The Canadian Journal of Psychiatry

First, to highlight the major differences among mental health acts in different Canadian jurisdictions as they relate to involuntary admission criteria, treatment authorization, review and appeal procedures, and conditional leave and community treatment orders. Second, to analyze the impact of these differences on the care that individuals with mental illness receive.

We examined the mental health act provisions of all Canadian jurisdictions to determine how the clinical management of a typical case would differ among jurisdictions. We used a statement of principles for mental health legislation endorsed by the Canadian Psychiatric Association to guide the analysis. We confirmed interpretation of each act and its implementation through key informant contact in each province and territory.

We found clinically significant differences among the provinces and territories on all major components of their mental health acts.

Provisions that prevent patients receiving appropriate clinical care can be found in some Canadian mental health acts. Alternate provisions that support appropriate clinical care, that respect the human rights and personal dignity of patients, and that are consistent with the Canadian Charter of Rights and Freedoms can be found in the legislation of other jurisdictions.

To review lithium's utility in the treatment of mood disorders.

We reviewed the safety, tolerability, teratogenicity, optimal dosing regimens, and mortality-lowering effects of lithium. Clinical relevance and scientific rigour determined which articles we selected for review.

Lithium is the paradigmatic treatment for bipolar disorder (BD). In treating BD, optimal maintenance plasma levels may be approximately 0.75 to 0.85 mEq/L. Although nephrogenic diabetes insipidus is not uncommon, irreversible renal failure due to lithium appears to be a rare, idiosyncratic event. Lithium-induced cardiovascular teratology appears to be less common than previously thought. Optimal lithium dosing may be once daily, this agent appears to bestow a robust suicide-lowering effect, and emerging data hint at neurotrophic and neuroprotective effects.

Lithium remains an effective and integral agent in the treatment of BD. Its ability to lower suicide rates in persons with BD warrants clinical attention.

This article reviews published studies on the use of lamotrigine in the treatment of bipolar disorder (BD).

We performed a Medline search to identify the literature data base available on double-blind, open-label studies and case series on the use of lamotrigine to treat BD.

Three double-blind studies, 3 open-label studies, and 2 case series have been conducted to date (n = 401 patients). Most patients were either nonresponders or partial responders to other mood stabilizers. Overall, 50% to 83% of the patients responded to lamotrigine; doses in the studies ranged from 50 to 400 mg daily. Switching to mania while on 200 mg of lamotrigine or more was extremely rare, and there were no reports of serious adverse effects during the study periods.

Lamotrigine is proving to be an effective agent in the treatment of BD and may be useful for patients who have not responded to other mood stabilizers.

To perform a retrospective survey of discharge medications at a tertiary care psychiatric facility and to assess the incidence of antipsychotic polypharmacy.

This is a retrospective survey that used the Department of Pharmacy's computer database to obtain relevant discharge information on all nongeriatric patients with schizophrenia discharged from Riverview Hospital between November 1, 1996 and October 31, 1998. From a total of 492 eligible patients, 229 met the inclusion criteria and formed the database for the survey.

The main finding of the survey was that 27.5% of our discharged patients diagnosed with schizophrenia left our facility on an antipsychotic polypharmacy regimen. Compared with patients discharged on a single antipsychotic, the pooled data revealed a significantly greater use of anticholinergic agents in those patients prescribed an antipsychotic polypharmacy regimen. Further, of the atypical agents, only risperidone showed a statistically significant reduction in dosage when coprescribed with a second antipsychotic.

Although antipsychotic polypharmacy persists today, as it has over the past 30 years, evidence-based data to support this controversial treatment strategy is lacking. As a result clinicians are relying on their clinical experience, and perhaps intuition, to design antipsychotic polypharmacy treatment protocols. Efforts should be made to replace subjective clinical impression with a more rational approach to antipsychotic polypharmacy—one that is based on pharmacodynamic and pharmacokinetic understanding of drug action.

The purpose of this study was to assess regional cerebral glucose metabolism in patients with schizophrenia who had never received antipsychotic medication and whose olfactory identification ability had been assessed. Two hypotheses were examined. First, the patients were compared with normal controls to determine whether differences in regional cerebral metabolism were apparent. Second, regional rates of metabolism were correlated with olfactory ability and the relation between them determined.

The patient (n = 26) and control (n = 32) subjects were scanned at rest using positron emission tomography (PET) after administration of ¹⁸F-fluorodeoxyglucose (FDG). In addition, the University of Pennsylvania Smell Identification Test was administered to each patient.

Patients with schizophrenia had reduced rates of glucose metabolism in the right and left thalamus that reached significance if not corrected for multiple comparisons. However, if a Bonferroni correction was applied over the 27 regions of interest, the differences were not significant. Scores on the Smell Identification Test were negatively correlated with 8 regions of interest. When scores were analyzed using multiple regression, the left frontal cortex and the medial parietal cortex were significant predictors.

