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

depression for years or even decades before the correct diagnosis is made [42-44]. The risk of misdiagnosis is even greater for those with milder forms of bipolar disorder, such as bipolar II disorder, cyclothymic disorder, and cyclic depression, and it is conceivable that many such patients are never correctly diagnosed. This is a matter of grave concern because, in addition to causing bipolar switching, antidepressants can worsen the course of disorders in the spectrum, sometimes with disastrous consequences [14, 40]. Fortuitously, the challenge of distinguishing bipolar spectrum disorders from unipolar depression can be circumvented by applying the MCNH hypothesis because the hypothesis is pathology-based rather than symptom-based. Treatment is aimed at reducing the excitability of the neurological system rather than specific symptoms. By addressing the root cause of psychiatric symptoms, all of the symptoms, including symptom-cycling, can be reduced simultaneously. According to the MCNH hypothesis, symptom-cycling is the consequence of aberrant circuit induction, a kind of neurological short-circuiting that occurs when pathologically hyperactive feeder circuits stimulate activity in circuits that would normally be less active [20, 22, 23]. Persons with inherently hyperexcitable neurological systems have a tendency to cycle both because their neuronal circuits have a propensity to become pathologically hyperactive and because their relatively hypoactive receiver circuits are themselves hyperexcitable. Also, because the frequency with which symptoms cycle would depend upon the total number of neuron-to-neuron connections, the MCNH hypothesis would predict that those patients with the most neurons would be the most rapid cyclers, whereas those with the least neurons would be the least rapid cyclers [22]. Patients with an intermediate number of neurons could experience cycles within cycles [22, 45, 46]. It is also possible that some cognitive-emotional states, such as intense grief, could keep the locus of hyperactivity stuck in one specific firing pattern, thus tending to prevent symptoms from cycling [19, 22]. Thus, using the MCNH hypothesis, it would not be the frequency of cycling nor even the presence of cycling that would guide medication selection but, rather, the excitability of the neurological system. IV. H ow to I dentify the N euronal H yperexcitability T rait I ndependent of P sychiatric S ymptomatology Although the ability to identify the neuronal hyperexcitability trait independent of psychiatric symptomatology had previously been lacking, an explosion of recent studies has identified an association between resting vital-sign measurements and the later development of various psychiatric conditions. In a longitudinal study involving more than one million men in Sweden, Latvala et al. [47] found that subtle elevations in resting heart rate (RHR) were predictive of the later development of generalized anxiety disorder, obsessive- compulsive disorder, and schizophrenia. Similarly, Blom et al. [48] found that adolescent girls with various emotional disorders had increased resting respiratory rates (RRR) in comparison to healthy controls. Persons with higher resting heart and respiratory rates have also been found to be at increased risk of developing a wide range of chronic medical conditions, including diabetes [49-52], high blood pressure [53-55], cardiovascular disease [56-61], cancer [62-64], dementia [65], and all- cause mortality [62, 66]. The subtle vital-sign elevations with which these disease processes are associated are thought to be the consequence of a tonic elevation in basal neurological activity in persons who inherit the genes for neuronal hyperexcitability [25]. In other words, neuronal hyperexcitability could be at the root of a wide range of chronic medical conditions in addition to various psychiatric conditions. Hypothetically, the reason that psychiatric symptoms tend to precede the development of diagnosable physical abnormalities is that the cognitive-emotional system is more expressive of neuronal excitation than other organs and systems of the body [67]. The physical consequences tend to be delayed because they express the gradual erosive effects of neuronal hyperexcitability, which can take years or even decades to occur [25, 68, 69]. The fundamental mechanism by which neuronal hyperexcitability is thought to drive these erosive effects is the same as that by which it is thought to drive the elevated vital signs: hyper-activation of the sympathetic nervous system [25]. Chronic sympathetic dominance, which maintains the body in a catabolic state, accelerates the aging process and increases one’s vulnerability to every disease process that chronic stress can drive. It has been estimated that, in the absence of any significant cardiorespiratory disease, confounding medications, or substances of abuse, an RHR above 75 beats/min or an RRR above 15 breaths/min is indicative of the neuronal hyperexcitability trait [22, 25]. In addition to providing an objective method of identifying the neuronal hyperexcitability trait, the association between resting vital signs and chronic illness could help explain why the lifespan of persons with severe mental illness tends to be so much shorter than the general population [25, 68, 69]. It also suggests that, in addition to reducing psychiatric symptoms, reducing the excitability of the neurological system could help postpone or even prevent the development of a wide range of chronic diseases. This idea is supported by the anecdotal observation that effective treatment with anticonvulsants frequently lowers resting heart and respiratory rate measurements quite significantly. In addition to simplifying diagnostics and guiding treatment, the MCNH hypothesis predicts that the vast majority of persons who struggle with 27 Year 2023 Global Journal of Medical Research Volume XXIII Issue III Version I ( D ) A © 2023 Global Journals A Precision Medicine Approach to the Treatment of Psychiatric Disorders