Soccer and brain jiggling

There is no news or surprise that strong hits to the head produce transient or permanent brain damage. But how about mild hits produced by light objects like, say, a volley ball or soccer ball?

During a game of soccer, a player is allowed to touch the ball with any part of his/her body minus the hands. Therefore, hitting the ball with the head, a.k.a. soccer heading, is a legal move and goals marked through such a move are thought to be most spectacular by the refined connoisseur.

A year back, in 2015, the United States Soccer Federation forbade the heading of the ball by children 10 years old and younger after a class-action lawsuit against them. There has been some data that soccer players display loss of brain matter that is associated with cognitive impairment, but such studies were correlational in nature.

Now, Di Virgilio et al. (2016) conducted a study designed to explore the consequences of soccer heading in more detail. They recruited 19 young amateur soccer players, mostly male, who were instructed to perform 20 rotational headings as if responding to corner kicks in a game. The ball was delivered by a machine at a speed of approximately 38 kph. The mean force of impact for the group was 13.1 ± 1.9 g. Immediately after the heading session and at 24 h, 48 h and 2 weeks post-heading, the authors performed a series of tests, among which are a transcranial magnetic stimulation (TMS) recording, a cognitive function assessment (by using the Cambridge Neuropsychological Test Automated Battery), and a postural control test.

Not being a TMS expert myself, I was wondering how do you record with a stimulator? TMS stimulates, it doesn’t measure anything. Or so I thought. The authors delivered brief  (1 ms) stimulating impulses to the brain area that controls the leg (primary motor cortex). Then they placed an electrode over the said muscle (rectus femoris or quadriceps femoris) and recorded how the muscle responded. Pretty neat. Moreover, the authors believe that they can make inferences about levels of inhibitory chemicals in the brain from the way the muscle responds. Namely, if the muscle is sluggish in responding to stimulation, then the brain released an inhibitory chemical, like GABA (gamma-amino butyric acid), hence calling this process corticomotor inhibition. Personally, I find this GABA inference a bit of a leap of faith, but, like I said, I am not fully versed in TMS studies so it may be well documented. Whether or not GABA is responsible for the muscle sluggishness, one thing is well documented though: this sluggishness is the most consistent finding in concussions.

The subjects had impaired short term and long term memory functions immediately after the ball heading, but not 24 h or more later. Also transient was the corticomotor inhibition. In other words, soccer ball heading results in measurable changes in brain function. Changes for the worst.

Even if these changes are transient, there is no knowing (as of yet) what prolonged ball heading might do. There is ample evidence that successive concussions have devastating effects on the brain. Granted, soccer heading does not produce concussions, at least in this paper’s setting, but I cannot think that even sub-concussion intensity brain disruption can be good for you.

On a lighter note, although the title of the paper features the word “soccer”, the rest o the paper refers to the game as “football”. I’ll let you guess the authors’ nationality or at least the continent of provenance ;).


Reference: Di Virgilio TG, Hunter A, Wilson L, Stewart W, Goodall S, Howatson G, Donaldson DI, & Ietswaart M. (Nov 2016, Epub 23 Oct 2016). Evidence for Acute Electrophysiological and Cognitive Changes Following Routine Soccer Heading. EBioMedicine, 13:66-71. PMID: 27789273, DOI: 10.1016/j.ebiom.2016.10.029. ARTICLE | FREE FULLTEXT PDF

By Neuronicus, 20 December 2016


Giving up? Your parvalbumin neurons may have something to do with it

Cartoon from, licensing unknown
Cartoon from Photobucket, licensing unknown.

One of the most ecologically-valid rodent models of depression is the learned helplessness paradigm. You get a rat or a mouse and you confine it in a cage with an electrified grid. Then you apply mild foot shocks at random intervals and of random duration for an hour (which is one session). The mouse initially tries to escape, but there is no escape; the whole floor is electrified. After a couple of sessions, the mouse doesn’t try to escape anymore; it gives up. Even when you put the mouse in a cage with an open door, so it can flee to no-pain freedom, it doesn’t attempt to do so. The interpretation is that the mouse has learned that it cannot control the environment, no matter what he does, he’s helpless, so why bother? Hence the name of the behavioral paradigm: learned helplessness.

All antidepressants on the market have been tested at one point or another against this paradigm; if the drug got the mouse to try to escape more, then the drug passed the test.

Just like in the higher vertebrate realm, there are a few animals who keep trying to escape longer than the others, before they too finally give up; we call these resilient.

Perova, Delevich, & Li (2015) looked at a type of neuron that may have something to do with the capacity of some of the mice to be resilient; the parvalbumin interneurons (PAI) from the medial prefrontal cortex (mPFC). These neurons produce GABA, the major inhibitory neurotransmitter in the brain, and modulates the activity of the nearby neurons. Thanks to the ability to genetically engineer mice to have a certain kind of cell fluoresce, the researchers were able to identify and subsequently record from and manipulate the function of the PAIs. These PAIs’ response to stimulation was weaker in helpless animals compared to resilient or controls. Also, inactivation of the PAI via a designer virus promotes helplessness.

Reference: Perova Z, Delevich K, & Li B (18 Feb 2015). Depression of Excitatory Synapses onto Parvalbumin Interneurons in the Medial Prefrontal Cortex in Susceptibility to Stress. The Journal of Neuroscience, 35(7):3201–3206. doi: 10.1523/JNEUROSCI.2670-14.2015. Article | FREE FULLTEXT PDF

By Neuronicus, 21 October 2015

Making new neurons from glia. Fully functional, too!

NeuroD1 transforms glial cells into neurons. Summary of the first portion of the Guo et al. (2014) paper.
Fig. 1. NeuroD1 transforms glial cells into neurons. Summary of the first portion of the Guo et al. (2014) paper.

Far more numerous than the neurons, the glial cells have many roles in the brain, one of which is protecting an injury site from being infected. In doing so, they fill up the injury space, but they also prohibit other neurons to grow there.

Guo et al. (2015) managed to turn these glial cells into neurons. Functioning neurons, that is, fully integrated within the rest of the brain network! They did it in a mouse model of stab injury and a mouse model of Alzeihmer’s in vivo. Because a mouse is not a man, they also metamorphosized human astrocytes into functioning glutamatergic neurons in a Petri dish, that is in vitro.

It is an elegant paper that crossed all the Ts and dotted all the Is. They went to a lot of double checking in different ways (see Fig. 1) to make sure their fantastic claim is for real (this kind of double, triple, quadruple checking is what gets a paper into the Big Name journals, like Cell). Needles to say, the findings show a tremendous therapeutic potential for people with central nervous system injuries, like paralyses, strokes, Alzheimer’s, Parkinson’s, Huntington, tumor resections, and many many more. Certainly worth a read!

Reference: Guo Z, Zhang L, Wu Z, Chen Y, Wang F, & Chen G (6 Feb 2014, Epub 19 Dec 2013). In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer’s disease model. Cell Stem Cell, 14(2):188-202. doi: 10.1016/j.stem.2013.12.001. Article | FREE FULLTEXT PDF | Cell cover

By Neuronicus, 18 October 2015