Tag Archives: psychology

Sweet talking the pain way

Sure, we’ve all heard about the importance of the mind-body connection for improving our running performance, but how many of us actually give credence to the idea? Many of us have experienced the strong influence of our mental state on our physical performance, though we may not always be aware of its impact. You’re probably familiar with one of these scenarios … a bad day at work is topped off with an equally miserable run, or a celebratory run after hearing some good news sends you soaring into that runner’s high. Well, just the other day, my run highlighted exactly how powerful our mental landscape can be at assuaging or preventing injuries.

hamstring-origin-tendinopatFor the past five months (or more accurately, 17 years if you consider the repeated flare-ups since I began running) I’ve been battling chronic, relentless hamstring / glute / hip tightness and pain. Call it what you will … the various docs I’ve seen have attributed it to anything and everything, from sciatica to piriformis syndrome to hamstring tendinopathy to good old-fashioned overuse and weakness. Regardless of these meaningless diagnoses, I’ve found no relief, despite my desperate treatment attempts with massage, foam-rolling, ART and acupuncture. And despite this failed therapy, I’ve continued to run through the pain, as any typically irrational running addict would do.

A twitter discussion, following a particularly traumatic (to the hamstring) 12-miler, got me thinking. @skorarunning pointed out “I’ve even read that rolling could cause tightness, as it’s a stress to the muscles & they could tighten as a safety mechanism”. @rickmerriam corroborated “Muscles tighten up to prevent joints from going into positions of vulnerability. #BuiltInProtectiveMechanism”.

As I started my run the next day and my hammie/glute/hip immediately tightened up (per usual), I thought back to these comments. Why was it cramping? What was it trying to protect itself against? For whatever reason, it was vulnerable, and – sensing the need to shield itself against some mysterious stressor – locked up in defense. The vision of an anxious child came to mind: unnecessarily frightened of a harmless, imaginary threat. ‘If only I could just convince my hamstring that the threat is not real … there’s no reason to ‘fear’ the run,’ I wished. And so I did. I had a chat with my leg and encouraged it to clam the heck down. To stop overreacting. There was no real danger. It was safe and strong and protected. At the slightest hint of tension, I sweet-talked the muscle into soft, loose submission. And to my complete astonishment, the muscle listened, sending me sailing comfortably and strongly through 8 pain-free miles.

Was it merely a coincidence? Would my hamstring have behaved had I not whispered soothing lullabies into into its, um, hammie-ears? This was but another experiment of one, and I will never know. But I do know our muscles activate in a beautifully orchestrated neuromuscular symphony, which is intimately connected with our central nervous system. It would not surprise me if the the cognitive superstar of the human nervous system – the brain – is charismatic enough to use its mental coercion to sway its fellow motor neurons into passive compliance.

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What does Work-Related Burnout do to the Brain?

Originally published on the PLOS Neuroscience Community

We’ve all experienced it – the fatigue, stress and irritability after a long day of work. For most, these feelings are fleeting, and are nothing a good night’s sleep or a cup of tea over a good book can’t remedy. But for others, the daily stress extends into weeks and months, and eventually into long-term burnout. The physical toll on the over-worked can be so extreme that occupational burnout is being increasingly recognized as a serious medical condition. While the behavioral symptoms – including problems with memory or concentration, mood imbalances, insomnia and body aches – are well documented, the consequences of chronic burnout on brain function, and how such neural changes give rise to emotional dysregulation, have been inadequately examined. A recent PLOS One study, by Amita Golkar and colleagues from the Karolinska Institute, sought to better understand how chronic work-related stress alters brain function and emotional processing. While their findings confirm that impaired emotional regulation has neurobiological roots, another expert in the field has raised the question of whether stress may affect additional neural circuits undetected here.

Assessing stress

Thirty-two individuals with chronic burnout and 61 healthy controls participated. The patients worked 60-70 hours per week, manifested symptoms including sleeplessness, fatigue, irritability, cognitive impairments or impaired working ability for at least a year, and had lost at least six months of work to sickness. Each participant completed two test sessions, including a startle response task to measure emotional regulation, and resting-state functional MRI to evaluate functional brain connectivity.

