This is Your Brain on Burnout

Post by Elisa Guma

What is burnout?

Chronic physical, emotional, or mental exhaustion, decreased motivation, lowered performance, and negative attitudes towards oneself and others are all symptoms of “burnout”. This syndrome is familiar to many professionals in high-stress, demanding jobs. Burnout is usually caused by work that demands continuous, long-term cognitive, emotional, or physical efforts in concert with a perceived lack of control in the face of a demanding workload, as well as a lack of adequate social support or poor self-care (Vladut et al., 2010). While work-related stress is often the cause, burnout can also occur in other areas of life, such as parenting, caretaking, or romantic relationships.

How does burnout affect the neuroendocrine system?

Chronic stress conditions like burnout can cause dysregulation of the neuroendocrine system through the hypothalamic-pituitary-adrenal (HPA) axis (Oosterholt et al., 2014). When faced with an acute stressor (ex: seeing a snake in the grass), the body responds by increasing cortisol concentrations in the body, triggering the fight or flight response. Once the threat has passed cortisol levels fall and return to baseline. However, in chronic stress conditions like burnout, the body is unable to bring cortisol levels back to baseline, which wreaks havoc on our body’s neuroendocrine system. Prolonged stress and chronically elevated cortisol levels can lead to abnormally low baseline cortisol levels, (Oosterholt et al., 2014), increasing inflammation in the body and the risk for heart disease, diabetes, high blood pressure, and vulnerability to illness (Toker et al., 2012). It can also increase susceptibility to anxiety, depression, or misuse of drugs and alcohol (Ogbonnaya UC et al., 2022).

How does burnout affect brain structure and function?

Chronic stress, a key underlying feature of burnout, has been associated with increasing risk for both mental health conditions and physical illness, as well as changes in brain structure and function (Miranda et al., 2022). Neuroimaging studies of individuals experiencing chronic occupational stress have shown alterations to limbic and paralimbic networks that are commonly observed in other chronic stress conditions such as post-traumatic stress disorder or childhood maltreatment (Savic 2015, Savic et al., 2018; Blix et al., 2013).  These include cortical thinning of the prefrontal cortex (PFC), implicated in higher-order executive function and decision-making, as well as reduced functional connectivity of the PFC to other brain regions. Importantly, some studies demonstrate that cortical thinning is more pronounced in females than males, highlighting potential sex-specific vulnerabilities (Savic 2015, Savic et al., 2018; Blix et al., 2013). Alterations to limbic structures have also been reported, including reduced anterior cingulate cortex volume, and reduced functional connectivity between that region and the amygdala (Golkar et al. 2014). Additional studies demonstrate that females under chronic stress have enlarged amygdala volume while males have enlarged caudate volume (Savic et al., 2018). Importantly, the magnitude of these changes has been associated with the degree of perceived stress, pointing to some potential dose-response relationship.  

Burnout has also been associated with cognitive deficits. Those experiencing burnout are more likely to have attentional lapses and memory impairments, with effects often more pronounced in women than men (Morgan et al., 2011; Deligkaris et al., 2014) and may have more trouble switching attention between visual stimuli than non-stressed controls (Deligkaris et al., 2014). These cognitive and attentional challenges may lead to difficulties with work performance and the ability to feel rewarded and satisfied by the work (Liston et al., 2009).

What’s the connection between burnout and depression?

The symptoms associated with burnout are like those of depression (Schonfeld et al., 2015). Interestingly, reduced serotonin binding in the anterior cingulate cortex, hippocampus, and anterior insular cortex (regions involved in emotional processing), has been reported in the brains of those undergoing chronic occupational stress (Jovanovic et al. 2011). These brain regions, along with the serotonin system are involved to some extent in the pathology of depression, highlighting possible mechanistic overlaps. Although this relationship requires further investigation, similar attentional-behavioral changes have been reported between individuals with burnout and those with depression (Liston et al., 2009).

While burnout and depression may be highly correlated, there are some important distinctions. Depression is currently a diagnosable mental health condition, whereas burnout is not (Schonfeld et al., 2015). Additionally, burnout occurs in response to situational stress, while depression is not necessarily triggered by a specific event. However, it’s important to note that both conditions can require professional help.

How can we bounce back from burnout?

Recognizing you have burnout is an important first step. Give yourself grace and take time to care for your mental health. This can include seeing a therapist, taking breaks throughout the workday, exercising, practicing mindfulness, and trying to foster better work-life balance by engaging in non-work-related activities and social connections (Maslach et al., 2015).

Previous research in rodents has found that chronic stress impairs attention-shifting ability in rats and damages neurons in the prefrontal cortex, but these deficits are reversed after three weeks of relaxation (Arnsten AFT, 2009). Similarly, longitudinal brain imaging studies in humans have shown that cortical thinning and decreased functional connectivity of the prefrontal cortex and attention impairments can be reversed when stress exposure is reduced (Savic, et al., 20018, Deligkaris et al., 2014). This suggests that even though the effects of burnout are quite deleterious on the brain and body, there is room for improvement if stressful conditions can be managed.

