PubMed Health⌕ Search

Biomedical subjects

S M Stahl

Publications and source records attributed to S M Stahl.

At least 19 recordsLinked to original sources
PubMed2007

Negative symptoms of schizophrenia: a problem that will not go away.

OBJECTIVE: Negative symptoms of schizophrenia are a common, enduring, and debilitating component of the psychopathology of schizophrenia. Although efforts thus far to elucidate a distinct schizophrenia subtype based upon negative symptoms have yielded mixed results, there are nevertheless neurobiological correlates of the negative symptom typology. METHOD: A review of nosology, typology, and assessment tools for determining core negative symptoms in schizophrenia. RESULTS: Negative symptoms can be difficult to evaluate objectively. Current rating scales 'capture' key domains of negative symptoms, in spite of considerable overlap between these domains. However, each objective assessment trades off methodological rigor and detail against brevity of assessment and ease of use. CONCLUSION: The description of new methods for measuring these devastating symptoms, coupled with the ongoing development of novel antipsychotics and agents that augment antipsychotics have fuelled renewed interest in the evaluation of negative symptoms and optimism that better treatments for negative symptoms can be found.

Activities of Daily Living↗
PubMed2004

A critical review of atypical antipsychotic utilization: comparing monotherapy with polypharmacy and augmentation.

The atypical antipsychotics risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole have become first-line treatment for schizophrenia because they reduce the positive symptoms of psychosis but do not have a high incidence of extrapyramidal symptoms. However, these agents, like other antipsychotics, may take as long as 16 or more weeks to produce a response, and even with prolonged treatment are unlikely to evoke responses greater than 50% improvement in symptoms. This has led to the experimental use of high atypical antipsychotic doses, antipsychotic polypharmacy, and augmentation with other psychotropic drugs, all of which occur commonly in clinical practice. This article reviews the current evidence for these increasingly common means of treating schizophrenia and psychosis, with particular emphasis on polypharmacy and augmentation. To date, there are only two controlled studies of antipsychotic polypharmacy involving an atypical antipsychotic; the rest of the data are uncontrolled trials and case reports that describe a mixture of positive and negative findings. One multicenter, double-blind trial shows a faster onset of action when divalproex is added to risperidone or olanzapine than with antipsychotic monotherapy. A small double-blind study demonstrates efficacy when lamotrigine is added to clozapine. The rest of the data on augmentation with anticonvulsants are uncontrolled, and most report adverse effects. With the exception of divalproex, there are currently no compelling data to justify the use of antipsychotic polypharmacy or augmentation. Existing evidence suggests that the best treatments for schizophrenia and psychosis may be long-term trials of a sequence of atypical antipsychotic monotherapies at therapeutic doses.

Acetates↗
PubMed2001

Effectiveness of St John's wort in major depression: a randomized controlled trial.

CONTEXT: Extracts of St John's wort are widely used to treat depression. Although more than 2 dozen clinical trials have been conducted with St John's wort, most have significant flaws in design and do not enable meaningful interpretation. OBJECTIVE: To compare the efficacy and safety of a standardized extract of St John's wort with placebo in outpatients with major depression. DESIGN AND SETTING: Randomized, double-blind, placebo-controlled clinical trial conducted between November 1998 and January 2000 in 11 academic medical centers in the United States. PARTICIPANTS: Two hundred adult outpatients (mean age, 42.4 years; 67.0% female; 85.9% white) diagnosed as having major depression and having a baseline Hamilton Rating Scale for Depression (HAM-D) score of at least 20. INTERVENTION: Participants completed a 1-week, single-blind run-in of placebo, then were randomly assigned to receive either St John's wort extract (n = 98; 900 mg/d for 4 weeks, increased to 1200 mg/d in the absence of an adequate response thereafter) or placebo (n = 102) for 8 weeks. MAIN OUTCOME MEASURES: The primary outcome measure was rate of change on the HAM-D over the treatment period. Secondary measures included the Beck Depression Inventory (BDI), Hamilton Rating Scale for Anxiety (HAM-A), the Global Assessment of Function (GAF) scale, and the Clinical Global Impression-Severity and -Improvement scales (CGI-S and CGI-I). RESULTS: The random coefficient analyses for the HAM-D, HAM-A, CGI-S, and CGI-I all showed significant effects for time but not for treatment or time-by-treatment interaction (for HAM-D scores, P<.001, P =.16, and P =.58, respectively). Analysis of covariance showed nonsignificant effects for BDI and GAF scores. The proportion of participants achieving an a priori definition of response did not differ between groups. The number reaching remission of illness was significantly higher with St John's wort than with placebo (P =.02), but the rates were very low in the full intention-to-treat analysis (14/98 [14.3%] vs 5/102 [4.9%], respectively). St John's wort was safe and well tolerated. Headache was the only adverse event that occurred with greater frequency with St John's wort than placebo (39/95 [41%] vs 25/100 [25%], respectively). CONCLUSION: In this study, St John's wort was not effective for treatment of major depression.

