Amusia and stroke

Although a complete musical anti-talent myself, that doesn’t prohibit me from fully enjoying the works of the masters in the art. When my family is out of earshot, I even bellow – because it cannot be called music – from the top of my lungs alongside the most famous tenors ever recorded. A couple of days ago I loaded one of my most eclectic playlists. While remembering my younger days as an Iron Maiden concert goer (I never said I listen only to classical music :D) and screaming the “Fear of the Dark” chorus, I wondered what’s new on the front of music processing in the brain.

And I found an interesting recent paper about amusia. Amusia is, as those of you with ancient Greek proclivities might have surmised, a deficit in the perception of music, mainly the pitch but sometimes rhythm and other aspects of music. A small percentage of the population is born with it, but a whooping 35 to 69% of stroke survivors exhibit the disorder.

So Sihvonen et al. (2016) decided to take a closer look at this phenomenon with the help of 77 stroke patients. These patients had an MRI scan within the first 3 weeks following stroke and another one 6 months poststroke. They also completed a behavioral test for amusia within the first 3 weeks following stroke and again 3 months later. For reasons undisclosed, and thus raising my eyebrows, the behavioral assessment was not performed at 6 months poststroke, nor an MRI at the 3 months follow-up. It would be nice to have had behavioral assessment with brain images at the same time because a lot can happen in weeks, let alone months after a stroke.

Nevertheless, the authors used a novel way to look at the brain pictures, called voxel-based lesion-symptom mapping (VLSM). Well, is not really novel, it’s been around for 15 years or so. Basically, to ascertain the function of a brain region, researchers either get people with a specific brain lesion and then look for a behavioral deficit or get a symptom and then they look for a brain lesion. Both approaches have distinct advantages but also disadvantages (see Bates et al., 2003). To overcome the disadvantages of these methods, enter the scene VLSM, which is a mathematical/statistical gimmick that allows you to explore the relationship between brain and function without forming preconceived ideas, i.e. without forcing dichotomous categories. They also looked at voxel-based morphometry (VBM), which a fancy way of saying they looked to see if the grey and white matter differ over time in the brains of their subjects.

After much analyses, Sihvonen et al. (2016) conclude that the damage to the right hemisphere is more likely conducive to amusia, as opposed to aphasia which is due mainly to damage to the left hemisphere. More specifically,

“damage to the right temporal areas, insula, and putamen forms the crucial neural substrate for acquired amusia after stroke. Persistent amusia is associated with further [grey matter] atrophy in the right superior temporal gyrus (STG) and middle temporal gyrus (MTG), locating more anteriorly for rhythm amusia and more posteriorly for pitch amusia.”

The more we know, the better chances we have to improve treatments for people.


unless you’re left-handed, then things are reversed.


1. Sihvonen AJ, Ripollés P, Leo V, Rodríguez-Fornells A, Soinila S, & Särkämö T. (24 Aug 2016). Neural Basis of Acquired Amusia and Its Recovery after Stroke. Journal of Neuroscience, 36(34):8872-8881. PMID: 27559169, DOI: 10.1523/JNEUROSCI.0709-16.2016. ARTICLE  | FULLTEXT PDF

2.Bates E, Wilson SM, Saygin AP, Dick F, Sereno MI, Knight RT, & Dronkers NF (May 2003). Voxel-based lesion-symptom mapping. Nature Neuroscience, 6(5):448-50. PMID: 12704393, DOI: 10.1038/nn1050. ARTICLE

By Neuronicus, 9 November 2016



The runner’s euphoria and opioids

The runner’s high is most likely due to release of the endorphins binding to the opioid receptors according to Boecker et al. (2008, doi: 10.1093/cercor/bhn013). Image courtesy of Pixabay.

We all know that exercise is good for you: it keeps you fit, it reduces stress and improves your mood. And also, sometimes, particularly after endurance running, it gets you high. The mechanism of euphoria reported by some runners after resistance training is unknown. Here is a nice paper trying to figure it out.

Boecker et al. (2008) scanned 10 trained male athletes at rest and after 2 hour worth of endurance running. By “trained athletes” they mean people that ran for 4-10 hours weekly for the past 2 years. The scanning was done using a positron emission tomograph (PET). The PET looks for a particular chemical that has been injected into the bloodstream of the subjects, in this case non-selective opioidergic ligand (it binds to all opioid receptors in the brain; morphine, for example, binds only to a subclass of the opioid receptors).

