What is Emotional Regulation?
Emotional regulation refers to the processes by which individuals influence which emotions they experience, when they experience them, and how they experience and express those emotions (Gross, 2015). Rather than simply "controlling" emotions or suppressing unpleasant feelings, emotional regulation encompasses a range of cognitive and behavioural strategies that help people adapt their emotional responses to meet the demands of different situations.
Importantly, emotional regulation is not about eliminating negative emotions. Emotions such as fear, sadness and anger are essential for survival, decision-making and social communication. Instead, effective emotional regulation involves responding to emotions in ways that are flexible and appropriate to the situation. Depending on the context, this may involve reducing the intensity of an emotional response, maintaining it, or even enhancing it when it serves a useful purpose (Gross, 2015).
Gross's (2015) process model proposes that emotions unfold over time rather than appearing instantaneously. Emotional responses emerge through a sequence of events in which a person encounters a situation, selects or modifies aspects of it, directs attention towards aspects of that situation, interprets or appraises its meaning, and subsequently generates emotional, behavioural and physiological responses. Understanding how these processes are implemented within the brain has become a major focus of neuroscience, with growing evidence suggesting that emotional regulation depends on the coordinated activity of distributed brain regions rather than working in isolation.
While each region has specialised functions, effective emotional regulation depends on coordinated communication between distributed brain regions rather than the activity of any single structure. Functional connectivity between brain regions such as the prefrontal cortex (PFC), amygdala, hippocampus and anterior cingulate cortex (ACC) enables emotional information to be evaluated, contextualised and regulated (Etkin et al., 2015).
One of the best-known structures involved in emotional regulation is the amygdala. The amygdala is involved more broadly in detecting emotionally salient information, rapidly evaluating potential threats, assigning emotional significance to experiences, and supporting emotional learning and memory (Phelps & LeDoux, 2005).
Once a stimulus has been flagged this way, the hippocampus plays an important role in linking memories and contextual information with the amygdala's emotional response. The hippocampus and PFC maintain reciprocal connectivity, often mediated by the amygdala, that determines whether an emotional response is appropriate to the current context (Jin & Maren, 2015).
Working alongside this, the ventromedial prefrontal cortex (vmPFC) works closely with the amygdala and hippocampus and is involved in evaluating the emotional significance of stimuli and integrating emotional and cognitive information (Roy et al., 2012).
Where the vmPFC integrates emotional and cognitive information, the dorsolateral prefrontal cortex (DLPFC) is primarily involved in cognitive reappraisal, the process of reinterpreting emotional situations to reduce their emotional impact (Buhle et al., 2014; Etkin et al., 2015).
Finally, the ACC oversees this whole exchange by monitoring emotional conflicts, detecting errors, and supporting cognitive control. It integrates emotional information from the amygdala and hippocampus with cognitive processes in the PFC, enabling top-down regulation of emotional responses (Ochsner & Gross, 2005).
Dysfunction in emotional regulation rarely stems from the failure of a single structure, but rather from disrupted communication between these interconnected regions.
In depression and anxiety disorders, disruption between the PFC and the amygdala is thought to underlie both exaggerated threat responses and reduced capacity for cognitive reappraisal, reflecting a broader breakdown in top-down regulatory control (Price & Drevets, 2010; Etkin et al., 2011).
A related but distinct pattern occurs in PTSD where disrupted coordination between the amygdala, hippocampus and vmPFC produces hyperactive threat/fear responses, while attenuated DLPFC activation is associated with greater symptom severity and poorer executive functioning, reflecting an imbalance between cognitive control and affective processing networks (Etkin & Wager, 2007; Aupperle et al., 2012).
In OCD, while dysfunction in the cortico-striatal circuitry remains central, dysfunction extends beyond to the amygdala, hippocampus, ACC and orbitofrontal cortex (OFC) impairing fear extinction, contributing to persistent obsessions, compulsions, and anxiety (Milad & Rauch, 2012).
Taken together, these conditions illustrate that psychiatric vulnerability reflects the integrity of distributed network communication rather than the isolated failure of any one region, reinforcing the view that the PFC, amygdala, hippocampus, and ACC function as a coordinated system for evaluating, contextualising, and regulating emotional experience (Etkin et al., 2015).
