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

Mind-Brain Interactions Figure 1: Schematic illustration of the mind (large white burst) communicating with the brain via the synchronization of mentally-induced magnetic fields (white radiations) and neurologically-induced magnetic fields (red radiations). b) Practical Application of Mind-Brain Dynamics to the Diagnosis and Treatment of Mental Illness The idea that the mind and the brain are two distinctly different entities that interact with each other could begin to explain how treatment with psychotherapy alone and medication alone can achieve similar results both psychologically and neurologically [46]. Therapies that are aimed directly at changing the way one thinks would have secondary affects on the brain because everything that is processed by the mind would simultaneously be processed by the brain. Conversely, therapies that are aimed directly at modulating brain function would have secondary effects on the mind because everything that is processed by the brain would simultaneously be processed by the mind. Thus, for example, cognitive-behavioral therapy, which changes the way one thinks and feels, would retrain circuits in the brain because changes in cognitive-emotional processing alter neuronal firing patterns. Conversely, pharmacological therapy, which modulates the activity of specific neuronal circuits, would retrain one’s thoughts and emotions because changes in neuronal signaling cause changes in mental and emotional processing. The big question when it comes to therapy, however, is which form would be most effective for which patient? To answer that question, one would first need to determine which of the two—the mind or the brain—was the primary driver of the symptoms. One would then need to determine which form of therapy, when used to treat the appropriate part of the cognitive- emotional system, would be best for which patient. However, the answer to both of these questions would depend upon an accurate understanding of what causes psychiatric symptoms to begin with. Although the precise cause of psychiatric symptoms remains unclear, an emerging hypothesis contends that psychiatric symptoms are driven by pathological hyperactivity in symptom-related circuits in the brain. According to the multi-circuit neuronal hyperexcitability (MCNH) hypothesis of psychiatric disorders, pathological hyperactivity in anxiety circuits causes elevated and persistent feelings of anxiety; pathological hyperactivity in depressive circuits causes elevated and persistent feelings of depression; and pathological hyperactivity in cognitive circuits causes racing thoughts and obsessional thinking [47]. Yet, that would still fall short of explaining why the symptom- related circuits in the brain become pathologically hyperactive. However, a possible answer to that question is supplied by the gene research. A number of large, multi- center gene association studies have found that persons who suffer from common psychiatric disorders, such as anxiety, depression, bipolar disorder, and schizophrenia, have gene variants whose protein products fail to adequately regulate the firing of neurons [48-61]. Now then, given that all of the most common psychiatric disorders are essentially different combinations of the same symptoms, it would not be unreasonable to think that all of these disorders could be rooted in a shared physiological abnormality; namely, neuronal hyperexcitability. Hyperexcitable neurons would just fire too easily and fail to shut off when they should. Indeed, this aligns with the neurophysiological abnormalities that have been 6 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