Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness

Michael Raymond Binder

doi:doi:10.11648/j.ajcem.20221002.11

| Peer-Reviewed

Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness

Michael Raymond Binder

Published in American Journal of Clinical and Experimental Medicine (Volume 10, Issue 2)

Received: 22 February 2022 Accepted: 11 March 2022 Published: 23 March 2022

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

Despite the enormous strides that have been made in neuroscience, the pathophysiology of psychiatric disorders remains unclear. Consequently, various forms of psychotherapy, pharmacotherapy, and neuromodulatory therapy continue to be applied without a clear understanding of what pathological process is being treated. However, an emerging hypothesis contends that psychiatric symptoms are the consequence of pathological hyperactivity in symptom-related circuits in the brain. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, persistent firing in anxiety circuits causes persistent feelings of anxiety; persistent firing in depressive circuits causes persistent feelings of depression; persistent firing in cognitive circuits causes ruminative and obsessive thoughts; etc… This pathological circuit-specific hyperactivity is believed to be caused by an inherent failure of the neurological system to self-regulate when perturbed by a psychological, emotional, or biological stressor. Based on this hypothesis, it would not be unreasonable to think that psychiatric symptoms, irrespective of which disorder was being treated, would respond favorably to any natural or medicinal intervention that reduces the excitability of the neurological system. Although the use of brain-calming drugs in psychiatry is not new, what is new is the idea of focusing their use on correcting a specific physiological abnormality that is believed to underlie the symptoms. This technique, which could be called “Focused Neuroregulation,” would differ from standard pharmacotherapy in that if one anticonvulsant failed to alleviate or only partially alleviated symptoms, another anticonvulsant would be substituted or added rather than turning to an off-target class of drugs. This approach is clinically valid because each anticonvulsant is structurally different, and there are multiple mechanisms (and receptors) through which the excitability of the neurological system can be therapeutically regulated. Also, anticonvulsants, unlike other classes of psychotropic drugs, tend to bring the system back into balance; hence the term “mood stabilizers.” Yet another benefit of Focused Neuroregulation is that it could help prevent or slow the progression of the many chronic health conditions that have been linked to an inherent hyperexcitability of the neurological system. In recognition of these potential benefits, and in an effort to avoid the many problems that are associated with the symptom-based treatment of psychiatric and related functional symptoms, the aim of this article is to incentivize the study of a more targeted approach to the treatment of mental illness and the prevention of chronic disease.

Published in	American Journal of Clinical and Experimental Medicine (Volume 10, Issue 2)
DOI	10.11648/j.ajcem.20221002.11
Page(s)	49-58
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

Neuronal Excitability, Neuronal Hyperexcitability, Pathophysiology of Psychiatric Disorders, Biomarkers of Disease, Fifth Vital Sign, Anticonvulsants, Neuroregulators, Preventive Medicine

