Schizophrenia Assignment 2

Due on:

email to: dmingay@dmingay.u-net.com


Discuss the various explanations for schizophrenia.


This essay will probably have to be at least 4.5 pages long. For each explanation in turn present the theory, the evidence to support the theory, and then a critique — how good is the theory and what criticisms can be levelled against it? When you have gone through each, make up your own mind, on the basis of the evidence for and against each, which is the most plausible explanation.

Reading:
Cardwell: p647-657
Rosenhan and Seligman: pp440-459
Gross: pp810/11 gives a brief introduction to RD Laing
Laing: “The Divided Self” Chapters 1, 2, 6, 9, 10, 11
(There’s a lot of sometimes difficult reading here. Don’t get bogged down in the technical and philosophical language — just skim read the difficult bits to get an idea of what he is saying and how he uses it to explain the case studies.)
PsychINFO: Try searching for ‘schizophrenia’, ‘cause’, ‘medical model’ etc.
The stuff below:

Schizophrenia: some things worth knowing

One of the A Level textbooks makes the criticism of Laing that there is no evidence for his theory. You might want to argue that a) Sanity, Madness and the Family, his third major book, contains 11 highly detailed case studies which clearly show, through close textual analysis, exactly the sorts of faulty communication patterns within families which cause confusion, mystification and eventually madness, and b) Basaglia, the director of Turin's mental hospital in the 1960s, read Laing and changed the way the hospital was run, integrating it into the local community. Levels of madness dropped, and the Italian government was so impressed that they put him in charge of the whole country's mental health system, which led to a huge drop in madness throughout the county. Levels rose again after the next election, when the conservatives won and opened up mental hospitals run on the same lines as previously (reported in Kotowicz).

The same A Level textbook says that Laing can be criticised because he blames the family for schizophrenia. This criticism is ludicrous, you might argue, since if the family is indeed to blame, then his theory can hardly be criticised for saying so. You would then go on to argue that this isn't what Laing said anyway; a) he wasn't interested in blaming anyone, since he's a psychiatrist and not a lawyer, and b) he said parents' behaviour wasn't their fault, since they are that way because of their parents, who are that way because of their parents, and so on back to when we were monkeys.

Boyle (2001) makes a variety of points about the general dodginess of the medical profession's approach to schizophrenia.

First, the medical profession decided to medicalise mental problems in the middle of the 19th century because mental asylums were private - and run pretty successfully by all accounts on behaviourist lines - and they saw they could therefore make some money out of making people believe that mental problems were medical ones. The discovery that general paresis was caused by the syphilis virus helped them immensely in this effort, although since then there has been no sound evidence that any other mental problem is caused by anything biological. Thus you could argue in an exam essay that the biomedical view is severely compromised by being based on financial considerations rather than an unbiased search for the truth of the matter.

Second, when the branch of medicine known as psychiatry was set up, it was largely ridiculed by proper doctors, so they had to mimic normal medical procedure to enhance their kudos. (This goes for all mental problems, not just schizophrenia.) Proper doctors 'diagnose' illnesses, and they do this by a statistical process whereby they identify a cluster of features (symptoms) which appear to 'go together'; they then need to show that this cluster is reliably associated with another feature which can be measured independently (signs). This is why when you have a proper illness, the GP won't rely on your reported subjective symptoms because these are generally unreliable but will send you for tests. Then a syndrome name is attached to the set of symptoms and signs. This syndrome name is a theoretical construct (in proper technical medicine, you don't 'have', for example, Down's Syndrome, you have a statistically-reliably co-occurring set of symptoms and signs to which the label Down's Syndrome has been attached). This label is accepted as being a temporary label which is open to change as more information comes in; for example, if new technology allows us to carry out tests which show that we have been grouping together two entirely separate diseases, which only appear similar at a surface level, we would then give them two different labels. From all this we can say two things: first, no reliable signs have been found for schizophrenia, so it is misleading to say that it is a syndrome in the first place. Second, the fact that what constitutes the 'symptoms' of schizophrenia keeps changing on a regular basis (various editions of DSM, ICD and others), and that the term 'schizophrenia' seems to encompass a huge range of different behaviours which may or may not 'go together' in real people goes against the normal medical idea of the label being temporary - rather, it is as if they have decided that there is a 'thing' called schizophrenia first, and then tried to decide what it is afterwards. DSM et al. try to decide what goes under each heading, rather than look for clusters and then put a label over it.

Third, genetic research is deeply flawed on several counts. A major twin study, quoted in all the literature, is Slater et al. (1953) which concluded that there was a high concordance between MZ twins which indicated that schizophrenia has a genetic aetiology. In fact, 27% of his sample were dead at the time of diagnosis (other less famous studies are even worse). Slater may have been clever, but how he managed to carry out extensive clinical diagnostic assessments of dead people without the help of medium is puzzling. Of the ones who were alive, he often made diagnoses such as:

[Man shouting through from kitchen quote from Boyle goes here]

Adoption studies fare no better. Kety (1975) is a major study of this type. It transpires that an 'unknown' number of participants had died before the study. This didn't put off the Dr Jacobsen who was recruited to interview them. He simply conducted what he called 'pseudo interviews': he looked at their hospital records, interviewed himself, and answered the way he imagined they might have answered. And they're calling their participants mad!

Gene mapping studies are even more dodgy. This technique looks for clusters of genes which are the same in schizophrenics but different from those of normals (who should in turn be the same as each other). If you run a Google search for 'schizophrenia gene' you find even on the first page 'evidence' from different studies which show it's on chromosomes 1, 3, 13 or 15 and Oct 5. So despite claiming to have found the schizophrenia gene, they all claim it's in a different place. Even more dodgy, and indeed scary, is that Rutter (Professor Sir Michael, if you please), the Oct 5 man, turns out to have warped view of scientific rigour. His statistician (Roberts, 2002) claims that Rutter would repeatedly reject samples which did not show a correlation, but publish results from the rare batches that did. Even a GCSE Maths student will tell you that if you take random samples often enough, some will show 'meaningful' patterns just by chance. Apparently, the same thing has been going on until recently at the University College London schizophrenia gene research laboratories (Morley, 2002).

Why then the widespread belief that schizophrenia has a genetic basis? Even Seligman et al. go for this idea. Boyle explains it in terms of Social Constructionist theory. How people learn to think about things they don't know about is often shaped by the way people perceived to be 'experts' talk about them (Foucault calls this 'discourse'). Gene 'experts', who are keen to keep research grants coming, will talk about not having found the genes responsible for schizophrenia 'yet', which is saying something very different from simply saying they haven't found them.

A quick recap on another thing which students seem to often forget immediately after my class on it:

The overlap problem. Various research claims to have shown that schizophrenics' brains are different in a variety of ways from those of normals. This often boils down to the size of specific sections of the brain (e.g., the hippocampus), which are smaller, on average, for schizophrenics. However, this is only the average - there are wide individual variations in the sizes of brain parts. For example, many normal people have hippocampuses which are smaller that those of some schizophrenics. If it was the case that brian size causes schizophrenia, why aren't the normal people with small hippocampuses schizophrenic, and the schizophrenics with relatively large hippocampuses normal?