Footnotes Disclosure The authors report no conflicts of interest in this work. References 1. A placebo-controlled comparison of antidepressant efficacy and effects on sexual function of sustained-release bupropion and sertraline.
Clin Ther. Burden of phase-specific sexual dysfunction with SSRIs. J Affect Disord. Iatrogenic sexual dysfunction and the protective withholding of information: in whose best interest? J Psychiatr Ment Health Nurs. Balon R. SSRI-associated sexual dysfunction. Am J Psychiatry. J Adv Nurs. Rothschild A. Sexual side effects of antidepressants. J Clin Psychiatry. Effects of antidepressant medication on sexual function: a controlled study.
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Eur Neuropsychopharmacol. Painful ejaculation associated with antidepressants in four patients. Michael A, Mayer C. Fluoxetine-induced anaesthesia of vagina and nipples. Neill JR. Penile anaesthesia associated with fluoxetine use. Genetial anaesthesia persistign six years after sertraline discontinuation.
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J Marital Sex Ther. A placebo-controlled, double-blind trial of ginkgo biloba for antidepressant-induced sexual dysfunction. Human Psychopharmacol. Nearly half of all people taking SSRIs stop taking them within six months.
This is a stunning noncompliance rate. The easy way out is a lot harder than it looks. If the pills are such an easy shortcut, why do people quit taking them? The high dropout rate speaks to fundamental questions about SSRIs: What are you willing to give up to have a "normal" life?
Is it sex? Is it the embarrassment of involuntary hand tremors? Is it a sound sleep? What abnormality are you willing to take on for the hope of normality? I lasted a little over a year on Luvox. I wanted out. Maybe I wanted sex without the oven mitts, maybe I was tired of the sores in my mouth or maybe I was just in denial -- it had been so long since I'd had an anxiety attack, maybe I thought I was "cured.
My doctor tapered me off slowly, reducing the dosage by 25 milligrams every few weeks. I stepped up my meditations, prayers and yoga -- I knew I couldn't just get off the pills and hope for the best. I figured if I had a plan I'd be strong enough to manage without pills.
I was wrong. The sisters of seizure rose slowly, rubbing their eyes from the long sleep. It wasn't long before they brandished their pickaxes again. Everything came back: the chest pains, the feelings of panic and dread, the rapid breathing, the wrenching fear that I was going insane. But the worst was my obsessive thinking about time.
It gathered like a squall. If I were balancing my checkbook, I'd stop in the middle to put away some books, then I'd stop in the middle of that to write a letter, which I'd interrupt to take on something else, all the while worried about what I hadn't completed. I was consumed with the idea that I was running out of time. I would stand in the shower, angry I wasn't soaping up fast enough. My doctor wrote on his prescription pad and handed it to me. He pressed the slip of paper on me. Ponce de Leon Avenue is one of Atlanta's oddest streets.
It's two lanes of decaying southern elegance and urban blight yielding to an in-town revival. Well, at least the symbolism is right, I remember thinking as I pulled up to Dr. Crowe's office. I stepped into a room whispered in earth tones.
Chris Crowe is a towering man, 6-foot-4, with twinkling blue eyes. He mitigated the threat of his height with a calm, soothing voice. Soon after we met he made a remark I'd never heard before from a psychologist: "We should be done in sessions. I immediately disliked him. I don't trust people who promise profound changes in a short time. But his steady, dignified and scientific view of what I was going through won me over -- that, and the fact that he described every symptom I suffered better than I could.
Crowe is a cognitive-behavioral therapist. The term is an oxymoron, juxtaposing two opposing views of psychology. Cognitive therapy was developed by Aaron Beck in Philadelphia in the '60s. Its basic premise is that misguided thoughts cause pathological anxiety. Change the thoughts, reduce the anxiety. Cognitive therapy broke from traditional psychotherapy by ignoring emotions and traumatic childhoods. It only cared about thoughts and beliefs. Behavioral therapy, on the other hand, sneered at every school of psychology.