References

[1]	Binder MR. The multi-circuit neuronal hyperexcitability hypothesis of psychiatric disorders. AJCEM 2019; 7 (1): 12-30.
[2]	Binder MR. Introducing the term “Neuroregulator” in Psychiatry. AJCEM 2019; 7 (3): 66-70.
[3]	Binder MR. FLASH Syndrome: tapping into the root of chronic illness. AJCEM 2020; 8 (6): 101-109.
[4]	McGovern PE, Zhang J, Tang J, et al. Fermented beverages of pre- and proto-historic China. PNAS 2004; 101 (51): 17593-17598.
[5]	Cavalieri D, McGovern PE, Hartl DL, Mortimer R, Polsinelli M. Evidence for S. cerevisiae fermentation in ancient wine (PDF). Journal of Molecular Evolution 2003; 57 (Suppl 1): S226–232.
[6]	Rosenberg EC, Tsien RW, Whalley BJ, Devinsky O. Cannabinoids and epilepsy. Neurotherapeutics 2015; 12 (4): 747–768.
[7]	Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: ∆9-tetrahydrocannabinol, cannabidiol and ∆9-tetrahydrocannabivarin. British Journal of Pharmacology 2008; 153 (2): 199–215.
[8]	Silvestro S, Mammana S, Cavalli E, Bramanti P, Amazon E. Use of cannabidiol in the treatment of epilepsy: Efficacy and security in clinical trials. Molecules 2019; 24 (8): 1459.
[9]	Pearce JMS. Bromide, the first effective antiepileptic agent. Journal of Neurology, Neurosurgery & Psychiatry 2001; 72 (3).
[10]	Ciccarone D. Stimulant abuse: pharmacology, cocaine, methamphetamine, treatment, attempts at pharmacotherapy. Prim Care 2011; 38 (1): 41-58.
[11]	Hillhouse TM, Porter JH. A brief history of the development of antidepressant drugs: from monoamines to glutamate. Exp Clin Psychopharmacol 2015; 23 (1): 1-21.
[12]	Ramachandraih CT, Subramanyam N, Bar KJ, Baker G, Yeragani VK. Antidepressants: from MAOIs to SSRIs and more. Indian Journal of Psychiatry 2011; 53 (2): 180-182.
[13]	Kreston R. (2016) The psychic energizer! the serendipitous discovery of the first antidepressant - Body Horrors. http://blogs.discovermagazine.com/bodyhorrors/2016/01/27/2 081/. (Accessed 10/2/18).
[14]	Sultan RS, Correll CU, Schoenbaum M, et al. National patterns of commonly prescribed psychotropic medications to young people. J Child Adolesc Psychopharmacol 2018; 28 (3): 158-165.
[15]	Brody DJ, Gu Q. Antidepressant use among adults: United States, 2015-2018. National Center for Health Statistics. NCHS Data Brief No. 377, September 2020.
[16]	Khedr EM, Elserogy Y, Fawzy M. Effect of psychotropic drugs on cortical excitability of patients with major depressive disorders: A transcranial magnetic stimulation study. Psychiatry Research 2020; 291: 113287.
[17]	Cooper DC, Moore SJ, Staff NP, Spruston N. Psychostimulant-induced plasticity of intrinsic neuronal excitability in ventral subiculum. J Neurosci 2003; 23 (30): 9937-9946.
[18]	Binder MR. The neuronal excitability spectrum: A new paradigm in the assessment, treatment, and prevention of mental illness and its relation to chronic disease. AJCEM 2021; 9 (6): 193-209.
[19]	Edvinsson D, Ekselius L. Long-term tolerability and safety of pharmacological treatment of adult attention-deficit/hyperactivity disorder: A 6-year prospective naturalistic study. J Clin Psychopharmacol 2018; 38 (4): 370-375.
[20]	Binder MR. Anticonvulsants: The psychotropic and medically protective drugs of the future. AJCEM 2021; 9 (5): 180-188.
[21]	Binder MR. Electrophysiology of seizure disorders may hold key to the pathophysiology of psychiatric disorders. AJCEM 2019; 7 (5): 103-110.
[22]	Volkow ND, Swanson JM. Does childhood treatment of ADHD with stimulant medication affect substance abuse in adulthood? Am J Psychiatry 2008; 165 (5): 553-555.
[23]	Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson, RJ. Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. J. Neuroscience 2007; 27 (33): 8877-8884.
