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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients aged 33--70 years (mean 49.5) underwent nightly recordings in the ICU and subsequently on the ward following acute myocardial infarction. Sleep patterns were analyzed according to night after infarct and ICU versus ward environment. Significant differences in nocturnal sleep patterns from matched controls initially after infarction included greater wakefulness, low REM sleep per cent, long REM latency, fewer REM periods, more awakenings, more stage shifts and decreased sleep efficiency. The usual circadian variation in HR was absent, and there was an estimated 8--10 h of unrecorded daytime sleep, which together suggested a quite generalized disruption of biological rhythms. With time, there was loss of daytime sleep, lowered nocturnal wakefulness and increased REM sleep. Slow-wave sleep (sometimes with very long duration delta waves) increased above normal over post-infarction nights 3--9, and sleep was otherwise renormalized by post-infarction night 9. No sudden sleep changes occurred with transfer from ICU to ward. The altered sleep patterns appeared mainly attributable to infarction itself. Twelve nocturnal anginal attacks occurred. Ten began in NREM sleep and two in REM periods without particularly intense phasic activity. Post-infarction nocturnal angina therefore appears to differ in pathogenesis from angina outside this period, which usually occurs in REM sleep. ECG changes could occur during sleep before awakening with pain, and overall decrease in ECG amplitude sometimes accompanied angina. Most attacks (10 of 12) occurred on post-infarction nights 4 and 5, indicating that undetermined that undetermined factors produce a secondary period of heightened risk at that time.
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PMID:Sleep patterns in the intensive care unit and on the ward after acute myocardial infarction. 7 74

Studies of the behavioral correlates of activity in reticular formation cells, usually performed in restrained animals, have found units whose discharge relates to sensory stimuli, pain and escape behavior, conditioning and habituation, arousal, complex motivational states, REM sleep, eye movements, respiration and locomotion. Units with these different behavioral correlates were found in the same anatomical areas. Most studies report that a large proportion of encountered cells related to the behavior being studied. If one adds up the reported percentages, the total far exceeds 100%. Therefore it appears that many investigators are looking at the same cells and reaching very different conclusions about their behavioral roles. On the basis of observations in unrestrained cats, it is hypothesized that discharge in most RF cells is primarily related to the excitation of small groups of muscles. This hypothesis can parsimoniously explain many previous observations on the behavioral correlates of these cells, and is consistent with anatomical, physiological and phylogenetic studies of the reticular formation. The hypothesized simplicity of reticular formation unit function is contrasted with the complexity of the behavioral functions mediated by the RF, and the implications of this contrast discussed.
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PMID:Behavioral functions of the reticular formation. 11 77

Two groups of young, healthy, nonathletic volunteers were subjected to selective sleep stage deprivation. Six subjects were deprived of stage 4 sleep and seven subjects of REM sleep. The stage 4 deprived group reported more musculoskeletal symptoms during the deprivation condition than did the REM deprived group. The stage 4 deprived group also showed a significant increase in muscle tenderness between the baseline and deprivation conditions and an altered pattern of overnight change in muscle tenderness in response to deprivation. The REM deprived group did not show either of these changes. These results are discussed in the light of the previously postulated relationship between NREM sleep disturbance and muscoloskeletal pain in patients with so-called "Fibrositis syndrome."
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PMID:Induction of neurasthenic musculoskeletal pain syndrome by selective sleep stage deprivation. 17 77

Sleep is a vital human physiologic process. Insomnia can be caused by obsession and depression states, pain, or worry over everyday problems. Because of their pharmacologic action, alcohol and high doses of soporifics used as remedies may produce REM-deficit sleep and actually prolong insomnia. If the true cause of sleeplessness is not recognized and properly treated, insomnia may develop into a severe sleep problem. Since benzodiazepines and chloral hydrate do not suppress REM sleep, they are the medications of choice in the therapy for insomnia.
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PMID:Insomnia and the physiology of sleep. 20 31

The relationship between REM sleep deprivation and pain threshold was measured using 36 Sprague-Dawley female rats. Relative to that of the controls, a significant lowering of threshold to painful electrical stimulation was observed during each of the post-treatment tests, i.e., immediate, and after 3- and 24-hr. recovery periods, for the animals which had been REM deprived.
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PMID:REM sleep deprivation and pain thresholds in rats. 21 74

