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)

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

While myoclonus awake and at rest, body rocking and marching in place have been occasionally reported to occur in idiopathic restless legs syndrome (RLS), it has not been previously noted that these clinical features occur frequently in a subpopulation of severely affected older RLS patients seeking medical attention for longstanding symptoms that have become progressively worse over the years. We studied 10 unrelated patients from this subpopulation and polysomnographically documented myoclonus while awake and at rest in 8, and intermittent night-time body rocking and marching in place in 6 by history and videotape. Also occurring frequently were the well-known clinical features of floor pacing, paresthesias, sleep disturbances, periodic movements of sleep (PMS), tendency for the signs and symptoms to be worse at night, and a family history suggestive of RLS.
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PMID:Frequent occurrence of myoclonus while awake and at rest, body rocking and marching in place in a subpopulation of patients with restless legs syndrome. 341 79

In a follow-up study (mean, approximately six months), nitrazepam was helpful in suppressing periodic movements in sleep (sleep-related myoclonus) and improving disturbed sleep physiology and daytime symptoms of 13 patients (mean age - 53 yr).
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PMID:Nitrazepam for periodic movements in sleep (sleep-related myoclonus). 395 52

Disturbed nocturnal sleep is considered a symptom of narcolepsy. Polysomnographic recordings of 57 consecutive narcoleptic patients were reviewed for evidence of disturbed sleep. When disrupted sleep was present, it was attributable to recognized sleep disorders: nocturnal myoclonus and sleep apnea. Comparison of standard polysomnographically derived parameters of patients who had narcolepsy without sleep apnea or nocturnal myoclonus with those of a normal control group, showed no evidence of disturbed sleep in the patient population. The narcoleptics that also had nocturnal myoclonus or upper airway sleep apnea did have disturbed sleep in comparison with the normals. Our data suggest disturbed sleep tends to develop in narcolpetic patients with age, but is not an inherent element of the narcolepsy syndrome.
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PMID:Narcolepsy and disturbed nocturnal sleep. 661 86

The advances in research on sleep an biological rhythms have recently been applied to the diagnosis and treatment of sleep disorders. A new clinical specialty has developed with the establishment of sleep disorder centers and a diagnostic classification of sleep and arousal disorders. This new nosological approach has evolved from an extensive base of new scientific information concerning descriptive polygraphic and analysis of clinical case series. Four major categories have been defined: (a) disorders of initiating and maintaining sleep (insomnias), (b) disorders of excessive somnolence, (c) disorders of the sleep-wake schedule, and (d) dysfunctions associated with sleep. Within this comprehensive classification certain major pathophysiological advances are described for the "insomnias." These include polysomnographic identification of altered sleep stage patterns in the major effective illnesses, insomnias related to hypnotic drugs and alcohol, sleep disturbances associated with sleep-induced respiratory impairment, and sleep-related periodic movements during sleep (nocturnal myoclonus). Excessive daytime somnolence is primarily associated with the hypersomnia sleep-apnea syndrome and with narcolepsy. The relationship between biological rhythms (chronobiology) and disorders of the human sleep-wake schedules is very actively investigated. The recognition that sleep length, internal organization, and timing within neurophysiological circadian time-keeping systems has lead to better diagnosis of these sleep-wake disorders and new chronotherapeutic regimens. Finally, increasing identification and description of "parasomnias," i.e. dysfunctions associated with sleep, has led sleep research into important new areas that are of general physiological interest. It is now clear that sleep disorders medicine has become a new scientific and clinical discipline in its own right.
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PMID:Sleep and its disorders. 701 38

Polygraphic recordings of the sleep of patients complaining of insomnia has led to recognition of specific patterns of disturbed sleep corresponding to different etiologies of insomnia. This study presents results of polygraphic recordings of the sleep of 26 patients with chronic pain for which no physical cause can be found. All 26 also complained of insomnia. Sleep parameters of this group were compared with those to two other groups also complaining of insomnia: 12 patients whose disturbed sleep was judged secondary to psychiatric disorder, and 16 patients with the subjective complaint of insomnia in whom no objective evidence of sleep disturbance could be demonstrated. The three groups differed significantly in terms of their sleep parameters. The pain patients slept less than the subjective insomnia patients. The sleep disturbance of the psychiatric patients was more severe than that of the chronic patients. Several chronic pain patients showed evidence of nocturnal myoclonus; several also showed alpha rhythm intrusions into their sleeping electroencephalograms. The study verifies that chronic pain patients do experience significant sleep disturbance and raises several questions concerning relationships among chronic pain, sleep disturbance, and psychiatric illness, particularly depression.
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PMID:Disturbed sleep in patients complaining of chronic pain. 708 3

