Acute sleep deprivation reduces amygdala-kindled seizure thresholds in cats.
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Biomedical subjects
Publications and source records attributed to M B Sterman.
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Recent advances in the diagnosis of epilepsy include the development of a clinically useful classification of epileptic seizures and the recognition of specific epileptic disorders. These advances have been aided by the advent of x-ray computed tomography, long-term electroencephalographic telemetry, and video monitoring. Techniques for functional imaging of the human brain promise even greater diagnostic capabilities. New antiepileptic drugs have improved medical management, and technical and theoretical advances in pharmacokinetics have permitted physicians to design balanced dosing for individual patients. Although currently underused, surgical treatment of partial complex epilepsy can be safe and effective when used appropriately. Operant conditioning of electroencephalography may become another practical alternative therapy. Contributions of basic research to understanding the complications of status epilepticus have influenced treatment protocols and greatly improved the prognosis of this potentially lethal condition.
Seventeen infants with unexplained prolonged apnea that has been designated near-miss sudden infant death syndrome were monitored for sleep and cardiorespiratory variables during a 12-hour, all-night recording session. Infants were matched for gestational age, sex, and age at recording with control infants. Respiratory variables studied included respiratory rate, respiratory variability, apnea duration, apnea density, and periodic breathing. No statistically significant differences were found in sleep state or respiratory variables between near-miss and control infants. Eight infants (47%) had no recurrence of prolonged apnea, whereas three (17.6%) had recurrent apneic episodes for six weeks to eight months following the original episode. No clinical or polygraphic finding predicted which infant would exhibit recurrent apnea. None of the infants was monitored at home. All infants were developing normally when examined at 1 to 2 years of age.
Twelve-hour, all-night polygraphic recordings were obtained from 25 normal infants at 1 week and 1, 2, 3, 4, and 6 months of age. The objectives of the study were to provide a description of the emerging temporal distribution of quiet sleep (QS), active sleep (AS), and motility, and to describe the maturation of a circadian influence upon heart rates. With increasing age, increased percentages of AS began to cluster toward the end of the night and increased percentages of QS toward the beginning. A circadian influence upon heart rates was observed in AS and indeterminate sleep prior to its existence in QS. At 2 and 3 months of age motility in AS and QS increased linearly during the night.
The normal succession of sleep and waking states through a night is disturbed in infants at risk for the sudden infant death syndrome. Compared with normal infants, siblings of the sudden infant death syndrome victims have longer intervals between active sleep epochs at particular times during the night in the newborn period and a decreased tendency to enter short waking periods at 2 and 3 months of age. The latter finding is interpreted as an increased tendency to remain asleep, or a relative failure to arouse from sleep in infants at risk.
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The author reviews the use of operant conditioning to alter electroencephalogram (EEG) patterns. A discrete rhythmic EEG pattern directly related to modulation of motor patterns (sensorimotor rhythm, SMR) was brought under voluntary control in the cat. This technique was modified for use in epileptic human volunteers in order to reduce motor seizures. The use of a newer experimental design and its successful application in one subject is described.
Neurophysiological evidence for a negative feedback loop in somatosensory thalamic nuclei has provided a basis for understanding the origins of rhythmic activity in the electroencephalogram (EEG) of sensorimotor cortex. Studies reviewed here suggest that state-specific activation of this mechanism is responsible both for a variable pattern of rhythmic frequencies during wakefulness and the spindle burst pattern during sleep. It is proposed further that these rhythms index immobility and a common set of physiological changes in sensorimotor function, including reduced excitability in both afferent and efferent pathways. It is hypothesized, therefore, that the closing of a thalamic "inhibitory gate" is indicated by the occurrence of these rhythms. While a greater resolution of specific relationships is necessary, the study of these EEG patterns clearly provides a measure of complex physiological events in the nervous system, and can be also useful in identifying functional abnormalities.
Power spectral analysis of spontaneous EEG activity recorded during non-rapid eye movement (REM) sleep was employed in an effort to identify characteristic EEG substrate abnormalities in epileptics. All-night polygraphic recordings were obtained from 10 poorly controlled subjects with mixed and generalized seizures. Similar data were obtained from 10 matched nonepileptic subjects. Continuous 10 min samples of non-REM sleep were identified at the beginning and end of these all-night recordings. EEG activity recorded during these periods from left sensorimotor and parieto-occipital bipolar leads was digitized, subjected to the fast Fourier transform, and then sorted into successive 4 Hz frequency bands between 0 and 23 Hz. Mean spectral density was determined for each frequency band from both samples in both groups. Comparison of these values disclosed both similarities and differences between the two groups. All subjects showed a significant "time-of-night effect," with power at 0-3, 4-7, and 8-11 Hz greater at the beginning of the night. This finding was related to a similar observation in developing infants and attributed to a circadian influence on neuronal generators. In group comparisons, epileptics showed selective differences in common when compared with nonepileptics. These differences were reduced when data from a small group of unmedicated epileptic subjects were partialled out. Medicated epileptics showed differences restricted to the early morning non-REM sleep sample, which included significantly greater power at 4-7 Hz and significantly lower power at 12-15 Hz. Unmedicated subjects showed these differences in both samples and also showed significantly greater power in the 0-3 Hz band. It was suggested that anticonvulsant medications may exert a general normalizing influence on EEG characteristics during sleep, particularly at the beginning of the night in proximity to their administration. The documentation of significant EEG deviations restricted to two basic rhythmic patterns during sleep suggests a disturbance of underlying thalamocortical mechanisms.
