Publications by authors named "Ronald A Remick"

Objective: The evidence that regular physical activity can treat depressive disorders is increasingly robust. However, motivating patients with depression to engage in physical activity can be challenging. Interdisciplinary group medical visits (GMVs) with an integrated physical activity component may be a novel means to support patients in becoming more active.

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Objective: To describe an alternative model of psychiatric outpatient care for patients with mood and anxiety disorders (the Mood Disorders Association of British Columbia Psychiatric Urgent Care Program or the MDA Program) using group medical visits (GMV) and (or) email communications in lieu of individual follow-up appointments.

Method: Annual costs of the MDA Program were compared with average costs of private psychiatrists offering outpatient care and patients being treated in a mental health centre. In addition, questionnaires as to patient satisfaction with the MDA Program intake, GMV experience, and family physician satisfaction with the MDA Program were administered.

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Objective: Access to outpatient psychiatric care remains problematic in Canada. We have been using group medical visits (GMV) to treat psychiatric outpatients with mood and anxiety disorders. Our study aimed to show that patients are similarly satisfied with GMV and individual psychiatric treatment, hence the concern that patients truly prefer individual treatment may be unfounded.

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Background: The many attempts that have been made to identify genes for bipolar disorder (BD) have met with limited success, which may reflect an inadequacy of diagnosis as an informative and biologically relevant phenotype for genetic studies. Here we have explored aspects of personality as quantitative phenotypes for bipolar disorder through the use of the Temperament and Character Inventory (TCI), which assesses personality in seven dimensions. Four temperament dimensions are assessed: novelty seeking (NS), harm avoidance (HA), reward dependence (RD), and persistence (PS).

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Background: The many attempts to identify genes for bipolar disorder (BD) have met with limited success, which has generally been attributed to genetic heterogeneity and small gene effects. However, it is also possible that the categorical phenotypes used in genetic studies of BD are not the most informative or biologically relevant. We have explored aspects of temperament as quantitative phenotypes for BD through the use of the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego Auto-questionnaire (TEMPS-A), which is designed to assess lifelong, milder aspects of bipolar symptomatology and defines five temperaments: hyperthymic, dysthymic, cyclothymic, irritable, and anxious.

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Bipolar disorder (BD) and attention deficit hyperactivity disorder (ADHD) exhibit remarkably high rates of comorbidity, as well as patterns of familial co-segregation. Epidemiological data suggests that these disorders either share a common genetic architecture or that ADHD features in BD may represent an etiologically distinct subtype. We previously used the Wender Utah Rating Scale (WURS) to assess ADHD features in BD families and identified three heritable factors relating to impulsivity, mood instability, and inattention.

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Article Synopsis
  • This study presents findings from a genome-wide linkage analysis of bipolar disorder using an independent sample of 34 family pedigrees.
  • It involves genotyping 229 family members with a total of 440 genetic markers to investigate familial patterns of bipolar disorder.
  • The results replicated some previous linkage findings on chromosomes 6 and 17, while other regions from earlier studies showed weak or no replication, suggesting complex genetic influences on the disorder.
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Higher rates of bipolar disorder amongst the first-degree relatives of probands with ADHD, and increased rates of ADHD in the relatives of bipolar probands have been reported in many studies. This suggests some commonality in the genetic basis for bipolar disorder and ADHD. We hypothesized that ADHD symptoms in bipolar disorder may access a quantitative subphenotype that is genetically less complex and therefore advantageous for mapping studies.

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Attempts to identify bipolar disorder (BP) genes have only enjoyed limited success. One potential cause for this problem is that the traditional categorical BP phenotypes currently used in genetic linkage studies are not the most informative, efficient, or biologically relevant. An alternative to these strict categorical BP phenotypes is quantitative BP phenotypes.

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Bipolar affective disorder (BPAD) is suspected to arise in part from malfunctions of the circadian system, a system that enables adaptation to a daily and seasonally cycling environment. Genetic variations altering functions of genes involved with the input to the circadian clock, in the molecular feedback loops constituting the circadian oscillatory mechanism itself, or in the regulatory output systems could influence BPAD as a result. Several human circadian system genes have been identified and localized recently, and a comparison with linkage hotspots for BPAD has revealed some correspondences.

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Background: The array of different diagnoses and clinical presentations seen in the family members of bipolar probands suggests a quantitative or spectrum phenotype. Consistent with this idea, it has been proposed that an underlying quantitative variation in temperament may be the primary phenotype that is genetically transmitted and that it in turn predisposes to bipolar disorder (BP). Choosing the appropriate phenotypic model for BP is crucial for success in genetic mapping studies.

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Bipolar disorder is associated with malfunctions of the circadian system, which regulates individual circadian rhythms and which enables the adaptation to a daily 24-h cycle and seasonal change. One of the human circadian clock genes, cryptochrome 1 (Cry1) (located on 12q23-q24.1) was analyzed because of its close correspondence to a linkage hotspot for bipolar disorder.

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Bipolar disorder is a major psychiatric disorder characterized by extreme mood states that alternate between mania and depression. Family, twin, and adoption studies indicate a genetic component to the disease, but the etiology is suspected to be complex, with multiple genes contributing to an increased susceptibility to the disorder. We have previously reported a genome scan in which a genome-wide maximum LOD score indicated evidence of linkage at the marker D22S278 at 22q13.

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THERE HAS BEEN SIGNIFICANT PROGRESS in the area of mood disorders over the last 2 decades, encompassing advances in our knowledge of epidemiology, diagnosis, pathogenesis and treatment. This article presents a clinically oriented update and review on the diagnosis and management of major depressive disorder.

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A controlled study on the cardiovascular safety of monoamine oxidase inhibitors (MAOI) during general anesthesia for electroconvulsive therapy (ECT) was completed. No serious changes in blood pressure, heart rate, or ectopic beats were noted in either the MAOI or control groups during ECT. Based on pharmacological data, a review of the literature, and these preliminary results, the recommended 2-week discontinuation of MAOI before ECT appears unwarranted.

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