Side effects vary among the individual drugs of this class and may include: * increased risk of bone fractures * akathisia *suicidal ideation (thoughts of suicide) and other risks (see below) Sexual dysfunction<unk> s can cause various types of sexual dysfunction such as anorgasmia, erectile dysfunction, diminished libido, genital numbness, and sexual anhedonia (pleasureless orgasm). Sexual problems are common with<unk> s. While initial trials showed side effects in 5-15% of users (based on spontaneous reporting by users), later studies (based on asking patients directly) have shown side effect rates from 36% to 98%. Poor sexual function is also one of the most common reasons people stop the medication. In some cases, symptoms of sexual dysfunction may persist after discontinuation of<unk> s. This combination of symptoms is sometimes referred to as Post-SSRI Sexual Dysfunction (PSSD). On the 11th of June 2019 the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency concluded that a possible relationship exists between<unk>  use and persistent sexual dysfunction after cessation of use. The committee concluded that a warning should be added to the label of<unk> s and SNRIs regarding this possible risk. The mechanism by which<unk> s may cause sexual side effects is not well understood . The range of possible mechanisms includes (1) nonspecific neurological effects (e.g., sedation) that globally impair behavior including sexual function; (2) specific effects on brain systems mediating sexual function; (3) specific effects on peripheral tissues and organs, such as the penis, that mediate sexual function; and (4) direct or indirect effects on hormones mediating sexual function. Management strategies include: for erectile dysfunction the addition of a PDE5 inhibitor such as sildenafil; for decreased libido, possibly adding or switching to bupropion; and for overall sexual dysfunction, switching to nefazodone. A number of non-SSRI drugs are not associated with sexual side effects (such as bupropion, mirtazapine, tianeptine, agomelatine and moclobemide). Several studies have suggested that<unk> s may adversely affect semen quality. While trazodone (an antidepressant with alpha adrenergic receptor blockade) is a notorious cause of priapism, cases of priapism have also been reported with certain<unk> s (e.g. fluoxetine, citalopram). Emotional blunting Certain antidepressants may cause emotional blunting, characterized by reduced intensity of both positive and negative emotions as well as symptoms of apathy, indifference, and amotivation. It may be experienced as either beneficial or detrimental depending on the situation. This side effect has been particularly associated with serotonergic antidepressants like<unk> s and SNRIs, but may be less with atypical antidepressants like bupropion, agomelatine, and vortioxetine. Higher doses of antidepressants seem to be more likely to produce emotional blunting than lower doses. It can be decreased by reducing dosage, discontinuing the medication, or switching to a different antidepressant that may have less propensity for causing this side effect. Violence Researcher David Healy and others have reviewed available data, concluding that<unk> s increase violent acts, in adults and children, both on therapy and during withdrawal. This view is also shared by some patient activist groups. Vision Acute narrow-angle glaucoma is the most common and important ocular side effect of<unk> s, and often goes misdiagnosed. Cardiac<unk> s do not appear to affect the risk of coronary heart disease (CHD) in those without a previous diagnosis of CHD. A large cohort study suggested no substantial increase in the risk of cardiac malformations attributable to<unk>  usage during the first trimester of pregnancy. A number of large studies of people without known pre-existing heart disease have reported no EKG changes related to<unk>  use. The recommended maximum daily dose of citalopram and escitalopram was reduced due to concerns with QT prolongation. In overdose, fluoxetine has been reported to cause sinus tachycardia, myocardial infarction, junctional rhythms and trigeminy. Some authors have suggested electrocardiographic monitoring in patients with severe pre-existing cardiovascular disease who are taking<unk> s. Bleeding<unk> s directly increase the risk of abnormal bleeding by lowering platelet<unk>  levels, which are essential to platelet-driven hemostasis.<unk> s interact with anticoagulants, like warfarin, and antiplatelet drugs, like aspirin. This includes an increased risk of GI bleeding, and post operative bleeding. The relative risk of intracranial bleeding is increased, but the absolute risk is very low.