It was concluded that 5 of the children with mothers with schizophrenia were diagnosed with the disease compared to none of the controls. As well as this 37 our of the 47 were given some kind of psychiatric diagnoses in comparison to 9 from the 50 controls. This study compared to that of the twin study focused slightly more on the environment rather than just the genetic links the child had with their parent. Chemical Imbalance also known as “The dopamine hypothesis” is early research that proposed that dopamine was produces in excess in individuals with schizophrenia. More recent research suggests that there are six times the density od the post synaptic receptor for dopamine and this leads to an overall increased excitation as more impulses are carried across the synapse.
The risk of inheriting schizophrenia ranges from about 10% for those who have one first-degree family member (mother, father, sister, brother) with the disease to about 40%-65% if the disease affects both parents and an identical twin. However,
Grilly had found people with Parkinson’s disease (low levels of dopamine) who were taking the drug L-dopa to raise their levels of dopamine were developing schizophrenic type symptoms. There is a flaw with one of the key pieces of evidence to support the dopamine hypothesis. The drugs used to treat schizophrenia by blocking the dopamine receptors can actually increases it as neurons struggle to compensate for the sudden deficiency. Haracz, in a review of post-mortem studies of schizophrenics, found that most of those studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death, unlike post-mortem of schizophrenics who hadn’t received medication these results showed that these individuals had normal levels of dopamine. Therefore, this evidence then in fact weakens the support for the dopamine hypothesis.
Another issue is test-retest reliability. Wilks (2003) found a correlation of +0.84 for testing schizophrenics using the RBAN over a period of 1-134 days which shows that the diagnosis for schizophrenia has high test-retest reliability. Also Prescott et al (1986) analysed the
(Catherine Harrison, PhD, January 10, 2008) B. Drugs that remedy or lessen effects Antipsychotic and atypical antipsychotic drugs are used to treat this disorder such as: Risperidone and Clozapine among others. C. How these drugs help These medications cannot “cure” the illness, but they can take away many of the symptoms or make them milder. In some cases, they can shorten the course of an episode of the illness as well. These medications affect neurotransmitters that allow communication between nerve cells.
A diagnosis can consist of hallucinations, delusions, strange behavior, lack of social skills, inability to feel pleasure, poverty of speech, and psychomotor retardation. There are many speculations about the causes of schizophrenia—some even believe that cannabis use (especially at such a young age) can increase the likelihood of forming it; along with a light body weight. Also, there are treatments out there for schizophrenia but the one that works the most effectively is an antipsychotic drug working in about 70% of patients. Only about 1 in 5 people recover from schizophrenia because some refuse the drugs or relapse from major stressors or the family
The first treatment in biological therapies is chemotherapy; this is the use of drugs to treat a mental illness. Under chemotherapy there are 3 main types of drugs; Antipsychotic, antidepressants and anxiolytic. Anti psychotic drugs are generally used for more severe mental health problems such as schizophrenia. They work by balancing chemicals in the brain such as dopamine as this is linked with there hallucinations. Antidepressants on the other hand by balancing neurotransmitters such as serotonin and epinephrine witch can cause depression if not sufficiently balanced.
Schizophrenia (SZ) is a complex disorder, for which biological explanations have been put forward, with varying degrees of success. One biological explanation which has been proposed for SZ is the Dopamine Hypothesis. This theory suggests that SZ results from over-activity in the brain dopamine (DA) systems. The excess in the brain’s DA systems is both an excess of DA being released from neurons into the synapse, and an excess of DA receptors, meaning that the excess DA released is absorbed into the nervous system. Schizophrenic patients also tend to have increased DA sensitivity, meaning that even if their brain’s DA systems were working at a ‘normal’ level their symptoms might still be present.
“It occurs in 10 percent of people who have a first-degree relative with the disorder, such as a parent, brother, or sister. People who have second-degree relatives (aunts, uncles, grandparents, or cousins) with the disease also develop schizophrenia more often than the general population” (Schizophrenia, 2009). There isn’t just one gene that is associated with schizophrenia, but scientists believe there are several genes that are linked to the disorder. “Other recent studies suggest that schizophrenia may result in part when a certain gene that is key to making important brain chemicals malfunctions. This problem may affect the part of the brain involved in developing higher functioning skills” (Schizophrenia, 2009).
However, research findings within the area of genetics and addiction are inconsistent. For example Noble conducted a meta-analysis and found that 48% of severe alcoholics, 32% of less severe alcoholics carried the A1 variant of the DRD2 gene. Several other studies have failed to find a similar link, this places doubt upon the reliability of the explanation and research findings. Neurotransmitters such as dopamine are also linked to addictive behaviour. According to the disease model addictive behaviour is initiated because drugs/alcohol stimulate the reward pathway within the brain which causes dopamine to be