Me apresuro a reirme de todo, ante el miedo de ser obligado a llorar por ello.
Δομήνικος Θεοτοκόπουλος , Sagrada Familia con Santa Ana, 1590.
The induction of mania by antidepressant treatments is often cited as support for a mood disorder dichotomy. When tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) were introduced, concepts of unipolar and bipolar depression were not in use, so that the treatment was oVered to all patients who met criteria for a depressive episode.
Manic episodes that appeared during the course of treatment were interpreted as a medication side-eVect. The reports did not recognize a personal history of mania nor cycling into mania as natural features of a depressive mood disorder. No direct experimental studies of this eVect were offered. After reviewing the literature of induced mania with antidepressant treatments, Goodwin and Jamison (1990) concluded:
In summary, absolutely incontrovertible evidence of antidepressant induced mania and cyclic induction is still lacking . . .
The available evidence strongly suggests, however, that antidepressant drugs can precipitate mania in some bipolar-I patients, especially those who respond to antidepressants, and that some bipolar-II patients appear to be vulnerable to hypomania while taking antidepressants. Although antidepressant-induced rapid cycling does occur in some patients, its frequency is not easy to determine, and therefore, the generalizability of the observation is unclear.
Since that review, little new evidence has been published. Assessments of the incidence of manic episodes in patients with depression oVer the conclusion that 10–15% will have a manic or hypomanic episode in the next decade. The reports recognize that the patients most likely to do so have a history of depressive disorders early in life or an initial psychotic depression or melancholia.
Cross-sectional clinical features do not distinguish a first recurrent depression from the initial depression in a manicdepressive course. A review of the databases of several pharmaceutical companies reported that the switch in unipolar patients was 11.2% for TCA, 3.7% for selective serotonin reuptake inhibitors (SSRIs), and 4.2% for placebo.
The Stanley Foundation bipolar network assessed the spontaneous and treatmentassociated switch rates in patients with bipolar depression. In a group of 258 outpatients examined for 1 year, the number of days depressed was three times greater than the number of days manic.
In a second study, 127 bipolar depressed patients were randomized to 10 weeks of augmentation of mood stabilizers with the non-TCAs bupropion, sertraline, or venlafaxine. They reported that 9.1% were associated with switches to hypomania. In 73 continuation-phase antidepressant trials, 16–19% were associated with manic and hypomanic switches. Despite the low switch rates that did not exceed natural switch rates in manic-depressive patients, the authors conclude that depression and depressive cycling are a substantial problem in intensively treated bipolar outpatients.
A consequence of the belief in the risks of antidepressant drugs is the intensive search for alternative treatments for bipolar depression. While the efficacy of lithium for the manic phase is established, its merits as an antidepressant received mixed reviews. The introduction of carbamazepine for mania encouraged a belief that mania resulted from the kindling of abnormal seizure-like activity and started a search for anticonvulsants as treatments for bipolar disorder.
Several anticonvulsants are now recommended as ‘‘mood stabilizers’’ in the long-term management of bipolar depression. The relatively weak therapeutic eVect of anticonvulsants as mood stabilizers, however, is reflected in the recommended algorithms requiring a complex polypharmacy of mood stabilizers, SSRI antidepressants, antipsychotic agents, and benzodiazepine sedatives for reasonable efficacy. Another tactic has been to recommend the combination of newly introduced agents such as olanzapine– fluoxetine. A more formal dependence on psychotherapy, now presented as psychoeducation, is also offered.
To optimize a treatment strategy for clinical practice, the National Institute for Mental Health has recently contracted with a consortium of medical centers to test a complex algorithm known as the STEP-BD. Despite the absence of experimental evidence, trials of antimanic agents among bipolar patients often cite drug-induced cycling, without accounting for natural cycling rates as a justification for the use of these agents.
Manic episodes that appeared during the course of treatment were interpreted as a medication side-eVect. The reports did not recognize a personal history of mania nor cycling into mania as natural features of a depressive mood disorder. No direct experimental studies of this eVect were offered. After reviewing the literature of induced mania with antidepressant treatments, Goodwin and Jamison (1990) concluded:
In summary, absolutely incontrovertible evidence of antidepressant induced mania and cyclic induction is still lacking . . .
The available evidence strongly suggests, however, that antidepressant drugs can precipitate mania in some bipolar-I patients, especially those who respond to antidepressants, and that some bipolar-II patients appear to be vulnerable to hypomania while taking antidepressants. Although antidepressant-induced rapid cycling does occur in some patients, its frequency is not easy to determine, and therefore, the generalizability of the observation is unclear.
Since that review, little new evidence has been published. Assessments of the incidence of manic episodes in patients with depression oVer the conclusion that 10–15% will have a manic or hypomanic episode in the next decade. The reports recognize that the patients most likely to do so have a history of depressive disorders early in life or an initial psychotic depression or melancholia.
Cross-sectional clinical features do not distinguish a first recurrent depression from the initial depression in a manicdepressive course. A review of the databases of several pharmaceutical companies reported that the switch in unipolar patients was 11.2% for TCA, 3.7% for selective serotonin reuptake inhibitors (SSRIs), and 4.2% for placebo.
The Stanley Foundation bipolar network assessed the spontaneous and treatmentassociated switch rates in patients with bipolar depression. In a group of 258 outpatients examined for 1 year, the number of days depressed was three times greater than the number of days manic.
In a second study, 127 bipolar depressed patients were randomized to 10 weeks of augmentation of mood stabilizers with the non-TCAs bupropion, sertraline, or venlafaxine. They reported that 9.1% were associated with switches to hypomania. In 73 continuation-phase antidepressant trials, 16–19% were associated with manic and hypomanic switches. Despite the low switch rates that did not exceed natural switch rates in manic-depressive patients, the authors conclude that depression and depressive cycling are a substantial problem in intensively treated bipolar outpatients.
A consequence of the belief in the risks of antidepressant drugs is the intensive search for alternative treatments for bipolar depression. While the efficacy of lithium for the manic phase is established, its merits as an antidepressant received mixed reviews. The introduction of carbamazepine for mania encouraged a belief that mania resulted from the kindling of abnormal seizure-like activity and started a search for anticonvulsants as treatments for bipolar disorder.
Several anticonvulsants are now recommended as ‘‘mood stabilizers’’ in the long-term management of bipolar depression. The relatively weak therapeutic eVect of anticonvulsants as mood stabilizers, however, is reflected in the recommended algorithms requiring a complex polypharmacy of mood stabilizers, SSRI antidepressants, antipsychotic agents, and benzodiazepine sedatives for reasonable efficacy. Another tactic has been to recommend the combination of newly introduced agents such as olanzapine– fluoxetine. A more formal dependence on psychotherapy, now presented as psychoeducation, is also offered.
To optimize a treatment strategy for clinical practice, the National Institute for Mental Health has recently contracted with a consortium of medical centers to test a complex algorithm known as the STEP-BD. Despite the absence of experimental evidence, trials of antimanic agents among bipolar patients often cite drug-induced cycling, without accounting for natural cycling rates as a justification for the use of these agents.
publié par C.R. à
7:48 AM
<< Accueil