Therapy-resistant depressions: biochemical and pharmacological considerations.
Two statements are presented here: 1) antidepressants increase the amount of MA at the central receptors, and 2) antidepressants are effective in some, but quite ineffective in other patients, even if they belong to the same diagnostic category. Three questions result from these statements: 1) Does a central MA deficiency occur in depressive patients? 2) If so, is this disorder present in only a proportion of the patients? 3) If so, can this explain the apparent selectivity of antidepressants in the sense that particularly MA-deficient patients benefit from this type of therapy? A tentative answer is given to these three questions. In depressive patients the cerebral MA turnover can be diminished. These disorders do not occur in all patients but seem to be confined to certain categories of depression. Diminution or non-diminution of the central MA turnover is a (not the) factor which determines whether antidepressant medication will succeed or fail. The theoretical and practical implications of these answers are discussed.
D000275:Adjustment Disorders / Q000378:metabolism; D000928:Antidepressive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001921:Brain / Q000378:metabolism; D003863:Depression / Q000134:cerebrospinal fluid / Q000188:drug therapy* / Q000378:metabolism; D004351:Drug Resistance; D006719:Homovanillic Acid / Q000134:cerebrospinal fluid; D006801:Humans; D006897:Hydroxyindoleacetic Acid / Q000134:cerebrospinal fluid; D008995:Monoamine Oxidase / Q000172:deficiency / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D011339:Probenecid; D011955:Receptors, Drug / Q000187:drug effects; D012701:Serotonin / Q000378:metabolism
D000928:Antidepressive Agents; D011955:Receptors, Drug; D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D008995:Monoamine Oxidase; D011339:Probenecid; D009638:Norepinephrine; D006719:Homovanillic Acid