Rate of OCD and sub-threshold OCD in bipolar disorder patients with first depressive episode.

Evidence indicates that obsessive-compulsive disorder (OCD) co-occurs with bipolar disorder (BD) at a higher rate than in the general population. Although there is a preliminary indication of a predominant aggregation of OCD in BD patients with bipolar depression (BP-D), no explicit evaluation has previously been undertaken. Using the Structured Clinical Interview for DSM-5 Axis-I disorders and appropriate rating scales, seventy-three BD patients experiencing their first depressive episode were screened for OCD and subthreshold OCD. Nineteen (26%) of the 73 participants in addition to BP-D also met DSM-5 criteria for OCD and 17 (23.2%) patients met criteria for sub-threshold OCD. No differences in demographic and clinical variables evaluated in the study were found between the BP-D patients with and without OCD. Limitations of the study included a relatively small sample size, cross-sectional design and inclusion of only hospitalized BP-D patients. Additional studies are warranted to better define the longitudinal course of comorbid BP-D/OCD, treatment approaches and outcomes of this challenging patient population. Explicit prospective comparison of the rate of DSM-5 OCD and subthreshold OCD in depressive versus manic episodes of bipolar disorder within the same patient is justified.

CD247, a novel T cell-derived diagnostic and prognostic biomarker for detecting disease progression and severity in patients with type 2 diabetes.

OBJECTIVE: We have previously shown that chronic inflammation results in immunosuppression associated with CD247 downregulation in T lymphocytes. Type 2 diabetes mellitus (T2DM) is known to be associated with chronic inflammation. We therefore sought to examine CD247 expression levels in patients with T2DM and to assess whether it can serve as a diagnostic and prognostic biomarker for disease complications and outcomes. RESEARCH DESIGN AND METHODS: Peripheral blood samples from 75 T2DM patients and 40 healthy control subjects were collected and analyzed for the expression level of CD247 in T lymphocytes. Subjects with T2DM underwent a medical interview with physical examination and were followed for an additional average of 19.2 ± 0.9 months to determine the occurrence of major adverse disease end points. The relationship between the level of CD247 expression and disease status at the time of blood draw and the ability of the marker to identify future complications was evaluated. RESULTS: We observed a significant reduction in CD247 expression levels in T lymphocytes of T2DM patients when compared with healthy volunteers. CD247 downregulation was associated with disease severity, complications, and the occurrence of future cardiovascular events, suggesting its potential use not only as a diagnostic but also as a prognostic biomarker. CONCLUSIONS: Our results suggest the use of CD247 as a biomarker in diabetic patients for evaluating the state of chronic inflammation that contributes to morbidity and mortality in this disease and for the prediction of future cardiovascular events.

The effect of reboxetine co-administration with olanzapine on metabolic and endocrine profile in schizophrenia patients.

RATIONALE: We previously demonstrated that the addition of the selective norepinephrine reuptake inhibitor reboxetine attenuates olanzapine-induced weight gain. Using the same study sample, we also sought to determine whether reboxetine's weight-attenuating effect was accompanied by a beneficial effect on metabolic and endocrine parameters relevant to antipsychotic-induced weight gain and obesity. METHOD: Blood samples at baseline and at the end of the 6-week trial were available for 54 participants who participated in previous double-blind, placebo-controlled studies of reboxetine (4 mg BID) addition to olanzapine-treated schizophrenia patients. Fasting glucose, lipid profile, insulin, leptin, cortisol, dehydroepiandrosterone (DHEA), prolactin, and thyroid-stimulating hormone (TSH) were analyzed. RESULTS: In contrast to the olanzapine/placebo group, the olanzapine/reboxetine group exhibited a reduction in blood triglyceride (p < 0.05) and leptin (p < 0.05) levels, and elevation in cortisol (p < 0.05) and DHEA (p < 0.008) levels. No significant between-group differences were detected in the changes in cholesterol, glucose, insulin, TSH, and prolactin. CONCLUSIONS: Reboxetine addition resulted in meaningful improvement of some metabolic and endocrine measures associated with olanzapine-induced weight gain. The potential role of reboxetine in the prevention of olanzapine-induced weight gain and cardio-metabolic morbidity merits further large-scale, long-term investigation.

Age matters: Young T lymphocytes offer better protection from myeloma proliferation.

