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BioSchizophrenia
Biological Explainations and Treatments for Schizophrenia- AQAB Unit 3
| Question | Answer |
|---|---|
| Gottesman (1991)- What were the concordance rates for Monozygotic, and Dizygotic twins for Scizophrenia? | Monozygotic Twins- 48% Dizygotic Twins- 17% |
| If the concordance rates for Scizophrenia twixt Monozygotic Twins is not 100%, what can we deduce from this? | That there must be some environmental influence, and that while genetics may have a significant influence on the development of the disease, it is not absolutely responsible, and is impacted by situational factors (see Diatheses Stress Model) |
| Dizygotic twins have a concordance rate of 17% for Schizophrenia, whilst siblings (a brother or a sister) had a 9% concordance rate (Gottesman 1991). What do these findings show us? | That similar upbringings must be an important factor in developing Schizophrenia, and therefore Social and Environmental, as well as genetic factors are important. |
| Name one limitation of family studies to look at concordance rates of Schizophrenia? | Family studies do not remove environmental influence, so it can be hard to establish cause and effect. |
| Tienari et al (1987)- 7% of adopted children with schizophrenic mothers developed schizophrenia, compared to 1.5% of matched controls. What can this tell us about genetic influence on the development of Schizophrenia? | This demonstrates SOME genetic link for the development of schizophrenia. In Gottesman's Meta Analysis, it was found that the offspring of one parent with schizophrenia would have a 13% concordance rate in developing the disease- supports Tienari. |
| Name one limitation of Adoption Studies such as Tienari et al.(1987) | Not all babies are adopted from birth, so many still have exposure to the parent at some point. It can be hard to distinguish how much this early exposure has an effect on the concordance rates of Schizophrenia. |
| Name one limitation of the Biological- Genetic explanation of Schizophrenia. | -No single gene has been identified as responsible for schizophrenia -The diagnostic criteria for Schizophrenia has changed, and many studies such as Tienari may be outdated and inaccurate. -Doesn't account for cases with no family history of the disea |
| What is the 'Dopamine Hypothesis'? | The theory that schizophrenia is caused by excess levels of the neurotransmitter- Dopamine within central areas of the brain: the Amygdala (Associated with the fear response),and the Hypothalamus (associated with regulation). |
| What does the Dopamine Hypothesis claim that Dopamine is responsible for within the brain? | Increasing the firing of neurons, enhances communication, and stimulates greater neural activity- which is associated with positive symptoms of Schizophrenia. |
| What is an example of indirect support for the Dopamine Hypothesis? | -Amphetamines and cocaine can cause positive symptoms (drug induced psychosis) or make symptoms worse in sufferers. -Post-mortem: More dopamine is found in the brains of sufferers (Iversen 1979) -Clorpromazine reduces dopamine, and so reduces + symptoms |
| What did Lindstrom et al.(1999) find in PET scans of Scizophrenics? | That L-Dopa (used to make dopamine) is taken up faster in sufferers than in controls. |
| More HVA was found in the urine of schizophrenia sufferers, but what is HVA? | Homovanillic Acid- A Bi-Product of Dopamine. This suggests that sufferers have more Dopamine in their bodies- supporting the Dopamine hypothesis. |
| What evidence to support the Dopamine Hypothesis was found using PET Scans (Wong 1986) in the brains of untreated patients, compared to normal/medicated control groups? | Higher density of dopamine receptors. |
| The dopamine hypothesis was investigated through CORRELATIONS of dopamine levels, and symptoms. But what problem is there with this method? | CORRELATION does not always equal CAUSATION, it merely states that there is a RELATIONSHIP between two variables. We cannot establish cause and effect through this method alone. |
| Brier (1995) contested the Dopamine Hypothesis- stating that Serotonin was also involved in the onset and symptoms of schizophrenia. But what does this mean that the dopamine hypothesis is? | Too simplistic, and not comprehensive enough. You can support this point using Atypical Antipsychotics, which also target serotonin levels within the brain, and evaluate by saying that these drugs are often more effective than conventional antipsychotics. |
| Dopamine abnormalities are not present in ALL schizophrenics. What does this mean for the Dopamine Hypothesis? | It cannot explain 100% of cases, therefore it cannot help ALL patients, and so may not be a useful explanation for schizophrenia. |
| The Dopamine Hypothesis cannot explain 'spontaneous' remission, what does this mean for the theory? | Dopamine Levels are unlikely to change so quickly, and so the theory cannot be used to explain ALL cases, and so it is not useful to explain schizophrenia. |
| Why would Davis et al. (1991) say that the Dopamine Hypothesis is NOT useful? | The diversity and types of symptoms in schizophrenia indicate that several neurotransmitters may be involved- not just Dopamine. |
| How can Amorphine (a Dopamine agonist) be used to refute the Dopamine Hypothesis? | It does not induce symptoms of schizophrenia, and so the heightened activity of dopamine is not always responsible for schizophrenic symptoms. |
| What did Jernigan et al.(1986)find in the structures of the limbic system of schizophrenic patients through post mortem and imaging studies? | Significant Cell Loss |
