Apathy

Le Heron et al. (2018) defines apathy as a marked reduction in goal-directed behavior. But in order to move, one must be motivated to do so. Therefore, a generalized form of impaired motivation also hallmarks apathy.

The authors compiled for us a nice mini-review combing through the literature of motivation in order to identify, if possible, the neurobiological mechanism(s) of apathy. First, they go very succinctly though the neuroscience of motivated behavior. Very succinctly, because there are literally hundreds of thousands of worthwhile pages out there on this subject. Although there are several other models proposed out-there, the authors’ new model on motivation includes the usual suspects (dopamine, striatum, prefrontal cortex, anterior cingulate cortex) and you can see it in the Fig. 1.

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Fig. 1 from Le Heron et al. (2018). The red underlining is mine because I really liked how well and succinctly the authors put a universal truth about the brain: “A single brain region likely contributes to more than one process, but with specialisation”. © Author(s) (or their employer(s)) 2018.

After this intro, the authors go on to showcasing findings from the effort-based decision-making field, which suggest that the dopamine-producing neurons from ventral tegmental area (VTA) are fundamental in choosing an action that requires high-effort for high-reward versus a low-effort for low-reward. Contrary to what Wikipedia tells you, a reduction, not an increase, in mesolimbic dopamine is associated with apathy, i.e. preferring a low-effort for low-reward activity.

Next, the authors focus on why are the apathetic… apathetic? Basically, they asked the question: “For the apathetic, is the reward too little or is the effort too high?” By looking at some cleverly designed experiments destined to parse out sensitivity to reward versus sensitivity to effort costs, the authors conclude that the apathetics are indeed sensitive to the reward, meaning they don’t find the rewards good enough for them to move.  Therefore, the answer is the reward is too little.

In a nutshell, apathetic people think “It’s not worth it, so I’m not willing to put in the effort to get it”. But if somehow they are made to judge the reward as good enough, to think “it’s worth it”, they are willing to work their darndest to get it, like everybody else.

The application of this is that in order to get people off the couch and do stuff you have to present them a reward that they consider worth moving for, in other words to motivate them. To which any practicing psychologist or counselor would say: “Duh! We’ve been saying that for ages. Glad that neuroscience finally caught up”.  Because it’s easy to say people need to get motivated, but much much harder to figure out how.

This was a difficult write for me and even I recognize the quality of this blogpost as crappy. That’s because, more or less, this paper is within my narrow specialization field. There are points where I disagree with the authors (some definitions of terms), there are points where things are way more nuanced than presented (dopamine findings in reward), and finally there are personal preferences (the interpretation of data from Parkinson’s disease studies). Plus, Salamone (the second-to-last author) is a big name in dopamine research, meaning I’m familiar with his past 20 years or so worth of publications, so I can infer certain salient implications (one dopamine hypothesis is about saliency, get it?).

It’s an interesting paper, but it’s definitely written for the specialist. Hurray (or boo, whatever would be your preference) for another model of dopamine function(s).

REFERENCE: Le Heron C, Holroyd CB, Salamone J, & Husain M (26 Oct 2018, Epub ahead of print). Brain mechanisms underlying apathy. Journal of Neurology, Neurosurgery & Psychiatry. pii: jnnp-2018-318265. doi: 10.1136/jnnp-2018-318265. PMID: 30366958 ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 24 November 2018

The good and the bad of abstinence

The nucleus accumbens, a key region involved in reward processing and addiction. Credit: Zou et al. (2015)
The nucleus accumbens, a key region involved in reward processing and addiction. Credit: Zou et al. (2015)

Consumption of addictive drugs changes your brain and these changes underlie the consequent dependence. It is very difficult to quit, and certainly it is not a matter of lack of will power that the majority of drug users have such a great difficulty in trying to quit. But what happens to the brains of the lucky few who managed to kick the addiction out the window? Are their brains reverting to their pre-addiction states? As the paper below shows, sadly, no. But there is hope.

Zhou et al. ( 2015) used resting state fMRI (which means scanning your brain without requiring you to perform any task) to investigate the brains of 30 healthy controls and 30 heroin-addicts who were abstinent from the drug for more than 3 years. Specifically, they looked to see if the connectivity of certain brain regions involved in addiction is different after such a long abstinence time.

The bad news is that the abstinents still had some abnormal connectivity (for specialists: “stronger functional connectivity between the nucleus accumbens and the right ventromedial prefrontal cortex and relatively weaker connectivity between the nucleus accumbens and the left putamen, left precuneus, and supplementary motor area” p. 1697).

The good news: the longer the abstinence time, the greater the strength of the connection between nucleus accumbens and putamen (first structure involved in reward processing, the second in habit-learning), suggesting a partial neural recovery.

The study has some limitations: technical (did not control for heartbeat and respiration), methodological (most of the heroin abstinents were smokers, another addiction) and theoretical (one brain area does not support only one function, so its connectivity shouldn’t be over interpreted). With the caveat that the connectivity differences observed do not in any way point to a cause and effect relationship – that is we don’t know if these differences existed before the first heroin intake and caused it or they appeared after as a result of drug consumption, I think the paper is still is worth reading.

Reference: Zou F, Wu X, Zhai T, Lei Y, Shao Y, Jin X, Tan S, Wu B, Wang L, Yang Z (November 2015, Epub 17 Aug 2015). Abnormal resting-state functional connectivity of the nucleus accumbens in multi-year abstinent heroin addicts. Journal of Neuroscience Research, 93(11):1693-702. doi: 10.1002/jnr.23608. Article | FREE PDF

By Neuronicus, 9 October 2015