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Obsessive compulsive symptoms are commonly reported in those with schizophrenia. Clozapine has previously been reported to induce, aggravate and alleviate these symptoms. It is unclear if these are similar to the symptoms experienced by those with obsessive compulsive disorder. This study describes the obsessive compulsive symptom profile of a population of patients with schizophrenia treated with clozapine (n=62) and compares this with patients with Obsessive Compulsive Disorder (n=35). All participants were attending an outpatient community mental health service. The Obsessive Compulsive Inventory (which measures the frequency and associated distress of a range of “behavioural” and “cognitive” symptoms), the Hospital Anxiety and Depression Scale and a demographic questionnaire were completed. In addition the schizophrenia group treated with clozapine completed the Brief Psychiatric Rating Scale. The OCD group reported significantly more symptoms for all OCI subscales compared to the clozapine group. Overall fourteen (22%) of the schizophrenia treated with clozapine group had clinically significant total OCI scores. Two (3%) had documented OCS pre clozapine. De novo OCS was reported in twelve (19%) cases. Nine (11%) had documented OC symptoms pre-clozapine while only two (3%) had symptoms after clozapine was initiated. In terms of OC symptom profile, the clozapine group scored highest on the Doubting scale, a cognitive symptom whereas the OCD group scored highest on Washing, a behavioural symptom. Both groups reported greater distress with cognitive rather than behavioural symptoms. Medication including clozapine dose was not correlated with symptom severity. Anxiety correlated highly with obsessive compulsive symptoms in the Clozapine group but not the OCD group. Within the Clozapine group, Obsessing correlated highly with Unusual Thought Content. Findings suggest that obsessive compulsive symptoms in the Clozapine group may reflect a subtype of 'schizo-obsessive' disorder.

Patients with schizophrenia have an approximately 10-fold higher risk for obsessive–compulsive symptoms (OCS) than the general population. A large subgroup seems to experience OCS as a consequence of second-generation antipsychotic agents (SGA), such as clozapine. So far little is known about underlying neural mechanisms. To investigate the role of SGA treatment on neural processing related to OCS in patients with schizophrenia, we stratified patients according to their monotherapy into 2 groups (group I: clozapine or olanzapine; group II: amisulpride or aripiprazole). We used an fMRI approach, applying a go/no-go task assessing inhibitory control and an n-back task measuring working memory. We enrolled 21 patients in group I and 19 patients in group II. Groups did not differ regarding age, sex, education or severity of psychotic symptoms. Frequency and severity of OCS were significantly higher in group I and were associated with pronounced deficits in specific cognitive abilities. Whereas brain activation patterns did not differ during working memory, group I showed significantly increased activation in the orbitofrontal cortex (OFC) during response inhibition. Alterations in OFC activation were associated with the severity of obsessions and mediated the association between SGA treatment and co-occurring OCS on a trend level. The main limitation of this study is its cross-sectional design. To our knowledge, this is the first imaging study conducted to elucidate SGA effects on neural systems related to OCS. We propose that alterations in brain functioning reflect a pathogenic mechanism in the development of SGA-induced OCS in patients with schizophrenia. Longitudinal studies and randomized interventions are needed to prove the suggested causal interrelations.

Rationale Phytocannabinoids are useful therapeutics for multiple applications including treatments of constipation, malaria, rheumatism, alleviation of intraocular pressure, emesis, anxiety and some neurological and neurodegenerative disorders. Consistent with these medicinal properties, extracted cannabinoids have recently gained much interest in research, and some are currently in advanced stages of clinical testing. Other constituents of Cannabis sativa , the hemp plant, however, remain relatively unexplored in vivo. These include cannabidiol (CBD), cannabidivarine (CBDV), Δ 9 -tetrahydrocannabivarin (Δ 9 -THCV) and cannabigerol (CBG). Objectives and methods We here determined pharmacokinetic profiles of the above phytocannabinoids after acute single-dose intraperitoneal and oral administration in mice and rats. The pharmacodynamic–pharmacokinetic relationship of CBD (120 mg/kg, ip and oral) was further assessed using a marble burying test in mice. Results All phytocannabinoids readily penetrated the blood–brain barrier and solutol, despite producing moderate behavioural anomalies, led to higher brain penetration than cremophor after oral, but not intraperitoneal exposure. In mice, cremophor-based intraperitoneal administration always attained higher plasma and brain concentrations, independent of substance given. In rats, oral administration offered higher brain concentrations for CBD (120 mg/kg) and CBDV (60 mg/kg), but not for Δ 9 -THCV (30 mg/kg) and CBG (120 mg/kg), for which the intraperitoneal route was more effective. CBD inhibited obsessive–compulsive behaviour in a time-dependent manner matching its pharmacokinetic profile. Conclusions These data provide important information on the brain and plasma exposure of new phytocannabinoids and guidance for the most efficacious administration route and time points for determination of drug effects under in vivo conditions.

