scholarly journals Increased Reactivity of the Mesolimbic Reward System after Ketamine Injection in Patients with Treatment-resistant Major Depressive Disorder

2019 ◽  
Vol 130 (6) ◽  
pp. 923-935 ◽  
Author(s):  
Virginie Sterpenich ◽  
Sonia Vidal ◽  
Jeremy Hofmeister ◽  
Giorgio Michalopoulos ◽  
Victor Bancila ◽  
...  
Keyword(s):  
Neural Networks ◽  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Ventral Tegmental Area ◽  
Emotional Processing ◽  
Judgment Task ◽  
Treatment Resistant ◽  
Major Depressive ◽  
Ventral Tegmental ◽  
The Impact

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Ketamine rapidly improves maladaptive mood states in major depressive disorder, and some of the neural substrates underlying this therapeutic effect have been identified. This study aimed to identify functional changes within neural networks that may underlie the impact of ketamine on both reward and emotional processing in patients with treatment-resistant major depression. Methods Ten adult patients with a Montgomery–Åsberg Depression Rating Scale score above 25 were enrolled to receive a single intravenous administration of ketamine (0.5 mg/kg). Patients’ performance along with related neural network activations were analyzed in a game-like reward task and in an emotional judgment task using functional magnetic resonance imaging 1 day before and 1 and 7 days after ketamine administration. Results A significant correlation (R2 = 0.46, P = 0.03) between the improvement of depression scores and the enhanced reaction time for positive items was found in the game-like reward task 1 day after ketamine administration. This enhanced sensitivity for rewarded items was accompanied by increased activity of reward-related brain regions, including the orbitofrontal cortex, ventral striatum, and the ventral tegmental area, an effect that persisted up to 1 week after ketamine injection. In the emotional judgment task, it was found that ketamine rapidly modified local brain activities in response to emotionally negative, positive, or neutral stimuli in the amygdala, insula, anterior cingulate cortex, and in the ventral tegmental area. Conclusions Single bolus ketamine administration rapidly triggers lasting changes in mesolimbic neural networks to improve pathologic reward and emotional processing in patients with major depressive disorder.

The impact of ‘cluster maintenance TMS’ on irritability occurring in major depressive disorder

2020 ◽  
pp. 103985622094303 ◽  
Author(s):  
Saxby Pridmore ◽  
Yvonne Turnier-Shea ◽  
Sheila Erger ◽  
Tamara May
Keyword(s):  
Major Depressive Disorder ◽  
Transcranial Magnetic Stimulation ◽  
Depressive Disorder ◽  
Magnetic Stimulation ◽  
Subjective Measure ◽  
Naturalistic Study ◽  
Treatment Resistant ◽  
Major Depressive ◽  
The Impact ◽  
Cluster Maintenance

Objective: To determine the impact of clustered maintenance transcranial magnetic stimulation (TMS) on irritability occurring in treatment-resistant major depressive disorder (MDD). Method: A naturalistic study of 106 courses that includes pre- and posttreatment assessments of subjective and objective depression and a subjective measure of irritability developed for this study. Results: Forty-six participants (35 females), mean age 43.2 years (14.3), completed 106 courses. There was a significant reduction in irritability and depression scores ( p < .001). The change in irritability scores was significantly correlated with the change in depression scores, r = .40, p < .001. Conclusion: TMS has the capacity to reduce the irritability co-occurring with treatment-resistant MDD, known to be responsive to TMS. This increases the possibility of using TMS in the treatment of irritability co-occurring with other disorders or standing alone (should irritability be categorized as a stand-alone disorder).

scholarly journals Impaired reward-related learning signals in remitted unmedicated patients with recurrent depression

Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2510-2522 ◽  
Author(s):  
Hanneke Geugies ◽  
Roel J T Mocking ◽  
Caroline A Figueroa ◽  
Paul F C Groot ◽  
Jan-Bernard C Marsman ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Ventral Tegmental Area ◽  
Ventral Striatum ◽  
Inverse Association ◽  
Healthy Controls ◽  
Temporal Difference ◽  
Recurrent Depression ◽  
Major Depressive ◽  
Ventral Tegmental

