Search PubMed⌕ Search

Biomedical subjects

R A Remick

Publications and source records attributed to R A Remick.

At least 37 records · Page 2Linked to original sources
PubMed1996

Genetic linkage study of bipolar disorder and the serotonin transporter.

The serotonin transporter (HTT) is an important candidate gene for the genetic transmission of bipolar disorder. It is the site of action of many antidepressants, and plays a key role in the regulation of serotonin neurotransmission. Many studies of affectively ill patients have found abnormalities in serotonin metabolism, and dysregulation of the transporter itself. The human serotonin transporter has been recently cloned and mapped to chromosome 17. We have identified a PstI RFLP at the HTT locus, and here report our examination of this polymorphism for possible linkage to bipolar disorder. Eighteen families were examined from three populations: the Old Order Amish, Iceland, and the general North American population. In addition to HTT, three other microsatellite markers were examined, which span an interval known to contain HTT. Linkage analyses were conducted under both dominant and recessive models, as well as both narrow (bipolar only) and broad (bipolar + recurrent unipolar) diagnostic models. Linkage could be excluded to HTT under all models examined. Linkage to the interval spanned by the microsatellites was similarly excluded under the dominant models. In two individual families, maximum lod scores of 1.02 and 0.84 were obtained at D17S798 and HTT, respectively. However, these data overall do not support the presence of a susceptibility locus for bipolar disorder near the serotonin transporter.

Bipolar Disorder↗
PubMed1996

Depression and multiple sclerosis.

The objective of the present study were (1) to ascertain the lifetime risk of a depression in a representative group of multiple sclerosis (MS) patients, (2) to assess the morbidity risks for depression among first-degree relatives of these MS patients, and (3) to compare these familial risks for first-degree relatives of MS patients with those for first-degree relatives of a primary depression population, i.e., depression but no MS. We psychiatrically evaluated 221 MS patients (index cases) using a structured clinical interview for the DSM-III-R and calculated the rate and lifetime risk of depression for these index cases using the product limit estimate of survival function. We obtained psychiatric histories for all first-degree relatives of index cases, and we calculated morbidity risks for depression for these relatives using the maximum likelihood approach and compared the risks using the likelihood ratio tests. Index cases had a 50.3% lifetime risk of depression. Morbidity risks for depression among first-degree relatives of index cases were decidedly lower when compared with morbidity risks among first-degree relatives of the reference population. Although there appears to be a very high rate of depression among MS patients, the data for their first-degree relatives do not support a clear genetic basis for this depression, or at least the same genetic basis that probably operates within families when depression occurs in the absence of MS.

Adolescent↗
PubMed1995

Bipolar disorder: evidence for a major locus.

Complex segregation analyses were conducted on families of bipolar I and bipolar II probands to delineate the mode of inheritance. The probands were ascertained from consecutive referrals to the Mood Disorder Service, University Hospital, University of British Columbia and diagnosed by DSM-III-R and Research Diagnostic Criteria. Data were available on over 1,500 first-degree relatives of the 186 Caucasian probands. The purpose of the analyses was to determine if, after correcting for age and birth cohort, there was evidence for a single major locus. Five models were fit to the data using the statistical package SAGE: i) dominant, ii) recessive, iii) arbitrary mendelian inheritance, iv) environmental, and v) no major effects. A single dominant, mendelian major locus was the best fitting of these models for the sample of bipolar I and II probands when only bipolar relatives were defined as affected (polygenic inheritance could not be tested). Adding recurrent major depression to the diagnosis "affected" for relatives reduced the evidence for a major locus effect. Our findings support the undertaking of linkage studies and are consistent with the analyses of the National Institutes of Mental Health (NIMH) Collaborative Study data by Rice et al. (Arch Gen Psychiatry 44: 441-447, 1987) and Blangero and Elston (Genet Epidemiol 6:221-227, 1989).

Bipolar Disorder↗
PubMed1994

Mood Disorder Service Genetic Database: morbidity risks for mood disorders in 3,942 first-degree relatives of 671 index cases with single depression, recurrent depression, bipolar I, or bipolar II.