We report the case of a 69 year-old female patient who was hospitalized for Diogenes syndrome, defined by marked self-neglect, social withdrawal and excessive hoarding, leading to squalor. Somatic causes were eliminated. Her personal history showed an eight-year depressive episode followed by a 20-year hypomanic episode without remission, followed by a persistent manic episode associated with Diogenes syndrome for four years. The Diogenes syndrome was successfully treated with mood stabilizers. Mood disorders – in particular chronic mania (i.e. a manic episode lasting more than two years) – should be considered in cases of Diogenes syndrome and in current classifications.

Background A 52-year old lady presented for admission with severe depression characterised by suicidal ideation and delusional belief. Case presentation Her treatment regime was reviewed and modified. The dilemma was whether she suffered from a psychotic depression with delusion or an obsessional disorder. She responded well to change of antipsychotic medication. Conclusions Her depression went in remission and her delusional belief decreased in intensity. She also gained reasonable insight into her problem. She is currently being followed up in the psychiatric outpatient clinic.

Dickey comments on the article \"Adult Baby Syndrome\" by Evcimen and Gratz.

This is the first longitudinal report on possible psychosis resulting from the juvenile onset of hypothyroidism. A 10-year follow-up in the case of a 13-year-old boy published in this journal in 1993 is presented. The patient presented with a diagnostic dilemma. Although psychosis resulting from hypothyroidism was the most parsimonious explanation of his symptoms (new-onset auditory hallucinations, severe obsessions, and severe hypothyroidism), a primary psychiatric disorder (obsessive-compulsive disorder [OCD] or psychotic depression) aggravated by hypothyroidism could not be excluded. The aim of this study was to illustrate that the diagnosis and clinical interrelationships can be clarified by longitudinal data. Follow-Up Data: The patient's symptoms responded optimally to a combination of fluvoxamine, risperidone, and levothyroxine (LT4, 300 μg daily). He was free from severe symptoms until age 21, when he discontinued all psychotropic medications while continuing with LT4. Over 2 months later, he was hospitalized for thoughts of hurting himself or others. In the hospital, his LT4 was discontinued and propranolol was started. He was discharged on multiple psychotropic medications, and was rehospitalized 6 days later for suicide risk. When LT4 (200 μg daily) was added to his psychotropic regimen, he partially responded and was discharged. The optimal response to treatment occurred only after he was placed on a combination of fluoxetine, risperidone, and LT4 (300 μg daily). The patient remained stable for up to 12 months of follow-up. Conclusions: This chronology suggests that the optimal treatment in this patient probably required three components: a Selective Serotonin Reuptake Inhibitor, (SSRI) risperidone, and LT4 (300 g daily). Each component was apparently necessary but not sufficient individually for the optimal response. The relapse after the discontinuation of fluvoxamine and risperidone (but not LT4) suggests the presence of a primary psychiatric disorder (OCD with depression). The failure to improve without an adequate dosage of LT4 suggests that hypothyroidism was probably an aggravating factor. This case illustrates the diagnostic difficulty in distinguishing between obsessions, depressive ruminations, and delusions inchildren and the need to consider hypothyroidism in the differential diagnosis of the sudden worsening of OCD, or in cases of new-onset psychosis in children and adolescents.

Family genetic and phenomenological studies support an interrelationship between Gilles de la Tourette syndrome (GTS) and obsessive-compulsive disorder (OCD). Some authors consider GTS as part of a serotonergically mediated cluster of OCD spectrum disorders. To study serotonergic mechanisms in GTS, the effect of the relatively selective 5-HT2c agonist meta-chlorophenylpiperazine (m-CPP) was assessed. We studied the behavioural effects of m-CPP on tics, obsessions, compulsions and impulsions of GTS. Twelve medication-free GTS patients (ten men, two women) were included in a single dose 0.5 mg/kg oral m-CPP challenge study with a double-blinded placebo-controlled cross-over design. Global symptom scores, target symptom scores as well as biochemical measures were followed up to 24 h after baseline. While m-CPP caused a significant rise in plasma cortisol and prolactin levels, no significant effects were found on the tics, obsessions and compulsions. Impulsions showed a trend to ameliorate. This study does not support a predominant role for 5-HT on the tics in GTS. The trend of impulsions to ameliorate after m-CPP can be interpreted as circumstantial support for impulsivity-related 5-HT hypofunctionality in GTS. However, the large variability of m-CPP plasma concentrations found in this study casts doubts upon the reliability of m-CPP as a probe for challenge studies.

Sorry, there is no abstract. Read the first few lines of the text instead! The arising of obsessive-compulsive (OC) symptoms during clozapine treatment of schizophrenia has been described by several clinicians although recently criticised [1-9]. Checking rituals and contamination obsessions with clozapine treatment were reported by Patil [10] in 1992, while Baker et al. [1] reported cleaning, washing, sexual and, again, contamination obsessions; Cassady and Thaker [2] added religious obsessions to the list. None of the patients had any prior history of OC symptoms. Cases have also been described where clozapine seems to have acted upon a pre-existing OC symptomatology [5].