ADVERTISEMENT
The Role of Rumination in Depression
Question:
What is the role of rumination in depression?
Along with negatively biased, emotional responses to changes and diminished capacity to experience pleasure, rumination is a key symptomatic manifestation of Major Depressive Disorder (MDD). We have briefly touched upon a related topic in our March blog dealing with the role of Default Mode Network (DMN) in depression. Today’s conversation will be more focused on the clinical relevance of the ruminative tendency in depression. We will briefly review a few seminal studies about the neurobiological underpinning of rumination in the context of MDD. A group of Stanford researchers made a very intriguing observation by combining utilization of the Ruminative Response Scale-RRS (a self-report measure of rumination), Beck Depression Inventory-II (BDI-II) and fMRI to evaluate a group of depressed patients. They found that depressed individuals who demonstrated a greater activation of Posterior Cingulate Cortex (PCC) and Dorsomedial Prefrontal Cortex (dmPFC), manifested high levels of maladaptive rumination. This includes recall of miserable autobiographical memories and mind-wandering and lower levels of adaptive self-reflection, compared to healthy controls ( 1 ).
These two formations, PCC and dmPFC, are the principal components of DMN (see above). Another group described increased connectivity between subgenual Anterior Cingulate Cortex (sgACC) and PCC in patients with MDD. SgACC is a part of another brain network, called the Salience Network (SN), which processes sensory information, signaling an important change in our internal or external environment, and converts it into a corresponding emotion. In context of depression, SN is likely to “over-read” potential for threat danger and loss and generates intense negative feelings. It appears that these two circuits, SN and DMN, are inappropriately linked together in depressed patients. High connectivity between sgACC (SN component) and PCC (a DMN structure) was significantly correlated with brooding and ruminations, as assessed by RRS ( 2 , 3 ). In other words, abnormally fused DMN and SN activity has emerged as a neural substrate for depressive ruminations. Several other studies offer supportive findings. One of them reported increased depressive ruminations associated with altered PCC connectivity in the first episode of MDD, compared to healthy controls ( 4 ), while yet another correlated elevated PCC and vmPFC function in depressed individuals with the severity of depression and feelings of hopelessness ( 5 ).
If this is so, should we not focus our therapeutic interventions on suppressing ruminative tendencies? A group of scientists from the United Kingdom has done exactly that, and with remarkable results! Forty-two depressed patients who have previously met the criteria for treatment refractory MDD were randomized to receive either 12 sessions of Rumination-Focused Cognitive Behavioral Therapy (RF-CBT) or Treatment as Usual (TAU) consisting of ongoing antidepressant maintenance and outpatient clinic visits. RF-CBT is a manual-based treatment approach combing behavioral activation and rumination-focused CBT. Rumination is framed as a form of avoidance, and functional analysis is used to help individuals realize that their rumination about negative self-experience is maladaptive. Patients are coached to replace ruminations with a more helpful style of thinking. Within a 26-week follow up 62 percent of individuals treated with RF-CBT achieved remission compared with only 21 percent of patients from the TAU group ( 6 ). The effect size for the RF-CBT group was calculated to be in a 0.94-1.1 range, a very effective treatment indeed! In some ways this study represents a pioneer effort, which successfully translated implications of neurobiological research into the origin of depressive symptoms into a robustly effective treatment modality.
References
1. Hamilton JP, Furman DJ, Chang C, Thomason ME, Dennis E, Gotlib IH. Default-mode and task-positive network activity in major depressive disorder: implications for adaptive and maladaptive rumination. Biological psychiatry. 2011;70(4):327-33.
2. Berman MG, Peltier S, Nee DE, Kross E, Deldin PJ, Jonides J. Depression, rumination and the default network. Soc Cogn Affect Neurosci. 2011;6(5):548-55.
3. Berman MG, Nee DE, Casement M, Kim HS, Deldin P, Kross E, et al. Neural and behavioral effects of interference resolution in depression and rumination. Cogn Affect Behav Neurosci. 2011;11(1):85-96.
4. Zhu X, Wang X, Xiao J, Liao J, Zhong M, Wang W, et al. Evidence of a Dissociation Pattern in Resting-State Default Mode Network Connectivity in First-Episode, Treatment-Naive Major Depression Patients. Biol Psychiatry. 2011.
5. Grimm S, Boesiger P, Beck J, Schuepbach D, Bermpohl F, Walter M, et al. Altered negative BOLD responses in the default-mode network during emotion processing in depressed subjects. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2009;34(4):932-843.
6. Watkins ER, Mullan E, Wingrove J, Rimes K, Steiner H, Bathurst N, et al. Rumination-focused cognitive-behavioural therapy for residual depression: phase II randomised controlled trial. Br J Psychiatry. 2011;199(4):317-22.
