Can’t or Won’t – An Introduction To Apathy.

 Megan Jackson | 19 DEC 2018

Often, when a person hears the word apathy, an image comes to mind. A glassy-eyed teenager scrolling vacantly through their phone while their parent looks on in despair. While comical, it does not reflect what apathy really is clinically: a complex symptom that has important clinical significance.

In 1956, a study was published describing a group of Americans released from Chinese prison camps following the Korean war1. As a reaction to the severe stress they had suffered during their time in prison, the men were observed to be ‘listless’, ‘indifferent’ and ‘lacking emotion’. The scientists decided to call this pattern of behaviours apathy. However, at this point, there was no formal way to measure apathy. It was acknowledged that it could manifest in varying degrees, but that was the extent of it. It was over 30 years before apathy was given a proper definition and recognised as a true clinical construct.

As time went on, scientists noticed that apathy doesn’t just arise from times of extreme stress, like time in a prison camp, but that it also appears in a variety of clinical disorders. A proper definition and a way of assessing apathy was needed. In 1990, Robert Marin defined apathy as ‘a loss of motivation not attributable to current emotional distress, cognitive impairment, or diminished level of consciousness’. As this is a bit of a mouthful, it was summarised as ‘A measurable reduction in goal-directed behaviour’. This definition makes it easy to imagine an individual who no longer cares about, likes, or wants anything and therefore does nothing. However, this is not always the case. There are different subtypes of apathy that each involve different brain regions and thought-processes, these are:

Cognitive – in which the individual does not have the cognitive ability to put a plan into action. This may be due to disruption to the dorsolateral prefrontal cortex.

Emotional-affective – in which the individual can’t link their behaviour or the behaviour of others with emotions. This may be due to disruption to the orbital-medial prefrontal cortex.

Auto-activation – in which the individual can no longer self-initiate actions. This may be due to disruption to parts of the globus pallidus.

It’s much easier to picture how the different types of apathy affect behaviour. Take Bob for example. Bob has apathy, yet Bob likes cake. When somebody asks Bob whether he would like cake he responds with a yes. However, Bob makes no move to go and get it. Bob still likes cake, but he can no longer process how to obtain that cake. He has cognitive apathy. In another example, Bob may want cake but does not want to get up and get it. However if someone told him to, he probably would go and get it. This is auto-activation apathy and is the most severe and the most common kind. If Bob could no longer associate cake with the feeling of happiness or pleasure, then he has emotional-affective apathy.

So, whatever subtype of apathy Bob has, he doesn’t get his cake. A shame, but this seems a little trivial. Should we really care about apathy? Absolutely! Imagine not being able to get out of your chair and do the things you once loved. Imagine not being able to feel emotions the way you used to. Love, joy, interest, humour – all muted. Think of the impact it would have on your family and friends. It severely diminishes quality of life, and greatly increases caregiver burden. It is extremely common in people with neurodegenerative diseases like dementia2, psychiatric disorders like schizophrenia3, and in people who’ve had a stroke4. It can even occur in otherwise healthy individuals.

Elderly people are particularly at risk, though scientists haven’t yet figured out why. Could it be altered brain chemistry? Inevitable degeneration of important brain areas? One potential explanation is that apathy is caused by a disruption to the body clock. Every person has a body clock, a tiny area of the brain called the suprachiasmatic nucleus, which controls the daily rhythms of our entire bodies like when we wake up, go to sleep, and a load of other really important physiological processes like hormone release. Disruption to the body clock can cause a whole host of health problems, from diabetes to psychiatric disorders like depression. Elderly people have disrupted daily rhythms compared to young, healthy people and it is possible that the prevalence of apathy in the elderly is explained by this disrupted body clock. Much more research is needed to find out if this is indeed the case and why!

Figuring out how or why apathy develops is a vital step in developing a treatment for it, and it’s important that we do. While apathy is often a symptom rather than a disease by itself, there’s now a greater emphasis on treating neurological disorders symptom by symptom rather than as a whole, because the underlying disease mechanisms are so complex. So, developing a treatment for apathy will benefit a whole host of people, from the elderly population, to people suffering from a wide range of neurological disorders.

Edited by Sam Berry & Chiara Casella


  • Chase, T.N., (2011) Apathy in neuropsychiatric disease: diagnosis, pathophysiology, and treatment Neurotox Res 266-78.
  • Chow, T.W., (2009) Apathy Symptom Profile and Behavioral Associations in Frontotemporal Dementia vs. Alzheimer’s Disease, Arch Neurol, 66(7); 88-83
  • Gillette M.U., (1999) Suprachiasmatic nucleus: the brain’s circadian clock, Recent Prog Horm Res. 54:33-58
  • Stassman, H.D. (1956) A Prisoner of War Syndrome: Apathy as a Reaction to Severe Stress, Am.J.Psyc., 112(12):998-1003
  • Willem van Dalen, J., (2013) Poststroke apathy, Stroke, 44:851-860.

