Neurocognitive endophenotypes of impulsivity and compulsivity: towards dimensional psychiatry

The disordered mind

Obsessive-compulsive personality disorder (OCPD) is an early-onset disorder characterized by perfectionism, need for control, and cognitive rigidity. Its nosological status is currently under review. Historically, OCPD has been conceptualized as bearing a close relationship with obsessive-compulsive disorder (OCD). In this article, we discuss the diagnosis of OCPD in anticipation of its review for the ICD-11, from the perspective of clinical utility, global applicability, and research planning. Considering the recent establishment of an obsessive-compulsive and related disorders (OCRD) category in DSM-5, we focus on the relationship between OCPD and the disorders that are currently thought to bear a close relationship with OCD, including DSM-5 OCRD, and other compulsive disorders such as eating disorder and autistic spectrum disorder (that were not included in the DSM-5 OCRD category), as well as with the personality disorders, focusing on nosological determinants such as phenomenology, course of illness, heritability, environmental risk factors, comorbidity, neurocognitive endophenotypes, and treatment response. Based on this analysis, we attempt to draw conclusions as to its optimal placement in diagnostic systems and draw attention to key research questions that could be explored in field trials.

Evidence in the literature indicates that neurocognitive impairments may represent endophenotypes in psychiatric disorders.ObjectiveThis study aimed to conduct a systematic review on executive functions as a potential neurocognitive endophenotype in anxiety disorder diagnosis according to the DSM-IV and DSM-5 classifications.MethodsA literature search of the LILACS, Cochrane Library, Index Psi Periódicos Técnico-Científicos, PubMed and PsycInfo databases was conducted, with no time limits. Of the 259 studies found, 14 were included in this review.ResultsOnly studies on obsessive-compulsive disorder (OCD) were found. The executive function components of decision-making, planning, response inhibition, behavioral reversal/alternation, reversal learning and set-shifting/cognitive flexibility were considered to be a neurocognitive endophenotypes in OCD.ConclusionFurther studies on executive functions as a neurocognitive endophenotype in other anxiety disorders are needed since these may have different neurocognitive endophenotypes and require other prevention and treatment approaches.

Neurocognitive endophenotypes in pediatric OCD probands, their unaffected parents and siblings

Obsessive Compulsive Disorder. Current Science and Clinical Practice, by Joseph Zohar (Ed.) Chichester, United Kingdom: Wiley-Blackwell, 2012, 339 Pages (ISBN 978-0-470-97432-2, US $100.00, Hardcover)Reviewed by K1ERON O'CONNORDOl: 10.l037/a003227IThis book is part of the World Psychiatric Association Current Science and Clinical Practice Series. It is unsurprisingly heavily biased toward a medical model of obsessive-compulsive disorder (OCD). Indeed, the author claims in the introduction that the book is a celebration of the second revolution in OCD, the building blocks of which are neurocognitive endophenotypes, brain imaging, genetics, and venturing beyond the serotonin hypothesis; the first revolution apparently having dispelled notions of OCD's psychological origins.The editor is a distinguished psychiatrist (Joseph Zohar) who has published widely in psychiatric journals, and the other 12 chapters are mostly written by eminent clinician-researchers. The book is divided into three sections. Section 1 highlights assessment and treatments with a first chapter on assessment by J. Menchon; followed by a chapter on pharmacotherapy (E. Decloedt and D. Stein); a third chapter on cognitive behaviour therapy (CBT) (M. Franklin, A. Goss, and J. March); a fourth chapter on electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), and deep brain stimulation (DBS) (R. Blom, M. Figee, N. Vulink, and D. Denys); and a fifth chapter on treatment resistance (S. Pallanti, G. Grassi, and A. Cantisani). Section 2 on clinical spotlights contains a chapter of subtype and spectrum issues (E. Hollander, S. Poskar, and A. Gerard) and paediatric OCD (D. Geller, A. Faro, A. Brown, and H. Levy). The section on research spotlights contains a chapter on methodological issues for treatment trials (S. Reghumandanan and N. Fineberg), neurotransmitters (A. Abudy, A. Juven-Wetzler, R. Sonnino, and J. Zohar), brain imaging (D. Rosenberg, P. Easter, and G. Michalopoulou), genetics (D. Pauls), and neurocognition (S. Chamberlain and L. Menzies).The strongest chapters of the book are certainly on somatic treatment, genetics, and the search for endophenotypes and pharmacology. One of the most informative chapters from a technical viewpoint describes the experimental use of ECT, TMS, and DBS in treatment-resistant OCD. Other chapters discuss newer hypotheses concerning the search for endotypes in family members of OCD and genetic risk factors. There is an informative discussion on the efficacy of serotonin reuptake inhibitors and newer hypotheses about the involvement of other neurotransmitter (e.g., dopaminergic) systems. However, despite the impressive array of studies reviewed, the above chapters end by concluding that findings are contradictory and puzzling and that future work is necessary to be conclusive. In other words, despite increased knowledge, the somatic and genetic keys to evaluating and treating OCD remain experimental and elusive. On the other hand, in the brain imaging chapter, the authors conclude that the clinical phenomenology, nosology, and treatment of OCD have been well established, so exciting times lie ahead (p. 267) for research focused on neuroimaging and genetic laboratory interactions seeking biomarkers.I would argue our understanding of clinical phenomenology, nosology, and optimal treatment are far from satisfactory, and missing from this book is any clear recognition of the importance of the psychological components in clinical phenomenology. After all, OCD is diagnosed on the basis of disordered thinking and behaving. Ironically, improving the clinical phenomenology through knowledge of its psychological form and content is likely to prove essential to unravel genetic markers because it will better define the phenotype. Likewise, a critical look at current nosology (DSM) and symptom subtyping would have been refreshing. Instead, the spectrum chapter considers OCD and associated disorders along a symptom dimension in which the core phenomenological features are repetitive behaviours. …

