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Mind-Brain Dynamics in the Pathophysiology of Psychiatric Disorders

Received: 11 March 2022    Accepted: 28 March 2022    Published: 9 April 2022
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Abstract

Short of a comprehensive understanding of psychiatric disorders, two parallel but phenomenologically different schools of thinking continue to guide treatment: the psychological school and the biological school. Yet both of these schools of thinking have major shortcomings. The psychological school does not explain how psychopathology is related to neuropathology, and the biological school does not explain how neuropathology is related to psychopathology. However, a new hypothesis contends that the mind and the brain influence each other. “Mind” in this sense does not refer to a psychic manifestation of complex neurological activity but rather an independent entity that has the ability to think, emote, and access memory either in connection with neurological activity or independent of it. An important consequence of this is that mental stress could hyperactivate the brain, and hyperactivity in the brain could cause mental stress, thus creating a vicious cycle of mutual overstimulation between the mind and the brain. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, psychiatric symptoms develop when normal thoughts and emotions become abnormally amplified, prolonged, or distorted by pathological hyperactivity in the related circuits in the brain. Although this pathological hyperactivity can sometimes be initiated by the brain alone, it is almost always initiated by a superimposition of mental and emotional stress upon an underlying hyperexcitability of the neurological system. This article will discuss how the interactions between the mind and the brain influence: 1) the development of psychiatric symptoms; 2) the nature of the psychiatric symptoms; and 3) the severity of the psychiatric symptoms. It will also discuss the possible means by which the cognitive-emotional system interacts with the neurological system and speculate about where, based on brain architecture and detailed clinical observations, that interaction occurs. Acquiring a better understanding of mind-brain dynamics could help solve the mystery of mental illness and allow clinicians to treat mental and neuropsychiatric disorders with greater precision and with greater success.

Published in American Journal of Psychiatry and Neuroscience (Volume 10, Issue 2)
DOI 10.11648/j.ajpn.20221002.11
Page(s) 48-62
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Mind-Brain Dynamics, Pathophysiology of Psychiatric Disorders, Neuronal Hyperexcitability, Diathesis-Stress Model of Mental Illness

