Posted by alexandra_k on November 25, 2005, at 20:57:00
In reply to Re: thanks for the thoughts., posted by alexandra_k on November 25, 2005, at 19:20:45
Okay. So some of my thoughts were a little off (in the above post).
Here is what Frith has to say:
'My purpose in this chapter is to outline the evidence for believing that schizophrenia results from a brain disorder. A recent and detailed account of some of this evidence may be found in Kerwin (1992)...
Nevertheless, it was believed that brain abnormalities would soon be found. This has proved to be more difficult than expected. Neuropathologists searched diligently and abnormalities were frequently reported, but they were never replicated. Indeed, schizophrenia eventually came to be known as "the graveyard of neuropathology" (Plum, 1972). I have known neuropathologists to remark facetiously that it is easy to recognise the brains from schizophrenic patients because they are the ones which look normal... (p.15)
It is not suprising, in such a climate, many people came to believe that there was no brain abnormality associated with schizophrenia...
There were two major reasons for the dramatic switch of opinion in recent years towards the belief that schizophrenia is essentially a disease of the brain. The first was the chance discovery of antipsychotic drugs and the subsequent demonstration of their association with the neurotransmitter, dopamine. The second was the development of quantitative rather than qualitative studies of brain structure... (p. 16)
There are two distinct types of effects of treatment with antipsychotics on the movement system. Many patients treated with these drugs show signs similar to those observed in patients with Parkinson's disease: tremor, stiffness, and an abnormal gait. These "Parkinsonian" side-effects appear soon after drug treatment commences and disappear when treatment is discontinued. They are a direct consequence of the effects of the drugs on the dopamine system (Marsden, Tarsy, & Baldessarini, 1975). We know that Parkinson's disease is a consequence of the loss of dopamine-containing nerve terminals in the striatum (Ehringer & Hornykiewicz, 1960). A similar, but temporary, lack of dopamine is produced by antipsychotic drugs. The Parkinsonian side-effects of these drugs are very common and many schizophrenic patients are given additional drugs (usually anticholinergics such as procylindine) in the belief that these drugs will combat these side effects.
In addition to these Parkinsonian side-effects there is another kind of movement disorder associated with anti-psychotic drug treatment known as "tardive dyskinesia" (Jeste & Wyall, 1982). The most striking signs of the syndrome are strange involountary movements of the mouth, tongue, and jaw (orofacial dyskinesia, buccal dyskinesia). These signs are widely believed to be the irreversible consequence of long-term treatment with antipsychotics. They are believed to continue and, perhaps, even to get worse when treatment with antipsychotics is discontinued. There is evidence, however, that these movement disorders were observed in chronic schizophrenic patients before antipsychotic treatment was available, and they can also be observed in patients today who have never been treated with antipsychotics (Owens, Johnstone, & Frith, 1982) (p.20).
Regarding structural changes (brain abnormalities). He does not talk about it being 'degenerative' in fact he argues that it is not, so sorry for misrepresenting him there. He says
'In the 1970's there was a technological breakthrough, which is continuing to revolutionise the study of the brain in man. Computerised axial tomography (CAT) permitted a detailed image of the brain to be obtained from a living subject. In particular it was possible to measure the size of the ventricles (the fluid-filled spaces in the middle of the brain).
Simple measurement of the cross-sectional area of the lateral ventricles revealed them to be significantly enlarged in schizophrenic patients (Johnstone et al., 1956). Furthermore, for the first time in neuropathological studies of schizophrenia, this result has been replicated repeatedly (Gattaz, Kohlmeyer, & Gasser, 1991). Of course, the difference is quantitative, not qualitative. It is not the case that all schizophrenic patients have abnormally large ventricles. Rather it is the case that the mean ventricle size of a group of schizophrenic patients is larger than that of a control group matched for age, sex, and socioeconomic status. At the most, perhaps 25% of chronic schizophrenics have abnormally large ventricles. Inevitably this quantitative difference was missed by the classical neuropathologists, who were seeking qualitative differences. From their point of view the discovery of enlarged ventricles in schizophrenia is not very satisfactory. The enlargement is certainly not unique to schizophrenia, it is also observed in a more exaggerated form in all kinds of organic dementia. Furthermore, the enlargement is not found in all schizophrenics. What, then, does it tell us about schizophrenia?
We might first consider whether enlarged ventricles are associated with a particular kind of schizophrenia in terms of signs and symptoms. (p.20)
We would expect them to be associated with a more "organic" picture. To some extent this is true. Enlarged ventricles are associated with involvountary movement disorders (Owens et al., 1985), a lack of response to drug treatment (Weinberger et al., 1980), and negative signs, rather than positive symptoms (Andreasen et al., 1982)...
There is evidence that the enlargement is more marked in the part of the ventricular system that lies within the temporal lobe (the temporal horn) particularly on the left side of the brain (Crow et al., 1989). Consistent with these observations, some studies have found that the hippocampus and the adjacent area of cortex, the parahippo-campal gyrus, are reduced in size in schizophrenia (Bogerts et al., 1985; Brown et al., 1986). Both of these structures are part of the temporal lobe. Here again the differences are quantitative rather than qualitative. The differences may well represent a general reduction in the size of temporal lobe structures of all patients relative to the distribution in the normal population. The overlap between patients and normal subjects is such, however, that the size of the brain structures cannot qualify as "markers" for schizophrenia. (p.23)
... Repeated scans or scans of schizophrenic patients who have been ill for different lengths of time have not provided any evidence that the ventricles become progressively larger (Gattaz et al., 1991). There are a few instances where patients happened to have received scans well before the onset of schizophrenia. These cases have been found to have had large ventricles even at that early time, well before the onset of symptoms (O'Callaghan et al., 1998; Weinberger, 1998). These results suggest that schizophrenia is not a neurodegenerative disease and that brain abnormalities, including enlarged ventricles, precede the onset of the illness' (p.24).
Hmm.Nature / Nurture...
Some people have more of a biological componant than others...
And by the sounds of it...
Those are the people who are more likely to develop TD regardless of whether they take AP's or not...Still...
Maybe thats not quite right?
The full reference is:
Owens, D.G.C., Johnstone, E.C., & Frith, C.D (1982) Spontaneous involountary disorders of movement. *Archives of General Psychiatry, 39* 452-461.
poster:alexandra_k
thread:581390
URL: http://www.dr-bob.org/babble/20051119/msgs/582219.html