In the context of a functional treatment for pain five patients had electrodes chronically implanted in the periaqueductal gray matter (PGM) and at the same time in thalamic nuclei. The spontaneous activity of these structures was analyzed in comparison with the simultaneously recorded scalp-EEG. The structure-specific differences between the activity of the PGM and the thalamic nuclei were pointed out. In waking state a close functional relation between the alpha-activity of the PGM and the scalp-EEG was found. Physiological sleep patterns were recorded in the mesencephalon earleir than at the surface. REM-phases were initiated by 4/sec rhythms in the PGM. During rapid eye movements sharp waves in the PGM appeared which are evidently related to the eye movements themselves. The findings are discussed in reference to the literature. Special emphasis is placed on the anatomical connexions between the explored mesencephalic and thalamic structures and the temporo-occipital cortex and on the role of ponto-mesencephalic structures in slow-wave-sleep and REM-sleep.
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PMID:[Macro-electrode recording in man's brain-stem 1. Electrical activity during wakefulness and nightsleep (author's transl)]. 21 77

Using 30 Sprague-Dawley female rats, threshold to pain was measured over the course of recovery from REM sleep deprivation. Relative to the untreated controls and to their own pretreatment thresholds, the REM-deprived animals showed significantly reduced pain thresholds which were still evident 96 hours after the termination of the REM deprivation. Possible implications of these data for research with analgesic drugs were noted.
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PMID:Pain thresholds in rats during recovery from REM sleep deprivation. 22 23

Six nocturnal polygraphic recordings were carried out in a young man with fibrillary chorea of Morvan, during the acute period of the disease. Sleep was remarkably fragmented by numerous and brief awakenings but the total sleep time fluctuated between 157 and 312 mins.; the sleep structure was altered by the almost total absence of stages 3,4 and REM. During the day, the subject had one or two periods of sleep (1-2 hours) and complained of being tired. The nocturnal awakenings were correlated by the patient with pain and burning dysaesthesiae of distal distribution that were more severe than those occurring during the day. The patient improved gradually, and five month later both sleep disturbances and other signs of disease had disappeared.
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PMID:[Sleep disturbances in a case of Morvan's chorea (author's transl)]. 103 32

Recent advances in the investigation of brain-gut interaction in irritable bowel syndrome (IBS) were reviewed. Brain is suggested to play an important role in the pathophysiology of IBS on the basis of the following evidence. (1) Stress often induces major symptoms of IBS patients (Drossman et al., 1982), simultaneously with colonic hypermotility (Fukudo et al., 1987) or dysmotility of the small intestine (Kumar et al., 1985). (2) IBS patients rarely express symptoms or small intestinal dysmotility during sleep (Kellow et al., 1990). (3) IBS patients complain of more pain with balloon distension of the colon or rectum than normal controls; visceral perception is enhanced in IBS (Whitehead et al., 1990). (4) IBS patients often show psychoneurotic symptoms and extra-colonic somatic symptoms (Young et al., 1976). (5) There are some animal (Williams et al, 1987) or human (Dinan et al, 1990) experiments which indicate the possible involvement of brain peptide or brain monoamine in IBS. (6) Dysrhythmia or increased beta power in electroencephalogram is observed more often in IBS patients than in the normal controls (Fukudo et al, 1991) in addition to abnormal REM sleep in IBS patients (Kumar et al., 1992). These observations support our hypothesis that not only the gut but also the brain show dysfunction and exaggerated responsivity to the stimuli in IBS. Further research on brain-gut interaction in IBS is warranted.
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PMID:[Brain-gut interactions in irritable bowel syndrome: physiological and psychological aspect]. 133 64

Rapid euthanasia of laboratory rodents without the use of anesthesia is a necessary research technique whenever there is the likelihood of anesthesia or stress interfering with the chemistry of the tissues under investigation. Decapitation has long been the procedure of choice under such circumstances. Recently, however, the American Veterinary Medical Association (AVMA) panel on euthanasia recommended that decapitation be avoided on the grounds that the decapitated head may be conscious and suffering for as much as 15 seconds. The panel further recommended that if decapitation was scientifically necessary, the decapitated head be immediately immersed in liquid nitrogen. These AVMA guidelines now enjoy regulatory status; the recommendation that decapitation be avoided has thus caused considerable difficulty for all research requiring rapid, anesthesia-free collection of tissues. The scientific validity of these recommendations is consequently a matter of great practical as well as theoretical importance. The decision to discourage decapitation appears to have been based on a single literature report claiming that the EEG of the decapitated head revealed conscious suffering for more than 10 seconds (Mikeska and Klemm 1976). This review carefully examines the scientific literature on this subject. It is concluded that the report by Mikeska and Klemm of EEG activation in the decapitated head is correct, but that this phenomenon is also seen when the decapitated head is under deep anesthesia, and in normal brains under ether anesthesia or during REM sleep. Hence these findings do not demonstrate either consciousness or the perception of pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Euthanasia by decapitation: evidence that this technique produces prompt, painless unconsciousness in laboratory rodents. 152 30


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