WCA Recommendations for the Long-Term Treatment of Obsessive-Compulsive Disorder in Adults

CNS Spectrums ◽  
2003 ◽  
Vol 8 (S1) ◽  
pp. 7-16 ◽  
Author(s):  
John H. Greist ◽  
Borwin Bandelow ◽  
Eric Hollander ◽  
Donatella Marazziti ◽  
Stuart A. Montgomery ◽  
...  

ABSTRACTWhat are the latest psychotherapeutic and pharmacotherapeutic treatment recommendations for obsessive-compulsive disorder (OCD)? OCD is a relatively common disorder with a lifetime prevalence of ~2% in the general population. It often has an early onset, usually in childhood or adolescence, and frequently becomes chronic and disabling if left untreated. High associated healthcare utilization and costs, and reduced productivity resulting in loss of earning, pose a huge economic burden to OCD patients and their families, employers, and society. OCD is characterized by the presence of obsessions and compulsions that are time-consuming, cause marked distress, or significantly interfere with a person's functioning. Most patients with OCD experience symptoms throughout their lives and benefit from long-term treatment. Both psychotherapy and pharmacotherapy are recommended, either alone or in combination, for the treatment of OCD. Cognitive-behavioral therapy is the psychotherapy of choice. Pharmacologic treatment options include the tricyclic antidepressant clomipramine and the selective serotonin reuptake inhibitors (SSRIs) citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline. These have all shown benefit in acute treatment trials; clomipramine, fluvoxamine, fluoxetine, and sertraline have also demonstrated benefit in long-term treatment trials (at least 24 weeks), and clomipramine, sertraline, and fluvoxamine have United States Food and Drug Administration approvals for use in children and adolescents. Available treatment guidelines recommend first-line use of an SSR1 (ie, fluoxetine, fluvoxamine, paroxetine, sertraline, or citalopram) in preference to clomipramine, due to the latter's less favorable adverse-event profile. Further, pharmacotherapy for a minimum of 1–2 years is recommended before very gradual withdrawal may be considered.

1998 ◽  
Vol 173 (S35) ◽  
pp. 13-20 ◽  
Author(s):  
H. G. Baumgarten ◽  
Z. Grozdanovic

Background Serotonin may play a role in the pathophysiology of obsessive-compulsive disorder (OCD) because of the anti-obsessional effect of selective serotonin reuptake inhibitors (SSRJs).Method The literature is reviewed on knowledge of the role of serotonergic neurons in brain function, studies on monoamine metabolites in cerebrospinal fluid (CSF), various stress neuropeptides, neuroendocrine and behavioural challenge after administration of direct and indirect serotomimetic compounds, and neuroanatomical data on brain circuits organising behaviour.Results In most of the OCD cases analysed, CSF 5-hydroxyindoleacetic acid and homovanillic acid concentrations do not significantly differ from age-corrected controls. However, a relationship appears to exist between pre-treatment levels of these metabolites and clinical response to drugs acting on the serotonin transporter. Abnormalities in CSF arginine vasopressin, corticotropin-releasing hormone, oxytocin and somatostatin levels have been reported in OCD. Long-term treatment with high-doses of clomipramine, fluvoxamine, and fluoxetine tend to correct these neuropeptide abnormalities.Conclusions We hypothesise that continuous treatment with SSRJs alters serotonin turnover and neuropeptide expression patterns in OCD-entertaining functional forebrain/midbrain circuits.


2004 ◽  
Vol 65 (10) ◽  
pp. 1365-1371 ◽  
Author(s):  
Giuseppe Maina ◽  
Umberto Albert ◽  
Virginio Salvi ◽  
Filippo Bogetto

Psych ◽  
2020 ◽  
Vol 2 (3) ◽  
pp. 174-185
Author(s):  
Hannah M. Kilian ◽  
Bettina H. Bewernick ◽  
Margaretha Klein ◽  
Dora M. Meyer ◽  
Susanne Spanier ◽  
...  

Deep brain stimulation (DBS) is currently under research for the treatment of psychiatric disorders, e.g., obsessive-compulsive disorder (OCD) and treatment-resistant depression (TRD). Since the application of DBS in psychiatry has been in use for about 20 years, it is necessary to evaluate its long-term use now. A main issue in the long-term treatment of DBS concerns the effects of a discontinuation of stimulation due to intended as well as unintended reasons. In this contribution, the literature describing discontinuation effects following DBS in OCD and TRD is reviewed. Furthermore, a patient is reported in depth who experienced an unintended discontinuation of supero-lateral medial forebrain bundle (slMFB) DBS for TRD. In this case, the battery was fully depleted without the patient noticing. DBS had led to a sustained response for seven years before discontinuation of stimulation for just several weeks caused a progressive worsening of depression. Altogether, the rapid occurrence of symptom worsening, the absence of a notification about the stimulation status and the difficulties to recapture antidepressant response represent important safety aspects. For a further understanding of the described effects, time courses until worsening of depression as well as biological mechanisms need to be investigated in double-blind controlled trials.


2003 ◽  
Vol 64 (9) ◽  
pp. 1113-1121 ◽  
Author(s):  
Eric Hollander ◽  
Andrea Allen ◽  
Martin Steiner ◽  
David E. Wheadon ◽  
Rosemary Oakes ◽  
...  

2002 ◽  
Vol 159 (1) ◽  
pp. 88-95 ◽  
Author(s):  
Lorrin M. Koran ◽  
Elizabeth Hackett ◽  
Arkady Rubin ◽  
Robert Wolkow ◽  
Delbert Robinson

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Manuel Arrojo-Romero ◽  
María Tajes Alonso ◽  
Jose de Leon

The treatment recommendations in obsessive-compulsive disorder (OCD) after lack of response to selective serotonin reuptake inhibitors (SSRIs) include augmentation with other drugs, particularly clomipramine, a more potent serotonin reuptake inhibitor (SRI), or antipsychotics. We present two cases of response to lamotrigine augmentation in treatment-refractory OCD; each received multiple SRI trials over a >10-year period. The first patient had eleven years of treatment with multiple combinations including clomipramine and SSRIs. She had a >50% decrease of Y-BOCS (from 29 to 14) by augmenting paroxetine (60 mg/day) with lamotrigine (100 mg/day). The second patient had 22 years of treatment with multiple combinations, including combinations of SSRIs with clomipramine and risperidone. She had an almost 50% decrease of Y-BOCS (from 30 to 16) and disappearance of tics by augmenting clomipramine (225 mg/d) with lamotrigine (200 mg/day). These two patients were characterized by lack of response to multiple treatments, making a placebo response to lamotrigine augmentation unlikely. Prospective randomized trials in treatment-resistant OCD patients who do not respond to combinations of SSRIs with clomipramine and/or antipsychotics are needed, including augmentation with lamotrigine. Until these trials are available, our cases suggest that clinicians may consider lamotrigine augmentation in such treatment-resistant OCD patients.


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