Transcranial Direct Current Stimulation (tDCS) is a non-invasive neuromodulation technique which passes a weak electrical current through scalp electrodes which modifies neuronal excitability and cortical activity (Thair et al., 2017). In depression, the anode is placed over the LDLPFC which is hypoactive producing an excitatory effect while the cathode is placed over the RDLPFC which is hyperactive producing an inhibitory effect (Sathappan et al., 2019). A meta -analysis of 23 randomized, sham-controlled trials found that active tDCS produced significantly greater improvements in depressive symptoms than sham stimulation, with response and remission rates roughly double those seen with sham (Razza et al., 2020). By directly correcting this hemispheric imbalance, tDCS offers one route back to the regulatory capacity that depression disrupts.
Neurofeedback is a form of biofeedback in which individuals learn to self-regulate their own brain activity in real time, using a continuous feedback signal typically presented as audio or visual cues that reflects ongoing changes in their brainwave patterns (Marzbani et al., 2016). In PTSD, one randomized controlled trial found that alpha-down neurofeedback training enhanced engagement of the DLPFC and improved integration within the brain's default mode network (Shaw et al., 2023). In terms of efficacy, a randomized, waitlist-controlled trial found that neurofeedback produced significantly greater reductions in PTSD symptoms than a waitlist control, with effect sizes comparable to the best evidence-based treatments for PTSD (van der Kolk et al., 2016). This suggests neurofeedback can help restore the very DLPFC engagement that PTSD leaves depleted.
Transcranial Magnetic Stimulation (TMS)
Transcranial magnetic stimulation (TMS) is a non-invasive neuromodulation technique that uses rapidly changing magnetic fields to influence activity in targeted brain regions. During treatment, a magnetic coil is placed on the scalp, delivering brief pulses that pass through the skull and induce electrical currents in underlying cortical tissue. Depending on the stimulation parameters, TMS can either increase or decrease cortical excitability (Klomjai et al., 2015).
Bilateral TMS for depression aims to restore frontal cortical asymmetry in MDD by applying high frequency stimulation to the LDLPFC to increases activity and low frequency stimulation to the RDLPC to decrease activity. A systematic review and meta-analysis by Berlim et al. (2013) found that bilateral rTMS significantly reduced depressive symptoms and achieved clinically meaningful response and remission rates, while remaining well tolerated. Like tDCS, TMS aims to restore balanced activity between the left and right DLPFC, helping to improve top-down regulation of emotional processing.
Edinoff et al. (2022) highlight the potential of TMS as a novel intervention for PTSD by targeting disrupted emotional regulation networks. The RDLPFC has been the most studied target, with evidence suggesting improvements in core PTSD symptoms, particularly hyperarousal and avoidance. By modulating DLPFC activity, TMS may enhance top-down control of limbic regions involved in fear processing.
Berlim et al. (2013) investigated the effects of TMS in the treatment of OCD, pooling results from 10 randomized, sham-controlled trials. Active rTMS produced a significant improvement in core OCD symptoms, with over a third of patients responding to treatment. Benefits were particularly evident following low-frequency stimulation of the orbitofrontal cortex (OFC) or supplementary motor area (SMA). Modest improvements in co-occurring anxiety and depressive symptoms were also observed with active treatment overall, highlighting the potential for rTMS to address the broader symptom burden associated with OCD.
Emotional regulation depends on distributed communication between the PFC, amygdala, hippocampus, and ACC rather than the isolated function of any single region. Dysfunction within this network, rather than damage to any one structure, underlies the emotional dysregulation observed in depression, anxiety disorders, PTSD, and OCD. Neuromodulation techniques such as tDCS, neurofeedback, and TMS target this network directly, aiming to restore balance. Current evidence indicates that these interventions can produce clinically meaningful symptom improvement across a range of conditions, though treatment protocols continue to be refined as understanding of the underlying circuitry develops.
Written by Niamh, Smart TMS Dublin Practitioner
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