Adult↗
PubMed2001

Reemergence of sexual dysfunction in patients with major depressive disorder: double-blind comparison of nefazodone and sertraline.

BACKGROUND: Several different classes of antidepressants have been associated with sexual adverse effects. This double-blind, randomized trial compared the effects of nefazodone and sertraline on reemergence of sexual dysfunction in depressed patients who had experienced sexual dysfunction as a result of sertraline treatment. Depressive symptoms were also monitored. METHOD: One hundred five patients with DSM-III-R major depressive episode who were experiencing sexual dysfunction attributable to sertraline (100 mg/day) were screened for entry. Eligible patients entered a 1-week washout period that was followed by a 7- to 10-day single-blind placebo phase. Patients without symptoms of sexual dysfunction at the end of the single-blind placebo phase were randomly assigned to receive double-blind treatment with either nefazodone (400 mg/day) or sertraline (100 mg/day) for 8 weeks. RESULTS: Nearly 3 times more sertraline-treated patients (76%; 25/33) experienced reemergence of sexual dysfunction (ejaculatory and/or orgasmic difficulty) than did nefazodone-treated patients (26%; 10/39) (p < .001). In addition, patients treated with nefazodone were more satisfied with their sexual functioning than were patients treated with sertraline. Both treatment groups demonstrated a similar and sustained improvement in depressive symptoms. Both drugs were well tolerated, and the overall incidence of adverse reactions was similar for both treatment groups; however, 9 sertraline-treated patients (26%) discontinued because of adverse events compared with 5 nefazodone-treated patients (12%). Of the patients discontinuing therapy for adverse events, 5 of the sertraline-treated patients did so because of sexual dysfunction reported as an adverse event, whereas only 1 of the nefazodone-treated patients discontinued therapy secondary to sexual dysfunction. CONCLUSION: In this sample of patients with major depression who had recovered from sexual dysfunction induced by treatment with sertraline, nefazodone treatment resulted in significantly less reemergence of sexual dysfunction than did renewed treatment with sertraline and provided continued antidepressant activity.

Adolescent↗
PubMed2001

Natural estrogen as an antidepressant for women.

Recent well-controlled studies suggest that estrogen has antidepressant actions in perimenopausal women. Estrogen may also have antidepressant actions in postpartum women and across the life cycle for women who are resistant to treatment with various antidepressants. The question, however, of which depressed women to treat with antidepressants, which with estrogen, and which with both remains unanswered.

Adolescent↗
PubMed2001

"Hit-and-run" actions at dopamine receptors, part 1: Mechanism of action of atypical antipsychotics.

Either 5-HT2A antagonism or fast dissociation from D2 receptors may define an atypical antipsychotic. To have little or no motor symptoms from an antipsychotic, it is clear that D2 receptor binding in the striatum must be less than that caused by conventional antipsychotics. Pure 5-HT2A antagonism by itself does not result in robust antipsychotic actions. However, 5-HT2A antagonism can reduce D2 antagonism and thereby reduce motor symptoms without reversing antipsychotic actions. If, however, this 5-HT2A antagonism is overwhelmed by too much D2 antagonism, it cannot result in such atypical antipsychotic actions. Another route to reducing D2 receptor binding appears to be to shorten binding time, also known as rapidly dissociating from the D2 receptor. Many of the agents with atypical antipsychotic clinical properties hit the D2 receptor hard enough to cause antipsychotic effects and then run before they cause extrapyramidal side effects.

Antipsychotic Agents↗