Volumetric MRI study of orbito-frontal cortex and thalamus in obsessive-compulsive personality disorder

Participants of expert group on CPG for Obsessive Compulsive Disorder Adarsh Tripathi, Om Prakash Singh, Paramjeet Singh, Tushar Jagawat, M, Aleem Siddiqui, K.K. Verma, D.M. Mathur INTRODUCTION Obsessive-compulsive disorder (OCD) is a common psychiatric illness with lifetime prevalence of 1-3% [1]. It is the fourth-most common psychiatric illness and a leading cause of disability. OCD is associated with significant impairment in functioning, quality of life and disability. If untreated, OCD is a chronic illness with a waxing and waning of symptoms. A recent meta-analysis of long-term naturalistic prospective studies demonstrated that nearly a half of patients experience remission with much higher rates of remission in Indian patients compared to those in the west [2]. Early diagnosis and appropriate treatment may improve outcomes. Despite OCD being a common mental illness, most seek treatment after several years of suffering. Those who suffer from OCD tend to be secretive about their symptoms and suffer from shame and embarrassment. Less than a third of OCD sufferers receive appropriate pharmacotherapy and even less receive evidence-based psychotherapy. Symptoms The hallmarks of OCD are presence of obsessions and compulsions. Obsessions are repetitive, unwanted, intrusive thoughts, images or urges that are mostly ego-dystonic and cause severe distress or anxiety. Compulsions (or rituals) are repetitive behaviours or mental acts that are performed in response to an obsession to reduce anxiety/distress or prevent a dreaded consequence. Obsessions and compulsions are time consuming, distressing and are often resisted unsuccessfully. Clinical manifestations of OCD are remarkably similar across cultures and geographic locations. Common obsessions and compulsions and symptom dimensions identified through factor-analytical studies are shown in Table 1.Table 1: Common symptoms of OCDDiagnosis Many people experience intrusive thoughts and exhibit repetitive behaviours. A diagnosis of OCD is made only if symptoms are time consuming (e.g., more than an hour per day), distressing or cause significant interference in functioning. This is reflected in DSM-5 diagnosis of OCD and in the upcoming ICD-11 [3]. The ICD-11 criteria for OCD are likely to be very similar to the DSM-5 criteria [34]. The ICD-11 may include an insight specifier along the same lines as DSM-5. There are sweeping changes to the description of OCD in the proposed ICD-11. Duration criteria and subtyping of OCD may be removed in the revision for lack of evidence and clinical relevance. In ICD-10, a diagnosis of OCD was discouraged in the presence of schizophrenia, tic disorder or depression. This criterion too may be removed paving the way to make a diagnosis of OCD even in the presence of these comorbid disorders. Another major change to the diagnosis of OCD is creation of OCD and related disorders in DSM-5 (and in the ICD-11) and exit from the group of anxiety disorders. Many disorders are included in this group: body dysmorphic disorder (BDD), trichotillomania (TTM), skin picking disorder, hoarding disorder, substance/medication-Induced obsessive-compulsive and related disorder and obsessive-compulsive and related disorder due to another medical condition. In the upcoming ICD-11, few other conditions find a place in this group that include tic disorders, hypochondriasis and olfactory reference syndrome. All these disorders are grouped together based on shared clinical features (e.g., repetitive behaviours), comorbidity patterns, familiality, neuropsychological deficits, treatment response and importantly shared brain circuitry abnormalities. Hoarding disorder which may not share many features with OCD is grouped along with OCD because of historical association with OCD and obsessive-compulsive personality disorder. Comorbidity OCD is often comorbid with other psychiatric disorders. It is important to assess all patients with OCD for associated psychiatric comorbidity since they may have an effect on treatment outcome if left untreated. Depression and anxiety disorders are present in over a half of patients seeking treatment for OCD. Common comorbid disorders are listed in Table 2. Those with early onset OCD, in particular those with onset in childhood have high rates of attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and tic disorders.Table 2: Comorbid disorders in OCDBipolar disorder, in particular type 2, is reported to be not uncommon in OCD [5]. Similarly, OCD is not uncommon in those with primary diagnosis of bipolar disorder [67]. OCD when comorbid with bipolar disorder tends to run an episodic course [8] with worsening of symptoms in depressive phases and improvement in hypomania/ mania phases. It is important to recognise OCD-bipolar comorbidity because of treatment implications. The specific