Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This clinical study of 62 patients with restless legs syndrome and associated anxious-depressed and other clinical states seems to indicate that caffeine is the major etiological factor in the causation of the restless legs syndrome. Anxiety, while modifying the subjective experience of the dysphoric sensation of restless legs, is not a causative factor. Caffeine is responsible for the increased nervous system arousal as well as for the direct peripheral contractile effect on the striated muscle. This arousal is often reflected psychologically in anxiety and sometimes depressive manifestations, insomnia, heightened proprioceptive awareness and physiologically in the toxic sensory experience of restless legs associated with increased neuromuscular reactivity which may include myoclonus and myokomia.
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PMID:Restless legs, anxiety and caffeinism. 69 85

The elderly have more organic sleep problems disturbing sleep and contributing to insomnia than younger individuals. The most common disorders afflicting the elderly are obstructive sleep apnea, restless legs syndrome, and nocturnal myoclonus. Poor sleep habits often aggravate or contribute to the ongoing difficulty with sleeping. In the depressed elderly, characteristic EEG changes occur that may help distinguish major depression from pseudodementia; however, it should be considered that pseudodementia may be a harbinger of primary dementia. A careful sleep history and often evaluation by polysomnography are central to the management of sleep problems in the elderly. In conjunction with treatment of any underlying organic sleep disorders, brief administration of short-acting benzodiazepine sedatives for sleep onset insomnia or rapid-acting intermediate half-life benzodiazepines for sleep maintenance insomnia can be quite helpful in the elderly, especially if behavioral techniques also are employed. Elimination of medications, alcohol, and caffeine, which disturb sleep, is also an important part of the treatment approach.
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PMID:Sleep disorders in geriatric patients. 160 Apr 90

In 1986, we reported two anatomoclinical observations of a familial condition that we called "fatal familial insomnia" (FFI). We now present the pedigree as well as the clinical and neuropathologic findings in five new subjects. The pedigree includes 288 members from six generations. Men and women are affected in a pattern consistent with an autosomal dominant inheritance. The age of onset of the disease varies between 37 and 61 years; the course averages 13 months with a range of 7 to 25 months. Progressive insomnia (polygraphically proven in two cases); autonomic disturbances including hyperhidrosis, hyperthermia, tachycardia, and hypertension; and motor abnormalities including ataxia, myoclonus, and pyramidal dysfunction, were present in every case, but with variable severity and time of presentation. Sleep and autonomic disorders were the earliest signs in two subjects, motor abnormalities were dominant in one, and others had intermediate clinical patterns. Pathologically, all the cases had severe atrophy of the anterior ventral and mediodorsal thalamic nuclei. Other thalamic nuclei were less severely and inconsistently affected. In addition, most of the cases had gliosis of the cerebral cortex, a moderate degree of cerebellar atrophy with "torpedoes," and severe atrophy of the inferior olivary nuclei. One case also showed spongy degeneration of the cerebral cortex. We conclude that all the lesions were primary, and that FFI is a multisystem disease in which the different structures are primarily affected with different severity. The insomnia appears to correlate best with the major thalamic pathology. The possibility that FFI belongs to the group identified as prion diseases or diseases transmitted by unconventional agents is examined.
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PMID:Fatal familial insomnia: clinical and pathologic study of five new cases. 173 58

Forty-eight chronic hemodialysis (HD) patients (pts) completed questionnaires that used linear analogue scales (LAS), yes/no responses, and demographic data collection to characterize sleep disorders. Twenty-five pts (52%) reported problems sleeping. These pts graded sleep problems significantly higher than those without sleep problems (6.5 +/- 3 vs. 1.8 +/- 2, p less than 0.001 by LAS). Those with sleep disorders were more likely to smoke cigarettes (13/25 vs. 6/23, p less than 0.05) and have bone pain (14/25 vs. 6/23, p less than 0.05). No differences among pts with and without sleep problems were seen in age, gender, time on dialysis, caffeine intake, pruritus, feelings of sadness, worry, or anxiety, or Kt/V values (1.5 +/- 0.2 vs. 1.4 +/- 0.2, p less than 0.13). Restless legs (84%), onset insomnia (76%), and nighttime (76%) and early A.M. waking (72%) characterized the sleep disorders; symptoms suggesting nocturnal myoclonus were less common (20%). We conclude that sleep disorders are common in HD pts and may be exacerbated by tobacco use, bone pain, and restless legs. Kt/V does not correlate with sleep disorders. Further examination of this problem, including formal sleep studies, is needed.
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PMID:Characterizing sleep disorders in chronic hemodialysis patients. 175 Dec 35