The rationale is as follows: if we see an increase in ligand binding, then the receptors were free, unoccupied, showing a reduction in the endogenous neurotransmitter, that is the substance that the brain produces for those receptors; if we see a decrease in the ligand binding it was because the receptors were occupied, meaning that there was an increase in the production of the endogenous neurotransmitter. The endogenous neurotransmitters for the opioid receptors are the endorphins (don’t confuse them with epinephrine a.k.a. adrenaline; different systems entirely).

After running, the subjects reported that they are euphoric and happy, but no change in other feelings (confusion, anger, sadness, fear etc.; there was a reduction in fear, but it was not significant). The scanning showed that it was less binding of the opioidergic ligand in many places in the brain (for the specialist, here you go: prefrontal/orbitofrontal cortices, dorsolateral prefrontal cortex, anterior and posterior cingulate cortex, insula and parahippocampal gyrus, sensorimotor/parietal regions, cerebellum and basal ganglia).

Regression analysis showed that there was a link between the euphoria feeling and the receptor occupancy: the more euphoric the people said they were, the more endorphines (i.e. endogenous opioids) they had bound in the brain. This study is the first to show this kind of link.

Reference: Boecker H, Sprenger T, Spilker ME, Henriksen G, Koppenhoefer M, Wagner KJ, Valet M, Berthele A, & Tolle TR. (Nov 2008, Epub 21 Feb 2008). The Runner’s High: Opioidergic Mechanisms in the Human Brain. Cerebral Cortex, 18:2523–2531. doi:10.1093/cercor/bhn013. Article | FREE FULLTEXT PDF

By Neuronicus, 28 November 2015


Pee now! NOW, I said! In a huge magnet. While we watch.

Photo credit: Free clipart from
Photo credit: Free clipart from

Like many studies that fill in unknown gaps in the body of knowledge, the paper below may not attract attention, except from the people in their narrow field. So let’s give it a little attention.

Michels et al. (2015) sought to map out the brain network underlying the control of urination using the fMRI. They got 22 healthy adult males and they gave them furosemide, which is a diuretic, and then asked them to drink as much water as they want until they need to urinate. During this, “a condom catheter was attached to the penis of each subject” (p. 3370), to monitor the urine flow while in scanner. Then the testing would not start, oh no. The subjects were then submitted to an ultrasound to make sure the bladder was full. Then they were asked again how much they really needed to go pee. Then they go in the scanner in a supine position, where they are told to wait, then to imagine the starting of urination (but don’t pee just yet!), and finally, finally allowed to urinate. But then, cruelly, told to stop only 3 second into the act. And then the scanner cycle would repeat. Their champion peers (I cannot avoid the pun, I’m sorry) managed to pee 15 times in the scanner. I wonder how many subjects peed sans cue… (authors don’t mention that).

Fig. 1 from Michels et al. (2015) depicting the fMRI scan paradigm, which consisted of 2 randomly alternating blocks.
Fig. 1 from Michels et al. (2015) depicting the fMRI scan paradigm, which consisted of 2 randomly alternating blocks. SDV = strong desire to void.

Amazingly, under these conditions, there were seven men who could not urinate in the scanner. Authors call these non-voiders, or, as we commonly know them, the shy bladders or the bashful kidneys. Not surprisingly, non-voiders had lower activity in the pontine micturition center (PMC), a brain area, which, as its name implies, is responsible for urination. Also not surprisingly – for me at least, the authors find this interesting -, the non-voiders showed increased activity in the anterior midcingulate cortex (aMCC), which is an area involved in control. I guess you need some steely control to not pee after all that. The aMCC inhibits the urination-facilitation brain regions, such as the PMC.

Anyway, the main finding of the study is a detailed map of micturition supraspinal mechanisms, which consists of a slew of structures, each with its own function. I had never known how complicated peeing and not-peeing are until I read this paper. Jokes and cringes aside, this study is a welcome addition to understanding how we control our bodily functions and where to start looking when this control fails, shedding new light on the interplay between reflex and control.

Reference: Michels, L., Blok, B. F., Gregorini, F., Kurz, M., Schurch, B., Kessler, T. M., Kollias, S., & Mehnert, U. (October 2015, Epub Jun 26 2014). Supraspinal Control of Urine Storage and Micturition in Men-An fMRI Study. Cerebral Cortex, 25(10): 3369-80. doi: 10.1093/cercor/bhu140. Article | FREE FULLTEXT PDF

By Neuronicus, 1 October 2015