Sertraline and akathisia: Spontaneous resolution

Olivera, Arturo A.

doi:10.1016/s0006-3223(96)00384-8

Cited by 15 publications

(3 citation statements)

References 3 publications

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“…In the treatment of affective disorders the focus with regard to akathisia has until recently been mainly on the antidepressant¯uoxetine, but other SSRIs have been reported to cause similar akathisia-like side effects (Lane, 1998;Baldwin, 2000;Hansen and Wilkinson, 2001;Olivera, 1992;Settle, 1994;Eberstein et al, 1996;Gerber and Lynd, 1998;Arya, 1994), although this has so far not been as well investigated and documented as with¯uoxe-tine. There could be two reasons for this, either that uoxetine is actually the most likely of the antidepressants to cause akathisia, or that¯uoxetine is the most widely used antidepressant drug and would therefore statistically be a more common cause of akathisia.…”

Section: Treatment With Neuroleptics and Antidepressantsmentioning

confidence: 99%

“…A considerable number of case reports and review articles listed by Lane have suggested this association, especially with selective serotonin reuptake inhibitors (Lane, 1998;Hansen and Wilkinson, 2001;Olivera, 1992;Gerber and Lynd, 1998). This paper will review the evidence base for this association and look into the possible link between drug-induced akathisia and suicidal behaviour (Lane, 1998;Lipinski et al, 1989;Rothschild and Locke, 1991;Hamilton and Opler, 1992).…”

Section: Introductionmentioning

confidence: 97%

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A critical review of akathisia, and its possible association with suicidal behaviour

Hansen

2001

Human Psychopharmacology

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The purpose of this paper was to make a critical review of akathisia, based on the principles of evidence-based medicine, and to explore a possible link between akathisia and suicidal behaviour (suicidal thinking, parasuicide and completed suicide). An extensive systematic search was carried out on three major databases, Embase, ClinPsych and Medline. Fifty-seven relevant references were found, and a further 26 references were reviewed after careful selection from the references of the original references. The Cochrane Library did not contain any systematic reviews on the subject. Akathisia can be caused by several different groups of drugs, but most frequently by antipsychotics and to a lesser extent antidepressants. Research into akathisia is made considerably more difficult by the lack of a universally agreed definition of the condition. The underlying pathophysiology is still far from clear, but the literature offers guidelines on less hazardous management regimes for patients. On the basis of the existing literature, akathisia cannot at this stage unequivocally be linked to suicidal behaviour. It is certain, however, that the condition of akathisia does cause considerable distress in an already vulnerable group of patients. Because it is largely avoidable, new, more rigorous strategies must be put in place to prevent it. Copyright 2001 John Wiley & Sons, Ltd.

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Section: Treatment With Neuroleptics and Antidepressantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

A critical review of akathisia, and its possible association with suicidal behaviour

Hansen

2001

Human Psychopharmacology

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“…Some patients treated with SSRIs may also experience cognitive symptoms such as mental slowing and decreased attention capability, psychological symptoms such as apathy and emotional blunting (Hoehn-Saric et al, 1990 and1991;Garland et al 2001;Opbroek et al 2002;Ellison and Stanziani, 1993;Bertschy and Vandel, 1993), and motor symptoms such as bruxism, akathisia and extrapyramidal symptoms (Adler and Angrist, 1995;Altshuler et al, 1994;Bauer et al, 1996;Bertschy and Vandel, 1993;Black and Uhde, 1992;Boffa and Lofchy, 2000;Bostwick and Jaffee, 1999;Chelben et al, 2001;Chong, 1995;Chong and Tan, 1996;Dave, 1994;Diler et al, 2002;Dominguez-Moran et al, 2001;Fleischhacker, 1991;Freidman, 1990;George and Trimble, 1993;Gerber and Lynd, 1998;Gill et al, 1997;Hansen, 2003;Klee and Kronig, 1993;Lambert et al, 1998;Lee and Nam, 2000;Lipinski et al, 1989;Lobbezoo et al, 2001;Maany and Dhopesh, 1990;Mander et al, 1994;Olivera, 1996Olivera, , 1997Opler, 1994;Perucca et al, 1997;Reccoppa et al, 1990;Romanelli et al, 1996;Settle, 1993;Shihabuddin and Rapport, 1994;...…”

Section: Side-effect Profilementioning

confidence: 99%

Monoaminergic‐based Pharmacotherapy for Depression

Papakostas¹,

Fava²

2005

Biology of Depression

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Although recent advances in neuropharmacology, neuroendocrinology, molecular biology, and pharmacogenetics have been instrumental in bringing about potential treatments for depression which are fundamentally unrelated to their predecessors, including substance P antagonists, glutaminergic agents, and corticotropinreleasing factor (CRF) antagonists, nevertheless it was agents that influenced the function of monoamine receptors and transporters that were discovered initially by serendipity and then developed as treatments for depression. The development of such compounds also served as a framework for the understanding of depression as a medical illness affecting brain functioning. As a result of these efforts, our field has gained further understanding of the role of monoamines in depression. In previous chapters, the relevance of monoamines in the underlying pathophysiology of depression was reviewed. In the following chapter we will focus on describing the contemporary role of monoaminergic agents in the treatment of depression. 6.

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