Reasons for Quitting Serotonin Reuptake Inhibitor Therapy: Paradoxical Psychological Side Effects and Patient Satisfaction

Bolling, Madelon Y.; Kohlenberg, Robert J.

doi:10.1159/000080392

Cited by 59 publications

(38 citation statements)

References 7 publications

(11 reference statements)

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“…63 Serotonergic drugs can inhibit goal-directed behaviour, including sex, pleasurable exercise, and curiosity. 64 Norepinephrine. NE increases activation to both positive and negative stimuli.…”

Section: Midbrain Inputsmentioning

confidence: 99%

Brain Illness and Creativity: Mechanisms and Treatment Risks

Flaherty

2011

Can J Psychiatry

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Highlights • Psychiatric and neurological drug choice may alter patients' creativity, sometimes in counterintuitive ways. • To preserve creativity, treatments that enhance dopaminergic function are more helpful than those that decrease dopaminergic function. • Traits that in stressful environments increase vulnerability to illness may, in permissive environments, help creativity. Brain diseases and their treatment may help or hurt creativity in ways that shape quality of life. Increased creative drive is associated with bipolar disorder, depression, psychosis, temporal lobe epilepsy, frontotemporal dementia, Parkinson disease treatments, and autism. Creativity depends on goal-driven approach motivation from midbrain dopaminergic systems. Fear-driven avoidance motivation is of less aid to creativity. When serotonin and norepinephrine lower motivation and flexible behaviour, they can inhibit creativity. Hemispheric lateralization and frontotemporal connections must interact to create new ideas and conceptual schemes. The right brain and temporal lobe contribute skill in novelty detection, while the left brain and frontal lobe foster approach motivation and more easily generate new patterns of action from the novel perceptions. Genes and phenotypes that increase plasticity and creativity in tolerant environments with relaxed selection pressure may confer risk in rigorous environments. Few papers substantively address this important but fraught topic. Antidepressants (ADs) that inhibit fear-driven motivation, such as selective serotonin reuptake inhibitors, sometimes inhibit goal-oriented motivation as well. ADs that boost goal-directed motivation, such as bupropion, may remediate this effect. Benzodiazepines and alcohol may be counterproductive. Although dopaminergic agonists sometimes stimulate creativity, their doing so may inappropriately disinhibit behaviour. Dopamine antagonists may suppress creative motivation; lithium and anticonvulsant mood stabilizers may do so less. Physical exercise and REM sleep may help creativity. Art therapy and psychotherapy are not well studied. Preserving creative motivation can help creativity and other aspects of well-being in all patients, not just artists or researchers.

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Section: Midbrain Inputsmentioning

confidence: 99%

Brain Illness and Creativity: Mechanisms and Treatment Risks

Flaherty

2011

Can J Psychiatry

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“…It is suggested that sexual dysfunction may contribute to patient noncompliance and this is important especially for the maintenance treatment of major depressive disorder (Bolling and Kohlenberg, 2004;Hirschfeld, 1999;Werneke et al, 2006). Quality of life is an important issue and includes sexual functioning (Williams et al, 2006) and concern about antidepressant-induced sexual dysfunction has continued to grow; however, the mechanism of action of sexual dysfunction associated with SSRIs is not well understood (Saiz-Ruiz et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Mirtazapine augmentation in depressed patients with sexual dysfunction due to selective serotonin reuptake inhibitors

Ozmenler

Karlıdere

Bozkurt

et al. 2008

Human Psychopharmacology

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“…And, as anybody who has studied ADM knows, management of ADM is a conflict-ridden business. Many patients are unwilling to take ADM; of those who do take it, many do not respond, while others who do respond develop intolerable side effects; finally, of those who respond with tolerable side effects, a good portion have their own ideas about how to take the medication and when to stop (Bolling & Kohlenberg, 2004).…”

Section: Resultsmentioning

confidence: 99%

Biologism is Behavior: A Commentary on Wong and Wyatt and Midkiff

Holman

Kohlenberg

2007

Behav. Soc. Iss.

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In response to Wong (2006) and Wyatt and Midkiff (2006), we argue that behaviors related to biologism-i.e., believing that biological explanations are more explanatory than they really are-and other aspects of biological psychiatry are susceptible to behavior analysis, and we explore the possibility of such an analysis with special attention to the interests of clinicians and clinical researchers. We also propose that behavior analysis, biology, and science in general may best be served by the adoption and promotion of a more philosophically and scientifically rigorous view of the interaction between biological and behavioral factors. Such a view would promote rational integration rather than opposition of theoretical systems. KEYWORDS: biology, behavior analysis, antidepressant medicationIn this commentary on Wong (2006) and Wyatt and Midkiff (2006), we argue two main points, both related to the broader discursive frame within which debate-whether scientific, clinical, or political-about the relative merits of biological and behavioral approaches takes place. The first point follows from Wyatt and Midkiff's statement that a "paradigm shift" away from the biological perspective would represent progress. For "paradigm shift," we read behavior change. We therefore discuss the nature of such a behavior change, focusing on concerns relevant to our own backgrounds and aims as clinicians and clinical researchers. This perspective emphasizes a pragmatic and humanistic application of behavior analytic principles in service of optimum clinical outcomes.The second point we wish to argue concerns the handling of the duality of biology and behavior itself-even when we recognize that duality as merely discursive, and especially in light of the massive complexity of the phenomenon that this duality tries to model. While this point elicits yawns from undergraduates, who are subjected to it again and again, we wish to repeat it here. Maintaining a simple duality of biology and behavior is simply not scientifically or philosophically responsible, and as clinicians and researchers (whether behavior analytic or not) guided by the super-ordinate principles of scientific method and pragmatism, we ought to articulate, carefully and consistently, a more rigorous view of their interactive union. Such a view does not exclude exposing the fallacies of the reigning biologism. But beyond these excesses, a more healthy dialogue, 1 Correspondence related to this article may be sent to gholman@u.washington.edu.

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Reasons for Quitting Serotonin Reuptake Inhibitor Therapy: Paradoxical Psychological Side Effects and Patient Satisfaction

Cited by 59 publications

References 7 publications

Brain Illness and Creativity: Mechanisms and Treatment Risks

Brain Illness and Creativity: Mechanisms and Treatment Risks

Mirtazapine augmentation in depressed patients with sexual dysfunction due to selective serotonin reuptake inhibitors

Biologism is Behavior: A Commentary on Wong and Wyatt and Midkiff

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