Theorem X: Mental Interactions are Physical Processes
A mother, seeing her beloved child wandering into the street and about to be hit by a speeding car, decides without hesitation to save her child by jumping into the street to protect her child even if that means risking her own life. Obviously, her love for the child must be able to affect her thinking, planning, and decision and cause her to carry out such a life-risking act. But how can the feeling of love affect other mental processes, such as thinking, planning, and deciding? The obvious mechanism is that, as mental processes are the information-processing parts of neural processes, interactions between mental processes occur by information transmissions between the involved neural processes via their synapses.
8.1. Mental Force
However, another possible mechanism that has long been suspected to exist and that some people still believe in is that mental processes interact between themselves directly, without utilizing the neural synaptic transmissions, by using a force that is not one of the four fundamental physical forces. This force may be called mental force or mental power. Let’s examine this force in more detail of how it probably works and what happens if it works.
To be a mental force, the force must be directly executable by mental processes and must affect other mental processes directly by itself. As a mental process is the information-processing part of a neural process (Theorem II), when the mental process is affected (or changed) by mental force, the neural process of the mental process must be affected (or changed) similarly too so that they remain in accordance with each other. This means that the mental force must be able to affect (change) the neural process physically. In detail, this means that the mental force must be able to affect membrane channels and synaptic channels of millions of neurons and move billions and billions of sodium, potassium, calcium, and/or chloride ions at the correct channels in a correct way (such as a correct amount of sodium, calcium, etc. ions are moved at the correct rate, in the correct direction, and at the correct time, in each and every channel in a concerted pattern) accurately so that appropriate polarizations or depolarizations occur at the right time and result in timely and appropriate action potentials or no action potentials of each of the millions of neurons in the involved neural circuit [1,2,3] so that the correct signaling pattern occurs in the circuit of the neural process.
The main questions about this mental force are
- What is the nature of this mental force?
- How can it affect various kinds of neuronal membrane and synaptic channels and move different kinds of ions?
- In affecting the membrane and synaptic channels and moving ions across channels, energy must be expended or gained. Where does this force draw energy from or channel the gained energy to, and how does it do that?
- How can this force know what the exact signaling pattern (such as what the exact signaling pattern of a decision to save a child) is to be created in what neural process in order that the desired mental process and qualia (such as a decision to save a child) occur? And how can this force know which neurons of the 100 billion neurons in the brain are the neurons of the neural process that is to be affected?
- How can this force affect millions/billions of neuronal membrane and synaptic channels in the neural circuit correctly, both spatially and temporally, so that the desired signaling pattern (in 4.) is created?
Evidently, to create a suitable signaling pattern in a correct neural process for a certain mental process to occur is not a simple physical process. But the mental force, if it really exists, must be able to do this. Up to the present time, however, there are no answers to how it can do this, and there is no physical evidence for this force either.
8.2. Mental process interactions
On the contrary, a lot of evidence supports that mental process interactions occur by signal transmissions through neural synaptic connections between the involved neural processes. Let’s examine how mental process interactions occur by this mean in more details. When one mental process (such as seeing a child in danger) occurs, the signaling pattern that is the information of this visual perception will be sent through synaptic connections to other neural processes of other mental processes. These signal-receiving neural processes will process this information and generate signaling patterns that are their specific information (i.e., a decision to save a child, emotion of fright, retrieval of relevant past knowledge and experiences of how to save the child, etc.). The generated signaling patterns, which are the generated information, will likewise be sent to related neural processes via neural synaptic transmissions and create successive signaling patterns that are successively processed information that will be sent to other related neural processes, and so on. Overall, because neural circuits are connected in some specific patterns and because synaptic junctions are capable of processing transmitted signals [2, 4-13], neural synaptic transmissions can “not only transmit but also process” information through the neural circuits and synapses. Thus, coherent mental process functions can occur via neural processes and neural synaptic transmissions.