BACKGROUND: The incidence and growth of cancer has been reported to increase with age and/or impaired T lymphocyte function. RESULTS: Consistent with these observations, we found that a monoclonal serum immunoglobulin (mIgG2b), rarely detectable after the injection of 5T33 murine multiple myeloma (MMM) cells into 3-4 month old wild-type C57BL/6 mice was seen more frequently in 18-20 month old wild-type C57BL/6 mice and in 3-4 month old Rag1-deficient C57BL/6 mice. These observations were confirmed and extended using more sensitive assays such as quantitation of splenic mRNA specific for the canonical 5T33 monoclonal IgG2b produced by 5T33 myeloma cells and the most sensitive assay, photon-imaging of mice injected with 5T33 cells, stably transfected with fire-fly luciferase gene (5T33L cells), which emit photons after the injection of luciferin. Furthermore, the proliferation of 5T33L myeloma cells in Rag1-deficient C57BL/6 mice was greater in mice which also received spleen T cells from 18-20 month old C57BL/6 wild-type mice compared to mice which received splenic T cells from 3-4 month old C57BL/6 wild-type mice. Thus, immune reconstitution of C57BL/6 mice with splenic T cells from young wild-type mice offered greater protection from progressive growth of 5T33L myeloma cells than did reconstitution with splenic T cells from old mice. CONCLUSIONS: Our findings support the hypothesis that age-associated changes in splenic T cell function contribute to the increased growth of 5T33 MMM cells in old compared to young C57BL/6 mice. Should similar processes occur in humans, increasing the anti-myeloma activity of T cells in old patients with multiple myeloma or transferring cryopreserved, young, autologous, T cells might benefit elderly patients with multiple myeloma.

Reducing antipsychotic-induced weight gain in schizophrenia: a double-blind placebo-controlled study of reboxetine-betahistine combination.

RATIONALE: Combination treatment with reboxetine, a selective norepinephrine reuptake inhibitor, and betahistine, a histamine H1 receptor agonist/H3 antagonist, was developed to produce complementary action in CNS pathways regulating appetite and body weight. In the present placebo-controlled study, we evaluated whether a reboxetine-betahistine combination attenuates olanzapine-induced weight gain in schizophrenia patients. METHOD: Forty-three inpatients with DSM-IV schizophrenic disorder participated in a randomized double-blind study. Reboxetine (4 mg/day) with betahistine (48 mg/day) (N = 29) or placebo (N = 14) was co-administered with olanzapine (10 mg/day) for 6 weeks. Mental status was assessed at baseline and endpoint with relevant rating scales. Intention-to-treat method was used for statistical analysis. RESULTS: Seven patients in the study group and four in the placebo group discontinued the trial. At the end of the trial, patients in the olanzapine/reboxetine + betahistine group gained significantly less weight than those in the olanzapine/placebo group [2.02 ± 2.37 and 4.77 ± 3.16 kg, respectively; t = 2. 89, degrees of freedom (df) = 41, p = 0.006]. The weight-attenuating effect of this combination was twofold larger than the weight-attenuating effect previously demonstrated with reboxetine alone. Significantly fewer patients in the study group than in the comparison group increased their initial weight by >7 %, the cutoff for clinically significant weight gain [3/29 (10.3 %) and 6/14 (42.9 %), respectively; χ (2) = 6.03, df = 1, p = 0.014]. The reboxetine-betahistine combination was safe and well tolerated. CONCLUSIONS: Reboxetine-betahistine combination produces a clinically meaningful attenuation of olanzapine-induced weight gain. These results justify direct comparison between the reboxetine-betahistine combination and reboxetine alone.

Age-of-onset of schizophrenic and obsessive-compulsive symptoms in patients with schizo-obsessive disorder.

