Can you tickle yourself?

As I said before, with so many science outlets out there, it’s hard to find something new and interesting to cover that hasn’t been covered already. Admittedly, sometimes some new paper comes out that is so funny or interesting that I too fall in line with the rest of them and cover it. But, most of the time, I try to bring you something that you won’t find it reported by other science journalists. So, I’m sacrificing the novelty for originality by choosing something from my absolutely huge article folder (about 20 000 papers).

And here is the gem for today, titled enticingly “Why can’t you tickle yourself?”. Blakemore, Wolpert & Frith (2000) review several papers on the subject, including some of their own, and arrive to the conclusion that the reason you can’t tickle yourself is because you expect it. Let me explain: when you do a movement that results in a sensation, you have a pretty accurate expectation of how that’s going to feel. This expectation then dampens the sensation, a process probably evolved to let you focus on more relevant things in the environment that on what you’re doing o yourself (don’t let your mind go all dirty now, ok?).

Mechanistically speaking, it goes like this: when you move your arm to tickle your foot, a copy of the motor command you gave to the arm (the authors call this “efference copy”) goes to a ‘predictor’ region of the brain (the authors believe this is the cerebellum) that generates an expectation (See Fig. 1). Once the movement has been completed, the actual sensation is compared to the expected one. If there is a discrepancy, you get tickled, if not, not so much. But, you might say, even when someone else is going to tickle me I have a pretty good idea what to expect, so where’s the discrepancy? Why do I still get tickled when I expect it? Because you can’t fool your brain that easily. The brain then says; “Alright, alright, we expect tickling. But do tell me this, where is that motor command? Hm? I didn’t get any!” So here is your discrepancy: when someone tickles you, there is the sensation, but no motor command, signals 1 and 2 from the diagram are missing.

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Fig. 1. My take on the tickling mechanism after Blakemore, Wolpert & Frith (2000). Credits. Picture: Sobotta 1909, Diagram: Neuronicus 2016. Data: Blakemore, Wolpert & Frith (2002). Overall: Public Domain

Likewise, when someone tickles you with your own hand, there is an attenuation of sensation, but is not completely disappeared, because there is some registration in the brain regarding the movement of your own arm, even if it was not a motor command initiated by you. So you get tickled just a little bit. The brain is no fool: is aware of who had done what and with whose hands (your dirty mind thought that, I didn’t say it!) .

This mechanism of comparing sensation with movement of self and others appears to be impaired in schizophrenia. So when these patients say that “I hear some voices and I can’t shut them up” or ” My hand moved of its own accord, I had no control over it”, it may be that they are not aware of initiating those movements, the self-monitoring mechanism is all wacky. Supporting this hypothesis, the authors conducted an fMRI experiment (Reference 2) where they showed that that the somatosensory and the anterior cingulate cortices show reduced activation when attempting to self-tickle as opposed to being tickled by the experimenter (please, stop that line of thinking…). Correspondingly, the behavioral portion of the experiment showed that the schizophrenics can tickle themselves. Go figure!

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Reference 1: Blakemore SJ, Wolpert D, & Frith C (3 Aug 2000). Why can’t you tickle yourself? Neuroreport, 11(11):R11-6. PMID: 10943682. ARTICLE FULLTEXT

Reference 2: Blakemore SJ, Smith J, Steel R, Johnstone CE, & Frith CD (Sep 2000, Epub 17 October 2000). The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: evidence for a breakdown in self-monitoring. Psychological Medicine, 30(5):1131-1139. PMID: 12027049. ARTICLE

By Neuronicus, 7 August 2016

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The culprit in methamphetamine-induced psychosis is very likely BDNF

Psychoses. Credit: NIH (Publication Number 15-4209) & Neuronicus.
Psychoses. Credit: NIH (Publication Number 15-4209) & Neuronicus. License: PD.

Methamphetamine prolonged use may lead to psychotic episodes in the absence of the drug. These episodes are persistent and closely resemble schizophrenia. One of the (many) molecules involved in both schizophrenia and meth abuse is BDNF (brain derived neurotrophic factor), a protein mainly known for its role in neurogenesis and long-term memory.

Lower BDNF levels have been observed in schizophrenia, therefore Manning et al. (2015) wondered if it’s also involved in meth-induced psychosis. So they got normal mice and mice that were genetically engineered to express lower levels of BDNF. They gave them meth for 3 weeks, with escalating doses form one week to the next. Interestingly, no meth on weekends, which made me rapidly scroll to the beginning of the paper and confirm my suspicion that the experiments were not done in USA; if they were, the grad students would not have had the weekends off and mice would have received meth every day, including weekends. Look how social customs can influence research! Anyway, social commentary aside, after the meth injections, the researchers let the mice untroubled for 2 more weeks. And then they tested them on a psychosis test.

