PubMed · 16110592
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Sachdev. 2005. Transcranial direct current stimulation in developing countries.. https://pubmed.ncbi.nlm.nih.gov/16110592/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Reanalyses of placebo-controlled trials reveal an increased risk of suicidal ideations or parasuicidal acts in children and adolescents under treatment with selective serotonin reuptake inhibitors (SSRI) or other antidepressants. Although no completed suicide was shown, these findings are the more important because, with the exception of fluoxetine, an evidence base for the efficacy of antidepressants is weak or lacking in this age group. For adults, there is no reason to doubt that antidepressants help to reduce suicides by shortening depressive episodes and preventing recurrence. A general and pronounced suicide-inducing effect of SSRI or other antidepressants can largely be excluded. On the other hand, in some vulnerable patients the risk of suicidal acts can increase, especially during the first days of antidepressant treatment. There is no evidence that this risk is higher with SSRI than with other antidepressants or nonpharmacological treatments. Safety in case of overdose is a strong argument favouring newer antidepressants over tri- and tetracyclic antidepressants in outpatients with unclear suicidality. The current widespread public discussions concering the risks of antidepressants is a risk in itself because confidence in treatment, compliance, and help seeking behaviour may get influenced negatively.
Sleep disorder is one of the major symptoms in depression. It can be a risk factor, predictor, or symptom of depressive episodes. Successful therapy of sleep disorder in severely depressed patients can be a problem of its own. So far, there are few data from systematic studies. Definite treatment recommendations and strategies do not exist. The use of sleeping aids is mainly based on clinical experience and arbitrary treatment preferences. This article tries to summarize the difficulties of a rational therapeutic approach to dyssomnia in depressive patients. In addition to medical treatment, the basics of sleep hygiene should be considered. From a pharmacological point of view, sedating antidepressants, short-term add-on benzodiazepines or nonbenzodiazepines, and long-term add-on low potency neuroleptics are considered appropriate treatments. The combination with atypical sedating antipsychotics or low-dose tricyclic antidepressants may be helpful. Drugs which primarily work through serotonin and noradrenalin have negative effects on sleeping disorders since they suppress REM sleep. In contrast to that, GABAergic, antihistaminic, and anticholinergic effects are beneficial for inducing and maintaining sleep. Half-time, pharmacodynamic and pharmacokinetic effects and interactions, and influence of the drugs on reaction time and personal well-being have to be considered.
The family of hydroxymethylglutaryl coenzyme A reductase inhibitors, collectively known as statins, are used clinically to reduce plasma cholesterol levels. Recent reports indicate that statin therapy is associated with a reduced risk of depression, although the mechanism underlying this antidepressant effect is unknown. Evidence suggests that increasing central BDNF activity plays an important role in the treatment of major depression. In the nervous system, the proteolytic cleavage of pro-BDNF, a BDNF precursor, to BDNF through the tissue-type plasminogen activator (tPA)-plasmin pathway represents one mechanism that can regulate the action of BDNF. In vitro studies have demonstrated that statins can induce tPA and inhibit plasminogen activator inhibitor-1, the major inhibitor of tPA. It is therefore possible that statins could act through the tPA-plasminogen pathway to increase BDNF and achieve an antidepressant effect. It is suggested that statins could be of therapeutic potential for patients with major depression: especially those that have an abnormality in the tPA-plasminogen pathway or comorbidities relating to cardiovascular disease. Furthermore, BDNF dysfunction has also been implicated in several other neuropsychiatric diseases, such as Alzheimer's disease, attention-deficit hyperactivity disorder and Rett syndrome. The potential use of statins in these diseases may warrant further exploration.