<unk> s are known to cause platelet dysfunction. This risk is greater in those who are also on anticoagulants, antiplatelet agents and NSAIDs (nonsteroidal anti-inflammatory drugs), as well as with the co-existence of underlying diseases such as cirrhosis of the liver or liver failure. Fracture risk Evidence from longitudinal, cross-sectional, and prospective cohort studies suggests an association between<unk>  usage at therapeutic doses and a decrease in bone mineral density, as well as increased fracture risk, a relationship that appears to persist even with adjuvant bisphosphonate therapy. However, because the relationship between<unk> s and fractures is based on observational data as opposed to prospective trials, the phenomenon is not definitively causal. There also appears to be an increase in fracture-inducing falls with<unk>  use, suggesting the need for increased attention to fall risk in elderly patients using the medication. The loss of bone density does not appear to occur in younger patients taking<unk> s. Bruxism<unk>  and SNRI antidepressants may cause jaw pain/jaw spasm reversible syndrome (although it is not common). Buspirone appears to be successful in treating bruxism on<unk> /SNRI induced jaw clenching. Discontinuation syndrome<unk>  reuptake inhibitors should not be abruptly discontinued after extended therapy, and whenever possible, should be tapered over several weeks to minimize discontinuation-related symptoms which may include nausea, headache, dizziness, chills, body aches, paresthesias, insomnia, and brain zaps. Paroxetine may produce discontinuation-related symptoms at a greater rate than other<unk> s, though qualitatively similar effects have been reported for all<unk> s. Discontinuation effects appear to be less for fluoxetine, perhaps owing to its long half-life and the natural tapering effect associated with its slow clearance from the body. One strategy for minimizing<unk>  discontinuation symptoms is to switch the patient to fluoxetine and then taper and discontinue the fluoxetine.<unk>  syndrome<unk>  syndrome is typically caused by the use of two or more serotonergic drugs, including<unk> s.<unk>  syndrome is a condition that can range from mild (most common) to deadly. Mild symptoms may consist of increased heart rate, fever, shivering, sweating, dilated pupils, myoclonus (intermittent jerking or twitching), as well as hyperreflexia. Concomitant use of<unk> s or SNRIs for depression with a triptan for migraine does not appear to heighten the risk of the<unk>  syndrome. Taking monoamine oxidase inhibitors (MAOIs) in combination with<unk> s can be fatal, since MAOIs disrupt monoamine oxidase, an enzyme which is needed to break down<unk>  and other neurotransmitters. Without monoamine oxidase, the body is unable to eliminate excess neurotransmitters, allowing them to build up to dangerous levels. The prognosis for recovery in a hospital setting is generally good if<unk>  syndrome is correctly identified. Treatment consists of discontinuing any serotonergic drugs and providing supportive care to manage agitation and hyperthermia, usually with benzodiazepines. Suicide risk Children and adolescents Meta analyses of short duration randomized clinical trials have found that<unk>  use is related to a higher risk of suicidal behavior in children and adolescents. For instance, a 2004 U.S. Food and Drug Administration (FDA) analysis of clinical trials on children with major depressive disorder found statistically significant increases of the risks of "possible suicidal ideation and suicidal behavior" by about 80%, and of agitation and hostility by about 130%. According to the FDA, the heightened risk of suicidality is within the first one to two months of treatment. The National Institute for Health and Care Excellence (NICE) places the excess risk in the "early stages of treatment". The European Psychiatric Association places the excess risk in the first two weeks of treatment and, based on a combination of epidemiological, prospective cohort, medical claims, and randomized clinical trial data, concludes that a protective effect dominates after this early period. A 2014 Cochrane review found that at six to nine months, suicidal ideation remained higher in children treated with antidepressants compared to those treated with psychological therapy. A recent comparison of aggression and hostility occurring during treatment with fluoxetine to placebo in children and adolescents found that no significant difference between the fluoxetine group and a placebo group. There is also evidence that higher rates of<unk>  prescriptions are associated with lower rates of suicide in children, though since the evidence is correlational, the true nature of the relationship is unclear. In 2004, the Medicines and Healthcare products Regulatory Agency (MHRA) in the United Kingdom judged fluoxetine (Prozac) to be the only antidepressant that offered a favorable risk-benefit ratio in children with depression, though it was also associated with a slight increase in the risk of self-harm and suicidal ideation. Only two<unk> s are licensed for use with children in the UK, sertraline (Zoloft) and fluvoxamine (Luvox), and only for the treatment of obsessive–compulsive disorder. Fluoxetine is not licensed for this use. Adults It is unclear whether<unk> s affect the risk of suicidal behavior in adults. * A 2005 meta-analysis of drug company data found no evidence that<unk> s increased the risk of suicide;
Selective serotonin reuptake inhibitor
Atypical antidepressant
Tricyclic antidepressant
Tetracyclic antidepressant
Heterocyclic antidepressant
Glycine reuptake inhibitor
Serotonin–dopamine reuptake inhibitor
Dopamine reuptake inhibitor