Farmakologi og REM søvn.

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REM sleep behavior disorder (RBD) is characterized by complex behavioral manifestations in response to dream content that may cause sleep disruption or injuries to the patient or the bed partner. In this case, the patients need treatment to control their symptoms. Pharmacologic agents have been reported to have positive and negative impacts on REM sleep muscle atonia and the motor behaviors associated with RBD. Clonazepam is efficacious and well tolerated by the majority of patients afflicted by RBD and should be considered as initial treatment. In patients at risk of falls who have cognitive impairment or who have obstructive sleep apneas, melatonin may be a good alternative to clonazepam. Anticholinesterase inhibitors and dopaminergic agents are not of clear benefit. Monoamine oxidase inhibitors, tricyclic antidepressants, serotonergic synaptic reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD. When these agents are prescribed to patients with neurodegenerative disorders or narcolepsy who are at risk of developing RBD, systematic follow-up may be warranted to detect the emergence of RBD symptoms.

Drugs with beneficial effects on RBD symptoms.

Clonazepam, a sedating benzodiazepine, is currently regarded as the treatment of choice for RBD (table 1). Two large case series have reported substantial improvement in the majority of patients treated with clonazepam.6,25 In the largest series, clonazepam showed complete benefit in 79% of patients, and partial benefit in an additional 11%.6 The initial dose is 0.5 mg at bedtime. If this is ineffective, doses can be increased to 1 or 2 mg. In most cases, a suppression of problematic sleep behaviors and nightmares is observed in the first week of treatment. Tolerance is infrequent and the beneficial effects of clonazepam usually persist for several years. Although the mechanism of action of clonazepam is unclear, it seems to work via suppression of clinical motor manifestations of REM sleep rather than reducing REM sleep muscle tone. On PSG, clonazepam reduced behavioral manifestations and decreased phasic EMG activity without restoring tonic REM sleep muscle activity.28 The beneficial effects of clonazepam have been attributed in part to its serotonergic properties.29 Clonazepam is ineffective in approximately 10% of patients.6,25 Additionally, although only a minority of patients notice significant side effects, clonazepam may increase the risk of confusion or falls in the elderly 30 and may induce or worsen obstructive sleep apnea. There have been no reports describing efficacy of other benzodiazepine medications in RBD. Alternative treatments may have to be considered

Published in Neuology: Volume 67(5) 12 September 2006

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Medisiner som trigger RBD:Drugs inducing or aggravating the symptoms of RBD.

Monoamine oxidase inhibitors, such as selegiline and phenelzine, have been reported to induce RBD symptoms both in patients with parkinsonism 54 and in healthy young subjects (table 3).55 Although one report documented a reduction of RBD symptoms following the administration of carbamazepine,56 a chemical agent sharing similarities with tricyclic antidepressants, the bulk of evidence over the past 30 years has suggested deleterious effects of tricyclic antidepressants on REM sleep muscle atonia, and induction of RBD symptoms in healthy subjects and in patients with psychiatric and neurologic disorders (table 3).15,57–62 There are similar reports of RBD symptoms being triggered by serotonergic synaptic reuptake inhibitors such as fluoxetine and mirtazapine.63,64 A systematic PSG study of patients taking newer serotonergic antidepressants, such as fluoxetine, paroxetine, citalopram, sertraline, and venlafaxine, found an increase in REM sleep EMG tonic activity compared to control subjects.65

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Medisiner som trigger RBD:Drugs inducing or aggravating the symptoms of RBD.

Monoamine oxidase inhibitors, such as selegiline and phenelzine, have been reported to induce RBD symptoms both in patients with parkinsonism 54 and in healthy young subjects (table 3).55 Although one report documented a reduction of RBD symptoms following the administration of carbamazepine,56 a chemical agent sharing similarities with tricyclic antidepressants, the bulk of evidence over the past 30 years has suggested deleterious effects of tricyclic antidepressants on REM sleep muscle atonia, and induction of RBD symptoms in healthy subjects and in patients with psychiatric and neurologic disorders (table 3).15,57–62 There are similar reports of RBD symptoms being triggered by serotonergic synaptic reuptake inhibitors such as fluoxetine and mirtazapine.63,64 A systematic PSG study of patients taking newer serotonergic antidepressants, such as fluoxetine, paroxetine, citalopram, sertraline, and venlafaxine, found an increase in REM sleep EMG tonic activity compared to control subjects.65

Jeg kan bare si en ting og det er at clonazepam har vært utrolig bra i forhold til mareritt som blir "levd ut". Svettetokter, roping, veiving med armer. Jeg kan også underskrive på at antihistaminer har forverret mareritt, tolvon/remeron,nozinan likeså.