Psychology Sz: Biological Explainations For Schziophernia

Front 1

Kendler et al

Back 1

Compelted a family study and found that if a first degree relative has SZ then you are 18x more likely to contract this mental condition yourself.

Front 2

Gottsman and Shields

Back 2

Found more specific concordance rates:
- Sibling has SZ = 6%
- One parent has SZ = 13%
- Both parents = 46%
This provides goos support for the role of genetics, as these concdance rates were simualr all over the world. This indicated culture has no bearing on the onset of SZ.

Front 3

Genain Case Study

Back 3

This family has two parents with SZ and all 4 daughters also had the condition, however of different types. Question what is the cause of different subtypes of SZ, as this would suggest this facotr could not be inherited. Furthermore, though this study give good detail, it cannot be generalised to others.

Front 4

Gottsman

Back 4

Twin study meta-analysis of 40 studies. Found consistently the MZ twins had concordance rates of 48% whereas DZ twins concoradance rates were 17%. This would suggest that genes has a 50% effect on the development of SZ. THis study shows high interater relaiblity of twin studies. This could be further improved by using single blind studies, so researcher baised can be reduced.

Front 5

Joseph

Back 5

Said that nature and nurture cannot be untangled from twin studies, as not only do they share the same enviorment, but MZ twins are more likely to be treated the same and share the same experences. Therefore causation cannot be determined.

Front 6

Kety

Back 6

5400 Danish children who had been adopted took part in this longitudinal study. Thye found 32% of children who developed SZ had a mother with the condition, with only 18% on children with SZ having no past genetic history. This shows that genetics increase the SZ risk, however some children still developed the condition without genes, which shows the enviroment plays a role. The genetic theory alone is reductionistic.

Front 7

Kringlen

Back 7

Believed that SZ levels of adopted children with SZ parents may be inaccurate, as adoptive parents are likely to be aware of the childs medical history. This raised the question, who would adopt a child like that?

Front 8

Miyakawa et al

Back 8

Turned on a gene in mice which produced the chemical calcuriun and found the negative SZ symptoms developed. This however cannot be extrapolated to humans and it is unsure whether the mice were showing SZ symptoms, as there is not accurate diagnosis tools for SZ in mice.

Front 9

Synder

Back 9

Believed that the dopomine hypothesis could be used to explain schizophernia. He suggested that over production of the neurotransmitter dopomine, which is linked to important brain functions such as memory and attention, leads to SZ.

Front 10

Cromer

Back 10

Said this could explian thought distubance, issues with perception and memory, thus providing a biological explianation for positive symptoms.

Front 11

Davidson

Back 11

Gave increasing levels of L-Dopa drug to pp's with Parkinsons suffers who normally suffer with a decreased level of dopomine. This drug increases dopomine levels, as as the dosaging increased SZ symptoms became prevelent. However, this is only a correlational study, so causation cannot be determined. This issue which cannot be overcome due to the ethical concerns with inducing SZ into a healht individaul.

Front 12

Haracz

Back 12

Believed the drugs given to SZ were the cause of this increased dopoimne level. Drugs blocked dopomine receptors sites, which lead to an increase in dopomine as the brain tried to compensate the changes. However, this was a post mortem study and therefore validity is lowered, as changes to the brain could occur after death. PET scans on living patients are a more reliable way of researching SZ.

Front 13

Torrey

Back 13

Suggested that the cause of SZ was changes in ventrical size. SZ pp's were found to have ventricals which were 15% larger than health pp's. This could be explained by increase production of cerebrospinal fluid.

Front 14

Bornstein

Back 14

Discovered that SZ with negative syptoms were more likely to have enlarged ventrical than those who showed positive symptoms.

Front 15

Lyon et al

Back 15

Suggested that anti-pyschotic medication could be the cause of changed brain strucutre. They found as the dosage increased the denstiy of the brain increased, which would lead to a increased ventrical gap.

Front 16

Buchsbaum et al

Back 16

Compared PET scans of healthy individuals and SZ. They found that the prefrontal cortex had lower metabolic rates in SZ pp's. The PFC is linked to emotion, therefore this finding could explain blunting and negative syptoms.

Front 17

Sudath et al

Back 17

Found that a MZ twin with sz had enlarged ventricals and a reduced aterior hypothalamus compared to the MZ twin without SZ. This supports the role for changing neuroatonomy causing SZ.

Front 18

Gottsman and Reily

Back 18

Sugested the diathesis stress model. This states that individauls develop a biological predispostion for sz as a result of genetics. The environment and stress then lead to sz developing. This explains individual differences.