Part A: Causes and Treatments of Schizophrenia.
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Part A: Causes and Treatments of Schizophrenia.
Schizophrenia is the disease that is most commonly associated with the concept of madness. It attacks about 1% of individuals of all races and cultural groups, typically beginning in adolescence or early adulthood. The major difficulty in studying and treating schizophrenia is accurately defining it. Its symptoms are complex and diverse; they overlap greatly with those of other psychiatric disorders, and they frequently change during the progression of the disorder. Also, various neurological disorders are associated with symptoms that might suggest a diagnosis of schizophrenia (Pinel 2007).
Schizophrenia is a severe psychiatric disorder, which typically produces life-long disability. Once considered to be a neurodegenerative disorder, schizophrenia is now most commonly viewed as a disorder of development. This view is supported by a lack of neurodegenerative processes during much of the course of the disease, and by the fact that affected individuals show cognitive and social impairment even before the first episode of the disease. The prevailing hypotheses postulate either an early developmental defect that develops into schizophrenia when normal maturational events occur during adolescence or early adulthood, or defects in late developmental events such as myelination or sexual maturation. Concordance rates are 41-65% in monozygotic twins, compared to 0-28% in dizygotic twins, leading to heritability estimates as high as 85%. Although it is clear that there are strong genetic factors, there is also evidence that environmental factors contribute significantly to schizophrenia. Numerous loci at different chromosomes have been linked to the disease, indicating that several genes underlie susceptibility to schizophrenia, but the identification of these genes has been very difficult. New techniques, including large-scale surveying of gene expression in brains of people with schizophrenia and genome-wide linkage analysis in isolated populations, have implicated the neuregulins and their receptors. While NRG1 is not the only candidate gene that predisposes an individual to schizophrenia, the extensive knowledge of the biological roles of the NRG1-erbB pathway provides an opportunity to gain new insight into the molecular and cellular mechanisms of the disease (Corfas, Roy, Buxbaum 2004).
The major difficulty in studying and treating schizophrenia is accurately defining it. Its symptoms are complex and diverse; they overlap greatly with those of other psychiatric disorders, and they frequently change during the progression of the disorder. Also, various neurological disorders are associated with symptoms that might suggest a diagnosis of schizophrenia. In recognition of the fact that the current definition of schizophrenia likely includes several different brain diseases, some experts prefer to use the plural form to refer to this disorder: the schizophrenias (Pinel 2007).
The following are common symptoms of schizophrenia, but none of them appears in all cases. Indeed, the recurrence of only two of these symptoms for one month is grounds for the diagnosis of schizophrenia Only one symptom is necessary for a diagnosis of schizophrenia if the person exhibits delusions that are particularly bizarre or hallucinations that include one voice providing a running commentary or two voices conversing (Pinel 2007).
Postmortem studies have identified abnormalities in the myelin sheath, oligodendroglia, and interstitial neurons in schizophrenic patients compared with those of healthy volunteers. Kraepelin postulates frontal and temporal lobe abnormalities to be central to the pathology of the disease. Recent postmortem and neuroimaging studies have provided a considerable amount of evidence for brain abnormalities in the frontal and temporal regions of the brain in schizophrenia. If the pathophysiology of schizophrenia reflects a disturbance in the white matter, then such abnormalities might be observed by using diffusion tensor imaging (DTI) because DTI metrics are sensitive to nerve fibre changes. To date, the uncinate fasciculus and superior longitudinal fasciculus, i.e. the pathways through the front temporal lobes, have been well investigated. Several previous studies have reported differences in DTI metrics between schizophrenic patients and healthy volunteers, but results have been inconsistent and differences between patients and volunteers have been observed not only in the front temporal lobes but also in the corpus callosum and cingulate cortex, and more widespread abnormalities in the brain have also been reported. These differences may be attributed, in part, to differences between individual patients (Ota 2009).
Traditional antipsychotics effectively control the hallucinations, delusions, and confusion of schizophrenia. This type of antipsychotic drug, such as haloperidol, chlorpromazine, and fluphenazine, has been available since the mid-1950s. These drugs primarily block dopamine receptors and are effective in treating the “positive” symptoms of schizophrenia. Side effects for antipsychotics may cause a patient to stop taking them. However, it is important to talk with your doctor before making any changes in medication since many side effects can be controlled. Be sure to weigh the risks against the potential benefits that antipsychotic drugs can provide. Mild side effects: dry mouth, blurred vision, constipation, drowsiness and dizziness. These side affects usually disappear a few weeks after the person starts treatment. More serious side effects: trouble with muscle control, muscle spasms or cramps in the head and neck, fidgeting or pacing, tremors and shuffling of the feet (much like those affecting people with Parkinsons disease). Side effects due to prolonged use of traditional antipsychotic medications: facial ticks, thrusting and rolling of the tongue, lip licking, panting and grimacing (Grohol 2006).
Part B: Biopsychologist perspective
After review Marys case the single mother who is having difficulty sleeping for the past month. First I will look at the International Classification of Sleep Disorders, (ICSD) diagnostic criteria for primary insomnia requires: (I) a predominant complaint of difficulty in initiating or maintaining sleep, or nonrestorative sleep, for at least 1 month; (ii) that the sleep disturbance (or associated daytime fatigue) causes clinically significant distress or impairment in social, occupational, or other important areas of functioning; (Hi) that the sleep disturbance does not occur exclusively during the course of another sleep disorder {e.g., narcolepsy, breathing-related sleep