Assessing the effects of bupropion SR on mood dimensions of depression

Tomarken, Andrew J.; Dichter, Gabriel S.; Freid, Cathryn M.; Addington, Stephanie; Shelton, Richard C.

doi:10.1016/s0165-0327(02)00306-3

Cited by 114 publications

(58 citation statements)

References 20 publications

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“…Other examples of DA agents effective in the treatment of MDD include the selective D 2 /D 3 receptor agonists pramipexole [292] and piribedil [293] the catechol-O-methyltransferase inhibitor tolcapone, [294], and the preferential presynaptic DA antagonist amisulpride, [295]. Particularly relevant in the present context are previous reports [290,296,297] that although both DA and non-DA agents can be used to effectively treat mood disorders, DA agents generally have superior effects on symptoms of anhedonia, specifically when compared with non-DA agents [19,298-300]. Tremblay and colleagues [226] reported that depressed patients had relatively greater increases in striatal and orbitofrontal cortex activation in response to emotional pictures after administration of dextroamphetamine (a stimulant associated with increased DA release).…”

Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

253

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Section: Reviewmentioning

confidence: 99%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

253

207

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“…However, there are very few studies evaluating the effects of antidepressant treatment on NA and PA reactivity in clinically depressed people. Two studies reported that both distress and anhedonia are affected by antidepressants (Tomarken et al, 2004;Dichter et al, 2005). Bhagwagar et al (2004) demonstrated that in individuals with a history of depression, antidepressant treatment normalized abnormal fear processing in the form of enhanced fear recognition.…”

Section: Introductionmentioning

confidence: 99%

Reduced Stress-Sensitivity or Increased Reward Experience: The Psychological Mechanism of Response to Antidepressant Medication

Wichers

Barge-Schaapveld

Nicolson

et al. 2008

Neuropsychopharmacol

126

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Depression has often been associated with increased negative affect reactivity to stress (Stress-Sensitivity) and reduced capacity to experience pleasure or positive affect (Reward Experience). To date, no studies have prospectively examined changes in StressSensitivity and Reward Experience following antidepressant treatment. The sample included 83 depressed patients and 22 healthy controls. A randomized controlled trial was carried out with patients receiving either imipramine or placebo for 6 weeks. At baseline and 6 weeks, patients and controls participated in an Experience Sampling procedure, prospectively measuring ecologically valid daily life appraisals of activities and mood states. The course of depression was assessed with the Hamilton Depression Rating Scale (HDRS). Multilevel linear regression analyses showed that patients had higher negative and lower positive appraisals of activities than controls. In addition, patients showed increased Stress-Sensitivity (negative affect reactivity to negatively appraised activities). Treatment with imipramine decreased Stress-Sensitivity and increased Reward Experience (positive affect reactivity to positively appraised activities). Changes in Stress-Sensitivity and Reward Experience were in part reducible to changes in the process of activity appraisal itself. However, increase in Reward Experience, but not decrease in Stress-Sensitivity, discriminated between patients who responded and those who did not, independent of changes in the process of activity appraisal itself. Response to treatment in depression may be conditional on restoration of hedonic capacity, the cerebral substrate of which requires further study in relation to antidepressant response. A search for (synergistic) antidepressant therapies specifically targeting ability to experience reward may be warranted.

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“…Shelton: My colleagues and I have identified at least 2 dominant domains of symptoms in depressed patients, the fatigue/anergia symptoms and the anxiety/ worry/rumination types of symptoms, and our data with bupropion 13 suggests that bupropion is robustly effective for anergia and not differentially effective from placebo for the anxiety-related symptoms. The problem that exists in pure randomized trials is that if we can identify 2 groups of people-anergic and anxious-after the initial phase of treatment and randomly assign them to one treatment or the other, we would probably get a washout of antidepressant effect, simply because some people in each group are going to respond to one treatment and some people to the other treatment.…”

Section: Dr Trivedimentioning

confidence: 70%

Use of Treatment Algorithms for Depression

Trivedi¹,

Fava

Marangell³

et al. 2006

J. Clin. Psychiatry

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The effectiveness of treatment algorithms rests on 3 principles. The 3 broad categories requiring special attention are (1) the determination of the need for sequential treatment algorithms; (2) what should be the placement of various treatment interventions in treatment algorithms with sequenced treatments, e.g., at what point should combination treatments and somatic treatments be included; and finally, (3) what the process or procedure is to implement algorithms in the clinical setting, e.g., the use of recently developed measurement-based care. 1 Dr. Osser: It is clear to me that there are significant differences between the likely outcome of people receiving treatment as usual (TAU) as opposed to algorithm-driven treatment. In the Texas Medication Algorithm Project (TMAP), 2 that difference was seen primarily in the first 3 months. An important factor in that difference was that the care coordinator identified patients who were not doing well and needed to move to the next step in the algorithm. For the next 9 months of the TMAP study, there was no widening of the difference between the algorithm group and the TAU group, suggesting that, from that point on, both groups did reasonably well (Figure 1). Dr. Trivedi: There is also evidence in primary care from Katon and colleagues, 3 which showed that guideline-driven care produces better outcome than TAU. Unützer and coworkers 4 found similar results. All of these studies have used care coordinators in the algorithm-driven treatment groups. The question becomes whether the better outcomes are related to the use of the care coordinator.Dr. Shelton: Dr. Trivedi, according to your TMAP article from 2004, 2 I agree that the first quarter is where the majority of change happens, but if you look at the end of a year of treatment, there still is a substantial difference between the TAU and the algorithm treatment patients. TAU patients did not catch up by the end of a year (see Figure 1), but the differences that are achieved are achieved primarily up front and then maintained throughout the year. Dr. Marangell: The data are fairly consistent in showing that algorithms result in not just better response rates, but improved patient satisfaction as well. Katon et al. 3 found that response rates were 74% with the algorithm versus 44% with TAU and that patients who received algorithmdriven treatment were more likely than patients who received TAU to rate their quality of care as good or excellent (93% vs. 75%).Dr. Fava: If you ask me whether there is a need for treatment algorithms in depression, I would say absolutely, but I question if we truly

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Assessing the effects of bupropion SR on mood dimensions of depression

Cited by 114 publications

References 20 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reduced Stress-Sensitivity or Increased Reward Experience: The Psychological Mechanism of Response to Antidepressant Medication

Use of Treatment Algorithms for Depression

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