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Query: UMLS:C0600097 (Sedation)
 1,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The psychiatric side effects of the major antihypertensive drugs other than reserpine are reviewed, including centrally acting drugs such as methyldopa and clonidine, peripheral adrenergic drugs such as guanethidine, beta-adrenoceptor blockers such as propranolol, and diuretics. Problems with differential diagnosis and with the interpretation of case reports make assessment of psychiatric side effects difficult. Sedation and sleep disturbances are the most common side effects, occurring with methyldopa, clonidine, and propranolol. Only methyldopa is clearly associated with depression. Other reported effects are toxic confusional states and psychotic reactions. These are rare, however, and no clear patterns of development have been recognized.
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PMID:Psychiatric side effects of antihypertensive drugs other than reserpine. 612 25

Mirtazapine is a unique antidepressant that refines the specificity of effects on noradrenergic and serotonergic systems. It is an antagonist of presynaptic alpha 2-adrenergic autoreceptors and heteroreceptors on both norepinephrine and serotonin (5-HT) presynaptic axons, plus is a potent antagonist of postsynaptic 5-HT2 and 5-HT3 receptors. The net outcome of these effects is increased noradrenergic activity together with specific increased serotonergic activity, especially at 5-HT1A receptors. This mechanism of action maintains equivalent antidepressant efficacy but minimizes many of the adverse effects common to both tricyclic antidepressants and selective serotonin reuptake inhibitors. Mirtazapine has an onset of clinical effect in 2-4 weeks similar to other antidepressants, although sleep disturbances and anxiety symptoms may improve in the first week of treatment. It has minimal cardiovascular and anticholinergic effects, and essentially lacks serotonergic effects such as gastrointestinal symptoms, insomnia, and sexual dysfunction. Sedation, increased appetite, and weight gain are more common with mirtazapine than with placebo. An elimination half-life of 20-40 hours enables once-daily bedtime dosing. The recommended initial dosage is 15 mg once/day at bedtime, with an effective daily dosage range of 15-45 mg. Cases of overdose of up to 975 mg caused significant sedation but no cardiovascular or respiratory effects or seizures.
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PMID:Mirtazapine: an antidepressant with noradrenergic and specific serotonergic effects. 901 62

Posttraumatic stress disorder (PTSD) symptoms may improve significantly with antidepressant medications, however some phenomena often remain refractory to the most commonly used treatments. Frequently, sleep disturbances, such as insomnia and nightmares, are symptoms of PTSD that are refractory to antidepressant treatment. Gabapentin, a novel anticonvulsant agent, has been of interest as a potential anxiolytic agent, but has not been evaluated in PTSD. We reviewed records of 30 consecutive patients who had been diagnosed with PTSD according to structured interviews and had received gabapentin as an adjunctive medication. For each patient, the target symptoms that led to the initiation of gabapentin treatment were identified. Using the most recent clinical data available, the change in target symptom severity following treatment was rated as unimproved, mildly improved, moderately improved, or markedly improved. The gabapentin was often first prescribed to facilitate sleep. The majority (77%) of patients showed moderate or greater improvement in duration of sleep, and most noted a decrease in the frequency of nightmares. The dose range was 300-3600 mg/day. Sedation and mild dizziness were the most commonly reported side effects. This retrospective study suggests that gabapentin may improve in particular sleep difficulties and also other symptoms associated with chronic PTSD. Prospective, controlled studies are needed to further investigate the effects of gabapentin on insomnia, nightmares, and other core PTSD symptoms.
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PMID:Gabapentin in PTSD: a retrospective, clinical series of adjunctive therapy. 1179 51