serotonin-reuptake inhibitors (SSRIs) traditionally used to treat OCD may induce switch to mania or rapid cycling course. Obsessive-compulsive symptoms and OCD are not uncommon in schizophrenia. Nearly a third of schizophrenia patients report OC symptoms or OCD. Presence of OCD may have a negative effect on the long-term course of schizophrenia. Therefore treatment of OCD with SSRIs and cognitive-behavior therapy (CBT)/behavior therapy (BT) may have to be considered although there is not much of systematic evidence supporting their efficacy in treatment of OCD in schizophrenia. COMMON INGREDIENTS OF MANAGEMENT PLAN Common ingredients of managing OCD include the following: Detailed assessment of symptoms and comorbid patterns including suicidal behaviours either by unstructured clinical interview alone or supplementation with structured assessments. Decision on setting for treatment (outpatient vs. inpatient care depending upon the severity, treatment resistance etc.) Detailed psychoeducation of the patient and family member (s) about OCD, its course and treatment options including duration of treatment. Choice of treatment: drugs vs. CBT vs. combination In the Indian context, SSRIs are first-line treatments preferred over CBT because of feasibility, affordability and limited number of trained therapists. CBT may be considered if SSRIs alone are not beneficial. Discussion on side-effects of drugs; in women risks vs. benefits of drugs during pregnancy and in the post-partum period Follow-up plan after initiating treatment ASSESSMENT AND EVALUATION In routine clinical practice, use of structured / semistructured interviews and rating scales may not be necessary. They are optional. However, they may be used when the clinician needs supplementary information. A list of useful instruments in the assessment of OCD is provided in Table 3.Table 3: Commonly used instruments to assess OCD (optional)The Yale-Brown Obsessive-Compulsive Scale (YBOCS) is the most widely used severity rating scale for OCD in both adults [9] and children [10] and is considered a gold standard instrument to measure severity of OCD. It is a 10-item observer-rating scale, also available as self-rated instrument. It measures the overall severity of obsessive-compulsive symptoms for the preceding week. The YBOCS is a global measure of symptoms and does not provide severity of individual symptom dimensions. A total score of ≥ 16 is considered to be indicative of clinically significant OCD. The YBOCS severity scale also has an associated symptom check list of 15 categories of obsessions and compulsions including miscellaneous symptoms. The checklist elicits both current (1 month) and past symptoms. On the YBOCS item-11 insight scale, the insight is graded as follows: 0 = excellent (fully rational thinking), 1= good insight (readily acknowledges absurdity or excessiveness but has some lingering doubts), 2 = fair insight (reluctantly admits absurdity, but waivers; has some unrealistic fear but no fixed conviction), 3 = poor insight (overvalued ideas; maintains they are not unreasonable or excessive, but acknowledges validity of contrary evidence), and 4 = lack of insight (delusional). A higher score on the Y–BOCS item-11 indicates poorer insight. FORMULATING A TREATMENT PLAN Formulating a treatment begins with correct diagnosis of OCD as per the DSM or ICD classificatory systems. When feasible a structured clinical interview is recommended to obtain a comprehensive account of patient's problems. Once a diagnosis is established, a detailed assessment of symptom profile is mandatory. Family members often accommodate patient's rituals and contribute to poor outcome. In most severely ill patients, an elaborate family assessment may be needed. Once assessment is complete, short-term and long-term goals of treatment have to be established. Enhancing treatment adherence is a vital aspect of formulating a treatment plan. It is important to educate patients about lag in the onset of action of drugs and that improvement may occur over several months of continuous treatment. Brief education about basic principles of psychotherapy should be explained if psychotherapy is being planned. Essentials of formulating a treatment plan are summarized in Table 4. All patients and their immediate family members should be provided psychoeducation about OCD (Table 5).Table 4: Essentials of formulating a treatment planTable 5: Components of psychoeducationCHOICE OF TREATMENT SETTINGS In the Indian scenario, treatment is either on an outpatient or an inpatient basis. Outpatient treatment is usually sufficient for most OCD patients who are mild to moderately ill and for those who are likely to be adherent to treatment. Patients may be followed-up at periodic intervals, initially once in a month or two and subsequently at longer intervals depending upon the response to treatment and tolerability and side-effects. Hospital treatment