Depression and unemployment: panel findings from the Epidemiologic Catchment Area study

Studies that have found an association between unemployment and psychological depression often fail to establish the direction of causal influence. Analyses of Epidemiologic Catchment Area panel data revealed that of employed respondents not diagnosed with major depression at first interview, those who became unemployed had over twice the risk of increased depressive symptoms and of becoming clinically depressed as those who continued employed. Although the increase in symptoms was statistically significant, the effect on clinical depression was not, possibly because of the low power of the test. The reverse causal path from clinical depression at Time 1 to becoming unemployed by Time 2 was not supported. The unemployment rate in the respondent's community at time of interview was not related directly to psychological depression but appeared associated indirectly with depression via its impact on the risk of becoming unemployed. Implications for policy and further research were discussed.     

Concerns regarding study of obsessive-compulsive disorder in dogs

Thromboembolism is rarely considered in discussions of the complications of blunt chest trauma. The few cases of thromboembolism that have been reported in this setting have occurred in association with significant myocardial damage. A previously fit 23 year old woman was admitted to the intensive care unit following a road traffic accident. A day later, left atrial thrombus was demonstrated by transoesophageal echocardiography in the absence of any other evidence of important myocardial injury. Anticoagulation with heparin was cautiously introduced in spite of her extensive injuries, and there were no consequent bleeding complications. At hospital discharge on day 18 she was entirely well. Full anticoagulation with warfarin was continued for a further eight weeks at which time follow up transoesophageal echocardiography showed complete resolution of the thrombus.     

Beliefs in obsessive-compulsive disorder

Several types of beliefs have been hypothesized to be associated with obsessive-compulsive disorder (OCD), including responsibility for harm, need to control thoughts, overestimates of threat, intolerance of uncertainty, and beliefs about the consequences of anxiety and capacity to cope. The present study compared 62 subjects with OCD, 45 with other anxiety disorders (AD) and 34 controls, using 3 measures of OCD-related beliefs. OCD subjects scored higher than AD and control samples on 2 general belief measures. A closer analysis of specific belief domains indicated that OCD subjects scored higher than AD and control subjects on all 6 specific belief domains (responsibility, control, estimation of threat, tolerance of uncertainty, beliefs about the consequences of anxiety, and the capacity to cope). Four of the 6 domains showed reasonable convergent and discriminant validity with measures of OCD symptoms compared to other psychopathology; anxiety and coping beliefs were the exceptions. In regression analyses, cognitive measures contributed significant explanatory power beyond mood state and worry with uncertainty predicting severity of OCD symptoms above all other belief domains. Further research on OCD-relevant belief domains in etiology, maintenance and treatment is warranted.     

A 2-year study of sertraline in the treatment of obsessive-compulsive disorder

The present study investigated the tolerability, safety profile, and anti-obsessional efficacy of sertraline, a selective serotonin reuptake inhibitor, during long-term treatment of patients with obsessive-compulsive disorder (OCD). Fifty-nine OCD patients who had completed a 1 year double-blind, fixed dose study comparing sertraline and placebo subsequently entered a 1-year open extension. Among the 51 patients who had been treated with sertraline during the double-blind phase, the mean total duration of sertraline treatment was 690 days. Only treatment responders who completed the 52-week double-blind treatment phase were permitted to enter the open extension. The higher rate (p < 0.02) of sertraline patients (51 out of 241) than of placebo patients (eight out of 84), who responded to treatment and entered the open-label phase is therefore consistent with the greater mean improvement observed in the sertraline group during double-blind treatment. Placebo responders differed from sertraline responders in that they were less impaired at baseline of the double-blind study [Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) of 18.5 versus 23.4] and they exhibited less improvement during double-blind treatment (-6.1 versus -11.4). In the open-label phase all patients received sertraline at a starting dose of 50 mg once a day, titrated in 50 mg increments to a maximum dose of 200 mg according to clinical response. At end-point the mean Y-BOCS score for all patients decreased by a further 3.6 points. Patients previously treated with placebo showed greater improvement after being switched to sertraline than those who received continued sertraline treatment. Patients who completed the study and received 2 full years of sertraline treatment (n = 38) exhibited a mean improvement of 15.6 points using the Y-BOCS. Sertraline was well tolerated during both the double-blind phase and the open extension, and the incidence of adverse experiences was generally reduced during the second year of treatment. Three patients discontinued open treatment because of adverse experiences. Long-term sertraline treatment did not appear to be associated with the emergence, increased incidence, or increased severity of adverse experiences or clinically significant abnormalities in laboratory tests, vital signs, or the electrocardiogram. The study supports the long-term safety and tolerability of sertraline over a 2-year treatment course and the sustained efficacy of sertraline in patients with OCD.     

