Pramipexole in treatment‐resistant depression: a 16‐week naturalistic study

Lattanzi, Lorenzo; Dell’Osso, Liliana; Cassano, Paolo; Pini, Stefano; Rucci, Paola; Houck, Patricia R.; Gemignani, A.; Battistini, Giulia; Bassi, A.; Abelli, Marianna; Cassano, Giovanni Battista

doi:10.1034/j.1399-5618.2002.01171.x

Cited by 129 publications

(68 citation statements)

References 21 publications

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“…We reported previously a 68% response rate to pramipexole augmentation in patients with TRD treated for up to 16 weeks [Lattanzi et al, 2002]. In the present study, we report rates of sustained remission and depressive recurrence with pramipexole, in TRD patients treated up to 1 year.…”

Section: Introductionsupporting

confidence: 57%

Pramipexole in treatment-resistant depression: An extended follow-up

et al. 2004

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We evaluated the long-term antidepressant safety and response of adjunctive pramipexole, a D2-D3 dopamine agonist, in the course of drug-resistant depression. Twenty-three patients with treatment-resistant major depressive episode (MDE) were followed up after a 16-week pramipexole add-on trial. Pramipexole was added to current treatment with TCA or SSRI, at increasing doses from 0.375-1.500 mg/day. The LIFE scale was administered at baseline of the acute trial, at Weeks 16, 32, and 48. Patients were analyzed for sustained remission (score=<2 at LIFE for at least 8 weeks) and recurrence (after remission score > =3 at LIFE for at least 2 weeks) of depression. Of 23 patients, 12 had major depression and 11 had bipolar depression (16 women; mean age=52.8 years). Mean age of onset and median duration of current MDE were 35.1 years and 6 months, respectively; all subjects had at least two prior MDEs. Mean pramipexole dose was 0.990 mg/day. Median duration of follow-up was 28 weeks. Mean baseline MADRS and CGI-S scores were 33.7+/-8.4 (sd) and 4.6+/-0.8, respectively. Median time to sustained remission from baseline was 10 weeks and overall 60.9% (14/23) of subjects recovered within Week 22. Recurrence of depression occurred in 35.7% (5/14) of remitters after Week 24 and within Week 28 from remission. Although there were no sleep attacks, two cases of hypomania and one case of psychotic mania occurred at Weeks 22, 24, and 30, respectively. Pramipexole augmentation of antidepressant treatment was relatively safe and presumably effective in the long-term course of treatment resistant depression.

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Section: Introductionsupporting

confidence: 57%

Pramipexole in treatment-resistant depression: An extended follow-up

et al. 2004

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“…Since pramipexole, a D 2 R/D 3 R agonist, is an effective treatment for depression in humans (Lattanzi et al, 2002;Ostow, 2002) and the antidepressants bupropion and nortriptyline have been used as aids for smoking cessation, as is proposed for BP 897 (Le Foll et al, 2003a), we used a forced swimming test to assess the potential anti-depressant-like effects of BP 897 that may have contributed to its blockade of expression of nicotine-induced CPP. This test is sensitive to the effects of bupropion (Cooper et al, 1980) and other antidepressant drugs (Porsolt et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

Dopamine D3 Receptor Ligands Block Nicotine-Induced Conditioned Place Preferences through a Mechanism that does not Involve Discriminative-Stimulus or Antidepressant-Like Effects

Foll

Sokoloff

Stark

et al. 2004

Neuropsychopharmacol

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Environmental stimuli previously paired with drug taking appear to play a critical role in nicotine dependence. Converging anatomical, pharmacological, and behavioral evidence implicates dopamine D 3 receptors (D 3 Rs) in the mechanisms underlying stimulus-controlled drug-seeking behavior. This study assessed the effects of BP 897, a D 3 R partial agonist and ST 198, a D 3 R antagonist, on nicotine-induced conditioned place preferences (CPPs), used as a measure of drug-seeking behavior, on food-maintained responding and on discrimination performance under a two-lever-choice nicotine discrimination procedure. BP 897 and ST 198 both blocked the expression of nicotine-induced CPP at doses selective for D 3 R. They had no effect on locomotor activity in the CPP apparatus and no significant effect on nicotine discrimination performance or food-maintained responding under the discrimination procedure. Involvement of antidepressant actions in the effects of BP 897 and ST 198 on CPP is unlikely, since we found no effect of D 3 R blockade with BP 897 or genetic depletion of D 3 Rs in a forced swimming test, used as a behavioral test for antidepressant activity. This suggests that D 3 R ligands reduce the motivational effects of nicotine by a mechanism distinct from those of nicotine replacement therapy and bupropion, the two currently used aids for smoking cessation in humans. These findings support the use of D 3 R ligands as aids for smoking cessation and indicate that their effects would be selective for those rewarding or reinforcing effects of nicotine that contribute to the maintenance of tobacco-smoking behavior, without affecting subjective responses to nicotine or producing any antidepressant-like effects.

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“…[1][2][3] Aside from its use for these neurologic conditions, PPX has also been shown to be efficacious in the treatment of major depressive disorder (MDD), both as a monotherapy 4,5 and as an augmenting agent in patients with treatment-resistant depression. [6][7][8] The efficacy of PPX against depressive symptoms was first noted in patients with Parkinson disease.…”

Section: Introductionmentioning

confidence: 99%