During the behavioral task, a series of neutral and negative pictures was shown, with each picture flashed before and after an instruction cue (Figure 1). For negative pictures, subjects were told to either up-regulate, down-regulate or maintain their emotional response to the image (i.e., to experience the second presentation as more, less or similarly emotionally charged as the first presentation). Neutral pictures were always paired with the instruction to maintain their emotional response. To assess how the cues affected participants’ physiological responses to the images, during each picture presentation the researchers administered an acoustic startle and measured eye-blink responses using electromyography. This allowed them to compare stress responses to an identical stimulus, differing only in how the participants manipulated their emotional reactions.

Figure 1. Startle responses were measured before and after an emotional regulation cue to the same picture. doi: 10.1371/journal.pone.0104550

Figure 1. Startle responses were measured before and after an emotional regulation cue to the same picture. doi: 10.1371/journal.pone.0104550

Burnout impairs emotional regulation

When they were told to maintain or up-regulate their emotional responses, the burnout and control groups showed similar startle responses (response to the post-cue picture – response to the pre-cue picture). But critically, during the down-regulate condition the burnout group not only exhibited a greater stress response than controls (Figure 2), but also reported less success at implementing the emotional regulation instructions to the negative images. Just from these behavioral findings, it’s clear that chronic stress can dramatically alter how we process negative emotions. In particular, the burnt-out workers demonstrated less control over their reactions to negative experiences, showing signs of elevated distress that they were unable to dampen.

Figure 2. Patients showed an exaggerated response to negative images when instructed to down-regulate their emotions. doi: 10.1371/journal.pone.0104550

Figure 2. Patients showed an exaggerated response to negative images when instructed to down-regulate their emotions. doi: 10.1371/journal.pone.0104550

Burnout alters limbic function

Given this strong evidence that something was awry in these patients’ emotional regulation circuitry, Golkar and colleagues next asked whether altered neural function might underlie their symptoms. Naturally, they looked to the limbic system, a brain network involved in processing emotion. They focused particularly on the amygdala, which is known to be critical for evoking fear and anxiety, and is enlarged in people with occupational stress. Here, functional connectivity during rest between the amygdala and several brain regions was altered in patients; most notably, connections were weaker with the prefrontal cortex and stronger with the insula. What’s more, the stronger the correlation of the amygdala with the insula or a thalamic/hypothalamic region, the higher the individual’s perceived stress. Finally, connectivity between the amygdala and the anterior cingulate correlated with participants’ ability to down-regulate their emotional response from the startle-response task.

Figure 3. Differences in functional connectivity with the amygdala between patients and controls. doi: 10.1371/journal.pone.0104550

Figure 3. Differences in functional connectivity with the amygdala between patients and controls. doi: 10.1371/journal.pone.0104550

The findings of Golkar and colleagues help to establish a concrete understanding of the cognitive and neural changes underlying a too-often overlooked serious health condition. These findings add credence to the subjective feeling of being overly sensitive to negativity, or unable to control emotions, when burnt out. Perhaps more importantly, they confirm that such emotional impairments indeed have neurobiological underpinnings – changes that fit in beautifully with our knowledge of how the brain processes emotion. A stress-related disconnect between the amygdala and the prefrontal cortex and anterior cingulate – even at rest – builds upon earlier studies showing reduced volume and altered task-evoked responses in these areas associated with stress. And chronic stress was further related to amygdala hyperconnectivity with the insula and thalamus/hypothalamus, key regions for eliciting a stress response.

Dissociating the neural effects of stress

However, this study leaves several questions unanswered and raises a few more. Given the complexity of the patients’ psychological conditions, there were most certainly numerous other physical and psychological differences between the groups that went undocumented and uncontrolled. In the future, closer examination of these possible confounds will help identify their unique neural and behavioral effects. Furthermore, in addition to functional changes in several expected regions, altered resting connectivity also occurred in two unexpected regions – the cerebellum and motor cortex. Whether these were false positives, or whether occupational stress may have additional underappreciated motor or cognitive consequence, remains to be seen.

Another perspective

Because of the study’s justifiable focus on connectivity with the amygdala, it’s unclear how specific or broad the neural changes associated with chronic stress may be. Tom Liu, a researcher studying resting-state brain connectivity at UC San Diego, who was not involved in this study, explains,

“This begs the question of what other connections might be different between the two groups or perhaps show even better correlation with the stress scores. The issue there is that because of the large number of potential connections, a researcher is very quickly faced with a large multiple comparisons problem – this is an open issue in the field.”