This study examined fetal heart rate (FHR) variables during maternal sleep in subsequent siblings of infants who died of sudden infant death syndrome (SIDS) and who are thus at increased statistical risk for SIDS, and controls. Four findings differentiated the tracings of subsequent siblings of SIDS infants and controls: 1) FHR variability in subsequent siblings of SIDS infants ranged between 11 and 25 beats/min, compared with 6 to 10 beats/min in controls (P less than .001). 2) Bradycardia was more frequent in subsequent siblings of SIDS infants. 3) FHR accelerations (more than 150 beats/min) followed by heart rates below 120 beats/min were elevated in subsequent siblings of SIDS infants (P less than .01). 4) Strong respiratory arrhythmia was more frequent in subsequent siblings of SIDS infants. These siblings exhibited more reactive FHR patterns. Although these data cannot be interpreted as clinical markers to identify the infant who will die of SIDS, they are compatible with the hypothesis that mild chronic hypoxia is associated with risk for SIDS.
This study was designed to provide normative data on fetal heart rate (FHR), FHR variability, accelerations, and decelerations during maternal sleep in the third trimester of pregnancy and to identify rhythmicity in FHR variability. Twenty-four polygraphic recordings were obtained in 16 pregnant women at 32 and 36 weeks' gestation. FHR parameters were not predictably influenced by maternal sleep states. Cyclic changes in FHR variability with median cycle length of 53 minutes were observed. Accelerations and decelerations occurred an average of 12.2 and 4 times per 100 minutes, respectively. Bradycardia and tachycardia persisting beyond 10 minutes were not seen. FHR variability ranged from marked to decreased within recordings of the same subject; this observation has implications for non-stress testing of the fetus.
The effects of amphetamine and pentobarbital upon electrographic state were studied in naive cats and cats with forebrain lesions that induce insomnia. Amphetamine increased alertness and decreased both slow wave sleep (SWS) and rapid eye movement (REM) sleep states for up to 12 h in both intact animals and cats with lesions. Pentobarbital inhibited REM sleep and alert states while increasing SWS and drowsy states in naive cats. The effect was mainly restricted to the first 8 h. In cats with forebrain lesions, the effects were similar except that the amount of REM sleep was significantly elevated. During a portion of the first 8 h, the tracing cannot be distinguished from a normal control sample. It is hypothesized that pentobarbital mimics the normal inhibitory influence of the intact forebrain and either induces or facilitates 'normal' sleep patterns in cats with forebrain lesions.
This report is a follow-up to a previous paper which described seizure rate changes with central cortical EEG feedback training in 8 poorly controlled epileptic subjects. Data examined here include associated training compliance and performance, sleep EEG spectra, clinical EEG and anticonvulsant blood levels. The study employed a double-cross-over, single blind ABA design applied to two subgroups of epileptic patients. Both groups had in common two training periods (A1, A2) in which either 12--15 c/sec (subgroup I, n = 4) or 18--23 c/sec (subgroup II, n = 4) was reinforced in the absence of 6--9 c/sec, movement or epileptiform discharge, and one training period (B) in which 6--9 c/sec was reinforced in the absence of 12--15 or 18--23 c/sec as well as movement and epileptiform discharge. Training periods occurred primarily in the home and lasted 3 months. Compliance with training instructions and response acquisition were demonstrated. Overall anticonvulsant blood levels were low and unrelated to EEG or seizure changes. Clinical EEG findings corresponded to sleep EEG and seizure rate outcomes. Power spectral analysis of sampled non-REM sleep from all-night EEG recordings obtained after each training phase indicated contingency specific changes which were limited to sensorimotor recordings in subgroup I and corresponded to the pattern of seizure rate changes in this group. EEG changes were also limited to sensorimotor cortex in subgroup II, but were linear and paralleled a progressive decrease in seizure rate. Both groups, however, showed the same pattern of EEG changes with seizure reductions; low and high frequencies were reduced and intermediate, rhythmic frequencies increased. Correlational analysis confirmed this relationship. The pattern, duration and topographic specificity of these changes suggested a normalization of sensorimotor EEG substrates related to the EEG feedback traning.