There is increasing evidence that genetic factors play a role in the etiology of mood disorders. As a result, relatives of affected individuals are more often asking about their own risks to develop a mood disorder. From 1988 to 1990, all consecutive, unrelated inpatients and outpatients (index cases) presenting to the Mood Disorders Service, Department of Psychiatry, University of British Columbia, had detailed family histories taken, thus creating the Mood Disorders Service Genetic Database. Diagnoses for index cases and their first-degree relatives were made according to Research Diagnostic Criteria and Family History Research Diagnostic Criteria respectively. Morbidity risks for mood disorders were calculated for first-degree relatives (parents, siblings, children--aged 10 and above) of all index cases with a diagnosis of single depression, recurrent depression, bipolar I, or bipolar II disorder. Morbidity risks were calculated using the maximum likelihood approach. Morbidity risk data are presented according to the sex and diagnosis for the index case in an easy reference format for risk counselling. The risks are presented twice, including and excluding data for "high-risk" families whose genetic pedigree is suggestive of "autosomal dominant" inheritance.

Age of Onset↗
PubMed1994

A Canadian multicentre placebo-controlled study of a fixed dose of brofaromine, a reversible selective MAO-A inhibitor, in the treatment of major depression.

In a 6-week double-blind study, 220 patients with major depression (mostly outpatients) were randomly assigned to receive a fixed dose of brofaromine 150 mg daily (n = 111) or placebo (n = 109) after a 1-week single-blind placebo washout. Except for the HAM-D sleep items, brofaromine was superior to placebo on measures of depression as determined by the four methods of assessing drug efficacy: (1) psychiatric symptom rating (HAM-D 17-item less the three sleep items); (2) self-rating scale (Beck Depression Inventory); (3) Clinical Global Assessment of Efficacy; and (4) drop-out rate due to lack of efficacy. Most commonly reported adverse events with brofaromine were: headache, nausea, dizziness and sleep disturbance. Brofaromine was found to be an effective antidepressant, superior to placebo with a good tolerability profile.

Adolescent↗
PubMed1994

A controlled study of light therapy for bulimia nervosa.

OBJECTIVE: Winter worsening of mood and eating symptoms, similar to that of seasonal affective disorder, has recently been reported in patients with bulimia nervosa. To assess the effectiveness of light therapy for treatment of bulimia nervosa, the authors conducted a study of light therapy during winter comparing an active (bright white light) condition to a control (dim red light) condition in bulimic patients who were not selected for a seasonal pattern of bulimia. METHOD: After a 2-week baseline assessment, 17 female patients with a DSM-III-R diagnosis of bulimia nervosa underwent early morning light treatment with 2 weeks of bright white light exposure (10,000 lux for 30 min/day) and 2 weeks of dim red light exposure (500 lux for 30 min/day) in a counterbalanced, crossover design. Outcome measures included daily binge/purge diaries, objective and subjective measures of mood, and the Eating Attitudes Test. Expectation of response for each condition was also assessed before treatment. RESULTS: Although pretreatment expectation ratings were similar for each condition, the bright white light condition was superior to the dim red light condition for all mood and eating outcome measures. Patients with "seasonal" bulimia (N = 7) had significantly greater improvement after the bright white light treatment than patients with nonseasonal bulimia (N = 10). No significant order effects were noted, nor differential effects for patients taking concurrent antidepressant medications (N = 4). CONCLUSIONS: These data suggest that bright white light therapy is an effective short-term treatment for both mood and eating disturbances associated with bulimia nervosa, although the therapeutic effect may be greater in those patients with a seasonal pattern.

Adult↗
PubMed1993

Depressive symptoms and family history in seasonal and nonseasonal mood disorders.