Further work will help clarify whether stress – or other differences between the groups – predominantly affects limbic circuitry or might also contribute to global brain changes. Liu points out,

“One aspect that would have been interesting to look at is whether there were any global differences between the two groups that could have accounted for the differences, as the authors did not perform global signal regression.”

For instance, two recent studies report altered global signal associated with schizophrenia and variance in vigilance.

Golkar et al. help to bridge the gap between the emotional dysregulation of workplace burnout and its long-term impact on brain function. Such work is a valuable step towards not only better understanding the brain’s response to stress, but also better equipping us to manage our emotional and brain health – even after a long day of work.


Blix E, Perski A, Berglund H and Savic I (2013). Long-Term Occupational Stress Is Associated with Regional Reductions in Brain Tissue Volumes. PLOS One 8(6): e64065. doi:10.1371/journal.pone.0064065

Davis M (1992). The role of the amygdala in fear and anxiety. Annu Rev Neurosci 15:353-75. doi: 10.1146/annurev.ne.15.030192.002033

Flynn FG, Benson DF and Ardila, A (1999). Anatomy of the insula functional and clinical correlates. Aphasiology 13(1): 55-78. http://dx.doi.org/10.1080/026870399402325

Herman JP and Cullinan WE (1997). Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis. Trends Neurosci 20(2):78-84. doi: 10.1016/S0166-2236(96)10069-2

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

Jovanovic H, Perski A, Berglund H amd Savic I (2011). Chronic stress is linked to 5-HT(1A) receptor changes and functional disintegration of the limbic networks. Neuroimage 55(3):1178-88. doi: 10.1016/j.neuroimage.2010.12.060

LeDoux JE (2000). Emotion Circuits in the Brain. Annu Rev Neurosci 23: 155-84. doi: 10.1146/annurev.neuro.23.1.155

Savic I (2013). Structural Changes of the Brain in Relation to Occupational Stress. Cereb Cortex. doi: 10.1093/cercor/bht348

Schutte N, Toppinen S, Kalimo R and Schaufeli W (2000). The factorial validity of the Maslach Burnout Inventory—General Survey (MBI—GS) across occupational groups and nations. J Occup Organ Psych, 73(1), 53-66. http://dx.doi.org/10.1348/096317900166877

Wong CW, Olafsson V, Tal O, Liu TT (2013). The amplitude of the resting-state fMRI global signal is related to EEG vigilance measures. Neuroimge, 83, 983-90. doi: 10.1016/j.neuroimage.2013.07.057

Yang GJ, Murray JD, Repovs G, Cole MW, Savic A, Glasser MF, Pittenger C, Krystal JH, Wang XJ, Pearlson GD, Glahn DC, Anticevic A (2014). Altered global brain signal in schizophrenia. PNAS, 111(20), 7438-43. doi: 10.1073/pnas.1405289111

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To the depressed brain, it’s all the same

If you’re among the 8-12% of the population who will suffer from depression during their lifetime 1, you’re painfully aware of its debilitating symptoms – hopelessness, indifference, emptiness. While it’s clear how depression radically affects one’s emotional state, emerging research is showing that the reaches of depression extend far beyond our mood. In fact, depression can disrupt basic cognitive functions, with a particularly devastating impact on memory 2. However, at present we don’t fully understand the brain processes that give rise to depression, never mind how they contribute to the disorder’s associated cognitive impairments. A recent study published by neuroscientists at Brigham Young University suggests that depression is associated with problems with a particular memory operation known as pattern separation.

Can you tell Buddy from Fuzzy? Thank your hippocampus

Yassa & Stark, 2011

Imagine your two neighbors both have black labs, one slightly smaller and fuzzier than the other. A part of your brain called the hippocampus registers the subtle differences between the dogs and creates distinct representations of the two. You recognize Buddy and Fuzzy as unique because your brain effectively pattern separated them, forming distinct memories of each. It is this process that the researchers speculated might go awry in depression.

Earlier studies have shown that depressed individuals have smaller 4 and less active 5 hippocampi during memory formation than non-depressed people. Although pattern separation is not the only memory function mediated by the hippocampus, depression symptoms can manifest as a tendency to overgeneralize, the opposite of pattern separating. The authors therefore wondered whether diminished pattern separation might lie at the heart of depression-related memory problems.