Obsessive-compulsive symptoms (OCS) are prevalent, persistent, clinically significant phenomena in schizophrenia. To facilitate the understanding of their temporal interrelationship, we assessed age-of-onset of schizophrenic and obsessive-compulsive symptoms among 133 patients admitted to Tirat Carmel Mental Health Center (Israel) during the years 1999-2010 who met DSM-IV criteria for both schizophrenic disorder and obsessive-compulsive disorder (OCD). The mean age-of-onset of the first clinically significant OCS was significantly earlier than the mean age-of onset of the first psychotic symptoms. An earlier onset of OCS was detected in men, but not in women. In sixty-four of 133 patients OCS preceded the first psychotic symptoms, in 37 patients OCS followed them, and in 32 patients OCS and psychotic symptoms occurred simultaneously. A sub-analysis of 52 first-episode schizophrenia patients revealed that OCS emerged approximately 3 years earlier than psychotic symptoms. Notably, schizo-obsessive patients had earlier mean age-of-onset of first psychotic symptoms than a comparative group of 113 non-OCD schizophrenia patients matched for age, gender and number of hospitalization. Earlier emergence of OCS than schizophrenic symptoms in schizo-obsessive patients suggests that they are independent of psychosis and are not consequent to schizophrenia. In addition, the presence of OCS seems to modify clinical features of schizophrenia accounting for earlier onset of first psychotic symptoms, however a replication of these findings is needed.

Effect of the selective norepinephrine reuptake inhibitor reboxetine on cognitive dysfunction in schizophrenia patients: an add-on, double-blind placebo-controlled study.

The noradrenergic (NE) system mediates cognitive dysfunction in schizophrenia patients, and the NE transporter represents a putative target for cognitive enhancing therapy. In a double-blind placebo-controlled study we evaluated the effect of add-on reboxetine (4 mg/day), a selective norepinephrine reuptake inhibitor (NRI), co-administered with atypical antipsychotic olanzapine (10 mg/day) on cognitive functioning in DSM-IV schizophrenia patients. The Automated Neuropsychological Assessment Metrics battery and Wisconsin Card Sorting Test were used to assess selective cognitive functions at baseline and endpoint (6 weeks). Clinical assessment was also performed. No between-group differences were found in neurocognitive tests, suggesting that reboxetine did not significantly change patients' cognitive performance compared to placebo. Reboxetine was well-tolerated and did not interfere with the therapeutic effect of olanzapine. Long-term studies using higher reboxetine dosages and alternative NRIs (e.g., atomoxetine) are needed to determine the role of NRIs as cognitive enhancers in patients with schizophrenia and other disorders associated with cognitive impairments.

Obsessive-compulsive symptom dimensions in schizophrenia patients with comorbid obsessive-compulsive disorder.

A substantial proportion of schizophrenia patients also exhibit obsessive-compulsive symptoms (OCS). We sought to determine whether the revealed symptom dimensions in OCD exist in schizophrenia patients with comorbid OCD. One hundred and ten patients who met DSM-IV criteria for both schizophrenia and OCD were recruited. Exploratory factor analysis of the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) checklist was conducted. The inter-relationship between the resulting factors and schizophrenia symptom dimensions, as assessed by the Schedule for the Assessment of Positive (SAPS) and Negative (SANS) Symptoms, was examined. The principal component analysis of 13 Y-BOCS checklist categories yielded a five-factor solution and accounted for 58.7% of the total variance: (1) aggressive, sexual, religious obsessions and counting, (2) symmetry and ordering/hoarding compulsions, (3) contamination and cleaning, (4) somatic obsession and repeating compulsion, (5) hoarding obsession and checking/repeating compulsions. The Y-BOCS symptom dimensions did not correlate with schizophrenia symptom dimensions. The five symptom dimensions are comparable to those revealed in "pure" OCD, and suggest the involvement of universal mechanisms in the pathogenesis of OCD regardless of the presence of schizophrenia.

Clinical characteristics of schizotypal-related obsessive-compulsive disorder.

In this study we compared 15 patients with DSM-IV obsessive-compulsive disorder (OCD) and schizotypal personality disorder (SPD) and 31 non-SPD OCD patients. OCD-SPD patients had poorer insight, more negative symptoms, lower functioning, more antipsychotic augmentation and more first-degree relatives with schizophrenia-spectrum disorders. A distinct clinical phenotype of OCD associated with SPD should be considered when investigating etiopathogenetic mechanisms.

Awareness of illness and insight into obsessive-compulsive symptoms in schizophrenia patients with obsessive-compulsive disorder.