Abstract One of the core symptoms of major depressive disorder is anhedonia, an inability to experience pleasure. In patients with major depressive disorder, a dysfunctional reward-system may exist, with blunted temporal difference reward-related learning signals in the ventral striatum and increased temporal difference-related (dopaminergic) activation in the ventral tegmental area. Anhedonia often remains as residual symptom during remission; however, it remains largely unknown whether the abovementioned reward systems are still dysfunctional when patients are in remission. We used a Pavlovian classical conditioning functional MRI task to explore the relationship between anhedonia and the temporal difference-related response of the ventral tegmental area and ventral striatum in medication-free remitted recurrent depression patients (n = 36) versus healthy control subjects (n = 27). Computational modelling was used to obtain the expected temporal difference errors during this task. Patients, compared to healthy controls, showed significantly increased temporal difference reward learning activation in the ventral tegmental area (PFWE,SVC = 0.028). No differences were observed between groups for ventral striatum activity. A group × anhedonia interaction [t(57) = −2.29, P = 0.026] indicated that in patients, higher anhedonia was associated with lower temporal difference activation in the ventral tegmental area, while in healthy controls higher anhedonia was associated with higher ventral tegmental area activation. These findings suggest impaired reward-related learning signals in the ventral tegmental area during remission in patients with depression. This merits further investigation to identify impaired reward-related learning as an endophenotype for recurrent depression. Moreover, the inverse association between reinforcement learning and anhedonia in patients implies an additional disturbing influence of anhedonia on reward-related learning or vice versa, suggesting that the level of anhedonia should be considered in behavioural treatments.

scholarly journals The Impact of BDNF Polymorphisms on Suicidality in Treatment-Resistant Major Depressive Disorder: A European Multicenter Study

2017 ◽  
Vol 20 (10) ◽  
pp. 782-787 ◽  
Author(s):  
Alexandra Schosser ◽  
Laura Carlberg ◽  
Raffaella Calati ◽  
Alessandro Serretti ◽  
Isabel Massat ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Multicenter Study ◽  
Treatment Resistant ◽  
Major Depressive ◽  
European Multicenter Study ◽  
The Impact

scholarly journals Cognition and Its Association with Psychosocial and Occupational Functioning during Treatment with Escitalopram in Patients with Major Depressive Disorder: A CAN-BIND-1 Report: La Cognition Et Son Association Avec Le Fonctionnement Psychosocial Et Professionnel Durant Le Traitement Par Escitalopram Chez Des Patients Souffrant De Trouble Dépressif Majeur: Une Étude Can-Bind-1

2020 ◽  
pp. 070674372097482
Author(s):  
Shane J. McInerney ◽  
Trisha Chakrabarty ◽  
Malgorzata Maciukiewicz ◽  
Benicio N. Frey ◽  
Glenda M. MacQueen ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Cognitive Functioning ◽  
Symptom Severity ◽  
Cognitive Change ◽  
Cognitive Domain ◽  
Depression Symptom ◽  
Major Depressive ◽  
Occupational Functioning ◽  
The Impact

Objectives: Major depressive disorder (MDD) is associated with impairments in both cognition and functioning. However, whether cognitive deficits significantly contribute to impaired psychosocial and occupational functioning, independent of other depressive symptoms, is not well established. We examined the relationship between cognitive performance and functioning in depressed patients before and after antidepressant treatment using secondary data from the first Canadian Biomarker Integration Network in Depression-1 study. Methods: Cognition was assessed at baseline in unmedicated, depressed participants with MDD ( n = 207) using the Central Nervous System Vital Signs computerized battery, psychosocial functioning with the Sheehan Disability Scale (SDS), and occupational functioning with the Lam Employment Absence and Productivity Scale (LEAPS). Cognition ( n = 181), SDS ( n = 175), and LEAPS ( n = 118) were reassessed after participants received 8 weeks of open-label escitalopram monotherapy. A series of linear regressions were conducted to determine (1) whether cognitive functioning was associated with psychosocial and occupational functioning prior to treatment, after adjusting for overall depressive symptom severity and (2) whether changes in cognitive functioning after an 8-week treatment phase were associated with changes in psychosocial and occupational functioning, after adjusting for changes in overall symptom severity. Results: Baseline global cognitive functioning, after adjusting for depression symptom severity and demographic variables, was associated with the SDS work/study subscale (β = −0.17; P = 0.03) and LEAPS productivity subscale (β = −0.17; P = 0.05), but not SDS total (β = 0.19; P = 0.12) or LEAPS total (β = 0.41; P = 0.17) scores. Although LEAPS and SDS scores showed significant improvements after 8 weeks of treatment ( P < 0.001), there were no significant associations between changes in cognitive domain scores and functional improvements. Conclusion: Cognition was associated with occupational functioning at baseline, but changes in cognition were not associated with psychosocial or occupational functional improvements following escitalopram treatment. We recommend the use of more comprehensive functional assessments to determine the impact of cognitive change on functional outcomes in future research.

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