All the good things must come to an end

…Everything is temporary

This, too, shall pass

There are countless variations to this theme, in part because idea is so central to the human condition, and in part, because it’s true. So, this course, too, is approaching its end and it’s time to look back and see what is is we have got.

In the beginning, I stated my interest in learning about correlation and causality in the physical 7 biological operations of brain and the mind contents. We started from the very basics, the topological structure of neurons and glia cells was the starting point, as well as the function of neuron cell membrane. To navigate the brain, a motherload of new terminology was introduced:

For some reason, it’s the brain has no up and down, but dorsal and ventral. Anterior and posterior are used for front and back, but sometimes substituted with rostral and caudal. Medial kind of makes sense, lateral is a bit vaguer, at least if I need to locate something like dorsolateral prefrontal cortex, Brodmann’s area 9. I mean, wouldn’t area 8 be even more dorso and still lateral enough to fit the description?

We also learned to name quite a few anatomic structures in the brain, which I generally enjoyed, as annoying as it was to try and wind basal ganglia into a 3D formation with the playdough… 😊

I was interested in how to regulate the sleep / arousal balance, as I’m suffering from insomnia. It appears serotonergic raphe nuclei play a role, as does the pineal body that secretes melatonin. Also, reticular formation regulates sleep and wakefulness, retinal ganglion cells have direct projections in the hypothalamus that sync sleep and wakefulness biorhythm. There would have been a whole chapter dedicated to brain rhythms and sleep, but it was left outside of the curriculum. I’ll read it on my own when I have time, maybe some night when the sleep escapes me once again… 😉

The brain is much about chemicals, neurotransmitters. We learned about inhibition and excitation, different types of direct and indirect receptor systems that are coded to specific neurotransmitters and can also be tampered with external chemistry, drugs.

Of senses, vision and hearing were central. Both produce a very subjective understanding of the world by definition (the said understanding being an illusion born in the brain), but sometimes the reality effect fails and the gaps in the perception are revealed. We investigated some particular types of conditions that produced very ambiguous perceptions among us hoi polloi of the lecture hall.

Motor cortex and the motor function received also their due attention. We learned the signal path from brain to muscles and what is involved before the motor cortex sends its commands and after. Many parts of the chain, again, revealed to be under conscious control and more or less automatical.

Finally, excursions have been made to EEG, MEG and imaging facilities, research and hospital alike, and we’ve also had a taste of TEM and tDCS modalities in tampering with the neurons firing probabilities. Now there’s only one little experiment to run before the exam and we’re done. Thank you everybody for your contribution! This has been an interesting journey and I hope to be able to continue it in another course in the future.

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Twice excursed

This week’s theme evolved around two excursions, one to the Aalto NeuroImaging AMI Centre facilities, and the other to Sooma Oy, Vallila. What did I learn? At AMI Centre we saw navigated transcranial magnetic stimulation (nTMS), and functional magnetic resonance imaging (fMRI) instrumentation, as well as behavioral studies facilities. I’ll focus on the TMS as it has something in common with the Sooma tDCS, even if the working principles differ greatly.

I’ve been interested in repetitive transcranial magnetic stimulation (rTMS) as a non-invasive method to “tune” the operation of brain. It is, among other things, a feasible method to treat severe cases of depression, as I’ve learned from my friends, Drs Fingelkurts (https://www.bm-science.com/), who have developed customized rTMS sequences for exactly that purpose. TMS pulsing increases the probability of neurons firing by inducing an electrical field in the targeted cortical region depolarizing superficial axons and activating cortical networks. (Klomjai, Katz and Lackmy-Vallée, 2015) I asked whether it would be feasible to combine rTMS treatment with simultaneous mental tasking that activates the same region of the brain, to increase the firing rate further. According to our tour guide this ought to work.