may be considered for those who are at high suicide risk, dangerous to self or others, and intolerant to side-effects. Many severely ill and treatment-resistant patients may require prolonged (2-3 months) hospitalization for intensive treatment with CBT and for rationalization of pharmacotherapy. Inpatient care may also be required for severe depression, mania or psychosis that may be comorbid with OCD. Admission in rehabilitation services may be necessary for some patients who may not have benefited from standard treatments including inpatient care. PHARMACOLOGICAL TREATMENT The clinical practice guideline is framed based on a review of relevant scientific literature. As a first step, we framed relevant questions which arise in the minds of the practitioner while treating a patient suffering from OCD. A literature search was conducted in PubMed to answer these questions. We also reviewed the existing guidelines on treatment of OCD [11121314]. After a thorough literature review, the treatment strategies were rated based on the Strength of Recommendation Taxonomy (SORT) [15]. Consistent evidence from multiple randomized controlled trials (RCT) constitutes the highest level of evidence for a recommendation. However, the external validity of RCTs has been questioned due to the rigid protocols in undertaking the studies. A practitioner may make a clinical decision based on the available evidence considering other relevant factors that influence the decision making process. A non-exhaustive list of these factors might include psychiatric and other medical comorbidities, previous treatment trials, affordability, accessibility, hypersensitivity, side-effect profile, patients' values etc. RELEVANT CLINICAL ISSUES First-line pharmacological treatment for OCD Meta-analyses of RCTs show that selective-serotonin reuptake inhibitors (SSRIs) are significantly more effective than placebo in the treatment of OCD [16]. SSRIs are associated with many adverse effects but are usually well tolerated. The only other medication which has shown to be consistently effective in OCD is the serotoninergic tricyclic antidepressant clomipramine. Clomipramine has been found to be significantly more effective than placebo in multiple RCTs and meta-analysis of RCTs [16]. Network meta-analysis comparing the efficacy of clomipramine vs. SSRIs failed to find any efficacy advantage over SSRIs [16]. Most head-to-head comparison trials have not found any significant difference between the efficacy of clomipramine and SSRIs [17]. Further, meta-analyses and individual RCTs have found that the tolerability of clomipramine is worse than that of SSRIs [1317]. The anticholinergic, cardiac and neurological side effects of clomipramine may be problematic in this regard. CONSIDERING THE CONSISTENT EFFICACY AND BETTER TOLERABILITY, GUIDELINES RECOMMEND SSRIs AS FIRST LINE TREATMENT FOR OCD (TABLE 6). Choice of SSRITable 6: Medications recommended as monotherapy in OCDMeta-analyses comparing the different SSRIs [16] and direct head-to-head comparisons [1718] have not shown superiority of any one SSRI over the other. SSRIs differ to some extent in their propensity to cause certain adverse effects and drug interactions. However, there is no unequivocal evidence to suggest that these differences may be clinically meaningful. Recently, concerns have been raised regarding cardiac adverse effects with high dose of citalopram, which is commonly used in OCD. Hence, high-dose citalopram may be used with caution in those with risk for arrhythmias. THE PRACTITIONER IS RECOMMENDED TO CHOOSE AN SSRI FOR AN INDIVIDUAL PATIENT BASED ON FACTORS SUCH AS PREVIOUS RESPONSE, COMORBIDITY, TOLERABILITY, ACCEPTABILITY, ADVERSE EFFECTS, COST AND DRUG INTERACTIONS. Dose of SSRI It is generally recommended that OCD be treated with a higher dose of SSRI than that used in depression (Table 5). A meta-analysis of fixed-dose comparison studies have found a greater efficacy with higher doses of SSRI (60-80 mg fluoxetine equivalent) compared to medium (40-50 mg fluoxetine equivalent) and low doses (20-30 mg fluoxetine equivalent) [19]. However, all three dose ranges were significantly more effective than placebo. The increased efficacy comes at the cost of poor tolerability as evidenced by increased dropouts due to adverse effects [19]. A review of individual fixed-dose comparison studies found that the dose-response relationship is more evident for escitalopram, fluoxetine and paroxetine, while it is less clear-cut for citalopram and sertraline [17]. Clomipramine has not been tested in such fixed dose comparison studies. However, most studies have employed a flexible dosing at 150-250 mg [17]. It should be remembered that there is likely to be inter-individual differences in pharmacokinetic profile of drugs due to intrinsic variations in drug metabolism and drug interactions. GUIDELINES RECOMMEND TREATMENT OF OCD WITH HIGHER DOSE OF SSRIs. HOWEVER, IF