Biological Explanations of Schizophrenia Below are the various biological explanations of Schizophrenia. It is your mission to find out about each one. Your research must include definitions, research and evaluation. Genetic Influences – see notes from lesson Biochemical explanations – the dopamine hypothesis If genetic factors important likely to exert influence on hardware of brain i.e. structural or biochemical abnormalities should be detectable in brains of those diagnosed as schizophrenic. The dopamine hypothesis – Interest in Neurotransmitter dopamine arose when it was found that phenothiazines (neuroleptics, anti-psychotic drugs which reduce symptoms of schiz) work by inhibiting DA activity and that L-Dopa (a synthetic DA-releasing drug) can induce symptoms resembling acute schiz in non-psychotic people. Studies of drugs like amphetamines and LSD, which are known to have an affect on the dopaminergic system, have provided further support. These drugs can induce states v similr to acute schiz in health yindividuals and can exacerbate symptoms in people who are already vulnerable. In a study by Munkvad (1966) behaviour similar to that found in schizophrenic was induced in rats by administering amphetamines. The effects were revered by neuroleptic drugs. Further support – post-mortems of schizophrenics. These have revealed a specific increase of Da in the left amygdale (Falkai et al 1988) and increased Da receptor density in the caudate nucleus putamen (Owen et al 1978) Given these findings and assuming Da is most important factor in the action of anti-psychotic drugs, then it’s be expected that Da metabolism is abnormal in patients with schizophrenia. With the development of PET scans – metabolic activity can now be monitored in live brains. PET scan research recorded by Wong et al (1986) revealed that Da receptor density in the caudate nuclei is indeed greater in those with schiz than in controls. However, this isn’t supported by subsequent studies. AO2 – is support for hypothesis (excess Da activity demonstrated in schiz - particularly those demonstrating +symptoms; drugs alleviate +symptoms, but not so effective with –symptoms) -effect of diff drugs on diff sub-types (its possible that the inconclusive findings in Da studies merely reflects the 2 sub-types of schiz (type I and II). Amphetamines worsen +symptoms assoc with acute schiz and lessen –symptoms assoc with chronic schiz, whilst phenothiazines (anti-psychotics) alleviate +sym but not effective with –sym) Casue or effect? Role of Da in other disorders – Da unlikely to be sole factor in schiz cus its also been implicated in mania and number of other mental disorders which have diff symptoms. Each of these disorders is alleviated by quite diff drugs, yet main evidence for role of Da in schiz is the effectiveness of phenothiazines in alleviating symptoms Brain structure Recent advances in tech have enabled examination of live brains of people with schiz. MRI’s show definite structural abnormalities in the brains of patients with schiz. Brown et al (1986) found decreased brain weight and enlarged ventricles (cavaties in brain which hold cerebrospinal fluid). Flaum et al (1995) also found enlarged ventricles, along with smaller thalamic, hippocampal and superior temporal volumes. Buchsbaum (1990) found abnormalities in the frontal and pre-frontal cortex, the basal ganglia, the hippocampus and the amygdale. As more MRI studies done, more abnormalities discovered. Structural abnormalities have been found more often in those with negative/chronic symptoms, rather than positive/acute symptoms, lending support to the belief that there are 2 types of schizz (type I (acute) and II (chronic)). An argument against this is that many people with acute symptoms later go on to develop chronic schiz, which could indicate a further degeneration of the brain rather than 2 types of schiz. The critical period for onset of schiz is not usually before adolescence. Therefore, if brain abnormalities precede the onset of clinical symptoms, this would confirm that schiz is a developmental disorder. Weinberger (1988) claims that, despite much research, the evidence is still inconclusive as the whether there are progressive structural brain changes prior to initial onset of schiz or whether they follow the onset of clinical symptoms. One of the main probs in trying to understand the causal direction is that, so far, brain imaging in relation to schiz has mainly been restricted to people who have already been diagnosed. A study of teenage monkeys (Castner et al, 1998) may shed some light on the debate. They subjected the monkeys to brain damaging X-rays during fetal development and found that they showed no ill effects during childhood, compared to a control, but at puberty they developed symptoms of schiz, such as hallucinations – ethical consids!! AO2 – conflicting findings about structural abnormalities (whilst MRI studies appear to provide conclusive evidence of structural abnormalities, its worth noting they don’t always agree on region