In part one I discussed the history (Click here for part I); part two discussed the diagnosis (click here for part II). This section discuses proposed causes and treatment of schizophrenia.
Etiology (Cause)
There is no defined cause for any form of schizophrenia although many have been proposed. Early in the conceptualization of the disorder bad or inconsistent parenting and influenza in the mother during pregnancy were offered as possible causal factors. While today the field of psychiatry has denounced explanations of the cause of schizophrenia as being related to child-rearing practices or early experiences of the child, the influenza explanation still receives some support (Cohen, 2003). However, today modern psychiatry has pronounced schizophrenia to be a “disease” that is biologically based (the typical psychiatric explanation for any mental state).
Two Major Causal Factors
Neurotransmitters
Two major factors are commonly believed to contribute to the cause of schizophrenia: First, it is generally acknowledged that schizophrenia is at least in part caused by an imbalance of neurotransmitters. The classical “dopamine hypothesis” of schizophrenia has asserted that there is a hyperactivity in dopaminergic transmission at the dopamine D2 receptor in the projections to the limbic system in the brain (Matthysse, 1974). Despite several limitations this hypothesis still remains the most popular of the neurochemical theories. The idea that dopamine was central in schizophrenia notion was initially supported by the observation that dopamine agonists (substances that increase dopamine in the brain) such as cocaine and amphetamines can induce psychosis in healthy subjects and aggravate psychotic symptoms in schizophrenics (Moncrieff, 2009). Several receptors have been implicated in schizophrenia, however it has been suggested that upregulation of D2 receptors could be the result of adaptation to antipsychotic medications. There have been some PET studies demonstrating no significant difference in D2 receptors between never treated schizophrenics and controls (Moncrieff, 2009). More recent evidence has indicated that other neurotransmitters are also affected in schizophrenics such as glutamate and serotonin (Cohen, 2003; Sadock & Sadock, 2007; Pinel, 2009). Of course much of this evidence has come from the recent development of the atypical neuroleptics whose main mechanism of action is not just the blocking of dopamine (Moncrieff, 2009; Pinel, 2009).
Heredity
The other line of evidence is heredity, suggesting genes play a role in the cause schizophrenia. However, it is still unclear if schizophrenia is the result of a single mutated gene, a series of mutated genes, or a mutated gene passed from parents. The concordance rate (the rate relatives share the disorder) between monozygotic (identical) twins for schizophrenia is around .5 in most studies (Cohen, 2003; Sadock & Sadock, 2007). Several groups of researchers have hypothesized that different genotypes are responsible for different manifestations of schizophrenia. For instance, certain genes, such as the WLK1 gene found on chromosome 22, are found to be more common in catatonic schizophrenics, whereas the NRG gene found on chromosome 8 has been discovered to have links to other forms of schizophrenia (Tosato, Dazzan, & Collier, (2005).
Schizophrenia has been shown to affect both cortical and subcortical brain tracts, especially in the anterior region of the brain. Gene mutations may explain why the brains of schizophrenics have larger ventricles and less gray matter; hoever, some researchers note that this finding is only consistent in schizophrenics treated with medications (Voruganti & Awad, 2006). However, concordance rates are not 100 percent so there appears to be more than just a genetic basis for schizophrenia. There is only about a 50 percent chance that an identical twin sibling of a person with schizophrenia will also have the disorder. But it has been observed that relatives of schizophrenics have higher rates of other disorders such as schizotypal personality disorder and other disorders.
Treatment
While the disorder was recognized in the 1800’s by Emil Krapelin, well into the 20th century the origin and treatment for the disorder was relatively puzzling. Early treatments included insulin shock therapy and frontal lobotomy; however, both of these treatments have long been dismissed (Cohen, 2003). Psychotherapy for schizophrenia today is rarely been considered a first line treatment and the first line treatments for schizophrenia today consist of neuroleptic or antipsychotic medications. Older drugs such as and Haldol primarily work as dopamine antagonists (block dopamine), whereas new atypical antipsychotics such as Risperadal and Clozipine affect dopamine and serotonin.Others also affect other neurotransmitters.
Of course problems with medications have been compliance and side effect profiles (Cohen, 2003). Older drugs are associated with side effects such as tardive dyskinesia (uncontrollable movements), whereas the atypical antipsychotic drugs have fewer side effects (but each drug still has a side effect profile). The side-effects of the medications often lead to their discontinuation by the patient and in some cases the side-effects can be permanent. All medications for schizophrenia take several weeks before they take effect (another problem for the dopamine hypothesis as dopamine is blocked soon after the drug is taken) and up to 20% of patients will not respond to medication at all (Hyman & Fenton, 2003).
Next Part Four: Other Investigations and Concluding Remarks (Click here for Part IV)
Rudy Hatfield - I am a clinical neuropsychologist with extensive experience in the assessment and treatment of neurological and psychiatric disorders. I ...
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