| What did Nasralla et al.(1986)find regarding the Corpus Callosum of Schizophrenic Patients? | Gender differences in the thickening of fibres in the Corpus Callosum is reversed in people with Schizophrenia. This could indicate possible communication problems between the two halves of the brain. |
| What did Andreasen et al (1986) find regarding the Frontal Lobes of Schizophrenic Patients? | Some schizophrenics, especially those that show flat emotion, loss of motivation and poverty of speech may have smaller frontal lobes (as well as Cerebellums and Craniums) than those without Schizophrenia. |
| The two halves of the brain in a normal control are assymmetrical, patricularly in the tempero-parietal area of the cortex. How is this different in Schizophrenic patients? | Post mortem and Imaging Studies have shown that this asymmetry is much LESS evident in Schizophrenics. |
| What did Torrey (2001) find with regards to the Ventricles of schizophrenic sufferers? | They were 15% larger than normal controls. |
| What did Suddath et al (1990) find with regards to structural abnormalities (particularly the bilateral hippocampus) in discordant twin pairs (one with Schizophrenia, one without)? | In 14/15 cases, the schizophrenic twin had a smaller Bilateral Hippocampus. Showing that when genotype is controlled for, there is significantly diminished brain volume in the twin with Schizophrenia. |
| Liddle(1996) found evidence of underactivity in the tempero-frontal areas of the cortex of Schizophrenics, what is this called? | Hydrofrontality |
| Berman (1992) compared blood flow to the frontal lobes of Schizophrenics and controls whilst carrying out a simple cognitive test and found what? | Blood flow INCREASED in controls, but DECREASED in Schizophrenics |
| What did Buchsbaum (1990) find in PET Scans of blood flow within the frontal regions of the brains of schizophrenics? | Considerably reduced blood flow. |
| What did Carpenter et al (1992) find that was consistent with frontal lobe abnormalities in Schizophrenics? | Reduced memory capacity. |
| What did Benes et al. (1986) find in the cortex of Schizophrenic sufferers? | Evidence of Neural Degeneration |
| Weinberger et al (1986) found decreased blood flow in what area of Schizophrenic brains? | The Cortex |
| Lewis (1990) examined 18 studies and found NO SIGNIFICANT LINK between enlarged ventricles and negative symptoms in Schizophrenics. What does this mean for the Neuroanatomical explanation of Schizophrenia? | We cannot say that it is the cause, if we do not find the same evidence across studies- there may be another cause. |
| We cannot tell whether Brain abnormalities are a result of schizophrenia, or if schizophrenia is a result of brain abnormalities. What does this mean for the neuroanatomical explanation of schizophrenia? | Because we cannot establish cause and effect, it may mean that the credibility of the theory is reduced, and so it is not a good explanation for schizophrenia. |
| The biological explanation ignores environmental influence, what does this mean for the theory? | It is reductionist, and though biology may contribute to a predisposition to Schizophrenia, it is perhaps best to consider the importance of social and environmental factors to learn why and how it emerges in some people, but not others. (Gottesman link) |
| What do conventional Anti-Psychotics do? | Reduce dopamine levels in the brain. |
| What are the two kinds of Conventional Anti-psychotics? | Phenothyazines- Clorpromazine (Thorazine) Butryphenones- Haloperidol (Haldol)- Most familiar and widely used butryphenones |
| What kind of symptoms are most responsive to Conventional Anti-Psychotics? | Positive symptoms such as: delusions, hallucinations, disorganised speech, and bizarre behaviour. |
| What effect does Clorpromazine have on agitated patients? | A therapeutic effect, and reduces the strength of hallucinations and delusions. |
| How does Clorpromazine (conventional anti-psychotic) work? | Blocks Dopamine receptors. |
| Why do conventional anti-psychotics need to be taken regularly? | Because symptoms may often recur, sometimes with greater severity. |
| Cole et al (1964) found what differences between sufferers that had had 6 weeks of conventional anti-psychotic treatment, and sufferers that were given a placebo? | Sufferers on medication showed a significant improvement, compared to sufferers on a placebo. |
| What contesting evidence did Loebel et al (1992) find about the recovery of sufferers on conventional anti-psychotics? | 16% failed to recover within twelve months of the first treatment on anti-psychotics. |
| What symptoms do Atypical Anti-psychotics work on? | Positive (things that are added due to the condition), and negative (things that are taken away because of the condition- e.g. social skills) |
| Name two types of Atypical Anti-Psychotics. | Clozapine and Risperidone |
| When is Clozapine effective? | In some Schizophrenics where symptoms do not improve on Halperidol (conventional anti psychotics). A patient maintained on Clozapine is less likely to show side effects related to involuntary movements (tardive diskenisia) |
| What do Atypical Anti-Psychotics (such as Clozapine and Risperidone) do? | Block dopamine receptors AND also alter serotonin neurotransmission. They also seem to effect other neurotransmitters too, such as Acetocholine-memory, Norephineprhrine, and Histamine- associated with swelling and allergic reactions. |
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nayahpross
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