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Biomedical subjects

Stephen M Stahl

Publications and source records attributed to Stephen M Stahl.

At least 19 recordsLinked to original sources
PubMed2003

A double-blind, placebo-controlled trial of clonazepam in obsessive-compulsive disorder.

Selective serotonin reuptake inhibitors (SSRIs) are currently the first-line pharmacological agents in treating obsessive-compulsive disorder (OCD). Appropriate treatment for OCD also involves cognitive behavioural therapy (CBT), including exposure and response prevention. As there is a time delay in seeing full therapeutic response, and not all patients tolerate SSRIs, there remains an unmet need for additional treatment approaches in OCD. In addition, most responders report only a partial reduction in symptoms. Clonazepam has demonstrated effectiveness in several preliminary reports in treating OCD. Twenty-seven patients with OCD were entered into a 10 week, double-blind, parallel design trial of clonazepam vs. placebo. Overall, only 3 out of 25 patients who had >/= 1 rating on clonazepam/placebo were judged to be treatment responders, by scoring a 1 (very much improved) or 2 (much improved) on the CGI improvement scale. Responders included 2 of 9 in the placebo group and 1 of 16 in the clonazepam group. No significant difference was found between clonazepam and placebo groups on responder/non responder status (Chi(2 )=1.39, df =1,24, p=0.238), nor on change in YBOCS, Ham-A, Ham-D or NIMH scales from beginning to last evaluation carried forward. These findings suggest that clonazepam is not effective as monotherapy in treating OCD. Its effectiveness in specific subgroups of OCD patients with co-morbid anxiety disorders or as an augmentation strategy added to SSRIs remains to be determined.

Adult↗
PubMed2003

Co-use of donepezil and hypnotics among Alzheimer's disease patients living in the community.

BACKGROUND: In clinical trials, sleep problems have been identified as side effects of donepezil, an acetylcholinesterase (AChE)-inhibiting medication for the treatment of Alzheimer's disease (AD). Poor sleep quality can exacerbate behavior problems among patients and add to the burden experienced by their caregivers. We examined the relationship between co-use of donepezil and hypnotics in a large sample of persons with AD living in the community. METHOD: This secondary data analysis used cross-sectional subjects from a multiwave, consumer-based survey of AD caregivers conducted in 1997 and 1998. Rates of hypnotic use among users and non-users of donepezil were compared using chi-square analysis for independent samples, and multivariate logistic regression was used to identify significant independent correlates of hypnotic use. RESULTS: A total of 2638 caregivers completed at least 1 study wave. Use of hypnotics was higher in the donepezil subgroup (9.78%) compared with subjects not taking this medication (3.93%). Multivariate analysis demonstrated that donepezil use was independently linked to increased hypnotic use after controlling for the potential confounding effects of disruptive behavior and depressive symptoms (adjusted odds ratio = 3.34, p <.001). CONCLUSION: In this large community sample, donepezil use was statistically linked to increased hypnotic use. Because sleep quality may be a critical issue for persons with AD and their caregivers, more rigorous evaluation of sleep problems linked to AChE-inhibitor treatment is indicated.

Aged↗
PubMed2003

The ups and downs of novel antiemetic drugs, part 1: substance P, 5-HT, and the neuropharmacology of vomiting.

ISSUE: Novel antiemetic agents such as the newly approved aprepitant (Emend) target receptors for substance P, known as neurokinin-1 (NK(1)) receptors. When NK(1) receptors are blocked in the vomiting center of the brainstem, chemotherapy-induced emesis is reduced. It is possible that blocking NK(1) receptors elsewhere in the CNS will lead to therapeutic actions in depression and other stress-related disorders.

Antiemetics↗
PubMed2003

The ups and downs of novel antiemetic drugs, part 2: an illustration.

ISSUE: Novel antiemetic drugs block either neurokinin-1 receptors or serotonin-3 receptors. Research into the neuropharmacology of vomiting is providing insight into the ways substance P and serotonin interact within the central nervous system that could lead to additional applications of neurokinin-1 antagonists for the treatment of depression and stress.

Antiemetics↗
PubMed2003

Neurotransmission of cognition, part 3. Mechanism of action of selective NRIs: both dopamine and norepinephrine increase in prefrontal cortex.

ISSUE: Selective norepinephrine reuptake inhibitors exploit the fact that dopamine transporters are absent in prefrontal cortex, so dopamine has to hitchhike a ride on the norepinephrine transporter in order to be inactivated. Thus, blocking norepinephrine transporters leads to an increase in both dopamine and norepinephrine levels in prefrontal cortex as well as improvement in cognition in attention-deficit/hyperactivity disorder.

Adrenergic Uptake Inhibitors↗
PubMed2002

Comparative efficacy between venlafaxine and SSRIs: a pooled analysis of patients with depression.