As I know meditation alleviates symptoms of depression, among many other things, (Creswell, 2017) it would be an interesting test combine meditation and rTMS. One outcome might be less rTMS treatment times needed for the same effect, and another, such an arrangement could make it easier to use meditation as a method of self-help after the rTMS is over. One hurdle to jump over is meditation is a skill that takes time to learn. For a depressed person, this might be an obstacle, as the initiative, and motivation to persist in something that may produce benefits in the future, is typically lacking. However, there are methods based on neurofeedback that might help to smooth the road.(Garrison et al., 2013; van Lutterveld et al., 2017) Please feel free to use my ideas! 😊

Our visit to Sooma in a way continued along the tracks of TMS in modifying electrical activity of the brain, this time using transcranial direct current stimulation (tDCS). I volunteered as a guinea pig for a demo where I got to put the Sooma cap on and my brain was fried for a short while with a small current between the electrodes. The electrode placement in the Sooma version is generic. In treating depression, one electrode is placed over the dorsolateral prefrontal cortex region (F3) that in a depressed individual typically shows pronounced activity, and the placement of the other I can’t remember. Maybe the current was turned too high, even if I didn’t feel any pain?  😉 In any case, the idea is to decrease the probability for firing in that region, thus alleviating depression symptoms. As in the TMS case, also in the case of tDCS, a superposition of synergetic mental tasking with the treatment might boost the process. Another idea that occurred to me was to combine qEEG analysis prior and after the treatment to the treatment plan. One would see in advance whether each particular case of depression indeed correlated with activity in the F3 region, and also whether the treatment was effective in decreasing the activity.

References

Creswell, J. D. (2017) ‘Mindfulness Interventions’, Annual Review of Psychology, 68(1), pp. 491–516. doi: 10.1146/annurev-psych-042716-051139.

Garrison, K. A., Santoyo, J. F., Davis, J. H., Thornhill, T. A., Kerr, C. E. and Brewer, J. A. (2013) ‘Effortless awareness: using real time neurofeedback to investigate correlates of posterior cingulate cortex activity in meditators’ self-report’, Frontiers in Human Neuroscience, 7(440), pp. 1–9. doi: 10.3389/fnhum.2013.00440.

Klomjai, W., Katz, R. and Lackmy-Vallée, A. (2015) ‘Basic principles of transcranial magnetic stimulation (TMS) and repetitive TMS (rTMS)’, Annals of Physical and Rehabilitation Medicine, 58(4), pp. 208–213. doi: 10.1016/j.rehab.2015.05.005.

van Lutterveld, R., Houlihan, S. D., Pal, P., Sacchet, M. D., McFarlane-Blake, C., Patel, P. R., Sullivan, J. S., Ossadtchi, A., Druker, S., Bauer, C. and Brewer, J. A. (2017) ‘Source-space EEG neurofeedback links subjective experience with brain activity during effortless awareness meditation’, NeuroImage. Elsevier Inc., 151, pp. 117–127. doi: 10.1016/j.neuroimage.2016.02.047.

 

 

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Motoring along

The workings of motor cortex have been on my mind since they pop up from neuroimaging studies on meditation every now and then. In Fox et al. meta-analysis on functional neuroimaging studies (Fox et al., 2016) that dealt with modalities of mindfulness meditation (plus mantra recitation, which isn’t part of mindfulness), premotor cortex and supplementary motor area exhibited activation (meta-analytic clusters). The activation was noted both in focused attention meditation modality (concentrating on body parts or following of breath) and open monitoring modality (observing thoughts and sensation without trying to interfere with them). The explanation for the activation originated from the idea that mental manipulation of objects activates the same areas that are involved in actual manipulation. I wonder if this has workable analogies in the mirror cell mechanism? On the other hand, activation has been observed in these region during a variety of mental task recruiting higher order cognitive functions and attention regulation, such as working memory, attentional control, mental imagery and conceptual reasoning. Therefore, meditation, an activity especially coupled with attention control, fits well into the image.

We learned that not only motor cortex, but also other areas of the brain send in some cases commands to the outside world. The tasks of higher and lower motor neurons and interneurons was discussed, as well as activation and the simultaneous inhibition of the antagonist muscles, in eg. biceps (flexion) and triceps (the antagonist, extension). A very interesting thing: the artificially induced crossed innervation of muscles, i.e. innervating slow muscle cells with fast motor neurons or vice versa, changes the action of the thus innervated cell to resemble the type of innervation. This led me to think, would it be possible to alter the muscle type distribution by tampering with the muscle innervation somehow? I assume I have mostly slow muscle cells and gaining strength and high speed has always been a challenge, but if one were to take a very fast runner to start with, would it be possible to increase the sunning speed beyond the inborn gifts of nature?