References
[1] Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2] Ritaccio AL, Bruner P, Schalk G. Electrical stimulation mapping of the brain: Basic principles and emerging alternatives. J Clin Neurophysiol 2018; 35 (2): 86-97.
[3] Penfield W. Epilepsy and surgical therapy. Archives of Neurology and Psychiatry 1936; 36 (3): 449-484.
[4] Aravanis AM, Wang L-P, Zhang F, et al. An optical neural interface: in vivo control of rodent motor cortex with integrated fiberoptic and optogenetic technology. Journal of Neural Engineering 2007; 4 (3).
[5] Boyden ES, Zang F, Bamberg E, Nagel G, Deisseroth K. Millisecond-timescale, genetically targeted optical control of neural activity. Nature Neuroscience 2005; 8: 1263-1268.
[6] Cerf M, Thiruvengadam N, Mormann F, et al. On-line, voluntary control of human temporal lobe neurons. Nature 2010; 467: 1104-1108.
[7] Ferreira MAR, O’Donovan MC, Sklar P. Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder. Nat Genet 2008; 40 (9): 1056-1058.
[8] Yuan A, Yi Z, Wang Q, et al. ANK3 as a risk gene for schizophrenia: new data in Han Chinese and meta analysis. Am J Med Genet B Neuropsychiatr Genet 2012; 159B (8): 997-1005.
[9] Green EK, Grozeva D, Jones I, et al., Wellcome Trust Case Control Consortium, Holmans, PA, Owen, MJ, O'Donovan, MC, Craddock N. The bipolar disorder risk allele at CACNA1C also confers risk of recurrent major depression and of schizophrenia. Mol Psychiatry 2010; 15 (10): 1016-1022.
[10] Lopez AY, Wang X, Xu M, et al. Ankyrin-G isoform imbalance and interneuronopathy link epilepsy and bipolar disorder. Mol Psychiatry 2017; 22 (10): 1464–1472.
[11] Goddard GV. Development of epileptic seizures through brain stimulation at low intensity. Nature 1967; 214: 1020-1021.
[12] Rose GM, Diamond DM, Pang K, Dunwiddie TV. Primed burst potentiation: lasting synaptic plasticity invoked by physiologically patterned stimulation. In: Haas HL, Buzsàki G. (eds) Synaptic plasticity in the hippocampus. Springer, Berlin, Heidelberg, 1988.
[13] Merker B. Consciousness without a cerebral cortex: A challenge for neuroscience and medicine. Behavioral and Brain Sciences 2007; 30 (1): 63-134.
[14] Kawkabani K. Preserved consciousness in the absence of a cerebral cortex, the legal and ethical implications of redefining consciousness and its neural correlates: A case for a subcortical system generating affective consciousness. Neuroscience and Neurobiology Commons, Honors Research Projects 2018; 734.
[15] (http://blogs.discovermagazine.com/seriouslyscience/2014/07/31/getting-heart-transplant-change-personality/#.WIYU0cu9KK0. Accessed 5/16/18).
[16] Caspi A, Houts RM, Ambler A, et al. Longitudinal assessment of mental health disorders and comorbidities across 4 decades among participants in the Dunedin Birth Cohort Study. JAMA Netw Open 2020; 3 (4): e203221.
[17] Post RM. Mechanisms of illness progression in the recurrent affective disorders. Neurotox Res 2010; 18 (3-4): 256-271.
[18] Moody RA. Life after life. Mockingbird Books, 1975.
[19] Long J. Evidence of the afterlife: The Science of near-death experiences. HarperOne, 1975.
[20] Parnia S, Spearpoint K, de Vos G. AWARE—AWAreness during resuscitation—A prospective study. Resuscitation 2014; 85: 1799-1805.
[21] Van Lommel P. Near-death experiences: the experience of the self as real and not as an illusion. Ann N Y Acad Sci 2011; 1234: 19-28.
[22] Freud S. (1915). The unconscious. SE, 14: 159-204.
[23] Fuchs E, Flügge G. Chronic social stress: effects on limbic brain structures. Physiology & Behavior 2003; 79 (3): 417- 427.
[24] Mehler B, Reimer B, Coughlin JF, Dusek JA. Impact of incremental increases in cognitive workload on physiological arousal and performance in young adult drivers. Transportation Research Record: Journal of the Transportation Research Board 2009; (2138): 6-12.
[25] Kahn DA, Sachs GS, Printz DJ, Carpenter D. Medication treatment of bipolar disorder 2000: A summary of the expert consensus guidelines. Journal of Psychiatric Practice 2000; 6 (4): 197-211.
[26] Akiskal HS. The bipolar spectrum: new concepts in classification and diagnosis. In: Grinspoon L, editor. Psychiatry Update; The American Psychiatric Association Annual Review. Vol. 2. Washington DC: American Psychiatric Press 1983, pp. 271–292.
[27] Binder MR. Electrophysiology of seizure disorders may hold key to the pathophysiology of psychiatric disorders. AJCEM 2019; 7 (5): 103-110.
[28] Binder MR. The Neuronal Excitability Spectrum: a new paradigm in the diagnosis, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM; 2021; 9 (6); 187-203.
[29] Perin R, Berger TK, Markram H. A synaptic organizing principle for cortical neuronal groups. PNAS 2011; 108 (13): 5419-5424.
[30] Yuan P, Monie M. Activity shapes neural circuit form and function: A historical perspective. Journal of Neuroscience 2020; 40 (5): 944-954.
[31] Henkel AW, Welzel O, Groemer T W, et al. Fluoxetine prevents stimulation-dependent fatigue of synaptic vesicle exocytosis in hippocampal neurons. Journal of Neurochemistry 2010; 114 (3): 697-705.
[32] Lubloy A, Kereszturi JL, Nemeth A, Mihalicza P. Exploring factors of diagnostic delay for patients with bipolar disorder: a population-based cohort study. BMC Psychiatry 2020; 20 (75).
[33] Binder MR. A pathophysiolgically-based approach to the treatment and prevention of mental illness and its related disorders. AJCEM 2021; 9 (6): 223-232.