[24]	Leuchter AF, Cook IA, Hunter AM, Cai C, Horvath S. Resting-state quantitative electroencephalography reveals increased neurophysiologic connectivity in depression. PLoS One 2012; 7 (2): 1-13. e32508.
[25]	Scangos KW, Khambhati AN, Daly PM, et al. Closed-loop neuromodulation in an individual with treatment-resistant depression. Nature Medicine 2021; 27: 1696-1700.
[26]	Khushboo SB. Antidepressants: mechanism of action, toxicity and possible amelioration. J Appl Biotechnol Bioeng 2017; 3 (5): 437-448.
[27]	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. Nueropharmacology 2012; 62 (2): 1111-1118.
[28]	Wang M, Ramos BP, Paspalas CD, et al. Alpha2A- adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex. Cell 2007; 129 (2): 397-410.
[29]	Grunze HCR. The effectiveness of anticonvulsants in psychiatric disorders. Dialogues Clin Neurosci 2008; 10 (1): 77-89.
[30]	D’Alessio L, Korman GP, Sarudiansky M, et al. Reducing allostatic load in depression and anxiety disorders: physical activity and yoga practice as add-on therapies. Front Psychiatry 2020.
[31]	Varvin S. Which patients should avoid psychoanalysis, and which professionals should avoid psychoanalytic training?: A critical evaluation. Scandinavian Psychoanalytic Review 2014; 26 (26): 109-122.
[32]	El-Mallakh RS, Vöhringer PA, Ostacher MM, et al. Antidepressants worsen rapid-cycling course in bipolar depression: A STEP-BD randomized clinical trial. Journal of Affective Disorders 2015; 184: 318-321.
[33]	Goldberg JF, Truman CJ. Antidepressant-induced mania: an overview of current controversies. Bipolar Disorders 2001; 5 (6).
[34]	Truman CJ, Goldberg JF, Ghaemi SN. Self-reported history of manic/hypomanic switch associated with antidepressant use: data from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD). J Clin Psychiatry 2007; 68 (10): 1472-1479.
[35]	Henry C, Sorbara F, Lacoste J, Gindre C, Leboyer M. Antidepressant-induced mania in bipolar patients: Identification of risk factors. J Clin Psychiatry 2001; 62 (4): 249-255.
[36]	Yamaguchi Y, Kimoto S, Nagahama T, Kishimoto T. Dosage-related nature of escitalopram treatment-emergent mania/hypomania: a case series. Neuropsychiatr Dis Treat 2018; 14: 2099-2104.
[37]	Binder MR. Neuronal hyperexcitability: the elusive but modifiable instigator of disease. AJCEM 2022; 10 (1): 1-7.
[38]	Binder MR. Neuronal hyperexcitability: significance, cause, and diversity of clinical expression. AJCEM 2021; 9 (5): 163-173.
[39]	De Hert M, Correll CU, Bobes J, et al. Physical illness in patients with severe mental disorders. I. Prevalence, impact of medications and disparities in health care. World Psychiatry 2011; 10 (1): 52-77.
[40]	Cailhol L, Francois M, Thalamas C, et al. Is borderline personality disorder only a mental health problem? Personality and Mental Health 2016; 10 (4): 328-336.
[41]	Wang QQ, Xu R, Volkow ND. Increased risk of COVID-19 infection and mortality in people with mental disorders: analysis from electronic health records in the United States. World Psychiatry 2020; 20 (1): 124-130.
[42]	Li L, Li F, Fortunati F, Krystal JH. Association of a prior psychiatric diagnosis with mortality among hospitalized patients with coronavirus disease 2019 (COVID-19) Infection. JAMA 2020; 3 (9): e2023282.
[43]	Binder MR. Gabapentin—the popular but controversial anticonvulsant drug may be zeroing in on the pathophysiology of disease. AJCEM 2021; 9 (4): 122-134.
[44]	Binder MR. Psychiatric and functional physical symptoms: the more telling “fifth” vital sign. AJCEM 2021; 9 (6): 233-237.
[45]	Heninger GR, Delgado PL, Charney DS. The revised monoamine theory of depression: a modulatory role for monoamines, based on new findings from monoamine depletion experiments in humans. Pharmacopsychiatry 1996; 29 (1): 2-11.