Nocturnal myoclonus has been identified as a cause of disturbed sleep and excessive daytime fatigue. To our knowledge, no therapy has heretofore been available to adequately control this problem. We identified this problem clinically in two patients; in one, the phenomenon was observed with a polygraphic sleep recording. Small doses of clonazepam, 1 mg, before retiring were found to specifically control the myoclonus and allow sleep patterns to return to normal.
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PMID:Clonazepam treatment of insomnia due to sleep myoclonus. 735 5

The nocturnal myoclonus syndrome (NMS) consists of stereotyped, repetitive jerks of the lower limbs that occur during sleep or wakefulness. NMS is often related with restless-legs syndrome (RLS) and can cause severe sleep disturbances and daytime sleepiness. The efficacy of dopamine agonists in the treatment points to a dopaminergic dysfunction in NMS. We investigated the central dopamine D2-receptor occupancy with [123I] labeled (S)-2-hydroxy-3-iodo-6-methoxy-([1-ethyl-2-pyrrolidinyl]methyl) benzamide (IBZM) (a highly selective CNS D2 dopamine receptor ligand) ([123I]IBZM) and single photon emission tomography (SPET) in 20 patients with NMS and in 10 healthy controls. In most of the patients with NMS there was a lower [123I]IBZM binding in the striatal structures compared to controls. The results indicate that NMS is related to a decrease of central D2-receptor occupancy.
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PMID:Nocturnal myoclonus syndrome (periodic movements in sleep) related to central dopamine D2-receptor alteration. 778 13

Angelman syndrome is an inherited disorder that includes severe mental retardation and epilepsy. Patients have no speech, puppet-like gait with jerky movements, hyperactivity, disturbed sleep, bouts of inappropriate laughter, a pronounced jaw, and widely spaced teeth. The syndrome results from deletion or mutation within maternal chromosome 15q11-q13. Considerable evidence suggests that the gene or genes responsible for Angelman syndrome are expressed only from the maternal chromosome 15, a situation known as parental imprinting. This epigenetic marking of certain regions of the parental genomes is characterized by parent-of-origin-specific allelic DNA methylation, allele-specific DNA replication timing, and physical pairing of the two chromosome 15 homologues. Imprinting is important for normal development, and its disregulation causes several human disorders. The epilepsy of Angelman syndrome has been studied and indicates a rather typical electroencephalographic abnormality with slowing and notched wave and spikes. Various types of seizures occur, usually including myoclonus and atypical absence. Variable severity among patients suggests potential molecular diversity in the genetic mechanism, possibly the involvement of more than one gene. Angelman syndrome can arise from the following molecular genetic defects: a deletion in 15q11-q13 that covers the Angelman gene or genes, mutations that alter imprinting, and paternal uni-parental disomy for the region. Another 20% or so of patients with clinical symptoms of Angelman syndrome have none of these three defects but are believed to have mutations in one or more genes in the region, and this may be familial. The UBE3A gene, which codes for the enzyme ubiquitin protein ligase involved in protein degradation and processing, has been found to be mutated in many but not all of patients with Angelman syndrome and can be considered a major Angelman candidate gene. Other potential candidate genes in the region include a cluster of three GABAA receptor subunits, which are involved in inhibitory synaptic transmission in the brain. The GABRB3 gene, which codes for the beta 3 subunit, is deleted in most persons with Angelman syndrome. The absence of this gene in mice causes craniofacial abnormalities and neurologic impairment with seizures. The exact role of UBE3A and GABRB3 in the syndrome and their imprinting status are under investigation.
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PMID:Parental imprinting and Angelman syndrome. 1051 31

It has been proposed that sleep disturbances, especially reduced delta sleep, are related to a poor outcome in schizophrenia. To determine whether long-term treatment with neuroleptics can promote sleep disturbances by increasing the risk of a nocturnal myoclonus syndrome (NMS) (=periodic movements in sleep) related insomnia, we performed all-night polysomnography in 10 chronically ill schizophrenic patients who had been under neuroleptic therapy for a mean of 27 years. NMS-related insomnia was detected in all 10 patients. Potential pathophysiological relationships between long-term neuroleptic therapy and NMS occurrence are discussed. Our findings suggest that long-term administration of neuroleptics favours the appearance of insomnia.
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PMID:Can chronic neuroleptic treatment promote sleep disturbances in elderly schizophrenic patients? 1067 48


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