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

mind and body. Through this relaxation processes, psychiatric symptoms are reduced and one’s self- confidence is increased. However, the neurological mechanism through which this healing takes place remains unclear. b) Medical Interventions i. Psychotropic Medications a. Antidepressants Antidepressants are the mainstay of treatment for anxiety, depression, and a number of related psychiatric disorders. The serendipitous discovery of the antidepressant effect back in the 1950s led to the monoamine hypothesis of depression, which posited that a deficiency of monoamines was the core abnormality in clinical depression [4]. Although this could not explain why the antihypertensive drug reserpine, which lowers the activity of monoamines, was likewise effective in reducing symptoms of depression [5], the monamine hypothesis has guided the use of antidepressants for more than fifty years. More recently, however, several other weaknesses of the monoamine hypothesis have been identified. Chief among these are its failure to explain how antidepressants can be effective in treating psychiatric disorders other than clinical depression [4]; why a depletion of serotonin precursors does not produce symptoms of depression in healthy subjects [6]; and why antidepressants can sometimes cause a paradoxical worsening or cycling of symptoms [7-10]. It also fails to explain how the purported abnormalities in monoamine transmission actually translate into depressive symptomatology [11]. b. Antipsychotics Also known as “major tranquilizers,” antipsychotic drugs were originally used to treat agitation, hallucinations, and delusions in schizophrenia. However, they are increasingly being used to augment the effects of antidepressants and mood stabilizers in the treatment of clinical depression and bipolar disorder. Pharmacologically, antipsychotic drugs exert a host of neuroinhibitory effects, including blockade of histamine, dopamine, norepinephrine, and acetylcholine receptors [12], and although dopamine is known to play an important role in auditory signaling [13], the precise mechanism by which antipsychotic drugs exert their wide-ranging therapeutic effects has heretofore remained unclear. c. Psychostimulants Although these drugs were initially used to treat ADHD, they are now being used to treat a variety of co- occurring symptoms, such as anxiety, depression, apathy, and drowsiness. Psychostimulants are thought to exert their therapeutic effects by increasing catecholaminergic transmission in the brain. However, as with antidepressants and antipsychotics, the precise mechanism by which their pharmacological effects translate into their cognitive-emotional effects remains unclear. d. Anticonvulsants More commonly known in psychiatry as “mood stabilizers,” the use of anticonvulsants is largely reserved for bipolar spectrum disorders because of their ability to stabilize mood. Although the precise mechanism by which they exert this clinical effect has heretofore remained unclear, anticonvulsants are known to reduce neuronal excitability by a number of mechanisms, including augmentation of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) [14], potentiation of GABA receptor activation [15], and reduction of sodium and calcium flux across neuronal membranes [16, 17]. e. Ketamine In recent years, ultra-low doses of the dissociative anesthetic ketamine have been found to exert some of the most rapid and robust antidepressant effects yet to be observed [18]. Unfortunately, however, ketamine is relatively short-acting, has a narrow therapeutic index, and can be cumbersome to administer [19]. With repeated dosing, it also carries the risk of cognitive impairment, tolerance, and withdrawal [19]. However, the rapid and robust therapeutic effects of ketamine have drawn intense interest to its pharmacological effects. The drug is known to be an antagonist of the excitatory neurotransmitter glutamate, thus implicating glutamate in the pathophysiology of depression and possibly other psychiatric disorders. f. Neuroactive Steroids Recognizing that the postpartum period is a time of both increased vulnerability to depression and sharp fall in serum progesterone levels, derivatives of progesterone are now being investigated for use in treating clinical depression and bipolar disorder [20-22]. Although preliminary data look promising, a potential limitation of these drugs is a loss of therapeutic effect over time. This concern is based on previous experience with other positive allosteric modulators of the GABA-A receptor, such as barbiturates, benzodiazepines, and sedative hypnotics, all of which carry the risk of tolerance, dependence, and withdrawal. However, the therapeutic success of GABA-A receptor modulators, which put a break on neuronal firing, reiterates the importance of calming the brain in the treatment of psychiatric disorders. ii. Somatic Therapies a. Electroconvulsive Therapy (ECT) Still regarded as the gold-standard in the treatment of clinical depression, ECT involves the intentional induction of seizure activity in the brain. Although the mechanism by which ECT exerts its therapeutic effects remains unclear, it is evident that clinical improvement occurs not during the seizure but in 3 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