Cite This Article

Plain Text BibTeX RIS

APA Style

Michael Raymond Binder. (2022). Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. American Journal of Clinical and Experimental Medicine, 10(2), 49-58. https://doi.org/10.11648/j.ajcem.20221002.11

Copy | Download

ACS Style

Michael Raymond Binder. Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. Am. J. Clin. Exp. Med. 2022, 10(2), 49-58. doi: 10.11648/j.ajcem.20221002.11

Copy | Download

AMA Style

Michael Raymond Binder. Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. Am J Clin Exp Med. 2022;10(2):49-58. doi: 10.11648/j.ajcem.20221002.11

Copy | Download

@article{10.11648/j.ajcem.20221002.11,
  author = {Michael Raymond Binder},
  title = {Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {10},
  number = {2},
  pages = {49-58},
  doi = {10.11648/j.ajcem.20221002.11},
  url = {https://doi.org/10.11648/j.ajcem.20221002.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20221002.11},
  abstract = {Despite the enormous strides that have been made in neuroscience, the pathophysiology of psychiatric disorders remains unclear. Consequently, various forms of psychotherapy, pharmacotherapy, and neuromodulatory therapy continue to be applied without a clear understanding of what pathological process is being treated. However, an emerging hypothesis contends that psychiatric symptoms are the consequence of pathological hyperactivity in symptom-related circuits in the brain. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, persistent firing in anxiety circuits causes persistent feelings of anxiety; persistent firing in depressive circuits causes persistent feelings of depression; persistent firing in cognitive circuits causes ruminative and obsessive thoughts; etc… This pathological circuit-specific hyperactivity is believed to be caused by an inherent failure of the neurological system to self-regulate when perturbed by a psychological, emotional, or biological stressor. Based on this hypothesis, it would not be unreasonable to think that psychiatric symptoms, irrespective of which disorder was being treated, would respond favorably to any natural or medicinal intervention that reduces the excitability of the neurological system. Although the use of brain-calming drugs in psychiatry is not new, what is new is the idea of focusing their use on correcting a specific physiological abnormality that is believed to underlie the symptoms. This technique, which could be called “Focused Neuroregulation,” would differ from standard pharmacotherapy in that if one anticonvulsant failed to alleviate or only partially alleviated symptoms, another anticonvulsant would be substituted or added rather than turning to an off-target class of drugs. This approach is clinically valid because each anticonvulsant is structurally different, and there are multiple mechanisms (and receptors) through which the excitability of the neurological system can be therapeutically regulated. Also, anticonvulsants, unlike other classes of psychotropic drugs, tend to bring the system back into balance; hence the term “mood stabilizers.” Yet another benefit of Focused Neuroregulation is that it could help prevent or slow the progression of the many chronic health conditions that have been linked to an inherent hyperexcitability of the neurological system. In recognition of these potential benefits, and in an effort to avoid the many problems that are associated with the symptom-based treatment of psychiatric and related functional symptoms, the aim of this article is to incentivize the study of a more targeted approach to the treatment of mental illness and the prevention of chronic disease.},
 year = {2022}
}