How do you measure psychosis in rodents? By inference, since the mouse will not grab your coat and tell you about the newly appeared hypnotizing wall pattern and the like. Basically, it was observed that psychotic people have a tendency to walk in a disorganized manner when given the opportunity to explore, a behavior that was also observed in rodents on amphetamines. This disorganized walk can be quantifies into an entropic index, which is thought to reflect occurrence of psychosis (I know, a lot of inferring. But you come up with a better model of psychosis in rodent!).

Manning et al. (2015) gave their mice amphetamine to mimic psychosis and then observed their behavior. And the results were that the genetically engineered mice to express less BDNF showed reduced psychosis (i.e. had a lower entropic index). In conclusion, the alteration of the BDNF pathway may be responsible for the development of psychosis in methamphetamine users.

Reference: Manning EE, Halberstadt AL, & van den Buuse M. (Epub 9 Oct 2015). BDNF-Deficient Mice Show Reduced Psychosis-Related Behaviors Following Chronic Methamphetamine. International Journal of Neuropsychopharmacology, 1–5. doi: 10.1093/ijnp/pyv116. Article | FREE FULLTEXT PDF

By Neuronicus, 9 November 2015

As nutty as Dali, as crazy as van Gogh

Left: Portrait of Salvador Dali (taken in Hôtel Meurice, Paris, by Allen Warren, 1972). Right: Self-portrait with bandaged ear and pipe (van Gogh, 1889). Courtesy of Wikipedia.
Left: Portrait of Salvador Dali (taken in Hôtel Meurice, Paris, by Allen Warren, 1972). Right: Self-portrait with bandaged ear and pipe (van Gogh, 1889). Courtesy of Wikipedia.

Having a brain disease means to have different scores on emotion, cognition, and behavior inventories than the population mean. Also different from the population mean is the ability of an artist to create evocative things. Whether is a piece of music or a painting (or in my case a simple straight line), whether we like it or not, most of us agree that we couldn’t have done it. Also, artists show a decrease in practical reasoning, just like the schizophrenics.

Power et al. (2015) sought to find out if there is a link between being creative and having schizophrenia or bipolar disorder. Lucky for them, the north-European countries keep detailed medical and genetic databases of their population: they had access to 5 databases from Iceland, Sweden, and Netherlands, featuring tens to hundreds of thousands of people.

The authors analyzed hundreds of thousands of individual genetic differences (i.e. SNPs = single nucleotide polymorphisms) that had been previously linked with schizophrenia or bipolar disorder. As a side note, some of this data was obtained by inviting citizens to voluntarily fill out a detailed medical questionnaire and donate blood for DNA analysis. A staggering amount of people agreed. I wonder how many would have done so in U.S.A….

Anyway, the authors defined creative individuals (artists) as “those having (or ever having had) positions in the fields of dance, film, music, theater, visual arts or writing” (online supplemental methods), including those teaching these subjects. And they found out that the same genetic makeup that increases the risk of developing schizophrenia or bipolar disorder also underlies creativity. This link was not explained by education, age, sex, or shared environment.

The study also knocked down an evolutionary explanation for the persistence of schizophrenia and bipolar disorders in the genetic pool. The hypothesis posits that we still have these devastating brain disorders because they come with the side effect of creativity that offsets their negative fitness; but that does not hold, as the artists in this study had less children than the average population. Authors did not offer an alternative speculation.

Reference: Power, R. A., Steinberg, S., Bjornsdottir, G., Rietveld, C. A., Abdellaoui, A., Nivard, M. M., Johannesson, M., Galesloot, T.E., Hottenga, J. J., Willemsen, G., Cesarini, D., Benjamin, D. J., Magnusson, P. K., Ullén, F., Tiemeier, H., Hofman, A., van Rooij, F. J., Walters, G. B., Sigurdsson, E., Thorgeirsson, T. E., Ingason, A., Helgason, A., Kong, A., Kiemeney, L. A., Koellinger, P., Boomsma, D. I., Gudbjartsson, D., Stefansson, H., & Stefansson K. (July 2015, Epub 8 June 2015). Polygenic risk scores for schizophrenia and bipolar disorder predict creativity. Nature Neuroscience, 8(7):953-5. doi: 10.1038/nn.4040. Article + Nature comment

By Neuronicus, 7 October 2015