OBJECTIVE: The authors' goal was to compare the symptoms and family history of seasonal affective disorder with those of nonseasonal mood disorders. METHOD: From a subspecialty mood disorders clinic, 34 patients with major depression, seasonal pattern (seasonal affective disorder), diagnosed with DSM-III-R criteria, were matched in age, sex, and diagnostic subtype (recurrent unipolar, bipolar I, or bipolar II) to 34 patients with nonseasonal mood disorders. Data on symptoms during the most recent depressive episode were obtained by chart review and compared by using chi-square tests. Family history data for first-degree relatives of patients with seasonal and nonseasonal mood disorders were gathered by using the family history method, and diagnoses were based on Family History Research Diagnostic Criteria. RESULTS: Patients with seasonal affective disorder reported significantly more hypersomnia, hyperphagia, and weight gain and reported less suicidal ideation and morning worsening of mood than the patients with nonseasonal mood disorders. No differences were found in family histories of mood disorders, other psychiatric disorders, and any psychiatric disorder between the groups with seasonal versus nonseasonal mood disorders. Alcoholism was found more frequently in the relatives of the patients with seasonal affective disorder. CONCLUSIONS: Differences in symptoms between seasonal and nonseasonal mood disorders provide some support for seasonal affective disorder as a diagnostic subtype of mood disorders. However, the genetic loading for mood disorders (of unspecified seasonality), as determined by the family history method, is similar for seasonal and nonseasonal mood disorders.

Adult↗
PubMed1993

Obtaining a family psychiatric history: is it worth the effort?

The purpose of this study was to determine whether, for first-degree relatives of patients presenting to a mood disorders clinic, family history information on psychiatric conditions collected by a psychiatrist and incorporated into the patient's medical records is as informative as that gathered during an interview specifically designed to collect family history data. The study group consisted of 472 first-degree relatives of 78 randomly selected index cases from a large mood disorders genetic database. Family history of psychiatric disorders recorded in regular psychiatric medical records ("clinician history"), and data obtained by a genetic counsellor administering specific family psychiatric history questionnaires to patients and multiple family informants ("family history") were compared using a kappa statistic. Good agreement between the two methods on the presence or absence of a psychiatric disorder was found among first-degree relatives of index cases, but poor agreement was found with respect to the presence or absence of a specific mood disorder diagnosis(es) in a relative. The results suggest that a clinician-generated family psychiatric history is sensitive to the presence or absence of a psychiatric disorder when compared to a more structured detailed genetic interview. However, for research purposes, a clinician-generated family psychiatric history of a specific mood disorder diagnosis, without supporting collateral information, may not be reliable for use in supporting a mood disorder diagnosis in a patient and/or his relatives.

Adult↗
PubMed1993

Brofaromine in depression: a Canadian multicenter placebo trial and a review of standard drug comparative studies.

Brofaromine is a new, reversible, and selective type-A monoamine oxidase inhibitor (MAOI) that also has serotonin reuptake inhibitory properties. Its dual pharmacologic effects offer promise in the treatment of a wide spectrum of depressed patients while producing less severe anticholinergic side effects in comparison with standard drugs. A multicenter, double-blind, placebo-controlled study including 220 patients was undertaken to evaluate the efficacy and safety of brofaromine in major depression. This study of a fixed-dose design and 6 weeks' duration found that brofaromine was significantly better than placebo on the Overall Evaluation of Efficacy, Beck self-rating scale, HAM-D Bech subscale, HAM-D total 14 items (minus the three sleep items), HAM-D depressed mood item and retardation factor, and worse than placebo on the insomnia items of HAM-D. Significantly more patients on placebo than on brofaromine did not complete the trial due to lack of efficacy. In comparative controlled studies (n = 899), brofaromine was found to be at least as efficacious as tricyclic antidepressants (imipramine) and standard MAOIs (tranylcypromine and phenelzine). Reductions of at least 50% in the HAM-D total score were seen in 58-66% of patients treated with either brofaromine or imipramine (n = 609). Brofaromine also was found to be of comparable efficacy to tranylcypromine in two clinical trials (n = 132), one of which included patients considered to have a treatment-resistant depression (n = 39). In another double-blind study that compared brofaromine (150 mg/day) to phenelzine (45 mg/day) (n = 158), there was no difference between brofaromine and phenelzine.

Adolescent↗
PubMed1992

The effects of ultraviolet-A wavelengths in light therapy for seasonal depression.