Acceptability of the atrial defibrillator is partly limited by concerns about shock related anxiety and discomfort. Sedation and/or automatic cardioversion therapy during sleep may ease shock discomfort and improve patient acceptability. Three atrial cardioversion techniques were compared: patient-activated cardioversion with sedation, automatic night cardioversion with sedation, and automatic night cardioversion without sedation. Sedation was oral midazolam (15 mg). Fifteen patients aged 60 +/- 13 years were assigned each strategy randomly for three consecutive episodes of persistent atrial fibrillation requiring cardioversion. Patients completed questionnaires for multiple parameters immediately and again at 24 hours postcardioversion. Atrial cardioversion strategies with oral sedation (patient-activated and automatic) significantly reduced shock recall by 77% (P < 0.005), therapy dissatisfaction by 57%-71% (P < 0.03), shock discomfort by 61%-73% (P < 0.01), shock pain by 79%-83% (P < 0.001), and shock intensity by 73%-77% (P < 0.03), compared to automatic night cardioversion without sedation (P < 0.02). Atrial shock pain was short-lived and caused little disruption to the patients' daily routines. Automatic night cardioversion without sedation, resulted in sleep disturbances not seen with the other strategies (42% vs 0%, P < 0.001) as well as concerns about future pain or discomfort. Twelve patients (80%) chose patient-activated cardioversion with sedation as their preferred treatment, and three (20%) remainder chose automatic night cardioversion with sedation. Ninety percent of patients chose automatic night cardioversion without sedation as the least acceptable therapy. Sedation significantly increases atrial shock acceptability regardless of cardioversion method. Shocks without sedation are significantly less acceptable to patients using the atrial defibrillators.
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PMID:Improving the acceptability of the atrial defibrillator: patient-activated cardioversion versus automatic night cardioversion with and without sedation (ADSAS 2). 1527 Oct 9

Patients with schizophrenia often suffer from sleep disturbances such as excessive sleeping and insomnia. Common medications for schizophrenia can have a sedative effect on patients. Not all antipsychotic medications have the same sedative effect, which is related to dosage and affinity for histamine H1 receptors. Studies have shown that, compared with conventional antipsychotics, atypical antipsychotics such as risperidone, olanzapine, quetiapine, and ziprasidone generally cause less sedation yet are as effective in controlling psychosis and agitation. Sedation can be troublesome to patients who are trying to become re-integrated into society and interfere with their treatment regimen. Both persistent sedation and chronic insomnia can be managed by the physician.
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PMID:Atypical antipsychotics: sleep, sedation, and efficacy. 1600 Oct 94

Antidepressants have long been recognized as a contributory factor to falls and many studies show an association between antidepressants and falls. There are extensive data for tricyclic antidepressants (TCAs) and related drugs, and for selective serotonin reuptake inhibitors (SSRIs), but few data for other classes of antidepressants. Sedation, insomnia and impaired sleep, nocturia, impaired postural reflexes and increased reaction times, orthostatic hypotension, cardiac rhythm and conduction disorders, and movement disorders have all been postulated as contributing factors to falls in patients taking antidepressants. Sleep disturbance is a cardinal feature of depression, and all antidepressants have effects on sleep. TCAs and related drugs cause marked sedation with daytime drowsiness. SSRIs and related drugs have an alerting effect, impairing sleep duration and quality and causing insomnia, which may result in nocturia and daytime drowsiness. Daytime drowsiness is a significant risk factor for falls, both in untreated depression and in depression treated with antidepressants. Clinically significant orthostatic hypotension is common with TCAs and related drugs, the older monoamine oxidase inhibitors and serotonin-norepinephrine reuptake inhibitors (SNRIs). It occurs less commonly with SSRIs, and rarely with moclobemide and bupropion, and is not reported as a significant adverse effect of hypericum (St John's wort). Cardiac rhythm and conduction disturbances are well recognized with TCAs, tetracyclics and SNRIs, but have also been reported with SSRIs. The contribution of antidepressant-induced conduction and rhythm disturbances to falls cannot be assessed with current data. There are insufficient data to exonerate any individual antidepressant or class of antidepressants as a potential cause of falls. The magnitude of the increased risk of falling with an antidepressant is about the same as the excess risk found in patients with untreated depression.
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PMID:Antidepressants and falls in the elderly. 1955 90