AN INDIVIDUAL PATIENT IS NOT ABLE TO TOLERATE HIGHER DOSE, LOW TO MEDIUM DOSE TREATMENT CAN BE CONSIDERED. Duration of trial and dose titration A recent meta-analysis of 17 RCTs found that SSRIs separate from placebo as early as 2 weeks and that majority of improvement occurs early on in the course of treatment [20]. However, improvements seen early in the course of treatment may not be always clinically meaningful. In many patients, clinically meaningful improvements may be seen only after weeks or months of treatment. It is recommended that an adequate trial of a SSRI (or clomipramine) should be at least for 12 weeks to account for the lag in the onset of action. The APA guidelines recommend upward titration to the maximum FDA-approved doses by 4-6 weeks and continuation in that dose for another 6-8 weeks or so to determine efficacy [11]. Certain clinical and biological predictors of treatment response to SSRIs have been identified but they are not robust predictors (Table 7).Table 7: Predictors of response to SSRIsGUIDELINES RECOMMEND CONTINUING MAXIMALLY TOLERATED EFFECTIVE DOSE OF A SSRI FOR AT LEAST 12 WEEKS FOR JUDGING ITS EFFICACY. GUIDELINES ALSO RECOMMEND DOSE ESCALATION TO EFFECTIVE DOSE RANGES WITHIN 4-6 WEEKS AND CONTINUATION IN THE SAME DOSE FOR ANOTHER 6-8 WEEKS. 2. Other medications that can be tried as monotherapy in OCD Venlafaxine, a serotonin-norepinephrine reuptake inhibitor with preferential serotonergic action, has been studied in comparison to paroxetine in a double blinded study and clomipramine in a single blinded study. The studies found no difference in the efficacy between venlafaxine and the comparator agents in acute control of OCD. Given the absence of evidence from placebo-controlled trials, venlafaxine is not the first-line treatment for OCD. Hence, the guidelines consider venlafaxine as a second-line monotherapy agent in the treatment of OCD. Mirtazapine has been studied as a monotherapy in two small open-label trials with inconsistent findings. Therefore, mirtazapine cannot be recommended as monotherapy in treatment of OCD. 3. Treatment strategy for non-responders to first-line treatment Definitions of treatment outcome [21] are given in Table 8. Estimates suggest that around 40-70% patients show an adequate response to a trial of SSRI with a remission rate of 10-40% [16]. Clinicians often face the subsequent challenge of partial and non-response to SSRIs. Continuing improvement has been noticed with prolonged trial of SSRIs as discussed above. Hence, the initial trial may be continued further if there is evidence of ongoing improvement. A general treatment algorithm for OCD and for non-responders to SSRIs is shown in Figures 1 and 2 respectively.Table 8: Definitions of treatment outcome in OCDFigure 1: Treatment algorithm for treating a patient with OCD. *First line treatment chosen based on feasibility and severity of illness, #CBT/BT- Cognitive behavior therapy/Behavior therapy, @SSRI – Selective serotonin reuptake inhibitor, %rTMSrepetitive transcranial magnetic stimulation, $ - tDCS- transcranial direct current stimulation. ** Preferred for severe OCDFigure 2: Strategies for non-responders to SSRIs. SSRI-Selective serotonin reuptake inhibitors, CBT/BT-Cognitive behavior therapy/behavior therapy, rTMS- repetitive transcranial magnetic stimulationa. Switching to another medication Switching to another first-line medication has been found to be effective; experts provide a rough estimate of 40-50% response rate for the second SSRI and decreasing response rates with further trials. Switching to a second SSRI is suggested for non-responders to a first SSRI. In partial responders, changing medication may entail loss of the response to the earlier medication. Hence, switching is recommended in partial responders only if there are severe persisting symptoms or upon failure of other augmenting strategies such as CBT and atypical antipsychotics. b. Switching / Augmenting with CBT/BT It is uncertain whether initiating a combination of BT/CBT simultaneously with SSRI is advantageous compared to either treatment alone. However, CBT/BT has been proven to be effective as an augmenter in partial/non-responders to SSRIs [182223]. Where feasible, CBT/BT is a potential first-line augmenting option for partial/non-responders to SSRI treatment. c. Augmenting with another medication (Table 9)Table 9: Pharmacological augmenting agents in medications have been commonly tried as to SSRIs. and have the are the most widely studied augmenting agents of SSRIs The literature on is with including small doses and duration of treatment with both and of treatment resistance etc. recent meta-analyses of RCTs on found that as a group was significantly more effective than placebo in decreasing YBOCS a third of patients to and are consistently found to be effective as augmenting The evidence for should be with caution as it was based on a single study. A