While personal-level interventions are necessary, there must be change at the organizational level as well. For example, managers should be trained to recognize signs of burnout in their staff and companies should be encouraged to improve the work environment and conditions to foster a supportive work culture (Vladut et al., 2010). Ideally, individuals recognize the first signs of burnout and take steps to intervene, but chronic stress that manifests into burnout can be challenging to handle on your own. Considering professional support when burnout becomes an issue should be encouraged.

References +

Arnsten AFT. (2009). Stress signalgin pathways that impair prefrontal cortex structure and fuction. Nature Reviews Neuroscience, 10: 410-422.

Blix, E., Perski, A., Berglund, H., & Savic, I. (2013). Long-term occupational stress is associated with regional reductions in brain tissue volumes. PLOS ONE 8: e64065. doi:10.1371/journal.pone.0064065

Deligkaris, P., Panagopoulou, E., Montgomery, A. J., & Masoura, E. (2014). Job burnout and cognitive functioning: A systematic review. Work & Stress, 28, 107–123. doi:10.1080/02678373.2014.909545

Golkar, A., Johansson, E., Kasahara, M., Osika, W., Perski, A., & Savic, I. (2014). The influence of work-related chronic stress on the regulation of emotion and on functional connectivity in the brain. PLOS ONE 9: e104550. doi:10.1371/journal.pone.0104550

Jovanovic, H, Perki, A, Berglund, H, Savic, I (2011). Chronic stress is linked to 5-HT1A receptor changes in functional disintegration of the limbic networks. Neuroimage, 55, 1178-1188.

Liston, C., McEwen, B. S., & Casey, BJ. (2009). Psychosocial stress reversibly disrupts prefrontal processing and attentional control. Proceedings of the National Academy of Sciences, 106, 912–917. doi:10.1073/pnas.0807041106

Miranda, F. (2022). The neural correlates of burnout: a systematic review. Digitala etenskapliga Arkivet.

Maslach, C., & M. P. Leiter, (Eds.). (2015). It’s time to take action on burnout. Burnout Research, 2, iv–v. doi:10.1016/j.burn.2015.05.002

Morgan, C. A., Russell, B., McNeil, J., Maxwell, J., Snyder, P. J., Southwick, S. M., & Pietrzak, R. H. (2011). Baseline burnout symptoms predict visuospatial executive function during survival school training in special operations military personnel. Journal of the International Neuropsychological Society, 17, 494–501. doi:10.1017/S1355617711000221

Ogbonnaya UC, Thiese MS, Allen J. (2022). Burnout and engagement’s relationship to drug abuse in laywers and law professionals. J Occup Environ Med, 64: 621-627.

Oosterholt, B. G., Maes, J. H., Van der Linden, D., Verbraak, M. J., & Kompier, M. A. (2015). Burnout and cortisol: Evidence for a lower cortisol awakening response in both clinical and nonclinical burnout. Journal of Psychosomatic Research, 78, 445–451. doi:10.1016/j.jpsychores.2014.11.003

Savic, I. (2015). Structural changes of the brain in relation to occupational stress. Cerebral Cortex, 25, 1554–1564. doi:10.1093/cercor/bht348

Savic, I, Perksi A, Osika, W. (2018). MRI shows that exhaustion syndrome due to chronic occupational stress is associated with partially reversible cerebral changes. Cerebral Cortex, 28: 894-906.

Schonfeld IS, Bianchi R. (2015). Burnout and depression: two entities or one? Journal of clinical psychology, 71:22-37.

Toker, S., Melamed, S., Berliner, S., Zeltser, D., & Shapira, I. (2012). Burnout and risk of coronary heart disease: A prospective study of 8838 employees. Psychosomatic Medicine, 74, 840–847. doi:10.1097/PSY.0b013e31826c3174

Vladut, CI., Kallay, E. (2010). Work stress, personal life, and burnout. Causes, consequences, possible remedies: a theoretical review. Cognition, Brain, Behaviour, 14, 261-280. https://www.proquest.com/docview/856042813?fromopenview=true&pq-origsite=gscholar

Spatial Computing as an Explanation for Working Memory Control

Post by Megan McCullough

The takeaway

Spatial computing, the process of using the spatial dimension in cortical networks to organize information, allows for working memory control. This novel idea for working memory computations helps to explain how the synchronized activity of millions of neurons can control individual pieces of information that are involved in working memory. 

What's the science?

Working memory describes the ability to hold information in mind for a short period of time and flexibly use it in the execution of cognitive tasks. Evidence suggests that a coordinated interplay of beta and gamma oscillations (neural oscillations at specific frequency bands) could contribute to this facet of cognition. Since neural oscillations involve the synchronized activity of millions of neurons, it is still unclear how they can facilitate controlled access to individual pieces of information involved in working memory. This week in Nature Communications, Lundqvist and colleagues provide a novel explanation for how the cortical networks manage working memory and then verify this hypothesis by analyzing neuronal activity in monkeys performing different working memory tasks. 

