part of the problem with those who critique the establishment is their tendency to over-exaggerate their case and use a substantial amount of rhetoric which undermines their credibility. while this book begins with some of that (and has some of this strategy dispersed within) it also contains a sophisticated analysis and critique of problems with the disease model of mental illness and biological treatments for them.

http://www.amazon.com/Toxic-Psychiat.../dp/0312113668

i haven't finished the book yet, but i have finished the section on schizophrenia. some of the claims that are made are:

- many years of searching for the neurological basis of schizophrenia were unsuccessful. (e.g., nazi scientists has brains on demand and they were unable to discover the neurological basis despite numerous autopsy's).

- since the development of neuroleptics (anti-psychotics) gross brain abnormalities have been found (enlarged ventricles, shrunken areas etc). seeing as these gross brain abnormalities were not described prior to the development of anti-psychotics (and they are gross, or extensive enough for them to have been visible to microscopic investigation upon autopsy) it seems reasonable to conclude that the gross neurological damage is caused by anti-psychotics.

- he describes what were taken to be the beneficial effects of lobotomy (by quoting those who advocated it). the beneficial effects were lack of interest / caring, lack of passion, muted emotional responses, not questioning and simply following orders and instructions (these look rather similar to the so called 'negative symptoms' of schizophrenia). the main beneficial effect of lobotomy is that the patients in the institutions were complacent and followed orders and didn't initiate much action off their own bat. lobotomy made them easier to manage, basically. it did not prevent their symptoms (e.g., delusions, hallucinations, thought disorder) rather it inhibited them from expressing their symptoms and by being so bothered by them.

- he describes how anti-psychotics were described as being a successful chemical alternative to lobotomy because it produced the same effects in subjects. he describes how lobotomy surgically cuts the frontal lobes and limbic system off from communication (inputs and outputs) with the rest of the brain and how neuroleptics chemically cuts the frontal lobes and limbic system (and the basil ganglia) off from inputs from the rest of the brain.

- he describes how the effects of chemical lobotomy are similar in mentally ill people, mentally 'normal' people, animals etc. the neuroleptic medications don't have the specific effect to rectify neurological damage (of which none has been found) rather they have the effect of disabling brain communication.

- he describes how chemical lobotomy (treatment with anti-psychotics) was thought to be preferable to physical lobotomy because chemical lobotomy was thought to be reversible (one could simply stop prescribing the medication).

- he provides studies to show that they don't help positive symptoms more than other seditives and that they weren't responsible for getting people out of institutions and living more productive lives (they were shuffled to other institutions such as nursing homes).

- he describes how tardive dyskinesia mimics a disease called 'lethargic encephalitus' and claims that the effect of neuroleptic medication is to cause this disease by creating neurological damage rather than to rectify neurological damage. (he cites studies where the non-neuroleptically treated control group didn't have a single case of movement disorder)

'Generally the profession tells the public and patients very little about tardive dyskinesia and greatly minimises the risk. A fortunate exception is psychiatrist Jack Gorman in his book 'The essential guide to psychiatric drugs (1990)'. He warns the potential patient, 'the risk of developing severe TD from antipsychotic drugs probably lies between 20% and 40%, but mild signs may appear in up to 70% of patents.'

- TD is caused by hyper-reactivity of the dopamine system in the basal ganglia area (where the hyper-reactivity is caused by the neuroleptic medication). One would expect that the dopamine system in the areas of the limbic system and the frontal lobes would also become hyper-reactive resulting in dementias (tardive dementia) and this is what is found.

- clozapine / clozaril doesn't supress dopamine transmission in the motor areas (basil ganglia) so isn't likely to cause movement disorder (TD). it does produce a profound lobotomy effect, however, and since it is more effective in blocking transmission to the frontal lobes one might expect more significant longer term to higher mental functions (tardive dementias).


hmm... something to think about...

(reasons to carefully examine the malfunction assumption methinks...)