep performance deficits upon awakening. Although divergence of SSS ratings and addition test performance across nights was suggestive, there was no conclusive evidence that sleep inertia is qualitatively different from "typical" sleepiness.

Adolescent↗
PubMed1994

Transitory and short-duration changes of sleep organization provoked by amygdaloid kindling in the cat: a daily 23-hour sleep recording study.

The effect of amygdaloid kindling on sleep organization was tested in chronically implanted cats on a 12:12 light-dark cycle. Electrical kindling stimuli were delivered to the amygdala every 2 h during the light period. Total sleep time and percentage, mean duration, and mean number, as well as the hourly accumulation of waking (W) and sleep (slow wave sleep I and II, and paradoxical sleep) episodes were assessed from daily 23-h sleep recordings, consisting of baseline control recordings, control recordings where cats were briefly alerted at 2-h intervals to mimic the kindling trials manipulation, and recordings on each kindling day. The kindling process was completed within six days achieving three to five consecutive fully kindled seizures. Analysis of total recording time showed that the kindling process enhanced W stage and diminished total sleep time only on the second kindling day. Analysis of light and dark periods demonstrated compensatory W and sleep changes during the dark periods. Hourly sleep stage time accumulation was slowed during kindling trials, but compensated while stimuli were suspended. All of these changes returned to baseline values at the end of kindling. No significant differences between changes induced by kindling and those produced by alerting trials were found. We conclude that sleep alterations can not be exclusively attributed to kindling development, and that sleep is able to become adapted to the focal and generalized seizures effect.

Amygdala↗