Obsessive-compulsive symptoms (OCS) have been revealed in a substantial proportion of schizophrenia patients. We sought to evaluate insight into OCS in schizo-obsessive patients. We evaluated insight into OCS and awareness of schizophrenia, using the Brown Assessment of Beliefs Scale (BABS) and the Scale to Assess Unawareness of Mental Disorder (SUMD), respectively. Fifty-seven inpatients that met DSM-IV criteria for both schizophrenia and OCD were recruited. To determine a possible modifying effect of OCS on the awareness of schizophrenia, we included a comparison group of non-OCD schizophrenia patients (N = 80). Nine (15.8%) schizo-obsessive patients revealed lack of insight into OCS, whereas a majority (48 patients, 84.2%) exhibited good or fair insight. In the schizo-obsessive group, insight into OCS positively correlated with awareness of schizophrenia but not with awareness of delusions. Roughly 40% of the schizo-obsessive and non-OCD schizophrenia patients revealed unawareness of schizophrenia. Our findings indicate that OCS in schizophrenia represent an identifiable dimension of psychopathology independent of core schizophrenia symptoms.

Neurological soft signs in schizophrenia patients with obsessive-compulsive disorder.

Obsessive-compulsive disorder is a prevalent and clinically significant phenomenon in schizophrenia patients. Both schizophrenia and obsessive-compulsive disorder (OCD) are considered to be neurodevelopmental disorders sharing dysfunctional frontal-subcortical circuitry. Using the Neurological Evaluation Scale (NES), the authors assessed neurological soft signs in 59 patients who met DSM-IV criteria for both schizophrenia and OCD. The two schizophrenia groups (with and without OCD) scored higher than the comparison group but did not significantly differ from one another on any of the NES subscales. The first-episode patients in both groups scored similarly to patients with repeated hospitalizations on all NES subscales. Notably, the OCD patients scored similarly to the two schizophrenia groups on the NES motor sequencing subscale. The author's findings support the notion that neurological soft signs are independent markers of brain dysfunction detectable early in the course of schizophrenia. However, they are of limited value as a putative endophenotype in a search for specific etiological mechanisms underlying a schizo-obsessive subgroup of schizophrenia.

Attenuating effect of reboxetine on appetite and weight gain in olanzapine-treated schizophrenia patients: a double-blind placebo-controlled study.

RATIONALE: Search for safe and effective strategies to diminish weight gain associated with second generation antipsychotics (SGAs) is imperative. In the present study, we sought to replicate our preliminary findings, which indicated that coadministration of the selective norepinephrine reuptake inhibitor reboxetine attenuates olanzapine-induced weight gain. MATERIALS AND METHOD: Fifty-nine patients hospitalized for first-episode DSM-IV schizophrenic disorder participated in this randomized double-blind study. Reboxetine (4 mg/day; 31 patients) or placebo (29 patients) was coadministered with olanzapine (10 mg/day) for 6 weeks. Analysis was by intention-to-treat. RESULTS: Nine patients in each group prematurely discontinued the trial. Olanzapine/reboxetine-treated patients showed a significantly lower increase in body weight (mean = 3.31 kg, SD = 2.73) than their olanzapine/placebo-treated counterparts (mean = 4.91 kg, SD = 2.45). Significantly fewer olanzapine/reboxetine-treated patients gained at least 7% of their initial weight, the cutoff for clinically significant weight gain (6 [19.4%] of 31 patients vs 13 [46.4%] of 28 patients). Seven (22.6%) olanzapine/reboxetine-treated patients compared to only one patient (3.6%) in the olanzapine/placebo group revealed no weight change or even modest weight loss. Appetite increase was significantly lower in the olanzapine/reboxetine than olanzapine/placebo group and was correlated with attenuation of weight gain. Reboxetine addition was safe and well tolerated. CONCLUSIONS: The results confirm that coadministration of reboxetine promotes a clinically meaningful attenuation of olanzapine-induced weight gain in schizophrenia patients. If substantiated in long-term studies, along with behavioral management and diet counseling, reboxetine may have a clinical utility in controlling SGA-induced weight gain.

Preferential aggregation of obsessive-compulsive spectrum disorders in schizophrenia patients with obsessive-compulsive disorder.