Citalopram in the treatment of obsessive-compulsive disorder: an open pilot study

PURPOSE: To evaluate QT dispersion in hypertensive patients, with and without left ventricular hypertrophy, and compare with normal persons. METHODS: Thirty eight patients (21 male and 17 female, age 55 +/- 15 years) underwent echocardiography and simultaneous 12 lead, vertically aligned, electrocardiogram at 50 mm/s speed. No patient was on antiarrhythmic therapy. There were 19 non-hypertensive patients that constituted the control group (G-I). Group II was constituted by the other 19 patients, who were hypertensives. This group was further divided in group II-A (9 patients without left ventricular hypertrophy) and group II-B (10 patients with left ventricular hypertrophy). QT dispersion was obtained by the difference between the longest and the shortest QT registered. RESULTS: QT dispersion was significantly increased on hypertensive patients, both with and without left ventricular hypertrophy, when compared to controls (G-I 31 +/- 9 ms, G-II 52 +/- 15 ms. P < 0.0001; G-IIa 46 +/- 10 ms and G-IIb 56 +/- 18 ms X G-I, p < 0.0005). In hypertensive patients, there was no statistically significant difference between group II-A and group II-B. CONCLUSION: We conclude that QT dispersion is significantly increased on hypertensive patients when compared to non-hypertensive individuals and that such increase, occurs before left ventricular hypertrophy develops. These findings suggest that, in hypertensive patients, electrical changes in left ventricular myocardium can precede structural and morphological abnormalities. Such findings offer new insights into the mechanisms related to enhanced mortality among hypertensive patients.     

Improvement predictors in obsessive-compulsive disorder. An event-related potential study

The maturation of HIV-1 virions is accomplished through the proteolytic cleavage of Gag and GagPol precursor polyproteins by the viral-encoded protease (PR). Since virions are assembled from unprocessed polyproteins, the intracellular activation of PR must be limited. An experimental system was established that allows the investigation of the intracellular regulation of PR activity. By expressing Gag in trans with the GagPol precursor, downregulation of the intracellular PR activity associated with GagPol was demonstrated. Inhibition of PR activity was dependent upon the context of PR expression. Sequences capable of mediating this inhibition were localized to capsid. A mechanism through which Gag regulates PR activity is proposed whereby the disproportionate synthesis of Gag inhibits the activation of PR in the cytoplasm. Further elucidation of the mechanism of intracellular inhibition of PR activity may facilitate the development of novel PR inhibitors capable of inhibiting viral replication in vivo.     

Cytokine production in obsessive-compulsive disorder

Cytokine production was previously demonstrated to be reduced in untreated major affective patients. In addition, recovery from depression following clomipramine (CMI) treatment was accompanied by the restoration of interleukin-1 beta (IL-1 beta) and interleukin-3-like activity (IL-3-LA) to normal range. In the present study we assessed the in vitro production of IL-1 beta IL-2, and IL-3-LA by peripheral blood mononuclear cells (PBMC) in 11 nondepressed patients with obsessive compulsive disorder (OCD) before and after 8 weeks of CMI treatment. Results were compared with those of 11 healthy subjects. CMI treatment induced a significant improvement in OCD symptoms. No alteration was observed in cytokine production in OCD patients before treatment as compared to control subjects. Moreover, 8 weeks of drug treatment had no effect on cytokine production. In conclusion, OCD per se, as well as CMI treatment, have no effect on interleukin production as measured in this study.     

Disgust implicated in obsessive-compulsive disorder

Psychiatric classificatory systems consider obsessions and compulsions as forms of anxiety disorder. However, the neurology of diseases associated with obsessive-compulsive symptoms suggests the involvement of fronto-striatal regions likely to be involved in the mediation of the emotion of disgust, suggesting that dysfunctions of disgust should be considered alongside anxiety in the pathogenesis of obsessive-compulsive behaviours. We therefore tested recognition of facial expressions of basic emotions (including disgust) by groups of participants with obsessive-compulsive disorder (OCD) and with Gilles de la Tourette's syndrome (GTS) with an without co-present obsessive-compulsive behaviours (GTS with OCB; GTS without OCB). A group of people suffering from panic disorder and generalized anxiety were also included in the study. Both groups with obsessive-compulsive symptoms (OCD; GTS with OCB) showed impaired recognition of facial expressions of disgust. Such problems were not evident in participants with panic disorder and generalized anxiety, or for participants with GTS without obsessions or compulsions, indicating that the deficit is closely related to the presence of obsessive-compulsive symptoms. Participants with OCD were able to assign words to emotion categories without difficulty, showing that their problem with disgust is linked to a failure to recognize this emotion in others and not a comprehension or response criterion effect. Impaired recognition of disgust is consistent with the neurology of OCD and with the idea that abnormal experience of disgust may be involved in the genesis of obsessions and compulsions.     