Ref

Fox, K. C. R., Dixon, M. L., Nijeboer, S., Girn, M., Floman, J. L., Lifshitz, M., Ellamil, M., Sedlmeier, P. and Christoff, K. (2016) ‘Functional neuroanatomy of meditation: A review and meta-analysis of 78 functional neuroimaging investigations’, Neuroscience & Biobehavioral Reviews. Elsevier Ltd, 65, pp. 208–228. doi: 10.1016/j.neubiorev.2016.03.021.

 

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… or so I’ve heard

Last week we heard some interesting things at the lecture, as is to be expected when the topic was hearing! 🙂 We learned that the tonotopic (i.e. cochleotopic) organization of auditory cortices resembles that or visual cortices, i.e. different information (sound frequencies) are handled at different locations in the brain, even if not in the region described in Figure 11.27 of the course book, which, we learned, has macque tonotopic organization pasted on human brain… Also, the dorsal and ventral signal processing paths, the “where and what” processing streams, respectively, are analogous to those of visual data processing.

We also discussed, how the brain needs to calibrate auditory location spotting with the help other senses, and how it takes time. This is in accordance with my own observation that young kids do not seem to be able to make sense of directional auditory information, which gives you an edge playing hide-and-seek – now need to be quiet when it’s your turn to run and hide. It would be interesting to test if, by altering the shapes of my own pinna sufficiently would result in the loss of directional hearing. Pulling my ears didn’t seem to suffice and produced traumatic memories from my own childhood (of exceeding my limits and being gently led back within bounds by my ear flaps). 😉

I found it very fascinating how clever engineering there is in in the ear, how the signal is amplified 20-fold, and how there are also safety mechanisms that protect the ear against too loud sounds. If there’s room for improvement, I’d vote faster protection mechanisms as there is a delay before the muscles that protect the hearing contract, as I’ve had the opportunity to learn firsthand. I wonder if some are more prone to develop hearing loss exposed to the same information and whether it’s due to the effectivity of the protective mechanisms or something else? I have some dips in the frequency band along with tinnitus, whereas some of my friend do not seem to suffer from such problems despite, even if they have run to more gigs without any hearing protection than I with earplugs.

The audiovisual integration part was very illuminating, the illusion of hearing “baa” as “faa” was very strong coupled with the visual data. I wonder if I can use this as an excuse the next time I fail to understand what my wife says: “ The visual cues very conflicting, dear, I got confused!”

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It’s as it seems to be

Vision is the dominant sense for most people, I dare say, even if I do remember my old grade school teacher telling he’d rather be blind than deaf. This week we looked into vision. I found the lecture stimulating and the discussion about split brain patients and the separate informing of right and left brain lobes utilizing the outer edges of visual field intriguing. It appears when the connection between right and left hemisphere is cut – the corpus callosum severed historically to treat epilepsy – both halves develop autonomous consciousnesses which may have conflicting interests. This has been found out in studies where the right hemisphere has been instructed to do something without the knowing of the left hemisphere and then the person (incl. both hemispheres) has been asked to explain the motivation for acting according to the instruction. The left hemisphere seems to be the one capable of forming speech and, surprisingly, very capable of doling out nonsensical explanations even without any knowledge for the real motivation. This amazing capability of fabricating post hoc explanations for our behavior is proposedly one of the mechanisms causing us to believe in free will even when we become conscious of our decisions only after the brain has already made the decision.

Vision carries a great reality effect, i.e. we intuitively believe things are as they seem. This, of course, is rather silly from the point of view that our vision is very limited (we only see a tiny sliver of the electromagnetic spectrum), subjective (among human population we see different things differently, and compared to other animal species, even more so), and prone to illusions, as was demonstrated in the lecture. Or maybe its analogous to Orwell’s Animal Farm: we all see the same thing the same way, some just see them more same way than the others? By the way, the dress was blue stripes on gold and the sneaker pink with white stripe! 😊

What wonders me, given the huge resources dedicated to vision in the human cortex, is how those resources are utilized in those people that are born blind?