It didn't care about thoughts, beliefs, insights or the unconscious. Skinner, behaviorism sees pathology as learned behavior. And, it posits, what is learned can be unlearned. A dog conditioned to salivate when a bell rings right before feeding can get unconditioned if the food no longer appears after the bell. No one has to put the dog on the couch to identify underlying food issues.
It's fairly remarkable that these two schools of thought, so radically different from each other, have turned out to be so mutually dependent as a treatment for anxiety disorder. Though few studies have compared cognitive-behavioral therapy with medications, the existing data suggest parity.
But medications are a hare to therapy's turtle. They provide faster relief, but they'll only get you to the finish line if you're willing to refill prescriptions for the rest of your life.
Stop the prescriptions and you stop the relief. Therapy, on the other hand, seems to be effective for years after the last session. No one knows what the noncompliance rate is for therapy relative to medication, but it's probably high, if my experience is any gauge.
There are no side effects to therapy -- but what it lacks in unintended consequences it makes up for with intentional pain. Behaviorism has a charming theory called "intentional exposure," which is a fancy way of saying that the way out of pain is to go through it, over and over and over again, until it goes away on its own.
Crowe incredulously. I did not want a lesson in Zen koans. After a few minutes, Dr. Crowe asked me to rank, on a scale of one to eight, how similar the breathing felt to the breathing in an actual anxiety attack. This sucks, I thought to myself. These symptoms are most often seen 1—9 days after a dose change, 78 , 79 where younger children may be at higher risk from activation syndrome with particular focus placed on mood and irritability.
Nevertheless, while such risk may have been higher in trials for depression relative to those for OCD, 81 providers must carefully monitor for increased suicidal ideation when administering SSRIs to children with OCD, especially considering the high comorbidity rate with depression, 82 — 84 which sometimes may go undetected given the difficulties in diagnosing pediatric internalizing disorders.
Other side effects associated with clomipramine include dry mouth, somnolence, dizziness, fatigue, tremor, weight gain, and constipation. Atypical antipsychotics have drawn the majority of attention among other agents in treatment for OCD, with particular attention given to their role in augmenting non- or partial-response to SRIs.
Some data support this practice among adults; one recent meta-analysis suggests such use to be considered after 12 weeks of incomplete response to two adequate trials of SRI therapy.
Further evidence beyond uncontrolled reports is required to justify its use in youngsters with OCD. A new direction in augmenting agents involves the glutamate modulators memantine and riluzole, which have had open trial support for treatment resistant OCD in youth, 94 — 96 with promising results.
While preliminary, these medications provide an alternative to the traditional serotonin hypothesis in pharmacotherapy for pediatric OCD. Other glutamate modulators such as n-acetylcysteine and glycine have been theorized to be of pharmaceutical use, but no evidence currently exists to support their efficacy in pediatric OCD. The two major classes of medication that have been indicated as efficacious with pediatric chronic tic disorders are dopamine antagonists typical and atypical , and alpha-2 agonists.
While no meta-analytic estimates exist with regard to the efficacy of these agents, the effect sizes of antipsychotics relative to placebo are larger than those for alpha-2 agonists. Typical antipsychotics were the first medications to display efficacy in controlled research for pediatric tic disorders, and thus have the broadest evidence base. Haloperidol has a long history in the treatment of CTDs, with evidence stretching back 50 years.
Dosage reduction can be used to manage these side effects. Side effects from typical antipsychotics that can be serious include tardive dyskinesia and neuroleptic malignant syndrome. For CTDs, much lower doses are used than those used for psychotic disorders.
For this reason and perhaps because of neurobiological differences, those with CTDs appear to have low risk for tardive dyskinesia. Pimozide, which is a less powerful antagonist of norepinephrine than haloperidol, has been employed in treatment for pediatric CTDs. Its efficacy has been established in RCTs, , with fewer adverse effects than haloperidol. However, it still presents with a substantial side effect profile including weight gain, akathisia, acute dystonia, QTc prolongation, tardive dyskinesia, and extrapyramidal effects.
