Sexual problems are highly prevalent in both men and women and are affected by, among other factors, mood state, interpersonal functioning, and psychotropic medications. The incidence of antidepressant-induced sexual dysfunction is difficult to estimate because of the potentially confounding effects of the illness itself, social and interpersonal comorbidities, medication effects, and design and assessment problems in most studies. Estimates of sexual dysfunction vary from a small percentage to more than 80%. This article reviews current evidence regarding sexual side effects of selective serotonin reuptake inhibitors (SSRIs). Among the sexual side effects most commonly associated with SSRIs are delayed ejaculation and absent or delayed orgasm. Sexual desire (libido) and arousal difficulties are also frequently reported, although the specific association of these disorders to SSRI use has not been consistently shown. The effects of SSRIs on sexual functioning seem strongly dose-related and may vary among the group according to serotonin and dopamine reuptake mechanisms, induction of prolactin release, anticholinergic effects, inhibition of nitric oxide synthetase, and propensity for accumulation over time. A variety of strategies have been reported in the management of SSRI-induced sexual dysfunction, including waiting for tolerance to develop, dosage reduction, drug holidays, substitution of another antidepressant drug, and various augmentation strategies with 5-hydroxytryptamine-2 (5-HT2), 5-HT3, and alpha2 adrenergic receptor antagonists, 5-HT1A and dopamine receptor agonists, and phosphodiesterase (PDE5) enzyme inhibitors. Sexual side effects of SSRIs should not be viewed as entirely negative; some studies have shown improved control of premature ejaculation in men. The impacts of sexual side effects of SSRIs on treatment compliance and on patients' quality of life are important clinical considerations.

Though relatively modest in size, this is the largest placebo-controlled trial done to date in patients with Parkinson disease (PD) and depression. Nortriptyline was efficacious in the treatment of depression and paroxetine CR was not. When compared directly, nortriptyline produced significantly more responders than did paroxetine CR. The trial suggests that depression in patients with PD is responsive to treatment and raises questions about the relative efficacy of dual reuptake inhibitors and selective serotonin reuptake inhibitors.

Objective Despite the negative effects of depression in Parkinson’s disease, there is currently no evidence-based standard of care. The purpose of this study was to examine the efficacy of individually-administered Cognitive Behavior Therapy (CBT) versus clinical monitoring (with no new treatment) for depression in this medical population. Methods Eighty depressed (DSM-IV criteria) patients with Parkinson’s disease participated in an NIH-sponsored randomized-controlled trial of CBT vs. clinical monitoring (1:1 ratio) in an academic medical center from April 2007 to July 2010. All patients concurrently continued under the care of their personal physicians on stable medication regimens. The Hamilton Depression Rating Scale (HAM-D 17) was the primary outcome. CBT was modified to meet the unique needs of the Parkinson’s population and provided for 10 weeks. Assessments were completed at baseline and 5 (midpoint), 10 (end of treatment), and 14 weeks (follow-up) post-randomization by blind raters. Results The CBT group reported greater reductions in depression (HAM-D 17) vs. clinical monitoring (P<.0001). At week 10, mean HAM-D change was 7.35 for CBT vs. 0.05 for clinical monitoring (P<.0001). CBT was also superior to clinical monitoring on several secondary outcomes (i.e., Beck Depression Inventory, anxiety, quality of life, coping, Parkinson’s disease symptom ratings). There were more treatment responders in the CBT group (56% vs. 8%, P<.0001). Conclusions CBT may be a viable approach for the treatment of depression in Parkinson’s disease. Further research is needed to replicate and extend these findings.

Mood disorders are the most common psychiatric problem associated with Parkinson's disease (PD), and have a negative impact on disability and quality of life. Accurate diagnosis of depressive disturbances in PD is critical and will facilitate the testing and use of new interventions; however, there are no clear diagnostic criteria for depressive disorders in PD. In their current form, strict Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria are difficult to use in PD and require attribution of specific symptoms to PD itself or the depressive syndrome. Additionally, DSM criteria for major depression and dysthymia exclude perhaps half of PD patients with comorbid clinically significant depression. This review summarizes an NIH-sponsored workshop and describes recommended changes to DSM diagnostic criteria for depression for use in PD. Participants also recommended: (1) an inclusive approach to symptom assessment to enhance reliability of ratings in PD and avoid the need to attribute symptoms to a particular cause; (2) the inclusion of subsyndromal depression in clinical research studies of depression of PD; (3) the specification of timing of assessments for PD patients with motor fluctuations; and (4) the use of informants for cognitively impaired patients. The proposed diagnostic criteria are provisional and intended to be defined further and validated but provide a common starting point for clinical research in PD-associated depression.