Role of serotonin in obsessive-compulsive disorder

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 (SSRIs). 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 SSRIs alters serotonin turnover and neuropeptide expression patterns in OCD-entertaining functional forebrain/midbrain circuits.     

Taking chances: problem gamblers and mental health disorders--results from the St. Louis Epidemiologic Catchment Area Study

OBJECTIVES: This study determined prevalence estimates of problem gambling and relationships to other psychiatric and substance use disorders. METHODS: In 1981, the Diagnostic Interview Schedule was used to collect epidemiological information on problem gambling and other disorders from 3004 adults in St. Louis, Mo. RESULTS: The lifetime prevalence of pathological gambling was 0.9%; 46% of those surveyed gambled recreationally. Problem gamblers (those reporting at least one gambling-related problem) were 9.2% of the sample and were predominately White (69%), male (78.2%), and young than nongamblers. They were at increased risk for several psychiatric diagnoses, especially for antisocial personality disorder, alcoholism, and tobacco dependence. CONCLUSIONS: Clinicians treating alcoholism and tobacco dependence may need to screen for problem gambling. Additional research in the context of increased gambling opportunities is needed.     

Neurosurgical treatment of obsessive-compulsive disorder

BACKGROUND: Case reports suggest that neurosurgical operations can improve symptoms in patients with severe treatment-refractory obsessive-compulsive disorder (OCD). However, it is unclear which procedure is best and which may produce the most side-effects. METHOD: I review the literature on the efficacy and complications of four frequently used neurosurgical procedures (cingulotomy, capsulotomy, limbic leucotomy and subcaudate tractotomy) that are used to treat refractory OCD. RESULTS: Since the vast majority of patients who underwent surgery were severely and chronically disabled, it is likely that these procedures were of assistance in alleviating some of their symptoms. It is currently impossible to determine which surgical procedure is the best for a particular patient. CONCLUSIONS: Despite a lack of controlled data and inconsistencies in the literature, it appears that when non-surgical treatments have failed to improve OCD symptoms significantly in severely ill patients, at least partial relief can be obtained by some people with OCD by neurosurgery. Results of cumulative studies strongly support the need for continued research in this area.     

Progress and therapeutic response in the obsessive-compulsive disorder

The purpose of the present work was to analyze the outcome of patients diagnosed of Obsessive Compulsive Disorder (OCD) after Hospital discharge from our Unit, focusing on therapeutical efficacy immediately after discharge and in the follow up, searching for good evolution predictors. We have studied 42 patients (26 females and 16 males) diagnosed of OCD according to ICD-9 diagnostic criteria, all patients were hospitalized during a seven years period 1981 and 1988. Therapeutical response was evaluated through a (1-4 punctuation) of a Clinical Global Impression Scale considering the changes from the moment the patient was hospitalized, the day of discharge and in the follow up (mean 4.1 years). 73.8% and 71.4% were considered as treatment "responders" the day discharged and in the follow up respectively. Through a multiple logistic regression, treatment with serotonergic drugs and insidious onset of the illness were identified as short-term treatment response predictors, while the absence of a previous obsessive personality was a long-term therapeutical response predictor. Our results show the efficacy of serotonergic drugs and the tact that the presence of a previous obsessive personality could have a prognostic value in OCD.     

A preliminary study of partial hospital management of severe obsessive-compulsive disorder

OBJECTIVE: The study examined the effectiveness of a partial hospital treatment program combining behavioral therapy, medication, and psychosocial intervention for severe and treatment-resistant obsessive-compulsive disorder. METHODS: A total of 58 patients with a primary diagnosis of obsessive-compulsive disorder who underwent treatment in a partial hospital program were assessed at baseline, at program discharge, and at six-, 12-, and 18-month follow-ups. Obsessive-compulsive symptoms, depression, anxiety symptoms, and global functioning were rated. RESULTS: The majority of patients (71 percent) met the criterion for a successful outcome, which was a 25 percent decrease in score on the Yale-Brown Obsessive Compulsive Scale (YBOCS). Fifty-five percent finished the program with YBOCS scores of 16 or less, indicating only mild symptoms. Most of these patients sustained their improvement at six, 12, and 18 months after discharge, and many showed further improvement with continued outpatient management. CONCLUSIONS: The partial hospital treatment program for obsessive-compulsive disorder appears to be an effective intervention that should be implemented and investigated further.     