[34] David Cunning. The Cambridge Companion to Descartes' Meditations. Cambridge University Press, 2014. p. 277. ISBN 978-1-107-72914-8.
[35] Pandya SK. Understanding brain, mind and soul: Contributions from neurology and neurosurgery. Mens Sana Monogr 2011; 9 (1): 129-149.
[36] Forbes N, Mahon B. Faraday, Maxwell, and the electromagnetic field: How two men revolutionized physics. Prometheus Books, New York, 2014.
[37] Xu Y, Jia Y, Ma J, Hayat T, Alsaedi A. Collective responses in electrical activities of neurons under field coupling. Sci Rep 2018; 8: 1349.
[38] Freud, S. (1924). A general introduction to psychoanalysis, trans. Joan Riviere.
[39] Dimkov P. Large-scale Brain Networks and Freudian Ego. ResearchGate 2018 https://www.researchgate.net/publication/326468259.
[40] Crick F. Function of the thalamic reticular complex: The searchlight hypothesis. Proceedings of the National Academy of Sciences 1984; 81: 4586-4590.
[41] Thomson AM, Lamy C. Functional maps of neocortical local circuitry. Front Neurosci 2007 https://doi.org/10.3389/neuro.01.1.1.002.2007
[42] Theyel BB, Llano AL, Sherman SM. The corticothalamocortical circuit drives higher-order cortex in the mouse. Nature Neuroscience 2010; 13: 84-88.
[43] Baroncelli L, Braschi C, Spolidoro M, et al. Brain Plasticity and Disease: A Matter of Inhibition. Neural Plasticity; 2011.
[44] Herrero MT, Insausti R, Estrada C. (2015) Reference Model in Neuroscience and Biobehavioral Psychology. Brain Mapping: An Encyclopedic Reference. Vol. 2: Anatomy and Physiology Systems: 219-242.
[45] Treisman A. Focused attention in the perception and retrieval of multidimensional stimuli. Perception & Psychophysics 1977; 22 (1): 1-11.
[46] Treisman A, Gelade GA. A feature integration theory of attention. Cognitive Psychology 1980; 12: 97-136.
[47] Treisman A, Schmidt H. Illusory conjunctions in the perception of objects. Cognitive Psychology 1982; 14: 107-141.
[48] Julesz B. Spacial nonlinearities in the instantaneous perception of textures with identical power spectra. Philosophical Transactions of the Royal Society of London B 1980; 290: 83-94.
[49] Julesz B. Textons, the elements of texture perception, and their interactions. Nature 1981; 290: 91-97.
[50] Bergen JR, Julesz B. Parallel versus serial processing in rapid pattern discrimination. Nature 1983; 303: 696-698.
[51] Kwasniak J. Looking at the thalamic reticular nucleus. http://charbonniers.org/2013/02/13/looking-at-the-thalamic- reticular-nucleus/. (Accessed 5/17/18).
[52] Llinas R, Jahnsen H. Electrophysiology of mammalian thalamic neurons in vitro. Nature (London) 1982; 297 (5865): 406-408.
[53] Jahnsen H, Llinas R. Electrophysiological properties of guinea-pig thalamic neurones: an in vitro study. J. Physiol 1984; 349 (1): 205-226.
[54] Jahnsen H, Llinas R. Ionic basis for the electro- responsiveness and oscillatory properties of guinea-pig thalamic neurones in vitro. J Physiol 1984; 349: 227-247.
[55] Erlij D, Acosta-García J, Rojas-Márquez M, et al. Dopamine D4 receptor stimulation in GABAergic projections of the globus pallidus to the reticular thalamic nucleus and the substantia nigra reticulata of the rat decreases locomotor activity. Neuropharmacology 2012; 62 (2): 1111-1118.
[56] Faraone SV. The pharmacology of amphetamine and methylphenidate: Relevance to the neurobiology of attention-deficit/hyperactivity disorder and other psychiatric comorbidities. Neuroscience & Behavioral Reviews 2018; 87: 255-270.
[57] Hargreave E (2006). The neuroplasticity phenomenon of kindling. http://hargreaves.swong.webfactional.com/kindle.htm. (Accessed 5/19/18).
[58] Begh M, Beghi E, and Cornaggia CM. Epilepsy in psychiatric disorders. In: Mula M. (eds) Neuropsychiatric Symptoms of Epilepsy. Neuropsychiatric symptoms of neurological disease. pp. 289-302. Springer, Cham Publishing Company, 2016. ISBN: 978-3-319-22158-8.
[59] Josephson CB, Lowerison M, Vallerand I, et al. Association of depression and treated depression with epilepsy and seizure outcomes: a multicohort analysis. JAMA Neurol 2017; 74 (5): 533-539.
[60] Binder MR. FLASH syndrome: tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[61] Anderson JW, Lambert EA, Sari CI. Cognitive function, health-related quality of life, and symptoms of depression and anxiety sensitivity are impaired in patients with the postural orthostatic tachycardia syndrome (POTS). Front Physiol 2014; 5: 230.
[62] Sender R, Fuchs S, Milo R. Revised estimates for the number of human and bacteria cells in the body. PLoS Biology 2016. https://doi.org/10.1371/journal.pbio.1002533.
[63] Pockett S. The electromagnetic field theory of consciousness: A testable hypothesis about the characteristics of conscious as opposed to non-conscious fields. Journal of Consciousness Studies 2012; 19 (11-12): 191-223.
[64] McFadden J. Synchronous firing and its influence on the brain’s electromagnetic field: Evidence for an electromagnetic theory of consciousness. JCS 2002; 9 (4): 23–50.
[65] McFadden J. Integrating information in the brain’s EM field: The cemi field theory of consciousness. Neuroscience of Consciousness 2020; 2020 (1).
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    Michael Raymond Binder. (2022). Mind-Brain Dynamics in the Pathophysiology of Psychiatric Disorders. American Journal of Psychiatry and Neuroscience, 10(2), 48-62. https://doi.org/10.11648/j.ajpn.20221002.11