Pattern separation to the test

To test their hypothesis, they had 98 adults perform a memory test that demanded pattern separation, and complete questionnaires evaluating depression, anxiety, sleep and exercise. Participants with higher depression scores performed significantly worse on the memory test than those with low depression scores, consistent with past studies. Critically, the depressed group had particular difficulty distinguishing a new item they had never seen from a similar one they previously encountered, indicating that they were pattern separating poorly. Furthermore, they found that the higher an individual’s depression score, the worse their pattern separation performance. Importantly, there was no correlation between pattern separation and anxiety, sleep or exercise, suggesting that the memory deficit was specifically related to depression, and not confounded by other associated factors.

But why don’t depressed brains pattern separate?

This study goes a step beyond prior work to identify what specific memory function is compromised in depression. Although the study didn’t examine the neurobiological processes underlying the pattern separation deficit, its findings provide a clear direction for further research.

Past studies suggest that newly born neurons in the hippocampus, produced by neurogenesis, contribute to pattern separation 6 and an association between reduced neurogenesis and “depression” in animals 7. If there are links between pattern separation and neurogenesis, neurogenesis and depression, and now depression and pattern separation, might a causal relationship exist among the three? The authors propose that depression could inhibit neurogenesis, thus impairing pattern separation. Alternatively, reduced neurogenesis (which can be regulated by numerous factors such as exercise, drugs or a rich environment) may induce depressive symptoms. Given the invasive nature of currently available methods to study neurogenesis, examining the effect of neurogenesis on human depression and memory is no easy feat (although some innovative folks recently devised a clever way to document human neurogenesis).

Can poor pattern separation make you sad?

But this study raises another, possibly more accessible, question over how pattern separation is involved in emotional regulation. Whereas the average person might readily discriminate between similar objects or experiences, someone suffering from depression would emphasize the similarities. A pathological tendency to excessively generalize could account for an unwarranted negative outlook.

“That last party was so awkward, I should just stop trying to be social.”

“I was bad at my last job, so I’ll certainly fail at any job I try”.

We’ll have to wait on future research to fully understand whether poor pattern separation contributes to a negative outlook, as well as the brain basis of memory impairments in depression. In the meantime, take a moment to notice the subtle differences around you – it just might make you happy.


1. Andrade L et al. 2003. The epidemiology of major depressive episodes: results from the International Consortium of Psychiatric Epidemiology (ICPE) Surveys. Int J Methods Psychiatr Res. 12:3-21.
2. Zakzanis KK et al. 1998. On the nature and pattern of neurocognitive function in major depressive disorder. Neuropsychiatry Neuropsychol Behav Neurol. 11:111-9.
3. Shelton DJ & Kirwan CB. 2013. A possible negative influence of depression on the ability to overcome memory interference. Behav Brain Research.
4. Videbech P & Ravnkilde B. 2004. Hippocampal volume and depression: A meta-analysis of MRI studies. Am J Psychiatry. 161:1957-66.
5. Fairhall SL et al. 2010. Memory related dysregulation of hippocampal function in major depressive disorder. Biol Psychol. 85:499-503.
6. Clelland CD et al. 2009. A functional role for adult hippocampal neurogenesis in spatial pattern separation. Science. 325:210-3.
7. Petrik D et al. 2012. The neurogenesis hypothesis of affective and anxiety disorders: are we mistaking the scaffolding for the building? Neuropharmacology. 62:21-34.

Shelton DJ & Kirwan CB (2013). A possible negative influence of depression on the ability to overcome memory interference Behavioral Brain Research DOI: 10.1016/j.bbr.2013.08.016

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Misophonia: Common sounds are all the rage

Click click click.

“Dear GOD, why does she keep doing that? Doesn’t she know how irritating that is? Has she no respect for the rest of us trying to work? Is she intentionally trying to piss me off?!”

Your blood pressure rises as you bite your lip, suppressing the urge to verbalize this inner dialogue. You take several deep breaths to assuage the flood of anxiety. The anger and stress slowly dissolve, replaced by shame as you realize just how irrational this emotional response was. After all, your coworker was simply … clicking her pen.