Issues in the monopharmacotherapy and polypharmacotherapy of obsessive-compulsive disorder

Polypharmacotherapy is again becoming common place in clinical practice. Obsessive-compulsive disorder (OCD) as a single primary diagnosis is responsive exclusively to the serotonin reuptake inhibitors (SRIs) and this fact forms the major evidence supporting a central role for 5-HT (serotonin) in the pathogenesis of the disorder. Presently, the highly potent serotonin reuptake inhibitors clomipramine, fluoxetine, fluvoxamine, and paroxetine are the only agents approved by the Food and Drug Administration (FDA) for OCD, but there is evidence that other SRIs, such as sertraline, are also effective. Because OCD is often treatment refractory and highly comorbid with other psychiatric disorders, the use of polypharmacotherapy can be justified. Other serotonergic medications such as lithium, buspirone, trazodone, or fenfluramine may be useful as adjuvant treatments in treatment-refractory OCD and adjuvant antipsychotics are useful in tic disorders, personality disorders, and psychotic disorders. The usefulness of polypharmacotherapy should be tempered by adverse effects including the serotonin syndrome, withdrawal phenomena, extrapyramidal side effects, and drug-drug interactions.     

Comparison of clinical characteristics in obsessive-compulsive disorder and body dysmorphic disorder

Recent research has suggested that body dysmorphic disorder (BDD) is part of the spectrum of obsessive-compulsive disorders. In order to determine the extent of similarity for psychopathology measures, patients diagnosed with BDD were compared to a group of patients diagnosed with obsessive-compulsive disorder (OCD) on obsessionality, compulsivity, overvalued ideas, depression, and anxiety. Results indicate that BDD patients are similar to OCD patients for measures of obsessionality and compulsivity when BDD symptoms are assessed as such. BDD and OCD patients were also similar for measures of depression, and state and trait anxiety. OCD patients had higher levels of anxiety when measuring common physical symptoms associated with this affective reaction. BDD patients had higher levels of overvalued ideas, but fewer obsessive and compulsive symptoms. Overall, the results suggest that BDD is a variant of OCD, with special considerations given to degree of belief conviction (overvalued ideas.     

Cognitive frontal lobe dysfunction in obsessive-compulsive disorder

BACKGROUND: There is evidence that dysfunction within associative frontostriatal circuits represents a feature of obsessive-compulsive disorder (OCD). Previous neuropsychologic studies have yielded diverging results, which may in part be explained by differences in the selection of subjects and methods. The present study focused on the question of cognitive frontal lobe performance in OCD. METHODS: Twenty-nine unmedicated OCD patients were compared to a double-size control group of normal subjects matched individually for age, sex, and intelligence. A series of 12 neuropsychologic tests was applied, most of which are thought to be sensitive to different aspects of cognitive frontal lobe function. RESULTS: OCD patients were unimpaired at tests of abstraction, problem solving, set-shifting, response inhibition, active memory search, and choice reaction speed. Deficits of approximately one standard deviation were observed at timed tests of verbal and nonverbal fluency, attentional processing, and weight sorting. CONCLUSIONS: OCD patients exhibited selective deficits in tasks involving controlled attentional processing and self-guided, spontaneous behavior. We discuss a link between this neuropsychologic profile and dysfunctioning within the anterior cingulate, but not the dorsolateral prefrontal circuit.     

Neuroimaging and frontal-subcortical circuitry in obsessive-compulsive disorder

BACKGROUND: Neuroimaging studies provide strong evidence that the pathophysiology of obsessive-compulsive disorder (OCD) involves abnormal functioning along specific frontal-subcortical brain circuits. METHOD: A literature search was carried out for all brain imaging studies of patients with OCD. We also reviewed the basic science literature on the functional neuroanatomy of cortico-basal ganglia circuits, and integrated this information with neuroimaging data in OCD to formulate a theoretical model of brain mediation of OCD symptoms and response to treatment. RESULTS: At least a subgroup of patients with OCD may have abnormal basal ganglia development. Functional neuroimaging studies indicate that OCD symptoms are associated with increased activity in orbitofrontal cortex, caudate nucleus, thalamus and anterior cingulate gyrus. CONCLUSIONS: OCD symptoms are mediated by hyperactivity in orbitofrontal-subcortical circuits, perhaps due to an imbalance of tone between direct and indirect striato-pallidal pathways. We present a model which describes how frontal-subcortical brain circuitry may mediate OCD symptomatology, and suggest a hypothesis for how successful treatments may ameliorate symptoms, via their effects on circuit activity.