Global Journal of Medical Research, A: Neurology & Nervous System, Volume 23 Issue 3

and focus on determining which psychiatric symptoms would be most responsive to focused neuroregulation. A high response rate would help validate the use of resting vital-signs as markers of neuronal hyperexcitability. Also, by calculating the fraction of patients who exceed the resting vital-sign cutoffs, insight could be gained into the epidemiology of neuronal hyperexcitability and the sensitivity of resting vital-sign measurements as biomarkers of the neuronal hyperexcitability trait. If promising, such pilot studies could be followed by head-to-head prospective studies comparing the short and long-term effectiveness of this objectively-based method of diagnosis and treatment to standard (symptom-based) treatment. Additionally, because resting vital signs appear to be constitutionally elevated in carriers of the neuronal hyperexcitability trait [93], prevention studies could be done to determine the benefits of prophylactic neuroregulator therapy in those members of severely affected families who have upper-end-of-normal resting vital signs but have not yet manifested any clear evidence of mental illness. Adjustments of prophylactic medication in such persons could be guided by the response of resting vital signs to the medication and by reassessing for signs and symptoms that may become more clinically apparent only after they are reduced. Also in these studies, the relative importance of resting vital signs as predictive markers of mental illness and the specificity of these markers could be determined by tracking the progress of siblings whose vital signs fell below the hypothesized cutoffs as well as those whose resting vital signs fell above the hypothesized cutoffs but who decided against prophylactic therapy. Finally, to validate the hypothesis that the vulnerability to developing any of a wide range of psychiatric and functional physical symptoms is rooted in polymorphisms of single gene loci, comprehensive family diagnostic studies could be performed to determine the inheritance pattern of these symptoms and their associated psychiatric disorders as a clinically heterogenous but genetically related group. A classic Mendelian distribution would provide further support for the MCNH hypothesis and potentially pave the way for future research using CRISPR-Cas9 technology [120], offering exciting possibilities for targeted gene therapies [121]. IX. C onclusion By recognizing the cognitive-emotional system as a dynamic interplay between mind and brain and reconceptualizing psychiatric symptoms as pathological hyperactivity in symptom-related circuitsin the brain, the MCNH hypothesis, in conjunction with resting vital-sign measurements, has the potential to revolutionize the treatment of mental illness. Rather than treating patients based on subjective assessments and personal skill sets, treatment selection could, for the first time, be based on quantitative biomarkers. Resting vital-sign measurements provide an objective, evidence-based, and easily accessible way to identify the neuronal hyperexcitability trait, an inherited neurophysiological abnormality that is hypothesized to be at the root of most psychiatric and functional physical symptoms. In addition to improving diagnostic accuracy and guiding treatment selection, targeting the neuronal hyperexcitability trait informs the use of focused neuroregulation, a safer, faster, and more effective treatment approach for those patients who are determined, based on resting vital-sign measurements, to have a biologically-based psychiatric disorder. By identifying the neuronal hyperexcitability trait, the challenge of overlapping and co-occurring psychiatric diagnoses is circumvented and the use of medications that have unpredictable, conflicting, and sometimes paradoxical effects can be minimized. Targeting the neuronal hyperexcitability trait also has the potential to ward off psychiatric symptoms before they even begin and reduce the risk of developing any of the wide range of chronic health conditions with which this highly prevalent trait has been associated. In short, the MCNH hypothesis, in conjunction with resting vital-sign measurements, has the potential to change the face of modern psychiatry by transforming the treatment of mental illness from a symptom-based practice to a biologically-based practice. By seizing this unprecedented opportunity, we can strive toward a future in which behavioral healthcare, like other fields of medicine, is aimed at specific pathological processes, thus streamlining care, speeding recovery, and overcoming the long-held stigma of mental illness. Conflicts of Interest The author declares that he has no competing interests. R eferences R éférences R eferencias 1. Insel TR, Wang PS. The STAR*D trial: Revealing the need for better treatments. Psychiatric Services 2009. https://doi.org/10.1176/ps.2009.60.11.1466. 2. Saxena S, Gorbis E, O’Neill J, et al. Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder. Mol Psychiatry 2009; 14 (2): 197-205. 3. Lazaridou A, Kim J, Cahalan CM, et al. Effects of cognitive-behavioral therapy (CBT) on brain connectivity supporting catastrophizing in fibromyalgia. Clin J Pain 2017; 33 (3): 215-221. 4. Hirschfeld R. History and evolution of the monoamine hypothesis of depression. Journal of Clinical Psychiatry 2000; 61 (6): 4-6. 5. Strawbridge R, Javed RR, Cave J, Jauhar S, Young AH. The effects of reserpine on depression: A systemic review. Journal of Psychopharmacology 2022. 11 Year 2023 Global Journal of Medical Research Volume XXIII Issue III Version I ( D ) A © 2023 Global Journals Untangling Psychology from Biology in the Treatment of Psychiatric Disorders