comparing and placebo of SSRI found that not separate from placebo in augmenting efficacy This study has raised questions on the efficacy of as an and have not been consistently found to be while other have not been studied Meta-analyses not any on adequate dose and duration of treatment should be used in low doses (e.g., mg of mg for a period of at least weeks for an adequate of in the should be considered after the benefits and risks of long-term BASED ON THE AND BE THE FIRST FOR PHARMACOLOGICAL agents There is a supporting the use of drugs in OCD. The agents have been studied in OCD found effective in 2 double blinded and one single blinded found effective in 2 double blinded RCTs effective in 2 small but inconsistent in two RCTs from three has to be studied BASED ON THE AND ITS BETTER TOLERABILITY, IS AS THE FIRST agents including and are reported to be effective and well in small RCTs However, due to the of the individual are recommended as second line augmenting agents along with evidence that clomipramine can be an effective augmenting Clomipramine and SSRI combination should be used with fluoxetine and as they may clomipramine related adverse effects cardiac serotonin due to pharmacokinetic interactions. Clomipramine of SSRI may be tried but adequate to be in the potential adverse effects of the Mirtazapine has been found to the response with no significant benefits and may be considered as an augmenting agent in partial responders and Other augmenting agents and have not been found effective and are not recommended as augmenting The and efficacy of and drugs have to be studied they are recommended for routine clinical has been found to have acute effects in a which needs and the strategy can be recommended for routine clinical Other strategies there to be some short-term benefits for clomipramine in treatment patients, the benefits are This is not available in and is not recommended at present for clinical There are a few trials the of higher than recommended doses of SSRIs to mg of mg of in This strategy should be considered and may be used only in patients after other OF of patients not to available pharmacological and and treatments the have been tried in has not been for the treatment of OCD. in the of and not provide evidence for the efficacy of Hence, is not recommended as a treatment for OCD and may be considered for the treatment of comorbid conditions severe and disorders, if 2. transcranial magnetic the of and of or decreasing their based on the of stimulation. The in OCD are usually not with available of has been tried in which have with other in OCD. trials of low or high over either have but low over supplementary and However, the evidence has not been very the have to be in with There is no evidence that effects for longer than the trial The guideline as an for further and not for routine clinical 3. direct current is another and which either or the of the depending on the of the There are only a few and an open-label trial on in OCD. It has to be more it can be recommended for clinical use in OCD. in specific of the which is to be in OCD. can be with the of or with the of and a of as are in treatment OCD in a few to the these are generally employed in treatment patients (Table in the of studies that around of patients improve over months There is some that may be more effective in OCD and that its efficacy may be similar to that of brain may be associated with short-term and adverse effects including personality and adverse effects although rates are not criteria for brain brain is a high of in the the of action is it is to for OCD has been in controlled studies of and A recent meta-analysis found a rate of with a YBOCS of around is an and is associated with and adverse Further, the needs to be which may be can be recommended in OCD patients (Table after regarding the and of the The are not in and the are only one aspect of a comprehensive treatment which should may be considered only in patients after of patients for treatment severity of illness and Patients should be explained about the of benefits and They should be by an of a a and a for for The treatment should be conducted of a of and with of adverse criteria for to are shown in Table FOR OCD (TABLE Cognitive / and in has been shown to be in the treatment of OCD All treatment guidelines have suggested the use of CBT as a first-line treatment CBT for OCD is a first-line treatment option for OCD. is the most important of CBT along with When are monotherapy may be recommended in mild to moderately ill In severely ill patients a combination of CBT and SSRI is CBT as an strategy It is uncertain whether initiating a combination of and SSRI is advantageous compared to either treatment alone. However, CBT/BT is found to be effective in augmenting SSRIs in partial/non-responders to SSRIs [34]. A recent study found CBT to be to and placebo in augmenting SSRIs in OCD Patients in the CBT group

