Subject(s)
Analgesics/therapeutic use , Calcium Channels/drug effects , Neuralgia/drug therapy , gamma-Aminobutyric Acid/analogs & derivatives , Analgesics/adverse effects , Central Nervous System/drug effects , Clinical Trials as Topic , Humans , Low Back Pain/drug therapy , Low Back Pain/etiology , Neuralgia/etiology , Pain Measurement , Pregabalin , Prospective Studies , Radiculopathy/drug therapy , Radiculopathy/etiology , Treatment Outcome , gamma-Aminobutyric Acid/adverse effects , gamma-Aminobutyric Acid/therapeutic useABSTRACT
This study aims to determine whether the newly introduced serotonin type 2 (5-HT2) antagonist nefazodone has serotonin (5-HT) transporter-blocking properties at clinical doses in depressed patients. Change in platelet 5-HT was used as an index of the cumulative peripheral 5-HT uptake blockade produced by nefazodone and selective serotonin reuptake inhibitors (SSRIs). Platelet 5-HT was measured before and during treatment with nefazodone (N = 6) or an SSRI (N = 10) in patients with major depression. Corresponding Hamilton Rating Scale for Depression (HAM-D) scores were also obtained over the course of the study. The results of the study demonstrated that the decrease from mean baseline platelet 5-HT after SSRI treatment was significantly greater than the change after nefazodone treatment (-88% vs. -3%; Mann-Whitney U-test, p = 0.0002). Pretreatment platelet 5-HT level, posttreatment platelet 5-HT level, nor the percent decrease in platelet 5-HT correlated with the percent change in HAM-D scores in either treatment group. In conclusion, therapeutic doses of nefazodone do not cause sustained 5-HT uptake inhibition at the platelet 5-HT transporter.