Evidence that mental process interactions occur via neural processes and neural synaptic transmissions is countless. Anything that affects neural transmission directly at the synapses or at the neural tracts that connect to the synapses can affect mental process interactions. Pharmacologically, CNS (central nervous system) active substances that interfere with neural synaptic transmission, such as psychedelic drugs, CNS stimulants, and tranquilizers, alter mental processes according to which neural synaptic transmissions they affect and how they affect them, and the results can be hallucination, excitation, tranquility, etc. [14-17]. In patients with CNS diseases that have neural synaptic transmission dysfunction such as bipolar disorder, major depression, anxiety disorders, Alzheimer’s disease, and Parkinson’s disease, drugs that can help correct or improve the abnormal neural synaptic transmission can correct or improve the functions of corresponding neural processes and mental processes, such as mood and cognition [18-24]. A transection of a CNS nerve tract can affect and be used to treat a mental disorder (such as depression), pain, epilepsy, etc. [25-28]. A corpus callosum transection, which is done in some cases of intractable epilepsy, has observable mental effects that is called “split-brain syndrome”, in which some mental processes on one side of the brain cannot communicate with mental processes on the other side of the brain and in which there is an impaired functional connectivity between some modules between the two hemispheres [29-34]. Diseases that damage neural tracts that connect neural processes disrupt signal communication between the involved neural processes (and thus the corresponding mental processes) and result in various syndromes depending on which connection is destroyed, such as a conduction aphasia, which occurs when the left hemisphere arcuate fasciculus (which connects the sensory and motor language areas) is destroyed [35,36]* (such as in the case of cerebral infarction), and pseudobulbar affect (uncontrollable crying or laughing), which occurs when the corticopontine–cerebellar circuits (which are the pathways of emotion control) are disrupted (such as in the case of stroke or motor neuron disease). Regarding neural processes, evidence that mental process interactions occur via neural processes has been discussed in section PM2.4. B, Chapter 1.
(*Conduction aphasia also occurs from lesions at other sites, such as at the posterior-most portion of the left planum temporale and supramarginal gyrus [38,39].)
8.3. Theorem X
Therefore, it can be concluded that mental interactions between mental processes are neural process interactions via neural synaptic transmissions. As generation and propagation of action potentials in neural processes (which involve functioning of neuronal membrane channels and movement of ions across channels, etc.) and in neural synaptic transmissions (which involve functioning of synaptic channels, releasing and binding of neurotransmitters, depolarizations or hyperpolarizations of the postsynaptic membranes, etc.)  are physical processes, it can be concluded that mental process interactions are physical processes. This theory asserts this as a theorem:
Theorem X. Mental interactions are physical processes.
This theorem indicates that mental process interactions or the activities of the mind can be described and predicted by physical laws. For example, the effects of love, hate, aspiration, etc. on other mental processes such as thinking, planning, or deciding are physical effects and can ultimately be described and predicted by physical laws. The predictions can be definite or probabilistic depending on the physical laws involved.
If all the factors involved in the processes of mental process interactions, such as the exact signaling patterns of the neural processes of the affecting mental processes and the exact response characteristics of the neural processes of the affected mental processes, are known, it will be predictable what the result is. For example, when a person is given a choice to choose between two things, such as a house or a car; if all the factors of the involved mental processes, their neural processes, and their interactions are known, it can be predicted, definitely or probabilistically, what he/she will choose.
- Mental interactions can be created, identified, measured qualitatively and quantitatively, monitored, changed, or destroyed by performing the respective action to only their neural signal transmissions. These actions on the neural signal transmissions are both necessary and sufficient for the respective actions on the mental interactions to occur, and these actions on anything else without having the actions on the neural signal transmissions will not result in the actions on the mental interactions.
- In any event or experiment, all predictions that are true for the neural signal transmissions will be simultaneously true for the mental interactions that depend on the neural signal transmissions, and the changes that occur in neural signal transmission and that occur in the mental interaction will be identical in quality, quantity, and temporal pattern.
- Byrne JH. Introduction to neurons and neuronal networks. Neuroscience Online. The University of Texas Health Science Center at Houston (UTHealth). Retrieved 2018 Feb 14 from http://nba.uth.tmc.edu/neuroscience/s1/introduction.html
- deCharms RC1, Zador A. Neural representation and the cortical code. Annu Rev Neurosci. 2000;23:613-647. http://www.cnbc.cmu.edu/~tai/readings/nature/zador_code.pdf
- Augustine GJ. Unit 1. Neural Signaling. In: Purves D, Augustine GJ, David Fitzpatrick D, Hall WC, Lamantia AS, McNamara JO, Williams SM, editors. Neuroscience. 3rd ed. Sunderland, Massachusetts: Sinauer Associates Inc; 2004. ISBN-13: 9780878937257 ISBN-10: 0878937250. Retrieved 2017 Nov 1from https://www.hse.ru/data/2011/06/22/1215686482/Neuroscience.pdf
- Ainsworth M, Lee S, Cunningham MO, Traub RD, Kopell NJ, Whittington MA. Rates and rhythms: A synergistic view of frequency and temporal coding in neuronal networks. Neuron. 2012 Aug 23;75(4):572-583. http://www.cell.com/neuron/fulltext/S0896-6273(12)00709-X
- Bohte SM. The evidence for neural information processing with precise spike-times: A survey. Nat Comput. June 2004 Jun;3(2):195–206. https://link.springer.com/article/10.1023/B:NACO.0000027755.02868.60
- Doetsch GS. Patterns in the brain. Neuronal population coding in the somatosensory system. Physiol Behav. 2000 Apr;69(1-2):187-201.