BACKGROUND: Serotonergic and adrenergic enhancement may be synergistic and more effective than serotonergic enhancement alone in treating depression. The dual serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine is a dual reuptake inhibitor that may therefore offer greater efficacy than selective serotonin reuptake inhibitors (SSRIs). METHODS: Data from eight randomized, double-blind, controlled studies were pooled to compare efficacy in depressed patients receiving venlafaxine/venlafaxine extended release (XR), SSRIs, or placebo for </=8 weeks. The mean changes from baseline in the 21-item Hamilton Rating Scale for Depression (HAM-D(21)), Montgomery-Asberg Depression Rating Scale (MADRS), and Clinical Global Impressions-Global Improvement (CGI-I) and CGI-Severity of Illness (CGI-S) item scores were compared, as were response rates derived from these scales. RESULTS: Statistically significant differences in mean HAM-D(21) score decrease between venlafaxine (14.5) and SSRIs (12.6) and between the active treatments and placebo (11.3) were observed. Venlafaxine significantly decreased the mean MADRS scores more than SSRIs (17.8 vs. 15.9), and both treatments were significantly better than placebo (12.9). The same pattern of significance for CGI-I, HAM-D(21), and MADRS response rates between venlafaxine (71%, 64%, and 67%, respectively), SSRIs (64%, 57%, and 59%, respectively), and placebo (50%, 42%, and 41%, respectively) was observed. CONCLUSIONS: Venlafaxine was significantly more effective than SSRIs in improving depression, perhaps due to enhancing both serotonin and norepinephrine.

Adult↗
PubMed2002

Some relationships among assessments of depression.

The Directions program provides an administratively efficient method to screen for psychological disorders in a primary-care setting (FOCUS), confirm the need for treatment, and monitor progress (COMPASS-PC). The instruments are psychometrically sound and grounded in an established theory of mental-health treatment. The present study reports the relationships between FOCUS, COMPASS-PC, and the Hamilton Depression scale for a sample of patients who have been diagnosed as major depressive disorder, dysthymia, or depressive syndrome by standardized criteria (i.e., SCID-IV and DSM-IV). Moreover, Focus and COMPASS-PC are evaluated for their ability to detect depression as defined by SCID-IV and DSM IV. Furthermore, we examine the relationship between the different instruments in their ability to measure response to treatment over time.

Adult↗
PubMed2002

Effects of reboxetine on anxiety, agitation, and insomnia: results of a pooled evaluation of randomized clinical trials.

Several recent clinical trials have established that reboxetine, a new selective norepinephrine reuptake inhibitor (selective NRI), is effective and safe for the treatment of major depression. However, the effects of reboxetine on specific symptoms of anxiety, agitation, and insomnia have not been reported. Data were obtained from nine short-term, double-blind, randomized clinical trials in patients with major depression. After initial titration, patients received reboxetine 8 to 10 mg per day. The effects on specific HAM-D symptoms of agitation, anxiety, and insomnia were compared between reboxetine-and placebo-treated patients. In addition, the incidence of treatment-emergent agitation, anxiety, and insomnia side effects with reboxetine were examined. Compared with placebo, the proportion of patients with improvement on the HAM-D agitation item and the HAM-D anxiety and insomnia factors from baseline was significantly greater with reboxetine at most assessment intervals. In general, the incidence of agitation-or anxiety-related side effects was comparable with reboxetine and placebo. Although reboxetine was associated with a significant (p < 0.05) increase in treatment-emergent insomnia reported as an adverse effect during the first week of treatment, very few reports of insomnia were made at subsequent evaluations. The incidence of treatment-emergent agitation or anxiety was comparable between treatment groups.

Adult↗
PubMed2002

The psychopharmacology of energy and fatigue.

ISSUE: Second only to depressed mood itself tiredness, low energy, and listlessness are the most common symptoms associated with depression. Recent understanding of interactions between monoaminergic neurons may help explain why some antidepressants may be more rapidly energy restoring than others.

Antidepressive Agents↗
PubMed2002

Selective actions on sleep or anxiety by exploiting GABA-A/benzodiazepine receptor subtypes.

The next generation of anxiolytics may be subtype-selective partial agonists at GABA-A receptors. By exploiting new psychopharmacologic principles, such as the targeting of receptor subtypes that have unique subunits and the partial activation of these subtypes with stabilizers, we may eventually have anxiolytics that are rapid acting, but without sedation, amnesia, or dependence.

Acetamides↗
PubMed2002

Does depression hurt?

Depression is an illness that causes symptoms in both the body and the brain, i.e., painful physical as well as emotional and vegetative symptoms. Ascending serotonergic and noradrenergic pathways may mediate the emotional and vegetative symptoms of depression and can potentially be targets of serotonin and norepinephrine reuptake inhibitors to obtain relief of these symptoms. Descending serotonergic and noradrenergic pathways may regulate the painful physical symptoms of depression, and when targeted by serotonin and norepinephrine reuptake inhibitors, relieve these symptoms as well. Selective serotonin reuptake inhibitors have a remission rate of 35%, and dual-action reuptake inhibitors have a 45% remission rate. Despite these results, the best treatment of depression currently recognizes the 3 types of symptoms and targets them all for complete remission no matter which drug is used.

Affective Symptoms↗