Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 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

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

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.
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PMID:Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines. 250 42

Sleep is disturbed in 90% of patients with major depression. Disordered sleep physiology may persist after clinical remission of depression, suggesting either that sleep disruption is a trait characteristic of recurrent depression or that depressed patients acquire new habits that perpetuate sleep-related problems. This article reviews the data suggesting a common pathophysiology between sleep and depression. It then focuses on a strategy for evaluating and treating sleep disruption in depressed patients. Treatment must have a conservative goal of restoring sleep quality to the pre-episode level. The treatment of sleep disruption relies primarily on optimal treatment of the depression itself. This includes evaluation and treatment of comorbid medical disorders, substance use (e.g., caffeine, alcohol), and sleep disorders (e.g., nocturnal myoclonus, sleep apnea). The effects of the different classes of antidepressant medications on sleep architecture are presented. Nonpharmacologic strategies for improving sleep, such as behavior modification, relaxation, and phototherapy, are discussed. Finally, the risks and benefits of hypnotic use in the depressed patient and a treatment algorithm for the acute and chronic use of hypnotics are considered.
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PMID:Treatment of sleep disturbances in depressed patients. 784 8

Caffeine is a natural alkaloid methylxanthine that is found in various plants such as coffee or tea. Symptoms of a severe overdose may present with hypokalemia, hyponatremia, ventricular arrhythmias, hypertension followed by hypotension, respiratory failure, seizures, rhabdomyolysis, ventricular fibrillation and finally circulatory collapse. A 21-year-old woman called for the ambulance herself soon after the ingestion of about 10,000 mg of caffeine. At the arrival of the ambulance, the patient went into cardiac arrest almost immediately. After a total resuscitation period of 34 min including seven counter-shocks and 2 mg epinephrine, the patient was stable enough to be transferred to the hospital. The patient soon went into VF again and received two more counter-shocks and 1 mg epinephrine and finally an intravenous bolus dose of 300 mg amiodarone. The initial arterial blood gas showed pH at 6.47, lactate at 33 mmol/l and potassium level at 2.3 mmol/l. Unfortunately, no blood samples for caffeine analysis were taken. Three days after hospital admission, the patient developed myoclonus, which did not respond to medical treatment. Excessive intake of caffeine may produce arrhythmias and pronounced hypokalemia and ensuing ventricular fibrillation. In case of counter-shock-resistant VF, it can be necessary to give an early loading dose of amiodarone. Furthermore, it may be beneficial to replace the potassium as early as possible. Epinephrine and buffer solutions used during resuscitation may further decrease blood potassium levels and should be administrated cautiously. Epinephrine can be replaced by other vasopressor drugs, such as vasopressin without effects on beta-receptors.
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PMID:A case of fatal caffeine poisoning. 2064 25

Sleep bruxism is a sleep-related movement disorder that can be responsible for various pains and dysfunctions in the orofacial region. The aim of the current case-control association study was to investigate the association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. Non-related participants were recruited and divided into either a sleep bruxism group (n = 66) or control group (n = 48) by clinical diagnoses and 3-night masseter electromyographic recordings by means of a portable miniature device. The Epworth Sleepiness Scale, Temperament and Character Inventory, NEO-Five Factor Inventory and custom-made questionnaires that asked about familial aggregation, alcohol intake, caffeine intake, cigarette smoking, past stressful life events, daytime tooth-contacting habit, temporomandibular disorder, daily headache, snoring, apnea/hypopnea symptoms, leg-restlessness symptoms and nocturnal-myoclonus symptoms were administered. In addition, 13 polymorphisms in four genes related to serotonergic neurotransmission (SLC6A4, HTR1A, HTR2A and HTR2C) were genotyped. These factors were compared between case (sleep bruxism) and control groups in order to select potential predictors of sleep-bruxism status. The statistical procedure selected five predictors: Epworth Sleepiness Scale, leg-restlessness symptoms, rs6313 genotypes, rs2770304 genotypes and rs4941573 genotypes. A multivariate stepwise logistic regression analysis between the selected predictors and sleep-bruxism status was then conducted. This analysis revealed that only the C allele carrier of HTR2A single nucleotide polymorphism rs6313 (102C>T) was associated significantly with an increased risk of sleep bruxism (odds ratio = 4.250, 95% confidence interval: 1.599-11.297, P = 0.004).This finding suggests a possible genetic contribution to the etiology of sleep bruxism.
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PMID:Association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. 2254 12

The current work is targeted to review the risks of gabapentin misuse, its potential interactions with other drugs, side effects and use contraindications. This review consists of a total of 99 biographical references (from the year 1983 to 2016). A publication search of PubMed was performed from January 1983 to December 2016. It included animal studies, clinical studies, case studies and reviews related to gabapentin misuse, potential interactions, side effects and use contraindications. The search terms were gabapentin, anticonvulsant and antiepileptic. In general, it seems that gabapentin has risks of being misused based on the increased level of prescriptions, related fatalities, recreational misuse and higher doses of self-administration. The main reasons for gabapentin misuse are as follows: getting high, alleviating opioid withdrawal symptoms and potentiating methadone effects. Some of the main substances that interact with gabapentin are morphine, caffeine, losartan, ethacrynic acid, phenytoin, mefloquine and magnesium oxide. Some of the side effects caused by gabapentin are teratogenicity, hypoventilation, respiratory failure and myopathy. Finally, reports in general contraindicate the use of gabapentin in conditions such as myasthenia gravis and myoclonus.
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PMID:Review about gabapentin misuse, interactions, contraindications and side effects. 2822 49