- Gardner B, Sporea I, Grüning A. Encoding spike patterns in multilayer spiking neural networks. arXiv.org. 2015. 2015 Mar 31. Retrieved 2018 Feb 8 from https://arxiv.org/pdf/1503.09129.pdf
- Gardner B. Learning spatio-temporally encoded pattern transformations in structured spiking neural networks [submitted for the Degree of Doctor of Philosophy from the University of Surrey. Department of Computer Science, Faculty of Engineering and Physical Sciences]. Guildford, Surrey: University of Surrey; 2016 Mar. Retrieved 2017 Feb 15 from https://pdfs.semanticscholar.org/31e6/6434a451c8955e294abd080de4de0087b263.pdf
- Gr¨uning A, Bohte SM. Spiking neural networks: Principles and challenges. ESANN 2014 proceedings, European Symposium on Artificial Neural Networks, Computational Intelligence and Machine Learning. Bruges (Belgium), 2014 Apr 23-25, i6doc.com publ., ISBN 978-287419095-7. Retrieved 2017 Feb 16 from https://homepages.cwi.nl/~sbohte/publication/es2014-13Gruning.pdf
- Masuda N, Aihara K. Dual coding hypotheses for neural information representation. Math Biosci. 2007 Jun;207(2):312-321.
- Ponulak F, Kasinski A. Introduction to spiking neural networks: Information processing, learning and applications. Acta Neurobiol Exp (Wars). 2011;71(4):409-433. PMID: 22237491. http://www.ane.pl/linkout.php?pii=7146
- Rolls ET, Treves A. The neuronal encoding of information in the brain. Prog Neurobiol. 2011 Nov;95(3):448-90.
- Sanger TD. Neural population codes. Curr Opin Neurobiol. 2003 Apr;13(2):238-249.
- Gardner DM, Baldessarini RJ, Waraich P. Modern antipsychotic drugs: A critical overview. CMAJ. 2005 Jun 21;172(13):1703–1711. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1150265/
- Griffin CE, Kaye AM, Bueno FR, Kaye AD. Benzodiazepine pharmacology and central nervous system–mediated effects. Ochsner J. 2013 Summer;13(2):214–223. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684331/
- Liechti M. Novel psychoactive substances (designer drugs): Overview and pharmacology of modulators of monoamine signaling. Swiss Med Wkly. 2015 Jan;145:w14043. doi: 10.4414/smw.2015.14043. eCollection 2015. https://smw.ch/article/doi/smw.2015.14043
- MC Mauri, Paletta S, Maffini M, Colasanti A, Dragogna F, Pace CD, et al. Clinical pharmacology of atypical antipsychotics: An update. EXCLI J. 2014;13:1163–1191. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4464358/
- Hauser RA. Early pharmacologic treatment in Parkinson’s disease. Am J Manag Care. 2010 Mar;16 Suppl Implications:S100-7. http://www.ajmc.com/journals/supplement/2010/a280_10mar_parkinsons/a280_10mar_hauser
- Magrinelli F, Picelli A, Tocco P, Federico A, Roncari L, Nicola Smania N, et al. Pathophysiology of motor dysfunction in Parkinson’s disease as the rationale for drug treatment and rehabilitation. Parkinsons Dis. 2016;2016:9832839. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913065/
- Muayqila T, Camicioli R. Systematic review and meta-analysis of combination therapy with cholinesterase inhibitors and memantine in Alzheimer’s disease and other dementias. Dement Geriatr Cogn Dis Extra. 2012 Jan-Dec;2(1):546–572. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522458/
- Müller T. Drug therapy in patients with Parkinson’s disease. Transl Neurodegener. 2012;1:10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514092/
- Nava-Mesa MO, Jiménez-Díaz L, Yajeya J, Navarro-Lopez JD. GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimer’s disease. Front Cell Neurosci.2014;8:167. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070063/
- P K Gillman. Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. Br J Pharmacol. 2007 Jul;151(6):737–748. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2014120/