OBJECTIVE: To validate a complex association between schizophrenia and obsessive-compulsive disorder (OCD). METHOD: We used the Structured Clinical Interview for DSM-IV Axis I disorders to compare the rate of OCD spectrum and additional Axis I disorders in 100 patients who met criteria for both schizophrenia and OCD, non-OCD schizophrenia (n = 100), and OCD (n = 35). RESULTS: There was a robust between-group difference in the number of patients with one or more OCD spectrum disorders (schizo-obsessive n = 30, compared with schizophrenia n = 8; P = 0.001), that is, higher rates of body dysmorphic (8% compared with 0%) and tic (16% compared with 4%) disorders. No difference was revealed in affective, anxiety, and substance use disorders. We found comparable rates of OCD spectrum disorders in the schizo-obsessive and OCD groups (30% and 42.8%, respectively; P = 0.32). CONCLUSION: Preferential aggregation of OCD spectrum disorders in the schizo-obsessive group supports this unique clinical association. Whether a schizo-obsessive interface represents comorbidity or a specific subtype of schizophrenia warrants further investigation.

Acute otitis media and mastoid growth.

CONCLUSIONS: This study implies that the hypothesis that acute otitis media (AOM) in infancy inhibits the growth of the mastoid system cannot be accepted. OBJECTIVE: To establish a relationship between AOM in children and their mastoid pneumatization development. PATIENTS AND METHODS: Lateral Schüller mastoid radiographs (LMRs) were measured in two groups of children at ages 2-11 years. Group A (n=116) had a history of recurrent AOM; group B (n=108) had no such history. Patients were treated in a private clinic. Data were analysed at Tel Aviv University. The patients had their LMR taken and measured planimetrically. LMR areas on left and right sides were compared in each group and age and were tested for possible differences using the paired Student's t test. When no left/right difference was detected, the values were averaged. Groups A and B were compared at different ages using two-tailed two-sample unequal variance and correlation coefficients. RESULTS: The analyses show that the LMR area became gradually and significantly larger with age in group A (R2=0.858; p<0.05). It did not develop significantly in group B.

Obsessive-compulsive disorder in bipolar disorder patients with first manic episode.

BACKGROUND: Evidence indicates that obsessive--compulsive disorder (OCD) co-occurs with schizophrenia and bipolar disorder (BD) at a higher rate than in the general population. The inflated rate of comorbidity may result from chronic illness, antipsychotic therapy or treatment-seeking behavior. To control for these factors we evaluated the prevalence of OCD in patients with first-episode acute mania who met DSM-IV criteria for BD-I, and compared them with our previously reported group of first-episode schizophrenia patients. METHOD: Fifty-six BD-I patients with a first-episode of acute mania were screened for OCD and additional comorbid disorders using the Structured Clinical Interview for DSM-IV Axis-I disorders and appropriate rating scales. RESULTS: Only one patient (1.8%) met DSM-IV criteria for OCD, and two (3.6%) met criteria for sub-threshold OCD. In contrast, there was a substantial aggregation of substance use disorders 32.1% (N=8), anxiety disorders, other than OCD 26.8% (N=15) and eating disorders 14.3% (N=8). LIMITATIONS: Small sample size, cross-sectional nature of the assessments and the inclusion of only BD-I patients. CONCLUSION: The rate of OCD in first-episode BD-I patients did not differ significantly from that found in the general population and was substantially lower than in previously reported first-episode schizophrenia patients (1.8% vs. 14%). We suggest that a preferential association of OCD with schizophrenia early in the course of illness represents a pathophysiological linkage between the two disorders, and putatively a specific schizo-obsessive subtype. In contrast, OCD in BD-I may stand for "true" comorbidity. Large-scale parallel comparative evaluations of comorbidity in BD-I and schizophrenia may contribute to the search for specific pathophysiological mechanisms of distinct comorbid-related subsets in either disorder.

Low-dose mirtazapine: a new option in the treatment of antipsychotic-induced akathisia. A randomized, double-blind, placebo- and propranolol-controlled trial.