of brain affected, e.g. Flaum et al (1995) found no abnormalities in temporal lobe regions wheras Woodruff et al (1997) found quite sig reductions in the temporal lobe compared with controls. Structural abnormalities as cause or affect? (Most studies using MRI techniques have been carried out on people already diagnosed – not clear whether structural abnormalities predisposed to schiz or whether onset of clinical symptoms cause structural changes. Types of study – (Prospective studies, which could shed light on the direction of causality have been carried out only on animals and is difficult to generalise to humans) Diathesis-stress model Well established that bi factors important, its clear that enviro influences also have role to play. 1 explanation that links bio vulnerability to environmental stressors is diathesis-stress model. Reasoning = certain individuals have a constitutional predisposition to the disorder, but will only develop schiz if they are exposed to stressful situations. The predisposition may be genetic and/or the result of illness or damage in early life. Stressful events in enviro, such a smajor life events, traumatic exp or dysfunctional families may act as a trigger in a high-risk individual. Support – prospective longitudinal studies. Even though such support is compelling for the importance of genetic factors, they’ve also shown tha schiz didn’t always develop in those thought to be genetically vulnerable – led to researchers back to the environmentin search of precipitating factors. The Finnish Adoption study (Tienari 1987) investigated environmental factors by assessing the quality of parenting through tests and interviews. All reported cases of schiz occurred in families rated as ‘disturbed.’ Furthermore, when the rearing enviro were rated as ‘healthy’ in the high-risk sample, the occurance of schiz was well below general population rates. However, cant be seen as evidence for purely enviro aetiology cus low-risk children from ‘disturbed’ families didn’t develop schiz. The Israeli high-risk study (Marcus 1987) investigated enviro factors by assessing the parents on hostility, inconsistency and over-involvement. All reported cases of schiz had poor parenting ratings. However, all these cases show sighns of neuropsychological abnormalities at time of initial assessment (13yrs prev)- raises qu whether the abnormalities had influenced the parent-child interaction Pregnancy and birth – birth complications, viral infections during births, season of birth Season of birth – Since late 1920s, it’s been noticed that an overwhelming high proportion of people diagnosed with schiz were born in winter and early spring (Hope-Simpson 1981). Bradbury & Miller (1985) conducted a review of evidence and found that this was borne out in most countries in N hempishere. A recent English + Wales study shows this has remained consistent over the latter half of the century (Procopio & Marriott, 1998). In S hemisphere countries, a high propostion diagnosed were born in July –Sept – i.e. their winter months. Viral infections – infections such as measles, scarlet fever, polio, diphtheria and pneumonia, and in particular, the virus Influenza A been assoc with schiz ( Torrey at al 1988, Torrey et al 1996). Influenza A is most prevalent in the winter and, if implicated, could explain high n of winter births in schiz. The suggestion is that if the mother is infected during pregnancy there is pre-birth exposure to the Influenza A virus. It is thought that the 25-30 week foetus is most vulnerable cus of accelerated growth in cerebral cortez at this time (Mednick et al 1988). It’s hypothesised that the viral infection enters the brain and gestated til its activated by hormonal changes in puberty. Or there may be a gradual degeneration of the brain which eventually becomes so severe that symptoms of schiz emerge. Further support from observation that through history, peaks in schoz diagnosis have corresponded with major flu epidemics (Torrey et al 1988). Birth complications – quite convincing evidence for both structural and neurochemical abnormalities in the brain of schizs but does they result from a genetic defect or birth complications? A longitudinal study by Dalman et al 1999 found sig links between birth complications and later dev’t of schiz, with pre-eclampsia being the most sig risk factor AO2 – methodological probs – studies such as Torrey (viral infec) based on corr data = caution to infer cause. The data are also based on DSM-II diagnostic criteria for schiz, which included a broader diagnostic range of patients than DSM-III onwards. -genetic predisposition – Torrey et al (1988) claimed the link between viral infec and schiz only occurs in those who are already predisposed. If that was the case – concordance rates in MZ would be 100% and poss DZ as they are in the uterus together and are both exposed to same viruses. -Birth complications sole cause? Unlikely that complications like pre-eclampsia are sole cause as this is a common prob yet not all infants become schiz.