How did they do it?

First, the authors proposed a novel explanation for how the flexible access to individual pieces of information (i.e., working memory items) encoded in the activity of millions of neurons can be controlled through spatial computing. According to this spatial computing model, the brain allocates distinct regions across the cortical network for distinct pieces of information held in working memory and then controls these areas through beta-gamma oscillations. The scattering of different items in working memory across network space allows them to be manipulated independently from one another; this explains the flexibility of information in working memory. Importantly, these regions are not static, but change over time to flexibly update the status of each item, for instance when it goes from being the most recent to the second most recent in a sequence.

The authors made four predictions about what they should observe if spatial computing were to be a plausible explanation for how the brain controls information in working memory. 

1. Specific information relevant to the task would be encoded by distinct patterns of beta and gamma oscillations.

2. Information would be spatially organized in the network.

3. Spatial patterns pertaining to the rules of the task would be consistent throughout tasks even if the individual information (specific working memory items) changed

4. Neural oscillations would influence the spiking activity of neurons so that they would respond to a mix of external stimuli and task-related context.

The authors then tested these predictions by analyzing beta and gamma burst activity as well as neuronal spiking during working memory tasks. Neurophysiological recordings were conducted from the prefrontal cortex of rhesus monkeys as they performed working memory tasks. The tasks involved the monkeys having to remember the sequence of objects or colored squares and selecting which object flashed in front of them matched a stimulus they were shown previously. 

What did they find?

The authors found evidence that supported their spatial computing hypothesis. The authors verified all the predictions; this shows that spatial computing is a plausible explanation for the selective control involved in working memory. Although individual neurons that encode working memory content are scattered around the cortex, there is a mechanism that activates patches of the network. These neurons are then able to flexibly access task-relevant information, which is reflected in the spatial and temporal patterns of beta and gamma activity. In other words, beta and gamma oscillations reflect how the information needed in the task flows spatially across the brain network. How the information flows could be different for different tasks even if the same working memory items are used. The authors found evidence for these differences in varying patterns of beta and gamma activity.  

What's the impact?

This study proposes and then provides evidence for spatial computing, a novel explanation for how the brain controls and influences working memory. This offers new research paths into the inner workings of the human mind. 

The Impact of Air Pollution on the Brain

Post by Christopher Chen 

The takeaway

Exposure to air pollution has been linked to negative effects on cardiovascular and respiratory health, but its impact on brain function remains unclear. Scientists discovered that short-term exposure to air pollution in controlled conditions negatively affected fMRI measurements of brain connectivity, suggesting that air pollution may be harming our brains. 

What's the science?

The harmful effects of traffic-related air pollution are well-documented, with numerous studies showing how exposure to air pollution harms cardiovascular and respiratory health. Further, researchers have linked air pollution to negative outcomes on brain health, with some reports suggesting that air pollution particles transmitted to the brain via the olfactory bulb may enhance neuroinflammation. However, the effects of traffic-related air pollution on the brain remain relatively unexplored, at least under controlled conditions. A recent article in Environmental Health investigated the effects of exposure to traffic-related air pollution on the brain and cognitive function. 

How did they do it?

Twenty-five healthy adults were selected and screened for inclusion in this study. They were then chosen at random to be initially exposed to either: diluted diesel exhaust (DE) or filtered air (FA) under double-blind conditions at the Air Pollution Exposure Lab at the University of British Columbia. Immediately before exposure, researchers measured brain activity using fMRI. Following initial fMRI measurement the two-hour exposure began with the participants lightly cycling on a stationary bike for fifteen minutes in order to generate a representative level of activity. Immediately following the two-hour exposure, brain activity was again measured using fMRI. Two weeks later, participants first exposed to DE were exposed to FA while those first exposed to FA were exposed to DE. 

Following the conclusion of the experimental portion of the study, investigators analyzed fMRI data for changes in the blood oxygen level-dependent (BOLD) signal following DE and FA exposure. Specifically, they focused on brain regions linked to the default mode network, a well-studied functional brain network involved in higher-level thinking skills and memory that includes regions that are active together during wakeful rest. 

What did they find?

The fMRI data revealed several key differences in brain activity following exposure to DE and FA. The fMRI data also showed that under control conditions (exposure to FA), subjects saw a significant increase post-exposure in brain activity in the right middle temporal gyrus and occipital fusiform gyrus, brain regions known to be linked to the default mode network. This increase was not present after DE exposure. Furthermore, when comparing widespread changes in brain connectivity, researchers showed that brain connectivity in FA conditions was significantly enhanced compared to DE conditions. In other words, there was decreased brain connectivity after DE exposure compared to after FA exposure, suggesting that the brain isn’t functioning as well after exposure to diesel air. 

What's the impact?

Investigators found that traffic-related air pollution decreased brain connectivity compared to exposure to clean air. Overall, these findings suggest that there are negative effects of short-term exposure to air pollution on the brain. Future studies are needed to examine pollution exposures over longer durations to better understand the long-term impact.