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Lost in Translation, emptiness is found

There are things too little to really merit attention, yet still big enough to be bothersome. Things that fly under the radar of consciousness only to appear when you are looking elsewhere and disappear you try and train your focus on them. What are those things, really? Sometimes they are just little concepts, words that sound familiar enough not to be really considered, even if they somehow fail to hold a concrete shape if you were asked to define them. Translational was one of those word for me:

Earlier this year I went through a bunch of papers on the effect of mindfulness on health and cognition. Among those, there was one entitled “A translational neuroscience perspective on mindfulness meditation as a prevention strategy” by Tang and Leve (2016). In the paper, they proposed “a translational prevention framework of mindfulness and its effects”, a sentence in which every word made sense on their own, but when put together, the significance escaped me. Now, upon learning in the lecture that translational is an alias for applied, there’s only the “prevention network” to decipher… 😉

Now, the point of this linguistic exercise is not to complain about the language of the paper, even if I sign to notion that difficult things should be explained using simple language (Feynman paraphrase: If you can’t explain it to your grandmother…). What the lecture brought vividly to my attention was how empty words really are on their own. Empty in the Buddhist sense of emptiness, i.e. not existing as absolutes on their own but merely as a collection of references, all depending on each other.

What has this principle of emptiness / interconnectedness got to do with neuroscience? If we begin zooming in from the interconnectedness of all living systems to interactions between humans, we end up inside a human brain where the neuron are vastly interconnected. Somewhere in this interconnectedness, consciousness emerges from neurons that in themselves are not conscious. And in this lecture, it fits beautifully to the mention in the summary slides (on the overall principle of neurotransmitter systems function): “Everything influences everything”. In fact SI system depicts similar principles in a greatly simplified manner:

https://en.wikipedia.org/wiki/International_System_of_Units#/media/File:Relations_between_New_SI_units_definitions.svg

If you find yourself interested in the concept of emptiness, there’s an excellent book, Emptiness and Joyfull Freedom, by Greg Goode (a philosopher) and Thomas Sander (a mathematician) that can be found on Amazon (https://www.amazon.com/Emptiness-Joyful-Freedom-Greg-Goode/dp/1908664363). For a short, refreshing poetic break, Thich Nath Hanh’s text “Interbeing” is a nice one (http://www.awakin.org/read/view.php?tid=222).

Ref.

Tang, Y. Y. and Leve, L. D. (2016) ‘A translational neuroscience perspective on mindfulness meditation as a prevention strategy’, Translational Behavioral Medicine, 6(1), pp. 63–72. doi: 10.1007/s13142-015-0360-x.

 

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Neurotransmitters and how to tamper with them

This week’s lecture went through different neurotransmitters as well as their receptors and receptor cascades. A lasting theme throughout the lecture was m-opioid receptors, which was started by discussing with how to block them using naloxone. Naloxone is a m-opioid receptors blocker (i.e. antagonist) that was originally developed as a remedy against opioid abuse, but has also been found effective against alcohol abuse. Alcohol activates many neurotransmitter systems, among them being GABA and endorphin systems which release dopamine into the reward pathway bringing about pleasurable feeling. Of these two, Naloxone targets the endorphin (i.e. endogenous morphine) system by binding to the m-opioid receptors. A note to myself: Remember to look closer into how naloxone affects craving. It appears it does so not directly but gradually extinguishing the pleasure felt while drinking.

We also went through the serotonine hypothesis, which is the basis for treating patients suffering from depression with selective serotonine re-uptake inhibitors (SSRI), a multibillion business. The serotonine hypothesis has been hotly contested, yet it still is the dogma by which millions of people worldwide are being treated.  Finland ranks in top ten with regard to how many antidepressant users we have per capita (70 / 1000), the number one being US (110 / 1000) [http://www.businessinsider.com/countries-largest-antidepressant-drug-users-2016-2?r=US&IR=T&IR=T].

I raised a point whether GABA levels can be increased via ingesting GABA enriched tea (fermenting tealeaves under nitrogen seems to produce GABA into the fermented leaves, see eg. http://worldteanews.com/tea-health-education/gaba-tea-and-the-hype-around-its-health-benefits for explanation in lay terms). I tried to do a literature survey but did not find too veritable evidence of the health benefits.

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Vagus is vaguely taking shape

If I thought last week that we were getting a lot of new terminology, this week has confirmed my impression indeed! After filling in the six pages of names for various brain parts, I have to say it may still take a while before they are memorized…

I did have some kensho moments, nevertheless, as some formations I’ve already bumped into managed to manifest and say hello among the crowd. I’ve been wrestling with insomnia for quite some time, waking up almost every night after 4 to 5 hours of sleep, and sleeping the rest of the night in intermittent chunks if at all. I’ve read about causes for insomnia and my symptoms fit rather nicely (if nice were a good term…) with descriptions of hyperarousal of the nervous system (Kay and Buysse, 2017): when I wake up in the middle of the night, my heart is beating fast and strong like somebody had ordered it turn up the heat and prepare for war.  It’s very curious how after years of meditation I do not really suffer from rumination – my mind is rather still – yet the restlessness has remained in my body as if it were a blind ghost of days done by not  finding its way to the next world.