BACKGROUND: Preliminary evidence indicates a beneficial effect of serotonin 2A (5-HT(2A)) receptor antagonists in antipsychotic-induced akathisia (AIA). We investigated the antiakathisia effect, safety, and tolerability of low-dose mirtazapine, an agent with marked 5-HT(2A) antagonism. METHODS: In a 7-day double-blind trial, 90 antipsychotic-treated patients meeting DSM-IV criteria for AIA were randomly assigned to mirtazapine (n = 30; 15 mg), propranolol (n = 30; 80 mg), or placebo (n = 30). Primary outcome measures were between-group differences in Barnes Akathisia Scale (BAS) global scores and in the proportion of responders (reduction of > or = 2 points on BAS). Analysis was by intention to treat. RESULTS: Twenty-four patients (26.6%) who were assigned treatment did not complete the study (7 mirtazapine, 8 propranolol, 9 placebo), due to lack of response (n = 19) and adverse events (n = 5). Both mirtazapine and propranolol significantly reduced AIA severity (BAS: -34% mirtazapine and -29% propranolol vs. placebo -11%; p = .012 and p = .023, respectively). Thirteen (43.3%) mirtazapine and 9 (30.0%) propranolol-treated patients versus 2 (6.7%) placebo-treated patients responded (the corresponding odds ratios 10.7 [95% confidence interval (CI), 2.1-53.3] and 6.0 [95% CI, 1.1-30.7]). Five (16.7%) of 30 propranolol-treated patients and none in the mirtazapine and placebo groups (p = .0195 for both) prematurely discontinued the study due to clinically significant hypotension or bradycardia. CONCLUSIONS: The comparable efficacy and better tolerability of low-dose mirtazapine versus propranolol, the current first-line treatment for AIA, position mirtazapine as a favorable candidate for the treatment of acute AIA and may improve current therapeutic practices.

Familial aggregation of schizophrenia-spectrum disorders and obsessive-compulsive associated disorders in schizophrenia probands with and without OCD.

A substantial proportion of schizophrenia patients also has obsessive-compulsive disorder (OCD). To further validate the clinical validity of a schizo-obsessive diagnostic entity, we assessed morbid risks for schizophrenia-spectrum disorders and OC-associated disorders in first-degree relatives of schizophrenia probands with and without OCD. Two groups of schizophrenia probands [with OCD (n = 57) and without OCD (n = 60)] and community-based controls (n = 50) were recruited. One hundred eighty two first-degree relatives of probands with OCD-schizophrenia, 210 relatives of non-OCD schizophrenia probands, and 165 relatives of community subjects were interviewed directly [59.3% (108/182), 51.9% (109/210), and 54.5% (90/165), respectively], using the Structured Clinical Interview for Axis-I DSM-IV Disorders and Axis II DSM-III-R Personality Disorders and the remaining relatives were interviewed indirectly, using the Family History Research Diagnostic Criteria. Relatives of OCD-schizophrenia probands had significantly higher morbid risks for OCD-schizophrenia (2.2% vs. 0%; P = 0.033) and OCPD (7.14% vs. 1.90%; P = 0.014), and a trend towards higher morbid risk for OCD (4.41% vs. 1.43%; P = 0.08) compared to relatives of non-OCD schizophrenia probands. When morbid risks for OCD, OCPD, and OCD-schizophrenia were pooled together, the significant between-group difference became robust (13.74% vs. 3.33%; P = 0.0002). In contrast, relatives of the two schizophrenia groups did not differ significantly in morbid risks for schizophrenia-spectrum disorders, mood disorders, or substance abuse disorders. A differential aggregation of OC-associated disorders in relatives of OCD-schizophrenia versus non-OCD schizophrenia probands, provides further support for the validity of a putative OCD-schizophrenia ("schizo-obsessive") diagnostic entity.

The effect of famotidine addition on olanzapine-induced weight gain in first-episode schizophrenia patients: a double-blind placebo-controlled pilot study.

Olanzapine treatment is associated with substantial weight gain. In this double-blind placebo-controlled study we evaluated whether the H2 antagonist famotidine may prevent/attenuate olanzapine-induced weight gain. Fourteen first-episode DSM-IV schizophrenia patients were randomly allocated to receive either famotidine (40 mg/day, n=7) or placebo (n=7) in addition to olanzapine (10 mg/day) for 6 weeks. All patients completed the trial. Patients in both groups showed a similar increase in body weight (olanzapine/famotidine: 4.8 (3.2) kg and olanzapine/placebo: 4.9 (1.6) kg, respectively; a between-group difference of 0.14 (1.3) kg). Four of seven (57.1%) patients in the olanzapine/famotidine group and three of seven (42.9%) in the olanzapine/placebo group gained at least 7% of their initial body weight, a cut-off for clinically significant weight gain. Famotidine addition was safe and well tolerated and did not interfere with olanzapine's therapeutic effect. In conclusion, famotidine (40 mg/day for 6 weeks) is not effective in preventing/attenuating weight gain in olanzapine-treated first-episode schizophrenia patients.