Additionally, interactions with antidepressant medications which are commonly employed with OCD, such as fluvoxamine have been observed, which presents substantial concern when working with comorbid conditions. Fluphenazine, which has antagonistic properties for both D1 and D2 receptors, is better tolerated than haloperidol with regard to sedation and extrapyramidal effects while showing similar efficacy to haloperidol in adults.
Despite its relatively more desirable side effect profile, fluphenazine still presents the risks of traditional neuroleptic adverse effects including akathisia, tardive dyskinesia, and extrapyramidal effects.
The more recently introduced atypical antipsychotics have now garnered a substantial evidence base with regard to efficacy for pediatric CTDs. The major advantage of atypical antipsychotics is the reduced risk of tardive dyskinesia and extrapyramidal symptoms associated with classic neuroleptics.
However, there are concerns about the safety and tolerability of these medications, especially with regard to increased levels of prolactin with the exceptions of aripiprazole, quetiapine, and clozapine , sedation, and metabolic effects which can lead to elevated glucose levels, increased appetite, and weight gain.
Ziprasidone has 5HT-2 and D2 antagonistic properties along with norepinephrine and 5HT reuptake inhibition. Additionally, while mild sedation has been observed. Olanzapine has displayed efficacy in children with CTDs in several open trials — and one small crossover trial. Sedation, nausea, headache, agitation, and insomnia have been observed as side effects; some weight gain has been observed, but to a lesser degree than other comparable agents. Quetiapine has empirical support from one open label trial, but lacks RCT evidence to support its use.
It is a weaker D2 antagonist than comparable medications, and thus its theoretical efficacy for CTDs is questioned. Abdominal discomfort, gastrointestinal upset, somnolence, and weight gain have been observed as common side effects. Given the observed side effects of atypical antipsychotics, careful observation of adverse effects is recommended.
With regard to metabolic effects, the American Diabetes Association has published monitoring guidelines for these agents. Correll 92 has recommended detailed monitoring schedules that include testing for glucose, lipids, and liver function at three months after treatment initiation and then every six months thereafter, and to evaluate for sedation and weight gain at each visit.
Additionally, symptoms of elevated prolactin can include menstrual interruption in females and breast tenderness in males and females, and merit further inquiry upon observation. Proactive management of such effects is recommended including adjusting dosing, changing medications, and monitoring of lifestyle habits eg, appropriate diet and exercise. The alpha-2 agonists clonidine and guanfacine have demonstrated efficacy in treating pediatric CTDs.
While observed effect sizes in treating CTDs have been lower than those for antipsychotics, the major benefits of the alpha-2 agonists relative to antipsychotics is their reduced side effect profile which does not include metabolic interference or extrapyramidal symptoms and their efficacy for comorbid ADHD. Common side effects reported with clonidine use include sedation, irritability, headaches, and dry mouth. However, given its short half-life, withdrawal symptoms such as temporary increases in blood pressure and heart rate have been reported.
Guanfacine is more highly selective for the alpha- 2-adrenergic receptors, which is hypothesized to be the reason for its improved side effect profile relative to clonidine with particular regard to sedation.
It also has a longer half-life than clonidine, reducing the risk of withdrawal effects and permitting for more convenient dosing which can be limited to twice per day. The efficacy of the anticonvulsant topiramate was recently supported through an RCT by Jankovic et al. Common observed side effects include somnolence, weight loss, and cognitive slowing. The anticonvulsant levetiracetam has shown open-label evidence for improving tics; , however, two small randomized crossover trials did not detect a tic-reducing effect.
Mecamylamine is a nicotine receptor agonist which has conflicting research support, where a retrospective case report series indicated some efficacy, but it did not demonstrate superiority to placebo in a well-designed RCT.
Other agents that interact with the dopaminergic system include metoclopramide, tetrabenazene, tiapride, sulpriride, and pergolide. Metaclopromide is a D2 antagonist which has traditionally been used for gastroesophageal reflux disease and as an anti-nausea agent, with side effects that can include sedation, increased appetite, and increased levels of prolactin, along with a risk of tardive dyskinesia and extrapyramidal symptoms. Tiapride is a benzamide that has some support through an RCT to improve tics compared to placebo, with hyperprolactinemia, somnolence, and weight gain as side effects of note.