Insomnia is one of the most common complaints encountered by the primary care physician. Yet, in many cases, physicians treat the symptom of insomnia rather than evaluating and treating the underlying causes of insomnia. Because the subjective complaint of insomnia does not always correlate with evidence of objective sleep disruption, a careful history and evaluation are required. Assessment of the duration of insomnia and quantification of the impact of nocturnal sleep disruption on daytime functioning provide the most reliable indices of severity. Primary insomnia may be due to a number of different causes, such as poor sleep hygiene or circadian rhythm disruption. Insomnia may also be the presenting symptom of other primary sleep disorders, such as sleep apnea syndrome or nocturnal myoclonus, or of a variety of medical or psychiatric illnesses. The treatment of the patient with insomnia should address the underlying cause, when identifiable. When the cause cannot be identified, treatment should be conservative; nonpharmacologic therapies should be used whenever possible. When pharmacologic approaches are indicated, short-acting benzodiazepines should be administered in concordance with strict prescribing guidelines. Frequent follow-up is necessary to ensure continued therapeutic efficacy of the prescribed therapy.
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PMID:Detection and assessment of insomnia. 179 May 41

Tonic and rhythmic activity of the masticatory muscles accompanied by a loud and grating or clicking sound characterizes bruxism, a well-recognized parasomnia. We describe a 63-year-old man who complained of insomnia due to repeated tongue nibbling during sleep. Nocturnal polysomnographic recordings showed brief (50-100-ms) myoclonic jerks of myloioideus and masseter muscles occurring during phase 1 of sleep and leading to troublesome tongue nibbling with arousal of the patient. Hypnograms showed reduction of phase 2 and absent phases 3-4 and REM. Different pharmacological treatments including clomipramine, benzodiazepines, and carbamazepine were ineffective. A purposive interdental plate was placed to prevent jaw closings during sleep: masticatory myoclonus still persisted, but it did not provoke arousals; insomnia disappeared and night hypnograms improved.
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PMID:Sleep-induced masticatory myoclonus: a rare parasomnia associated with insomnia. 181 24

We report 38 consecutive patients referred to a sleep disorder clinic who on diagnostic polysomnography showed excessive amounts of brief fragmentary myoclonus throughout all stages of NREM sleep. Almost all patients were male despite a reasonably equal sex distribution of referral. The phenomenon was found associated with sleep-related respiratory problems, periodic movements in sleep (PMS), narcolepsy, intermittent hypersomnia and (rarely) insomnia. It also occurred associated with excessive daytime sleepiness (EDS) as an isolated polysomnographic finding apart from some degree of sleep fragmentation.
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PMID:Excessive fragmentary myoclonus in NREM sleep: a report of 38 cases. 241 Feb 21

A 72-year-old man with a 30-year complaint of intractable insomnia had a positive family history of depression. He first came to psychiatric attention in 1958, after attacking his wife. He was prescribed barbiturates, and later was given meprobamate and nitrazepam, but with no effect on his complaint. The patient tended to increase the dosage of any drug given, of his own accord. EEG sleep recording confirmed the diagnosis of nocturnal myoclonus. It was hoped that at the case conference further treatment stratagems would be suggested.
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PMID:Thirty years' war: a battle with insomnia. 257 8

Clonazepam (1 mg h.s.) and temazepam (30 mg h.s.) were studied in 10 patients diagnosed as having insomnia with nocturnal myoclonus. Each subject underwent two nocturnal polysomnographic recordings while drug-free, two during treatment with clonazepam, and two during treatment with temazepam. Treatment sessions were 7 days long, and recordings were done on nights 6 and 7 of the treatment sessions. A 14-day washout period separated the treatment sessions. The order of drugs used in the first and second treatment sessions was randomized. Objective and subjective sleep laboratory data showed that both drugs improved the sleep of patients with insomnia in association with nocturnal myoclonus. Neither drug significantly reduced the number of nocturnal myoclonic events. Sleep changes were consistent with those produced by sedative benzodiazepines in general. Thus, the data support clinical reports that clonazepam, a benzodiazepine marketed for the indication of seizure, is useful in improving sleep disturbances associated with nocturnal myoclonus. Temazepam, a benzodiazepine marketed for the indication of insomnia, was found to be a suitable alternative to clonazepam in the treatment of insomnia associated with nocturnal myoclonus. The present data and other studies suggest the need for a model that explains why leg movements and sleep disturbances may wax and wane independently.
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PMID:Nocturnal myoclonus: treatment efficacy of clonazepam and temazepam. 287 85

Two patients complaining of insomnia had sleep-related periodic leg movements (nocturnal myoclonus) on polysomnographic evaluation. Both also complained of cold feet and had abnormal peripheral pulse examinations. Treatment with phenoxybenzamine, alpha-adrenergic blocker, normalized the peripheral pulse responses, reduced the complaint of insomnia, and reduced the sleep related leg movements but resulted in only mild sleep improvements. Peripheral pulse examinations of ten other patients with sleep-related periodic leg movements revealed abnormal responses in four. From these and other results, it is hypothesized that the sympathetic nervous system may mediate the periodicity of sleep related periodic leg movements.
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PMID:Peripheral vasoconstriction in patients with sleep related periodic leg movements. 289 66


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