Copy | Download

TY  - JOUR
T1  - Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness
AU  - Michael Raymond Binder
Y1  - 2022/03/23
PY  - 2022
N1  - https://doi.org/10.11648/j.ajcem.20221002.11
DO  - 10.11648/j.ajcem.20221002.11
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 49
EP  - 58
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20221002.11
AB  - Despite the enormous strides that have been made in neuroscience, the pathophysiology of psychiatric disorders remains unclear. Consequently, various forms of psychotherapy, pharmacotherapy, and neuromodulatory therapy continue to be applied without a clear understanding of what pathological process is being treated. However, an emerging hypothesis contends that psychiatric symptoms are the consequence of pathological hyperactivity in symptom-related circuits in the brain. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, persistent firing in anxiety circuits causes persistent feelings of anxiety; persistent firing in depressive circuits causes persistent feelings of depression; persistent firing in cognitive circuits causes ruminative and obsessive thoughts; etc… This pathological circuit-specific hyperactivity is believed to be caused by an inherent failure of the neurological system to self-regulate when perturbed by a psychological, emotional, or biological stressor. Based on this hypothesis, it would not be unreasonable to think that psychiatric symptoms, irrespective of which disorder was being treated, would respond favorably to any natural or medicinal intervention that reduces the excitability of the neurological system. Although the use of brain-calming drugs in psychiatry is not new, what is new is the idea of focusing their use on correcting a specific physiological abnormality that is believed to underlie the symptoms. This technique, which could be called “Focused Neuroregulation,” would differ from standard pharmacotherapy in that if one anticonvulsant failed to alleviate or only partially alleviated symptoms, another anticonvulsant would be substituted or added rather than turning to an off-target class of drugs. This approach is clinically valid because each anticonvulsant is structurally different, and there are multiple mechanisms (and receptors) through which the excitability of the neurological system can be therapeutically regulated. Also, anticonvulsants, unlike other classes of psychotropic drugs, tend to bring the system back into balance; hence the term “mood stabilizers.” Yet another benefit of Focused Neuroregulation is that it could help prevent or slow the progression of the many chronic health conditions that have been linked to an inherent hyperexcitability of the neurological system. In recognition of these potential benefits, and in an effort to avoid the many problems that are associated with the symptom-based treatment of psychiatric and related functional symptoms, the aim of this article is to incentivize the study of a more targeted approach to the treatment of mental illness and the prevention of chronic disease.
VL  - 10
IS  - 2
ER  -

Copy | Download

Author Information

Michael Raymond Binder

Department of Psychiatry, North Shore University Health System, Highland Park Hospital, Highland Park, USA

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Michael Raymond Binder. (2022). Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. American Journal of Clinical and Experimental Medicine, 10(2), 49-58. https://doi.org/10.11648/j.ajcem.20221002.11

Copy | Download

ACS Style

Michael Raymond Binder. Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. Am. J. Clin. Exp. Med. 2022, 10(2), 49-58. doi: 10.11648/j.ajcem.20221002.11

Copy | Download

AMA Style

Michael Raymond Binder. Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness. Am J Clin Exp Med. 2022;10(2):49-58. doi: 10.11648/j.ajcem.20221002.11

Copy | Download

@article{10.11648/j.ajcem.20221002.11,
  author = {Michael Raymond Binder},
  title = {Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness},
  journal = {American Journal of Clinical and Experimental Medicine},
  volume = {10},
  number = {2},
  pages = {49-58},
  doi = {10.11648/j.ajcem.20221002.11},
  url = {https://doi.org/10.11648/j.ajcem.20221002.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20221002.11},
  abstract = {Despite the enormous strides that have been made in neuroscience, the pathophysiology of psychiatric disorders remains unclear. Consequently, various forms of psychotherapy, pharmacotherapy, and neuromodulatory therapy continue to be applied without a clear understanding of what pathological process is being treated. However, an emerging hypothesis contends that psychiatric symptoms are the consequence of pathological hyperactivity in symptom-related circuits in the brain. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, persistent firing in anxiety circuits causes persistent feelings of anxiety; persistent firing in depressive circuits causes persistent feelings of depression; persistent firing in cognitive circuits causes ruminative and obsessive thoughts; etc… This pathological circuit-specific hyperactivity is believed to be caused by an inherent failure of the neurological system to self-regulate when perturbed by a psychological, emotional, or biological stressor. Based on this hypothesis, it would not be unreasonable to think that psychiatric symptoms, irrespective of which disorder was being treated, would respond favorably to any natural or medicinal intervention that reduces the excitability of the neurological system. Although the use of brain-calming drugs in psychiatry is not new, what is new is the idea of focusing their use on correcting a specific physiological abnormality that is believed to underlie the symptoms. This technique, which could be called “Focused Neuroregulation,” would differ from standard pharmacotherapy in that if one anticonvulsant failed to alleviate or only partially alleviated symptoms, another anticonvulsant would be substituted or added rather than turning to an off-target class of drugs. This approach is clinically valid because each anticonvulsant is structurally different, and there are multiple mechanisms (and receptors) through which the excitability of the neurological system can be therapeutically regulated. Also, anticonvulsants, unlike other classes of psychotropic drugs, tend to bring the system back into balance; hence the term “mood stabilizers.” Yet another benefit of Focused Neuroregulation is that it could help prevent or slow the progression of the many chronic health conditions that have been linked to an inherent hyperexcitability of the neurological system. In recognition of these potential benefits, and in an effort to avoid the many problems that are associated with the symptom-based treatment of psychiatric and related functional symptoms, the aim of this article is to incentivize the study of a more targeted approach to the treatment of mental illness and the prevention of chronic disease.},
 year = {2022}
}