The healing power of companionship

Shireene Kalbassi | 11 MAY 2018

When it comes to the recovery of wounds and other medical conditions, most people probably think of hospital beds, antibiotics, and maybe some stitches. What probably doesn’t come to mind is the role that companionship may play in speeding up the healing process.

And yet, studies in humans have shown a link between increased companionship and enhanced recovery prospects (Bae et al 2001, Boden-Albala et al 2005).

So why should it be that social interaction influences the recovery process? Well, in social species, social interaction leads to the release of the hormone known as oxytocin, AKA the “love hormone”. This hormone is released from the pituitary gland, located in the brain. Increased levels of oxytocin have been associated with lower levels of stress response hormones, such as cortisol and corticosterone, and high levels of these stress response hormones have been shown to lead to impaired healing (Padgett et al 1998, DeVries  et al 2002, Heinrichs et al 2003, Ebrecht et al 2004).

This link between social interaction, oxytocin, stress hormones and recovery has been explored in studies, such as the work of Detillion et al (2004). Here, the authors investigated how companionship impacts wound healing in stressed and non-stressed hamsters. The role of companionship was explored by comparing socially isolated hamsters to ‘socially housed’ hamsters, that share a home environment with another hamster. Stressed hamsters were physically restrained to induce a stress response, while non-stressed hamsters did not undergo physical restraint.

In order to understand how these factors relate, the authors therefore compared four different groups: hamsters that were socially isolated and stressed, hamsters that were socially housed and stressed, hamsters that were socially isolated and non-stressed, and hamsters that were socially housed and non-stressed.

The hamsters that were socially isolated and stressed showed decreased wound healing and increased cortisol levels, when compared to socially housed hamsters or non-stressed socially isolated hamsters. Furthermore, when a blocker of oxytocin was given to socially housed hamsters decreased wound healing was observed, while supplementing stressed hamsters with oxytocin lead to increased wound healing and lower levels of cortisol.

So it seems that when social animals interact oxytocin is released, which reduces the levels of stress hormones, leading to increased wound healing.

But what if there is more to the story than this? These studies, and others like it, demonstrate a relationship between companionship and wound healing, but how might factors relating to social interaction impact recovery?

Venna et al (2014) explored the recovery of mice that were given a brain occlusion, where part of the blood supply of the brain is shut off to try to replicate the damage seen in stroke. However, in this study the mice were either socially isolated, paired with another stroke mouse, or paired with a healthy partner. When assessing recovery, the authors looked at multiple parameters including death rates, recovery of movement, and new neuron growth. The authors observed that, as expected, socially isolated stroke mice showed the lowest rates of recovery. Interestingly, stroke mice that were housed with other stroke mice showed decreased recovery rates when compared to stroke mice that were housed with a healthy partner.

So why should the health status of the partner influence the healing process of the mice? The work of Venna et al did not assess if the amount of social contact between stroke mice that were housed with another stroke mouse was equal to that of stroke mice that were housed with a healthy partner, which may explain the discrepancy seen between the two groups. Exploration of this could lead to better understanding of whether the quantity of social interaction may be leading to decreased recovery rates in the stroke mice housed with other stroke mice groups, or if the decreased recovery may be due to other factors.

Regardless, it appears that social interaction may not be a simple box to tick when it comes to enhancing the recovery process but is instead dynamic in nature. And while nothing can replace proper medical care and attention, companionship may have a role in speeding up the recovery process.  

If you want to know more about the use of animals in research, please click here.