Obsessive-compulsive disorder (OCD) is a debilitating heritable neuropsychiatric condition. Attempts to delineate genetic contributions in OCD have met with limited success, with an ongoing search for neurocognitive endophenotypes. In this study, an attempt has been made to study and compare the neurocognitive functioning of patients with OCD, their first-degree relatives (FDRs) and healthy controls. A cross-sectional design study was carried out with thirty dyads of patients with OCD, their FDRs and thirty matched healthy controls and screened using Mini International Neuropsychiatric Interview, Verbal Adult Intelligence Scale, Yale Brown Obsessive-Compulsive Scale, Montgomery Åsberg Depression Rating Scale, International Personality Disorder Examination (Anankastic personality scale).Tests of National Institute of Mental Health and Neurosciences Neuropsychological Battery were used to assess domains of attention, verbal memory, visual memory, set-shifting, response inhibition, planning and visuoconstructive abilities. spss version 14.0 was used for descriptive and analytical data analysis. There were no statistically significant differences between patients with OCD and their FDRs on neurocognitive domains of delayed verbal recall, set-shifting, response inhibition and visuoconstructive abilities (P > 0.05) which were impaired compared with healthy controls. Significant differences (P < 0.05) on domains of attention, planning time and visual memory were noted between FDRs and patients. The present study supports set-shifting and inhibitory control and proposes visuoconstructive abilities and delayed verbal recall as potential endophenotypes for OCD.