Although light therapy is a recognized effective treatment for seasonal affective disorder (SAD), there has been little research into the critical wavelengths of light that produce the antidepressant effect. Previous studies found conflicting results for the importance of the ultraviolet (UV) spectrum in the therapeutic effect of light therapy. To assess the clinical effects of UV-A wavelengths (315-400 nm), we studied 33 depressed SAD patients diagnosed with structured interviews by DSM-IIIR criteria. Following a baseline week, patients underwent 2 weeks of 2500 lux light therapy for 2 h daily (06:00-08:00). Light therapy consisted of cool-white fluorescent light with the addition of a special UV-A fluorescent tube. Patients were randomized to wear glasses during light therapy that either blocked (UV-blocked condition) or passed (UV-A condition) wavelengths below 400 nm. Both treatments significantly reduced all depression ratings, but no differences were found between the UV-A and UV-blocked conditions. We conclude that the UV-A spectrum does not increase the antidepressant response of light therapy. Given the potential side effects of chronic UV exposure, clinical application of light therapy should use light sources that have the UV spectrum filtered.

Adult↗
PubMed1991

Low electrooculographic ratios in patients with seasonal affective disorder.

OBJECTIVE: Changes in retinal sensitivity to light have been hypothesized as etiological in seasonal affective disorder. This study was undertaken to investigate sensitivity to light in seasonal affective disorder using electrooculography (EOG), an objective measure of retinal light response. METHOD: In a mood disorders clinic, 19 depressed, drug-free patients with seasonal affective disorder, diagnosed by DSM-III-R criteria, were compared with 19 age- and sex-matched normal comparison subjects. All subjects had identical EOG testing performed during the winter. EOG (Arden) ratios were calculated from the EOG data. RESULTS According to multivariate analysis of variance, the EOG ratios in the patients with seasonal affective disorder were significantly lower than those of the normal comparison subjects, although there was considerable overlap in EOG ratios between patients and comparison subjects. CONCLUSIONS: These results suggest that seasonal affective disorder is associated with subtle retinal abnormalities at the level of the photoreceptor/retinal pigment epithelium complex, consistent with subsensitivity to light. A limitation of this study is that the retinal origins of the EOG response are nonspecific and still not completely elucidated.

Adult↗
PubMed1991

Ultraviolet versus non-ultraviolet light therapy for seasonal affective disorder.

Although light therapy has been shown to be effective in the treatment of seasonal affective disorder (SAD), little research has been done to determine which light wavelengths affect treatment outcome. In this triple crossover study the authors compared 1 week of light therapy in which bright (2500 lux), full-spectrum fluorescent light, with and without blockade of the ultraviolet (UV) spectrum, was used with a dim (500 lux) light control in 11 SAD patients. The dim light condition had no significant antidepressant effects as measured by the Hamilton Rating Scale for Depression (HAM-D), the Beck Depression Inventory (BDI), and an atypical depressive symptom (ATYP) score. The UV-light condition significantly reduced HAM-D, BDI, and ATYP scores, whereas the UV-blocked condition significantly reduced only the ATYP score. These results suggest that the UV-spectrum in light therapy may have a differential effect on typical and atypical symptoms in SAD.

Depressive Disorder↗
PubMed1990

Dichotic perception and memory following electroconvulsive treatment for depression.

Verbal and visuospatial memory and dichotic listening performance were examined in 15 acutely depressed patients with no history of ECT, 17 depressed patients currently in remission, 15 remitted depressed patients who had received ECT six months or more in the past, and 20 normal controls. The neuropsychological functioning of an additional group of 10 acutely depressed patients was also studied before and two weeks after ECT. The results revealed some evidence of logical and autobiographical memory impairment two weeks following ECT, but no evidence that ECT impaired dichotic listening ability. Rather, a normalisation of hemispheric laterality was apparent on the dichotic listening task following ECT and the concomitant relief from depression. There was also no evidence of cognitive dysfunction on any task in individuals who were tested six months or more following their last ECT treatment.

Adult↗