Running head: DISCOVERING SCHIZOPHRENIA

Discovering Schizophrenia

Schizophrenia, a psychiatric disease that is generally associated with the idea of madness was first identified as a discrete mental illness by Dr. Kraepelin in 1887. In fact, Schizophrenia has been traced to Egypt, as far back as the second millennium before Christ. Depression, dementia, as well as thought disturbances that are typical in schizophrenia are described in detail in the Book of Hearts (Emile). Any television show or movie that tries to reenact a psychiatric ward usually has all its characters depicting the general symptoms associated with schizophrenia. The common symptoms of schizophrenia include hallucinations, bizarre delusions, incoherent thought, and generally odd behavior (Pinel, 2007). Positive schizophrenic symptoms of incoherence, hallucinations, and delusions are caused by an increase in neural activity, while negative schizophrenic symptoms such as lack of affect, cognitive deficits, and poverty of speech are caused by brain damage (Pinel, 2007). The difficulties of diagnosing this disease are that the symptoms range so far in assortment and complexity that they can sometimes overlap and include other psychiatric disorders. Nevertheless, once any one of these general associated symptoms have reoccurred for over eight months a diagnosis of schizophrenia can be made.
The first drugs used to try to treat both positive and negative schizophrenic symptoms were chlorpromazine and reserpine. Although reserpine is no longer used because of rapid reduction in an individual’s blood pressure, both drugs severally reduced schizophrenic symptoms and sparked the dopamine theory of schizophrenia. The neural basis of schizophrenia is centered primarily on the dopamine theory of schizophrenia. Basically, the dopamine theory of schizophrenia is a theory that “schizophrenia is caused by too much dopamine and, conversely, that anti-schizophrenic drugs exert their effects by decreasing dopamine levels” (Pinel, 2007, p.484). Both chlorpromazine and reserpine alienated the transmission of dopamine at dopamine synapses, but both did so in different manners. Pinel (2007) explains that reserpine alienated the transmission of dopamine at dopamine synapses by “depleting the brain of dopamine,” and chlorpromazine did so by “binding to dopamine receptors” (p.484). According to Pinel (2007), chlorpromazine is “a receptor blocker at dopamine synapses that binds to dopamine receptors without activating them” that in turn “keeps dopamine from activating dopamine receptors” (p.484).
Although the dopamine theory seems like a very reasonable explanation to the causes and treatment of schizophrenia, there are still several key findings, such as affected areas of the brain, which prompt alterations to this theory. The most current version of the dopamine theory of schizophrenia holds that “excessive activity at D2 receptors is involved in the disorder but there are other, as yet unidentified, causal factors” (Pinel, 2007, p.486). One key finding exposes that there are receptors other than D2 receptors involved in schizophrenia. Pinel (2007) explains that “the most compelling evidence that D2 receptors are not the sole mechanism underlying schizophrenia came from the development of antischizophrenic drugs that are not primarily D2 receptor blockers” (p.486). Another finding points out that it takes several weeks of neuroleptic therapy to alleviate schizophrenic symptoms (Pinel, 2007). Within a few hours, neuroleptics effectively block activity at D2 receptors, yet it takes weeks, even months, for schizophrenic symptoms to assuage (Pinel, 2007). Pinel (2007) clarifies that this “time lag indicates that the blockage of D2 receptors is not the specific mechanism of the neuroleptics’ therapeutic effect, but blocking D2 receptors triggers some slow-developing compensatory change in the brain that is the key factor of the therapeutic effect” (p.487).
In hopes