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Biomedical subjects

S M Stahl

Publications and source records attributed to S M Stahl.

At least 19 recordsLinked to original sources
PubMed1999

Safety profile of sustained-release bupropion in depression: results of three clinical trials.

This series of studies was undertaken to assess the safety profile of sustained-release (SR) bupropion in the treatment of depressed outpatients. Adults with a diagnosis of major depression were evaluated in 1 of 3 multicenter, randomized, double-masked, parallel-group, placebo-controlled trials conducted in private-practice psychiatric outpatient clinics. Following a 1-week, single-masked, placebo lead-in period, patients received bupropion SR for 8 weeks (study 1: 150 or 300 mg/d; study 2: 100, 200, 300, or 400 mg/d; study 3: 50 to 150 or 100 to 300 mg/d). Safety assessments included monitoring adverse events, patient discontinuation rates, changes in weight, vital signs, and clinical laboratory test results. Across studies, the most frequently reported adverse events were headache, dry mouth, and nausea. The incidence of adverse events was similar (< or =5% difference) between the bupropion SR and placebo groups, with the exception of dry mouth (bupropion SR, 16%; placebo, 7%). Dry mouth, nausea, and insomnia occurred significantly more often in bupropion SR-treated patients than in patients who received placebo (P<0.05). Nearly all (94% to 99%) adverse events reported in these studies were mild or moderate. Less than 10% of patients in either group discontinued treatment prematurely because of adverse events, and no deaths or serious drug-related adverse events were reported. Sexual dysfunction was reported as an adverse event by <1% of patients in either group. Bupropion SR was associated with dose-related weight loss in all 3 studies. No consistent patterns of change were observed in vital signs or in the results of clinical laboratory tests. Data from these 3 clinical trials demonstrate the favorable safety profile of bupropion SR in the treatment of depressed outpatients.

Adolescent↗
PubMed1999

Substance P and the neurokinins: novel peptide neurotransmitters in psychopharmacology.

A new neurotransmitter system is a family of 3 related peptides known as neurokinins. The best known of these is substance P. The others are known simply as neurokinin A and neurokinin B. The specific receptor subtypes that correspond to these 3 neurokinins are neurokinin 1 receptors for substance P, neurokinin 2 receptors for neurokinin A, and neurokinin 3 receptors for neurokinin B. These neurotransmitters appear to play a key role in the regulation of emotions, and antagonists of their receptors may be novel psychotropic drugs of the future.

Humans↗
PubMed1999

Antipsychotic polypharmacy, Part 1: Therapeutic option or dirty little secret?

Antipsychotic polypharmacy is a surprisingly frequent occurrence that can be both justified and unjustifed, depending on how it is used. To the extent that this phenomenon has been unrecognized and is not being studied, it is a "dirty little secret." To the extent that careful clinicians have uncovered a useful strategy for boosting the effectiveness of available antipsychotic monotherapies, it represents an opportunity to improve the outcomes of patients with psychotic illnesses.

Antipsychotic Agents↗
PubMed1999

Molecular neurobiology for practicing psychiatrists, part 2: how neurotransmitters activate second messenger systems.

Chemical neurotransmission begins when receptor occupancy by a neurotransmitter is converted into an intracellular second messenger that carries the information from the neurotransmitter deep into the target neuron. For clinicians, it is this transfer of neurotransmitter information all the way to the genome that hypothetically explains the therapeutic actions of many psychotropic drugs. This also accounts for why drugs that modify neurotransmission may take time to fully develop their clinical actions.

GTP-Binding Proteins↗
PubMed1999

Selecting an atypical antipsychotic by combining clinical experience with guidelines from clinical trials.

Three atypical antipsychotics are currently considered to be first-line therapies for schizophrenia, namely risperidone, olanzapine, and quetiapine. Deciding which one of these agents to choose for any given patient can be a daunting task because head-to-head comparisons of these 3 agents are just beginning, and most published trials are comparisons with typical antipsychotics, not with another atypical antipsychotic. Furthermore, results from clinical trials often do not match findings from clinical practice. Thus, guidelines for selection and use of the atypical antipsychotics are evolving from controlled studies as well as from clinical judgment based on the practical use of these agents once they have entered clinical practice. The atypical properties of first-line atypical antipsychotics as well as clozapine are reviewed here, with clinical pearls and dosing tips for each based upon a consensus of information from both clinical trials and clinical practice. The conventional antipsychotic loxapine is also reviewed and proposed as a potentially valuable agent to augment atypical antipsychotics when patients do not experience an acceptable treatment response from monotherapy with an atypical antipsychotic. By integrating information from clinical trials and clinical practice, the prescriber can be in a better position to choose which atypical antipsychotic to select for any given patient.

Animals↗
PubMed1999

Molecular neurobiology for practicing psychiatrists, part 3: how second messengers "turn on" genes by activating protein kinases and transcription factors.

One of the most important advances in molecular neurobiology of relevance to the practicing psychiatrist is how an intracellular second messenger can "turn on" genes by activating first a protein kinase enzyme and then a transcription factor. Failure to turn on the right genes may lead to psychiatric illnesses. Causing the appropriate genes to turn on may be the therapeutic mechanism of action of many current and future psychotropic drugs.

Enzyme Activation↗
PubMed1999

Molecular neurobiology for practicing psychiatrists, part 4: transferring the message of chemical neurotransmission from presynaptic neurotransmitter to postsynaptic gene expression.

Neurotransmitters activate genes in their target neurons by precipitating a molecular cascade, which may be the ultimate consequence of chemical neurotransmission. When this transfer is aberrant, a mental disorder may be manifest. When drugs act upon neurons to change gene expression, this could lead to therapeutic actions, side effects, and the long-term consequences of drug abuse.

Gene Expression↗
PubMed1998

Cholinesterase inhibitors for Alzheimer's disease.

New cholinesterase inhibitors capable of slowing the progression of Alzheimer's disease are being introduced at a rapid pace. In prescribing these drugs and setting realistic expectations for outcome, it is necessary to understand that they affect cholinergic activity in other tissues as well as the brain. They may be most effective when used in combination with other drugs.

Alzheimer Disease↗