Analysis of information sources in references of the Wikipedia article "Selective serotonin reuptake inhibitor" in English language version.
The commonly used method of estimating the 'response' to drug treatment in clinical trials of antidepressants (arbitrarily set at a 50% reduction in symptoms), involves the categorisation of continuous data from symptom scales, and therefore does not provide an independent arbiter of clinical significance. Moreover, this method can exaggerate small differences between interventions such as antidepressants and placebo [28], and statisticians note that it can distort data and should be avoided [29], [30]. Response rates in double-blind antidepressant trials are typically about 50% in the drug groups and 35% in the placebo groups (e.g., [31], [32]). This 15% difference is often defended as clinically significant because 15% of depressed people who get better on antidepressants would not have gotten better on a placebo. However, a 50% reduction in symptoms is close to the mean and median of drug improvement rates in placebo-controlled antidepressant trials [31], [32], [33] and thus near the apex of the distribution curve. Thus, with an SD of 8 in change scores, a 15% difference in response rates is about (an odds ratio of 1.86, a relative risk of 0.77, and an NNT of 7) is exactly what one would expect from a mean 3-point difference in HAM-D scores [28]. Lack of response does not mean that the patient has not improved; it means that the improvement has been less, by as little as one point, than the arbitrary criterion chosen for defining a therapeutic response.
Another common flaw is to report efficacy based on drug-placebo differences in response and remission rates (27). To come at binary constructs such as response and remission, continuous symptom rating scales are dichotomized along arbitrary cut-offs. However, methodologists have vigorously advised against the use of dichotomization (28–30) because it produces, among others, systematically inflated effect sizes (31–33).
Buspirone, a non-benzodiazepine anxiolytic, have even demonstrated enhancement of sexual function in certain individuals. For this reason, they have been proposed as augmentation agents (antidotes) or substitution agents in patients with emerging sexual dysfunction after treatment with antidepressants.
There is still no definitive treatment for PSSD. Low-power laser irradiation and phototherapy have shown some promising results.
The commonly used method of estimating the 'response' to drug treatment in clinical trials of antidepressants (arbitrarily set at a 50% reduction in symptoms), involves the categorisation of continuous data from symptom scales, and therefore does not provide an independent arbiter of clinical significance. Moreover, this method can exaggerate small differences between interventions such as antidepressants and placebo [28], and statisticians note that it can distort data and should be avoided [29], [30]. Response rates in double-blind antidepressant trials are typically about 50% in the drug groups and 35% in the placebo groups (e.g., [31], [32]). This 15% difference is often defended as clinically significant because 15% of depressed people who get better on antidepressants would not have gotten better on a placebo. However, a 50% reduction in symptoms is close to the mean and median of drug improvement rates in placebo-controlled antidepressant trials [31], [32], [33] and thus near the apex of the distribution curve. Thus, with an SD of 8 in change scores, a 15% difference in response rates is about (an odds ratio of 1.86, a relative risk of 0.77, and an NNT of 7) is exactly what one would expect from a mean 3-point difference in HAM-D scores [28]. Lack of response does not mean that the patient has not improved; it means that the improvement has been less, by as little as one point, than the arbitrary criterion chosen for defining a therapeutic response.
Another common flaw is to report efficacy based on drug-placebo differences in response and remission rates (27). To come at binary constructs such as response and remission, continuous symptom rating scales are dichotomized along arbitrary cut-offs. However, methodologists have vigorously advised against the use of dichotomization (28–30) because it produces, among others, systematically inflated effect sizes (31–33).
Buspirone, a non-benzodiazepine anxiolytic, have even demonstrated enhancement of sexual function in certain individuals. For this reason, they have been proposed as augmentation agents (antidotes) or substitution agents in patients with emerging sexual dysfunction after treatment with antidepressants.
There is still no definitive treatment for PSSD. Low-power laser irradiation and phototherapy have shown some promising results.
Another common flaw is to report efficacy based on drug-placebo differences in response and remission rates (27). To come at binary constructs such as response and remission, continuous symptom rating scales are dichotomized along arbitrary cut-offs. However, methodologists have vigorously advised against the use of dichotomization (28–30) because it produces, among others, systematically inflated effect sizes (31–33).