The finding of reduced metabolism in the thalami is consistent with some of the previous literature, whereas the negative correlations between specific regions and olfactory function are not consistent with studies using activation paradigms.

To determine whether juvenile obsessive–compulsive disorder (OCD) is familial and whether the rate of Tourette syndrome (TS) and tic disorders is higher among relatives of patients with OCD than among relatives of controls subjects.

We assessed first-degree relatives of 35 juvenile OCD probands (aged 16 years or less) and 34 matched, psychiatrically unaffected control subjects, using the Diagnostic Interview for Children and Adolescents–Revised (DICA-R) (unpublished), a Questionnaire for tic disorders, the Children's Version of Leyton's Obsessional Inventory (CV-LOI), and the Children's Version of the Yale-Brown Obsessive Compulsive Scale (CY-BOCS). Similarly, we assessed adult relatives, using the Schedule for Clinical Assessment in Neuropsychiatry (SCAN), Leyton's Obsessional Inventory (LOI), the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), and a Questionnaire for tic disorders. The diagnoses were determined by consensus, using DSM-III-R criteria. We calculated age-corrected morbid risk, using Weinberg's method.

The morbid risk for OCD among the relatives of OCD probands was 4.96%, while none of the relatives of unaffected control subjects had OCD. We did not diagnose TS in any of the relatives of either OCD probands or control subjects. We diagnosed chronic motor tic disorders in only 1 of the relatives of OCD probands, while none of the relatives of control subjects had any tic disorder.

Most juvenile cases of OCD are nonfamilial and unrelated to tic disorders, while only a few are familial. There is a need to re-examine the issue of familiality in cases of OCD, as well as its relation to TS, using larger community samples to better understand the hypotheses of familial transmission and comorbidity with tic disorders.

The purpose of this communication is to alert psychiatrists to the difficulties of translating results of group difference obtained from large, randomized clinical trials to the treatment of individual patients.

Reported discrepancies between a) clinical trial participants and general psychiatric patients, b) clinical trial investigators and general clinicians, and c) study trial and usual clinic conditions were assessed.

The results confirm that important differences exist in all 3 areas.

Recommendations for researchers include more complete assessments of factors that account for individual difference, an appraisal of outcomes more important to patients than symptom scores, and the use of statistical methods that permit the evaluation of individual difference. Recommendations for clinicians include a careful differentiation of results obtained in different phases of clinical trials and a clear appreciation of the different purposes of those trials. Clinicians should also appreciate that short-term effectiveness is not the same as long-term outcome and that aggregate scores may not apply to individual patients.

This study evaluates the clinical response to olanzapine used in association with selective serotonin reuptake inhibitors (SSRIs) or clomipramine in treatment-resistant obsessive–compulsive disorder (OCD).

We describe the cases of 9 patients with serotonin uptake inhibitor-resistant OCD who were given an open-label adjunctive treatment of olanzapine for a minimum of 6 weeks. The response was assessed by using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and the Clinical Global Impression Scale (CGI).

Six patients showed improvement of symptoms after the augmentation with olanzapine. One patient (treated with clomipramine) discontinued olanzapine due to side effects, and another 2 did not respond.

Olanzapine augmentation of SSRIs in treating OCD showed a good (two-thirds) response rate, and it could therefore be considered as a treatment option when conventional therapies have failed.

In vitro studies report that valproic acid causes an increase in HIV-1 replication. This retrospective study examines a sample of patients with HIV disease and behavioural disturbances, for which the treatment of choice is divalproex sodium (DVP), to determine whether DVP causes an increase in HIV-1 replication.

A chart and database review identified 15 patients with HIV disease presenting with either 1) mania or hypomania or 2) dementia with mania or with hypomania or behavioural disturbances. HIV-1 viral load was compared before and after mood stabilizer initiation.

Eleven patients started therapy with DVP, and 4 patients declined treatment with a mood stabilizer. Nine of the 11 patients taking DVP were also receiving antiretroviral therapy. HIV-1 viral load did not increase in 6 of the 9 patients who had measurements between 1 week and 3.5 months after DVP initiation. No follow-up was available for the other 3 patients. Of the 2 patients receiving DVP but not antiretroviral medication, 1 had an increase of 0.17 log in HIV-1 viral load at 4 months. No follow-up record was available for the second patient. The 4 patients not taking DVP were all on antiretroviral therapy; viral loads in 2 of them remained nondetectable over 3 to 4 months, and 1 had an increase of 0.32 log in HIV-1 viral load at 3 months. No follow-up record was available for the fourth patient.

These preliminary data suggest that, in the presence of effective antiretroviral therapy, HIV-1 viral load appears not to be adversely affected by the administration of DVP. The results for the patients receiving DVP in the absence of antiretroviral medication remain indeterminate. Further prospective study is required.