Now I know where the vagus nerve is lurking, and I intend to pore deeper into it’s function in controlling the balance of autonomic nervous system. I’ve already experimented with breathing techniques which seem to be helping, possibly by increasing vagal activity via respiratory sinus arrhythmia. (Tsai et al., 2015) I’ll write more about it in the coming blog entries when I have had time to look a little closer into the papers that I have found covering the subject.

REFs

Kay, D. and Buysse, D. (2017) ‘Hyperarousal and Beyond: New Insights to the Pathophysiology of Insomnia Disorder through Functional Neuroimaging Studies’, Brain Sciences, 7(3), pp. 1–19. doi: 10.3390/brainsci7030023.

Tsai, H. J., Kuo, T. B. J., Lee, G. S. and Yang, C. C. H. (2015) ‘Efficacy of paced breathing for insomnia: Enhances vagal activity and improves sleep quality’, Psychophysiology, 52(3), pp. 388–396. doi: 10.1111/psyp.12333.

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Second week, neurons, glia, playdough

This week we continued along the route in deciphering the function of the brain by first investigating the topological structure and function of neurons and glia cells, and then zooming closer to the cell membrane. It’s said that the human brain is the most complex thing in the known universe, and this started to reflect also in the lecture; new terminology abounded and it was getting tougher to try and follow the meaning of all the new concepts and how they were linked to each other.  Perhaps it would have helped if among the numerous slides there had been one or two explaining the structure and purpose of the lecture and maybe even one drawing together the most important concepts?

The exercise session was entertaining and informative. It’s much easier to remember where each functional region in the brain is after you’ve once baked a brain on your own, even if only from playdough. I wish I had better 3D model of the brain at my disposal as from brainstem upwards it was getting harder to place structures in their proper place. If anybody has a free or reasonably priced app for Android or Windows to recommend, I’d be interested!

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Learning diary – 1st lecture

Alas, yet another learning diary blog for the course Structure and Operation of Human Brain at Aalto University! First introductory lecture is down, several more to go. Feels rather weird to be participating a course after so many years since I’ve last actively studied new subjects under lectured settings. Weird, but refreshing! To paraphrase one of my gurus, Matti Nykänen, progress has progressed: the teaching methods seem to have evolved since the early iron age what with the propagation of learning diaries, excursions, and the paradigm shift from mumbling stone idols to actual interaction. Very nice! The course seems to be structured carefully as well as resourced properly – I’ve yet to see another with two professors and so many assistants at the service of the learning.

The Big Questions, oh yeah! Having pondered them myself to quite some extent, the promise of digging deeper into these is fetching! Keen on meditation, I’ve spend a lot of time with “Who am I?” and “What am I?”, classical questions of many traditions such as Zen Buddhism and Advaita Vedānta. I have experience of how these questions feel, when I present them to myself, let my mind calm down and wait for the answer, and have also read of the neural correlates they have been linked to. It will be good to hear

Speaking of correlates, I’m also looking forward to gaining a deeper understanding of the diffuse boundary between correlation and causality. I’ve read of the effects of physically tampering with the brain, such as severing the corpus callosum, and of damages caused by illnesses and accidents limited to specific regions of the brain, and how they are manifested on the behavioral level. From such data, it would be very alluring to draw hard mechanistic assumptions of the brain a “mere” machinery – flip this switch and that light goes on. But to what degree this really applies?

New pieces of information I found very interesting were the bits related to color blindness. The idea of us as homunculi living inside of our bodies observing the very separate, external world, is a strongly held intuition. It’s easy to feel that reality is outside and that our senses rely information of it to us as it is. This belief of externality of reality is, per eastern meditative traditions, one source for suffering.  Vision is a very strong sense modality with great reality effect, even if visible spectrum is but a tiny fragment of electromagnetic radiation that surrounds us. I knew animals and humans see colors differently depending on species, and that some women have receptor for four colors instead of the typical three, but I hadn’t heard of color blind people with only one colorblind eye. This offers a very nice access to subjective experience of colors!

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