Comparison of clinical characteristics and comorbidity in schizophrenia patients with and without obsessive-compulsive disorder: schizophrenic and OC symptoms in schizophrenia.

BACKGROUND: Since a substantial proportion of schizophrenia patients has symptoms of obsessive-compulsive disorder (OCD), we sought to provide a phenomenological characterization of a schizophrenia subgroup with OCD. METHOD: A consecutive sample of patients who met DSM-IV criteria for both schizophrenia and OCD (N = 55) was compared with 55 schizophrenia patients without OCD matched for age and number of hospitalizations. Structured Clinical Interview for DSM-IV Axis I psychiatric disorders (SCID-I), including a specific module for tic disorders based on DSM-IV criteria, Scales for the Assessment of Positive and Negative Symptoms, Yale-Brown Obsessive-Compulsive Scale, Clinical Global Impressions scale, and Hamilton Rating Scale for Depression were used. RESULTS: Schizophrenia patients with OCD (N = 55) had lower positive dimension scores than schizophrenia patients without OCD (N = 55) (p =.01). Two subgroups of schizo-obsessive patients were identified: OCD independent of schizophrenia symptoms and OCD partially overlapping positive schizophrenia symptoms. Schizophrenia patients with OCD had more SCID-detectable OCD-spectrum disorder, primarily body dysmorphic disorder and chronic tic disorders. More schizophrenia patients with OCD were treated with either add-on serotonin reuptake inhibitors or clozapine. CONCLUSION: Schizophrenia patients with OCD differ from their non-OCD-schizophrenia counterparts in severity of schizophrenia symptoms, co-occurrence of OCD-spectrum disorders, and pharmacotherapy. These findings and the identification of 2 subgroups of schizo-obsessive patients support the validity of this unique clinical entity and may facilitate the establishment of diagnostic criteria for a schizo-obsessive subtype of schizophrenia.

Efficacy of low-dose mirtazapine in neuroleptic-induced akathisia: a double-blind randomized placebo-controlled pilot study.

The nonselective serotonin (5-HT)-2A antagonists ritanserin, mianserin, and cyproheptadine were found efficacious in neuroleptic-induced akathisia (NIA). Mirtazapine is structurally and pharmacologically similar to mianserin, and the authors sought to determine its anti-NIA activity. Twenty-six neuroleptic-treated schizophrenic patients with DSM-IV diagnosis of NIA received add-on mirtazapine (15 mg/day) or placebo for 5 days in a double-blind design. Patients were assessed at baseline and days 3 and 5 with the Barnes Akathisia Scale (BAS), Positive and Negative Symptom Scale, Hamilton Rating Scale for Depression, and Simpson-Angus Scale for parkinsonism. Analysis of covariance with repeated measurements revealed significant group x time effects in favor of the mirtazapine group in both completers (n = 10 in each group) and intent-to-treat analysis (n = 13 in each group) for the BAS global subscale (F [1, 17] = 14.87, p = 0.001, and F [1, 23] = 13.24, p = 0.01, respectively) and objective subscale (F [1, 17] = 8.25, p = 0.011, and F [1, 23] = 7.35, p = 0.012, respectively) and borderline significant superiority for the BAS subjective subscale (F [1, 17] = 4.39, p = 0.051, and F [1, 23] = 4.12, p = 0.054, respectively) and distress subscale (F [1, 17] = 4.21, p = 0.056, and F [1, 23] = 3.80, p = 0.064, respectively). Significantly more mirtazapine-than placebo-treated patients (53.8% [7/13] vs. 7.7% [1/13], respectively; chi2 = 8.3, p = 0.004) met operational response criterion, a reduction of at least two points on the BAS global subscale. Mirtazapine treatment was associated with modest improvement of psychotic and parkinsonian symptoms. Mild sedation was the only side effect. Our study demonstrated that mirtazapine (15 mg/day) is an efficacious and well-tolerated therapeutic option in NIA. Marked 5HT2A/2C antagonistic activity of mirtazapine apparently accounts for its anti-NIA activity. The role of mirtazapine in the treatment of akathisia induced by atypical antipsychotic agents merits further investigation.