- Racagni G, Popoli M. Cellular and molecular mechanisms in the long-term action of antidepressants. Dialogues Clin Neurosci. 2008 Dec;10(4):385–400. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181899/
- Gallay MN, Moser D, Rossi F, Pourtehrani P, MagaraAE, Kowalski M, et al. Incisionless transcranial MR-guided focused ultrasound in essential tremor: Cerebellothalamic tractotomy. J Ther Ultrasound. 2016;4:5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4752806/
- Shah DB, Pesiridou A, Baltuch GH, Malone DA, O’Reardon JJ. Functional neurosurgery in the treatment of severe obsessive compulsive disorder and major depression: Overview of disease circuits and therapeutic targeting for the clinician. Psychiatry (Edgmont). 2008 Sep;5(9):24–33. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687086/
- Stigsdotter-Broman L, Olsson I, Flink R, Rydenhag B, Malmgren K. Long-term follow-up after callosotomy—A prospective, population based, observational study. Epilepsia. 2014 Feb;55(2):316–321. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4165268/
- Volpini M, Giacobbe P, Cosgrove GR, Levitt A, Lozano AM, Lipsman N. The history and future of ablative neurosurgery for major depressive disorder. Stereotact Funct Neurosurg. 2017;95(4):216-228. https://www.karger.com/Article/FullText/478025
- Pinto Y1, Neville DA, Otten M, Corballis PM, Lamme VA, de Haan EH. Split brain: Divided perception but undivided consciousness. Brain. 2017 May;140(5):1231-1237. https://academic.oup.com/brain/article/140/5/1231/2951052
- Pinto Y, de Haan EHF, Lamme VAF. The split-brain phenomenon revisited: A single conscious agent with split perception. Trends Cogn Sci. 2017 Nov;21(11):835-851.
- Roland JL, Snyder AZ, Hacker CD, Mitra A, Shimony JS, Limbrick DD, et al. On the role of the corpus callosum in interhemispheric functional connectivity in humans. Proc Natl Acad Sci U S A. 2017 Dec;114(50):13278–13283. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5740665/
- Uddin LQ, Mooshagian E, Zaidel E, Scheres A, Margulies DS, Kelly AMC, et al. Residual functional connectivity in the split-brain revealed with resting-state fMRI. Neuroreport. 2008 May;19(7):703–709. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640406/
- Volz LJ,Gazzaniga MS. Interaction in isolation: 50 years of insights from split-brain research. Brain. 2017 Jul;140(7):2051–2060. https://academic.oup.com/brain/article-abstract/140/7/2051/3892700
- Wolman D. A tale of two halves. Nature, 2012 Mar;483:260–263. doi:10.1038/483260a. http://www.nature.com/news/the-split-brain-a-tale-of-two-halves-1.10213
- Jones OP, Prejawa S, Hope TMH, Oberhuber M, Seghier ML, Leff AP, et al. Sensory-to-motor integration during auditory repetition: A combined fMRI and lesion study. Front Hum Neurosci. 2014;8:24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3908611/
- Marchina S, Zhu LL, Norton A, Zipse L, Wan CY, Schlaug G. Impairment of speech production predicted by lesion load of the left arcuate fasciculus. Stroke. 2011 Aug;42(8):2251–2256. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3167233/
- Floeter MK, Katipally R, Kim MP, Schanz O, Stephen M, Danielian L, et al. Impaired corticopontocerebellar tracts underlie pseudobulbar affect in motor neuron disorders. Neurology. 2014 Aug;83(7):620–627. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141995/
- Buchsbaum BR, Baldo J, Okada K, Berman KF, Dronkers N, D’Esposito M, et al. Conduction aphasia, sensory-motor Integration, and phonological short-term memory – an aggregate analysis of lesion and fMRI data. Brain Lang. 2011 Dec;119(3):119–128. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090694/
- Fujii M, Maesawa S, Ishiai S, Iwami K, Futamura M, Saito K. Neural basis of language: An overview of an evolving model. Neurol Med Chir (Tokyo). 2016 Jul;56(7):379–386. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945596/