Though still in infancy, the field of psychiatric genetics holds great potential to contribute to the development of new diagnostic and therapeutic options to treat these disorders. Among a large number of existing neurotransmitter systems, the serotonin system dysfunction has been implicated in many psychiatric disorders and therapeutic efficacy of many drugs is also thought to be based on modulation of serotonin. Serotonin transporter gene polymorphism is one of the most extensively studied polymorphisms in psychiatric behavioral genetics. In this article, we review the status of evidence for association between the serotonin gene polymorphism and some common mental disorders like affective disorders, post-traumatic stress disorder, obsessive-compulsive disorder, suicide, autism, and other anxiety and personality disorders. Going beyond traditional association studies, gene-environment interaction, currently gaining momentum, is also discussed in the review. While the existing information of psychiatric genetics is inadequate for putting into practice genetic testing in the diagnostic work-up of the psychiatric patient, if consistent in future research attempts, such results can be of great help to improve the clinical care of a vast majority of patients suffering from such disorders.

Dissociation of decision making under ambiguity and decision making under risk: a neurocognitive endophenotype candidate for obsessive-compulsive disorder.

Compensatory Frontoparietal Activity During Working Memory: An Endophenotype of Obsessive-Compulsive Disorder

The Behavior of Eating Glass, With Radiological Findings: A Case of Pica

Practice Parameter for the Assessment and Treatment of Children and Adolescents With Obsessive-Compulsive Disorder

Objective: The prevalence rate of obsessive-compulsive disorder (OCD) was found to be higher in women during pregnancy and puerperium than that estimated in the general population. Additionally, the symptomatology of OCD shows several variations during the lifetime of women. Objective of the current study was to examine the clinical characteristics and comorbidity with other anxiety and mood disorders of pregnancy-onset obsessive-compulsive disorder (POCD) and to investigate factors related to POCD. Method: The study sample was composed of three groups. The first group (POCD group) included 20 consecutive pregnant women meeting the criteria of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) for OCD, showing an onset of OCD during their current pregnancy. The second group (non-OCD group) consisted of 207 consecutive pregnant women without any mood or anxiety disorders to assess factors associated with POCD. In addition, the study included a control group to compare the symptoms of POCD and non-pregnancy-onset OCD. The control group was composed of 40 nonpregnant female outpatients with OCD. Type and severity of obsessive-compulsive symptoms were assessed with the Yale-Brown Obsessive-Compulsive Scale (YBOCS). OCD and other anxiety or mood disorders were determined by means of the Structured Clinical Interview for DSM-IV (SCID-I). Comorbid axis II disorders were diagnosed with the Structured Clinical Interview for DSM-III-R Personality Disorders (SCID-II). Results: The mean onset time of OCD in the POCD group was 13.3±6.35 (week5-28) gestational weeks. OCD occurred during the first trimester of pregnancy in 9 women (45%), during the second trimester in 10 (50%) women, and during the third trimester in 1 (5%) woman. The most common obsessions were contamination (n=16, 80%) and symmetry/exactness (n=6, 30%), and the most common compulsions were cleaning/ washing (n=16, 80%) and checking (n=12, 60%) in POCD. Thirteen (65%) of the pregnant OCD patients met the criteria for a mood or anxiety disorder. Generalized anxiety disorder was the most frequently diagnosed axis I disorder (40%, n=8). The independent factors associated with POCD were cigarette smoking (p=0.002), the existence of an anxiety disorder at onset of pregnancy (p=0.000), and obsessive-compulsive personality disorder (p=0.003). Conclusion: The present study suggests that POCD presents similar clinical characteristics with nonpregnancy-onset OCD. Mood or anxiety disorder comorbidity is observed in more than half of the women with POCD. Additionally, pregnant women who have at least one of 3 factors (cigarette smoking, the existence of an anxiety disorder at onset of pregnancy, and obsessive-compulsive personality disorder) seem to be at risk for POCD.

In science, whenever a lower level explanation is sufficient, it becomes paramount. This paper addresses the proposition that the same will happen for human behaviour. The author considers differen...