Copy | Download

TY  - JOUR
T1  - Focused Neuroregulation in the Treatment and Prevention of Mental and Physical Illness
AU  - Michael Raymond Binder
Y1  - 2022/03/23
PY  - 2022
N1  - https://doi.org/10.11648/j.ajcem.20221002.11
DO  - 10.11648/j.ajcem.20221002.11
T2  - American Journal of Clinical and Experimental Medicine
JF  - American Journal of Clinical and Experimental Medicine
JO  - American Journal of Clinical and Experimental Medicine
SP  - 49
EP  - 58
PB  - Science Publishing Group
SN  - 2330-8133
UR  - https://doi.org/10.11648/j.ajcem.20221002.11
AB  - Despite the enormous strides that have been made in neuroscience, the pathophysiology of psychiatric disorders remains unclear. Consequently, various forms of psychotherapy, pharmacotherapy, and neuromodulatory therapy continue to be applied without a clear understanding of what pathological process is being treated. However, an emerging hypothesis contends that psychiatric symptoms are the consequence of pathological hyperactivity in symptom-related circuits in the brain. According to the Multi-Circuit Neuronal Hyperexcitability (MCNH) Hypothesis of Psychiatric Disorders, persistent firing in anxiety circuits causes persistent feelings of anxiety; persistent firing in depressive circuits causes persistent feelings of depression; persistent firing in cognitive circuits causes ruminative and obsessive thoughts; etc… This pathological circuit-specific hyperactivity is believed to be caused by an inherent failure of the neurological system to self-regulate when perturbed by a psychological, emotional, or biological stressor. Based on this hypothesis, it would not be unreasonable to think that psychiatric symptoms, irrespective of which disorder was being treated, would respond favorably to any natural or medicinal intervention that reduces the excitability of the neurological system. Although the use of brain-calming drugs in psychiatry is not new, what is new is the idea of focusing their use on correcting a specific physiological abnormality that is believed to underlie the symptoms. This technique, which could be called “Focused Neuroregulation,” would differ from standard pharmacotherapy in that if one anticonvulsant failed to alleviate or only partially alleviated symptoms, another anticonvulsant would be substituted or added rather than turning to an off-target class of drugs. This approach is clinically valid because each anticonvulsant is structurally different, and there are multiple mechanisms (and receptors) through which the excitability of the neurological system can be therapeutically regulated. Also, anticonvulsants, unlike other classes of psychotropic drugs, tend to bring the system back into balance; hence the term “mood stabilizers.” Yet another benefit of Focused Neuroregulation is that it could help prevent or slow the progression of the many chronic health conditions that have been linked to an inherent hyperexcitability of the neurological system. In recognition of these potential benefits, and in an effort to avoid the many problems that are associated with the symptom-based treatment of psychiatric and related functional symptoms, the aim of this article is to incentivize the study of a more targeted approach to the treatment of mental illness and the prevention of chronic disease.
VL  - 10
IS  - 2
ER  -

Copy | Download