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    Michael Raymond Binder. Mind-Brain Dynamics in the Pathophysiology of Psychiatric Disorders. Am. J. Psychiatry Neurosci. 2022, 10(2), 48-62. doi: 10.11648/j.ajpn.20221002.11

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    AMA Style

    Michael Raymond Binder. Mind-Brain Dynamics in the Pathophysiology of Psychiatric Disorders. Am J Psychiatry Neurosci. 2022;10(2):48-62. doi: 10.11648/j.ajpn.20221002.11

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  • @article{10.11648/j.ajpn.20221002.11,
      author = {Michael Raymond Binder},
      title = {Mind-Brain Dynamics in the Pathophysiology of Psychiatric Disorders},
      journal = {American Journal of Psychiatry and Neuroscience},
      volume = {10},
      number = {2},
      pages = {48-62},
      doi = {10.11648/j.ajpn.20221002.11},
      url = {https://doi.org/10.11648/j.ajpn.20221002.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajpn.20221002.11},
      abstract = {Short of a comprehensive understanding of psychiatric disorders, two parallel but phenomenologically different schools of thinking continue to guide treatment: the psychological school and the biological school. Yet both of these schools of thinking have major shortcomings. The psychological school does not explain how psychopathology is related to neuropathology, and the biological school does not explain how neuropathology is related to psychopathology. However, a new hypothesis contends that the mind and the brain influence each other. “Mind” in this sense does not refer to a psychic manifestation of complex neurological activity but rather an independent entity that has the ability to think, emote, and access memory either in connection with neurological activity or independent of it. An important consequence of this is that mental stress could hyperactivate the brain, and hyperactivity in the brain could cause mental stress, thus creating a vicious cycle of mutual overstimulation between the mind and the brain. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, psychiatric symptoms develop when normal thoughts and emotions become abnormally amplified, prolonged, or distorted by pathological hyperactivity in the related circuits in the brain. Although this pathological hyperactivity can sometimes be initiated by the brain alone, it is almost always initiated by a superimposition of mental and emotional stress upon an underlying hyperexcitability of the neurological system. This article will discuss how the interactions between the mind and the brain influence: 1) the development of psychiatric symptoms; 2) the nature of the psychiatric symptoms; and 3) the severity of the psychiatric symptoms. It will also discuss the possible means by which the cognitive-emotional system interacts with the neurological system and speculate about where, based on brain architecture and detailed clinical observations, that interaction occurs. Acquiring a better understanding of mind-brain dynamics could help solve the mystery of mental illness and allow clinicians to treat mental and neuropsychiatric disorders with greater precision and with greater success.},
     year = {2022}
    }
    

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Author Information
  • Department of Psychiatry, NorthShore University HealthSystem, Highland Park Hospital, Highland Park, USA

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