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

sleep hygiene as “non-negotiable first steps” in the treatment of major depressive disorder [70]. Another important factor to consider is that the majority of studies that compare the effectiveness of psychotherapy alone to pharmacotherapy alone involve the use of antidepressants, and antidepressants are not the appropriate treatment for neuronal hyperexcitability [67, 71, 72]. Still, such studies yield comparable results [73], an observation that calls psychotherapy into question as much as the use of antidepressants. That is not to say that psychotherapy, as a therapeutic tool, is unhelpful, but only to say that most persons who seek psychotherapy would be better served if they were to simultaneously be assessed for neuronal hyperexcitability. If this common condition could be identified and treated successfully early in the course of psychotherapy, the distorting element of the patient’s distress would be minimized, and the therapy could focus more on matters that truly were rooted in psychology, such as attitude, values, and priorities. Some of the aforementioned psychotherapeutic techniques do just that, whereas others analyze the patient’s distressing thoughts and emotions. What all of the psychotherapeutic techniques have in common, however, is that they aim to reduce intrapsychic tension. Reducing intrapsychic tension has both direct and indirect benefits; it benefits the mind directly by bringing psychological relief, and it benefits the brain indirectly by reducing mental stimulation of the brain. However, as previously discussed, intrapsychic tension can be difficult to reduce when the pathologically hyperactive brain is keeping the mind bathed in stress. That underscores the importance of pharmacotherapy. If the brain could be quieted directly through anticonvulsant drugs (or any of the aforementioned medical therapies), the interference from the brain would be reduced, thus explaining why medical therapy tends to work faster than psychotherapy [46] but not as well as when combined with psychotherapy [74]. Notwithstanding the potential benefits of medical therapy, it should be noted that antidepressants, psychostimulants, and some of the other medical therapies that were referenced earlier stimulate some parts of the brain while calming others. For example, SSRIs increase neuronal firing in the cerebral cortex [75] but reduce neuronal firing in the amygdala [76], and rTMS can be used to either stimulate or inhibit the activity of specific neuronal circuits [77, 78]. Although increasing the activity of specific circuits can be therapeutic, it can also be counter-therapeutic, depending on how it affects the circuit-specific imbalances that are driving the patient’s symptoms. This is the MCNH explanation for the paradoxical effects that neuroactivating medical therapies, particularly antidepressant and psychostimulant therapies, can have. With these two classes of drugs topping the list of the most commonly prescribed medications, and the prevalence of psychiatric and substance use disorders at epidemic proportions, the need to better understand how these drugs and other medical therapies are affecting the mind and brain is evident. IV. A ssessing the R elative I mportance of the N euronal H yperexcitability T rait But even if neuronal hyperexcitability were at the root of psychiatric symptoms, it would not discount the importance of numerous other factors, such as family upbringing, childhood trauma, ongoing stressors, and personal choices. However, an analysis of the family pedigrees of persons who exhibit signs of mental illness is quite revealing. Although family, twin, and adoption studies have historically failed to identify a classic Mendelian pattern of inheritance for any of the common psychiatric disorders, a reconceptualization of psychiatric symptomsas the symptomatic expression of the neuronal hyperexcitability trait does reveal a classic Mendelian distribution. That distribution is strikingly autosomal dominant! [47]. In other words, in those families that are affected, probands who develop either subsyndromal or more obvious signs and symptoms of mental illness, such as a diagnosable psychiatric, functional physical, or substance use disorder, almost always appear in a classic autosomal dominant distribution. Moreover, a predictable subset of children in these families are completely unaffected despite being raised in the same households by the same parents. These so-called “survivors,” who typically appear in an autosomal recessive distribution, are presumably those who did not inherit one of the gene variants that have been linked to neuronal hyperexcitability. These observations combine to suggest that: 1) all of the most common psychiatric and functional physical disorders are rooted in the same biological abnormality; 2) all of these disorders may be driven by polymorphisms of a single gene locus; and 3) the hypothesized abnormality may be the most important predisposing factor in the development of these disorders. While recognizing their profound importance, these observations should be interpreted with caution because they are based on informally- obtained family pedigrees (approximately 300) rather than tightly controlled studies [67, 79]. V. T he C hallenge of I dentifying the N euronal H yperexcitability T rait Although the phenomenon of neuronal hyperexcitability as a possible driver of psychiatric symptoms has been described previously [47, 80], its significance has been sorely overlooked. This is largely due to the elusive nature of the neuronal hyperexcitability trait. The reasons for the difficulty 8 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