For most of us, sounds such as pen-clicking, chewing or whistling are everyday elements of a neutral auditory landscape that go largely unnoticed. But for a small portion of the population, such common sounds evoke extreme rage, disgust or anxiety. The first such cases were documented just over a decade ago, when the condition was coined misophonia, literally “hatred of sound”. Since then, thousands of self-diagnosed misophonics have sought comfort and advice from online support groups. Misophonia is gaining increasing attention by psychiatrists who believe it should be recognized as an official psychiatric disorder 1 and neuroscientists curious about how nervous system dysfunction may contribute to the condition. As a first step, a team of psychologists sought to better characterize misophonia in their study recently published in Frontiers in Human Neuroscience 2.


The researchers conducted a series of extensive interviews with eleven self-reported misophonics to characterize their trigger sounds, environmental features that exacerbate their reactions, and personal thoughts and coping strategies. Despite the small sample size and the somewhat anecdotal nature of the data, the study reports some interesting common threads. Most participants reported that symptoms first appeared in childhood and either continued or worsened over the years. Chances are, just today you’ve probably made some of the very sounds misophonics report as most maddening, including eating or chewing, pen clicking, footsteps, finger tapping or whistling. And depending on who you are, your innocent walk down the hall or your chipper whistle may have sent a nearby misophonic into a horrified rage; 82% claimed that their discomfort is only set off by certain people, while none were bothered by making the sounds themselves. Although the victims of such noxious sounds may not outwardly display their horror, internally they’re feeling intense anxiety, anger, irritation or physical pressure, thinking that your sounds are rude or disgusting, and experiencing high blood pressure or a racing heart rate. In fact, underneath their blank expression, they just might be thinking … (yup. These were actual thoughts reported by study participants):

“I want to punch this person”
“I hate this person”
“Would you shut up?”

But don’t dismiss misophonia as an extreme case of hateful intolerance. Misophonics are acutely aware that they focus abnormally on sounds. Their agony can be so extreme that it forces them to avoid certain social situations and can even elicit suicidal thoughts. Their self-directed thoughts clearly reflect this inner struggle:

“Why am I like this?”
“I envy people who aren’t bothered by sounds”

Hot and bothered

Might misophonics simply be a crew of melodramatic hypochondriacs? To determine whether participants actually demonstrate physical signs of “sound hate”, the researchers measured the skin conductance reponse (fancy term for sweat production) to a variety of sounds and images. To no surprise, the misophonics reported greater discomfort than controls to sounds but not to images. Justifying their claims, they also produced a greater skin conductance response than controls to sounds than images, and this reponse was positively correlated with subjective aversion to sounds.

The misophonic brain

But sweat can tell only so much about a disorder that is likely neurological in origin. To understand why misophonia occurs, in addition to what it is, scientists will need to look beyond skin-deep, into the brain. To date, no research has directly studied the neurobiological basis of misophonia, although testable hypotheses are in the works. One prevailing theory has emerged from the similarities between misophonia and another intriguing condition that has long fascinated scientists – synesthesia. synesthesiaMuch as misophonics abnormally associate sounds with intense emotions, synesthetes experience aberrant associations between sensations; for example, associating letters with colors, or months with spatial positions. It’s believed that this atypical sensory integration arises from enhanced interactions between the brain’s sensory networks. In support of this idea, neuroimaging studies have shown activation of the color-selective visual area V4 when synesthetes hear words 3, and increased structural connectivity between implicated sensory regions 4. If misophonia arises from similar processes, it might be generated from excessive cross-talk between the brain’s auditory and limbic systems. This is an enticing theory indeed, but it is just a theory. The obvious next step is to test whether, in fact, misophonics abnormally activate limbic regions in response to trigger sounds, or show increased connectivity between limbic structures and auditory cortex.

Until we better understand the disorder, why not keep those closet misophonics in mind at your next lunch? Chomp your sandwhich a tad quieter and you just might save someone’s sanity.


1. Schroder A et al. 2013. Misophonia: Diagnostic criteria for a new psychiatric disorder. PLoS One. 8.
2. Edelstein M et al. 2013. Misophonia: physiological investigations and case descriptions. Front Hum Neurosci. 7:296.
3. Nunn JA et al. 2002. Functional magnetic resonance imaging of synesthesia: activation of V4/V8 by spoken words. Nat Neuro. 5:371-5.
4. Zamm A et al. 2013. Pathways to seeing music: enhanced structural connectivity in colored-music synesthesia. Neuroimage. 74:359-66.

Edelstein M, Brang D, Rouw R, & Ramachandran VS (2013). Misophonia: physiological investigations and case descriptions. Frontiers in human neuroscience, 7 PMID: 23805089

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