Sulpiride is similar to tiapride, and has some support through retrospective studies to improve tics in adults. While clomipramine has demonstrated modestly superior outcomes relative to SSRIs, its side effects especially its cardiovascular effects limit its frontline use. The main choices among pharmacotherapy options for pediatric CTDs include neuroleptics, atypical antipsychotics, and alpha-2 agonists.
While neuroleptics have the most robust evidence base with regard to efficacy for pediatric CTDs, they also have a significant side effect profile. Thus, atypical antipsychotics and alpha-2 agonists have emerged as first-line pharmacotherapy options for pediatric CTDs, , with neuroleptics reserved for treatment refractory cases with marked impairment.
Like with medications for pediatric OCD, it is important to balance side effects with efficacy and it is recommended to increase dosages conservatively. Controlled evidence for pharmacotherapy options in the treatment of pediatric tic disorders.
For youth with CTDs, tics generally run a waxing and waning course, with many youth experiencing remission of tics by age Given these observations, the option of no treatment or behavioral therapy should be considered in the context of presenting severity versus the side effects of the medication employed, with particular consideration given to habit reversal training HRT.
The central components of HRT involve creating awareness of premonitory urges in context and then implementing incompatible competing behaviors, such as contracting the muscle opposite of the tic. For example, a child may learn to identify that he has an eye-blinking tic when sitting in class, become able to identify it each time it happens, and then invoke a response where he consciously uses his eye muscles to hold his eyes open when feeling such an urge.
Comorbid conditions in children present complexity in the context of therapeutic management for clinicians. Unfortunately, comorbidity is the rule rather than the exception in the clinical presentation of children with OCD and CTDs, and may be associated with attenuated response and remission rates. In general, the state of current psychopharmacological practice when presented with comorbidity for children with OCD and tics is to use the agent that is appropriate for each condition if pharmacotherapy is needed, while considering the possible negative or positive effects that the agent may have on comorbid conditions.
On the other hand, with regard to comorbid ADHD and CTDs, while there is some evidence that stimulants may exacerbate tics and anxiety in children with CTDs, , a meta-analysis by Bloch et al indicates that this effect may be dependent on the specific agent and dosing, and one multisite RCT found roughly equal tic increases when using methylphenidate, clonidine, or placebo.
Additionally, there is some evidence that risperidone and aripiprazole may have positive effects on anxiety symptoms, , , which is hypothesized to be a consequence of their action on 5HT receptors, and is a further consideration when treating comorbid CTDs and OCD. The goal of this review has been to discuss the current state of research on pharmacotherapy for pediatric OCD and CTDs, to provide an overview for clinical practice, and to demarcate current limitations in the literature to identify future research directions.
While pharmacotherapy is associated with generally positive treatment response, no current medication consistently achieves the more stringent criterion of symptom remission.
Even with CBT for pediatric OCD the most efficacious intervention reviewed , a significant proportion of children remain symptomatic following treatment. For CTDs, identifying and evaluating safe and effective alternatives to neuroleptics and atypical antipsychotics are indicated, with the use of alpha-2 agonists and topiramate as a starting point.
Across disorders, identifying moderators and mediators of response and side effects is of critical importance to facilitate treatment individualization. Identifying which populations respond better to a certain medicine or which patient groups are less likely to experience side effects from a particular agent could assist in improved idiographic care. With regard to contemporary agents, more comparative work between medications in a randomized fashion could allow for direct comparisons of efficacy and adverse event rates.
One further consideration is that that these medications are not prescribed in a vacuum, but are administered in the context of integrated behavioral healthcare. Careful weighing of the benefits and risks relative to the degree of impairment is of foremost importance when employing medications is needed, with particular regard given to available behavioral interventions.
In the presence of heterogeneity among family reactions to the pathology, clinicians can foster a supportive but disciplined approach towards implementing the chosen intervention. Compared to only 25 years ago, a marked increase in pharmacotherapy interventions have become available for children with OCD and CTDs to intervene for these debilitating conditions.
