The prevalence of psychiatric disorders in the United States is at a level that demands greater understanding of the mechanisms involved in the disorders and the drugs commonly concerned in treatment. Consequently, about 1% of the general population is affected by schizophrenia, 6% for depression, .07% of children develop Tourette syndrome, and about 25% of the population is affected by some type of anxiety disorder in their lifetime (Pinel, 2007). Indeed Johann Wolfgang von Goethe, who influenced men such as Hegel, Schelling, and Darwin, once said, “We do not have to visit a madhouse to find disordered minds; our planet is the mental institution of the universe” (Goethe, n.d., p. 3). Contained within these statistics and this quote is an implied mandate to better comprehend the psychiatric disorders in question, the associated diseases, and the drugs used to combat the symptoms and even cure the illnesses.
Schizophrenia is really an umbrella term in most people’s minds today and is most closely associated with madness or insanity. In truth though, schizophrenia does not require such a broad definition as madness or insanity but rather can be narrowed to those who suffer from bizarre delusions, inappropriate responses to emotional stimuli, hallucinations, incoherent thoughts, and temporary catatonia (Pinel, 2007). Schizophrenia usually begins in adolescence or early adulthood and has been shown to be caused by both a genetic predisposition and environmental factors. Treatment of schizophrenia has traditionally centered on neuroleptics, which retard the sensitivity of dopamine receptors, specifically one called D2. Over-activity at D2 receptors is highly implicated in cases of schizophrenia, thus the binding of these receptors has an anti-schizophrenic effect. Phenothiazines such as chlorpromazine, reserpine, and spiroperidol bind effectively to both D1 and D2 receptors, but other neuroleptics such as butyrophenones only bind to D2 receptors. And yet still others, such as clozapine, don’t even bind to D2 receptors but only D1 and D4 receptors. Furthermore, research has confirmed that it is not the binding of dopamine receptors, per se, that causes the anti-schizophrenic effects, but rather that the binding starts a chain of yet unknown events which eventually leads to alleviation of symptoms. There is also sufficient evidence to maintain that dopamine is not the only causal agent involved in schizophrenia, but rather some yet unknown neural mechanism might be at play. Also, severe brain damage is involved in those that have suffered from schizophrenia for some time. Moreover, neuroleptics have been associated with Parkinson’s disease-like side-effects such as tremors at rest and a decrease involuntary movement. Only atypical neuroleptics, such as clozapine which do not bind to D2 receptors, do not show Parkinson’s disease-like side-effects. Also, many who have been on neuroleptics for some time develop a tolerance which renders them ineffective.
Affective disorders, such as depression and mania, can be caused by either stress or can even have no apparent cause at all. Depression and mania sit at opposite poles of the emotional spectrum. Depression is characterized as a psychotic disorder of emotions and usually entails emotional stupors and even temporary catatonia; whereas, mania is usually associated with overconfidence and impulsivity. In studies of identical twins, a 60% concordance rate has been observed even when the twins did not live together. Clearly, there is an environmental as well as genetic component to the development of depression. The first drugs to treat affective disorders were monoamine oxidase inhibitors (MAO) which, like the name, inhibit the activity of monoamine oxidase. However, these drugs also cause a higher rate of strokes when coupled with high levels of cheese, wine, or pickles. Coincidentally, post-stroke mania has been observed in patients with lesions in the non-dominant hemisphere (Fenn, George, 1999) A safer alternative to MAO inhibitors would be tricyclical antidepressants because they inhibit the re-uptake of both serotonin and norepinephrine without the dangerous side-effects. The most widely regarded theory of affective disorders, the monoamine theory of depression, explains that under-activity at serotonergic and noradrenergic synapses is the main cause of depression. Drugs such as selective monoamine-reuptake inhibitors, (Prozac, Paxil, etc…) selective norepinephrine-reuptake inhibitors, (Reboxetine) and drugs that block the uptake of more than one monoamine neurotransmitter (Wellbutrin) all work by increasing the levels of serotonin and norepinephrine in the brain. Conversely, lithium does not block any neurotransmitters but is labeled a mood stabilizer because it stops the rapid transition between depression and mania in bipolar affective disorder. Furthermore, those who suffer from depression have been shown to display brain damage in the amygdala and the prefrontal cortex, which may contribute to the disorder.
Anxiety disorders are varied in type and treatment but can be subdivided into five major categories: generalized anxiety disorders, phobic anxiety disorders, panic disorders, obsessive-compulsive disorders, and posttraumatic stress disorders. These disorders are usually tied to recent traumatic events or a particular object or situation, with the exception of generalized anxiety disorder which is characterized by anxiety in the absence of any external stimuli. Benzodiazepines, such as Valium and Librium, are the most prescribed treatment for anxiety disorders, and their effectiveness is predicated on their agonist action on GABAA receptors. These drugs are however very addictive and cause many side-effects, such as nausea, sedation, and tremors. Serotonin agonists on the other hand, such as buspirone, have the binding effects of benzodiazepines without the sedation and relaxation; however, they still include nausea and can cause insomnia. Selective serotonin re-uptake inhibitors, which are also used for the treatment of affective disorders, are also used to alleviate the symptoms of anxiety disorders. The neural basis for anxiety disorders seems to lie in the high concentration of GABAA receptors in the amygdala and would explain the effectiveness of benzodiazepines.
Tourette syndrome is characterized by tics, which can be displayed as eye blinking and involuntary head movement or even hitting and uttering obscenities. Treatments for this type of disorder are mostly concerned with ancillary emotional problems such as anxiety and depression. Grossman, Harrison, & Mostofsky (1986) maintain that, “…Tourette patients are in considerable psychological distress” (p. 288). In their case study of 29 people diagnosed with Tourette syndrome, they found persistent schizophrenia, depression, and psychasthenia according to the MMPI scales. Usually, neuroleptics, those that bind to D2 receptors, are prescribed to combat the effects of Tourette syndrome, but no conclusive study has verified the effectiveness of said drugs on alleviating the symptoms of the syndrome. Furthermore, Tourette syndrome is associated with abnormalities in the basal ganglia, areas of the limbic system, and associated cortex.
In conclusion, the treatment of all of the aforementioned disorders seems to center on the binding of neural receptor in the brain in order to increase or decrease certain neurotransmitters. Nonetheless, the binding of said receptors seems to only treat the symptoms of the disorders rather than curing the patient of the disorder. Much more research is needed to ascertain the direct neural mechanisms involved in these disorders before scientists can begin to understand the complex interplay between the genetic predisposition and environmental factors which bring about these disorders.
Fenn, D., George, K. (1999). Post-stroke mania late in life involving the left hemisphere. Australian & New Zealand Journal of Psychiatry, 33(4), 598-600. Retrieved July 19, 2008, from EBSCOhost database.
Goethe, J. W. (n.d.). Retrieved July 20, 2008, from Quoteland Web site:
Grossman, H. Y., Harrison, R. H., Mostofsky, D. I. (1986). Psychological aspects of gilles de la tourette syndrome. Journal of Clinical Psychology, 42(2), 228-235. Retrieved July 19, 2008, from EBSCOhost database.
Pinel, J. P. J. (2007). Basics of biopsychology. Boston, MA: Allyn and Bacon.