Edited By Sophie Waldron & Monika śledziowska


  • Bae, S.C., Hashimoto, H.I.D.E.K.I., Karlson, E.W., Liang, M.H. and Daltroy, L.H., 2001. Variable effects of social support by race, economic status, and disease activity in systemic lupus erythematosus. The Journal of Rheumatology, 28(6), pp.1245-125
  • Boden-Albala, B., Litwak, E., Elkind, M.S.V., Rundek, T. and Sacco, R.L., 2005. Social isolation and outcomes post stroke. Neurology, 64(11), pp.1888-1892
  • Padgett, D.A., Marucha, P.T. and Sheridan, J.F., 1998. Restraint stress slows cutaneous wound healing in mice. Brain, behavior, and immunity, 12(1), pp.64-73.
  • DeVries, A.C., 2002. Interaction among social environment, the hypothalamic–pituitary–adrenal axis, and behavior. Hormones and Behavior, 41(4), pp.405-413.
  • Heinrichs, M., Baumgartner, T., Kirschbaum, C. and Ehlert, U., 2003. Social support and oxytocin interact to suppress cortisol and subjective responses to psychosocial stress. Biological psychiatry, 54(12), pp.1389-1398.
  • Ebrecht, M., Hextall, J., Kirtley, L.G., Taylor, A., Dyson, M. and Weinman, J., 2004. Perceived stress and cortisol levels predict speed of wound healing in healthy male adults. Psychoneuroendocrinology, 29(6), pp.798-809.
  • Detillion, C.E., Craft, T.K., Glasper, E.R., Prendergast, B.J. and DeVries, A.C., 2004. Social facilitation of wound healing. Psychoneuroendocrinology, 29(8), pp.1004-1011.
  • Glasper, E.R. and DeVries, A.C., 2005. Social structure influences effects of pair-housing on wound healing. Brain, behavior, and immunity, 19(1), pp.61-68
  • Venna, V.R., Xu, Y., Doran, S.J., Patrizz, A. and McCullough, L.D., 2014. Social interaction plays a critical role in neurogenesis and recovery after stroke. Translational psychiatry, 4(1), p.e351

♥ Achy-breaky heart? Try touchy-feely brain! ♥

Laura Smith | 14 FEB 2017

As today is Valentine’s day, let’s get a bit touchy-feely. Whether you’re looking forward to a date with your significant other; planning to profess your feelings to a special someone; or hoping your soulmate will sweep you off your feet, you’d probably like to share a romantic caress. But what happens in the brain when we anticipate touching the one we desire? Using functional magnetic resonance imaging (fMRI), scientists in Italy set out to answer just that question. Isn’t that convenient!

fMRI uses the same principle as standard MRI: a large, very powerful electromagnet detects differences in the magnetic properties of different bodily tissues, and some fancy maths turns these signals into pictures. In fMRI, people in the scanner perform tasks, and scientists can locate brain areas where activity levels change in response to this.

In their fMRI study, published in the journal Frontiers in Behavioural Neuroscience, Ebisch, Ferri & Gallese (2014) wanted to find out if how much someone loved their partner was reflected in their brain activity when they anticipated caressing them. Participants in the MRI scanner were instructed to affectionately touch either a ball or their partner’s hand, which were both placed close to them.  They received a “touch” or “do not touch” instruction 3 seconds after they were told which item to touch (the hand or the ball). Therefore, they would anticipate performing the touch each time, which would involve a change in brain activity.  The task was performed many times but, 67% of the time, participants were asked not to perform the touch.

Participants also completed the Passionate Love Scale (PLS) (Hatfield & Sprecher, 1986) : a 15-item questionnaire measuring the intensity of their desire for their partner from “extremely cool” to “extremely passionate”, so that the researchers could see whether it was related to the changes in brain activity.  There was such a relationship in the right posterior insula: an area of cortex believed to act as a processing-hub for information about the body’s current physiological state (Augustine, 1996) .  Insula activity decreased during anticipation of touching but the more passionate the love, the less deactivation there was for anticipation of romantic but not non-romantic touching. So, when participants’ desire for their partners was higher, there was more neural response to anticipation of touching the partner versus the ball.  Additionally, insula activity increased when touches were actually performed, and significantly moreso for romantic versus non-romantic touches.


Location of right posterior insula. Retrieved from Ebisch et al. (2014)1

The insula interacts with brain areas involved in bodily sensation (Zweynert et al., 2011) , in particular the somatosensory cortex.  This area’s activity in response to touch was previously shown to be influenced by anticipation of a reward (Pleger et al., 2008). Taking this into account, the researchers suggest that the posterior insula, via its connection with somatosensory cortex, may influence how we actually experience touches. As such, because desire for the partner was associated with less insula deactivation during anticipation of touching them, it may be that wanting to touch someone actually makes the experience of doing so all the more pleasant.

So spare a thought for your clever insula today, and have a happy Valentine’s day.


  • Augustine, JR. (1996). Circuitry and functional aspects of the insular lobe in primates including humans. Brain Res. Rev., 22, 229-244.
  • Ebisch SJ, Ferri F & Gallese V. (2014). Touching moments: desire modulates the neural anticipation of active romantic caress.
  • Hatfield E. & Sprecher S. (1986). Measuring passionate love in intimate relations. Adolescence, 9, 383-410.
  • Pleger B, Blankenburg F, Ruff C, Driver J & Dolan R. (2008). Reward facilitates tactile judgments and modulates hemodynamic responses in human primary somatosensory cortex. Neurophysiol., 39, A9.
  • Zweynert S, Pade JP, Wustenberg T et al. (2011). Motivational salience modulates hippocampal repetition suppression and functional connectivity in humans. Hum. Neurosci, 5, 144.

Featured image by Alex Van