This has provided an array of efficacious interventions for youth with markedly reduced side effect profiles, although much progress still remains to be made. Given this expansion of treatment options, the major decisions in clinical pharmacotherapy come down to a balance of efficacy and adverse effects in the context of functional impairment and available psychosocial interventions. Managing these variables in the context of the evidence base for each approach will foster improved child outcomes.
This manuscript has been read and approved by all authors. This paper is unique and not under consideration by any other publication and has not been published elsewhere. The authors confirm that they have permission to reproduce any copyrighted material. De Nadai and Mr. McGuire report no financial relationships with commercial interests.
Storch has received consultancy fees from Prophase Inc. Lewin has received consultancy fees from Prophase Inc. She receives textbook honorarium from Lawrence Erlbaum. National Center for Biotechnology Information , U. J Cent Nerv Syst Dis.
Published online Jun 1. Alessandro S. De Nadai , 1 Eric A. Storch , 1, 2, 3 Joseph F. McGuire , 1 Adam B. Lewin , 2, 3 and Tanya K. Murphy 2, 3. Find articles by Alessandro S. De Nadai. Eric A. Find articles by Eric A. Joseph F. Find articles by Joseph F. Adam B. Find articles by Adam B. Tanya K. Find articles by Tanya K. Author information Copyright and License information Disclaimer. Corresponding author email: ude. This is an open access article.
Unrestricted non-commercial use is permitted provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract In recent years, much progress has been made in pharmacotherapy for pediatric obsessive-compulsive disorder OCD and chronic tic disorders CTDs. Keywords: obsessive-compulsive disorder, tic disorders, Tourette disorder, psychopharmacology.
Introduction Obsessive-compulsive disorder OCD and chronic tic disorders CTDs can be highly impairing conditions which affect a wide range of youth. Pharmacotherapy Options for the Treatment of Pediatric OCD Selective reuptake inhibitor SRI medications have received the majority of research with pediatric OCD, which encompass the selective serotonin reuptake inhibitors SSRIs and a specific tricyclic antidepressant clomipramine , and over 1, patients are now available for comparison in meta-analysis.
Other Agents Atypical antipsychotics have drawn the majority of attention among other agents in treatment for OCD, with particular attention given to their role in augmenting non- or partial-response to SRIs.
Pharmacotherapy Options for the Treatment of Pediatric Chronic Tic Disorders The two major classes of medication that have been indicated as efficacious with pediatric chronic tic disorders are dopamine antagonists typical and atypical , and alpha-2 agonists. Typical Antipsychotics Typical antipsychotics were the first medications to display efficacy in controlled research for pediatric tic disorders, and thus have the broadest evidence base.
Atypical Antipsychotics Second Generation Antipsychotics The more recently introduced atypical antipsychotics have now garnered a substantial evidence base with regard to efficacy for pediatric CTDs.
Alpha-2 Agonists The alpha-2 agonists clonidine and guanfacine have demonstrated efficacy in treating pediatric CTDs. Table 1 Controlled evidence for pharmacotherapy options in the treatment of pediatric OCD.
Open in a separate window. Clinical management of pediatric chronic tic disorders The main choices among pharmacotherapy options for pediatric CTDs include neuroleptics, atypical antipsychotics, and alpha-2 agonists. Table 2 Controlled evidence for pharmacotherapy options in the treatment of pediatric tic disorders.
Medication class Advantages Disadvantages Medication Supporting research Dose range employed Duration Outcomes a Neuroleptics Most robust evidence base in demonstrating efficacy for tics Potential side effects include tardive dyskinesia and extrapyramidal symptoms Pimozide Sallee et al Bruggeman et al Gilbert et al 0. Clinical management of common comorbid conditions Comorbid conditions in children present complexity in the context of therapeutic management for clinicians.
Conclusion The goal of this review has been to discuss the current state of research on pharmacotherapy for pediatric OCD and CTDs, to provide an overview for clinical practice, and to demarcate current limitations in the literature to identify future research directions.
Footnotes Disclosures This manuscript has been read and approved by all authors. References 1. The international prevalence, epidemiology, and clinical phenomenology of Tourette syndrome: a cross-cultural perspective.
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