- Anonymous
"You may be only one person in the world, but you may also be the world to one person." author unknown
Introduction
There have been many problems with psychiatric drugs.
"This study demonstrates that chronic treatment with neuroleptics-not schizophrenia itself-significantly increases the risk of more frequent, earlier, and accelerated development of neurofibrillary pathology in the brains of elderly schizophrenics." WISNIEWSKI HM, CONSTANTINIDIS J, WEGIEL J, BOBINSKI M, TARNAWSKI M (1994)
This quote is from the ISI Web of Knowledge (31).
Harrison (1999)
Harrison (1) has been riding a dead horse called the neurodevelopmental theory. This theory has been repeatedly proven wrong by findings of gliosis and by longitudinal studies. Ref. 32, which came out after Harrison's review, reports progressive brain volume changes in schizophrenia. The progressive tissue loss supports a neurodegenerative theory. He should have known this because Ref. 33 was one of his references. Ref. 33 also shows progressive brain tissue loss.
Stevens (1981, 1982)
Stevens has also been riding a dead horse, but it has been a different dead horse. Stevens flirted with the virus theory for schizophrenia, another theory that has been proven wrong. Stevens (5, 6, 7) has reported gliosis, which is compatible with either a virus or a metabolic toxin. In Ref. 28 she favored the virus theory. However, no such virus has ever been found. Ref. 30 found an "agent" that was toxic in the cerebrospinal fluid of schizophrenics. However, all tests for a virus failed. The "agent" appeared to have been a metabolic toxin.
Mesa of Cuba and Torrey of the US also favor the virus theory. Mesa has found "particles", but these particles might be a chemical rather than a virus.
The full text may be seen for free for the 1982 paper. It is on the Archives of General Psychiatry website. This was a brilliant paper.
Alzheimer (1897)
Perhaps the first brilliant paper on this subject using microscopy was Alzheimer's 1897 paper on "dementia praecox" (8). Unfortunately this paper never seems to have been translated into English. He reported cytoplasmic pallor, the disappearance of cortical pyramidal cells in the 3rd layer, and other findings. It was not until the early 20th century that he published his famous paper on the disease that now bears his name.
Kraepelin (1919)
Kraepelin's book (9) was written earlier in German, but was translated into English in 1919. Kraepelin, influenced by Alzheimer & Nissl, described lipoid accumulation and and atrophy or cortcal neurons in "dementia praecox", which was the term then used for what is now called "schizophrenia".
Buscaino (1920, 1952)
Vito Maria Buscaino is now deceased, unfortunatley. His son carried on his work for a while, but his son might also be deceased. I have not seen any articles by the younger Buscaino in years. Buscaino blamed schizophrenia on a toxic amine. My view is that he was correct and ahead of his time. He also reported neuropathology in the disease that is now called schizophrenia. In 1952 he reported pathology in the liver, which he thought was caused by the amine.
In 1920 (10) he reported disintegrating plaques in the white matter, the formation of metachromatic globules, and other findings. The globus pallidus showed pathology in catatonia.
Josephy (1930. 1952)
Josephy (11) reported sclerosis, lipoid accumulation in pyramidal neurons in layer 2 prefrontal cortex and hippocampus, calcification in pallidum, neuroglial nodules, and glial change in striatum, thalamus, and brainstem. This confirms Alzheimer except that Alzheimer's findings were only in the cortex. The lipoid accumulation may be a very important clue to what is going on. My view is that fat deposits may reflect the fact that the cells are overeating one or more macronutrients, probably due to a transport error.
In 1931 Spielmeyer (12) confirmed the lipoid accumulation in the third cortical layer. This suggests a neurodegenerative disease.
Dide (1934)
This French scientist reported pathology in the hypothalamus (13). He found hypertrophy and dystrophy of neurons. Hypertrophy means enlargement. This is consistent with the neurons overeating some macronutrient(s). He found glial plaques. The consistent positive findings of gliosis demonstrate that a toxic factor is at work. This supports Buscaino's theory.
Morgan & Gregory (1935)
Morgan & Gregory (14) confirmed Dide. They found degenerative changes and gliosis in the hypothalamus. The hypothalamus is an important subcortical structure.
Vogt & Vogt (1952)
Vogt & Vogt (15) reported clusters of cells with vacuolation. Since vacuoles in animal cells usually represent food (although in plant cells they may hold water), this supports the theory of macronutrients flooding the cells. Pathology was seen in the cytoplasm. Positive findings were in the dorsomedial thalamus, anterior cingulate gyrus, 3rd temporal convolution, and globus pallidus. The globus pallidus is in the basal ganglia, which are now known to be high in dopamine. This supports dopamine theories for schizophrenia. It supports Buscaino's theory of a toxic amine.
Von Buttlar-Brentano (1952)
This brilliant German scientist reported positive findings confirming the Vogts (16). She found pathology in the nucleus basalis, sometimes called the substantia innominata, and in other areas.
Conclusions
The year 1952 was a banner year for the neuropathology of schizophrenia because a big symposium on the subject was held in Rome. Almost all work presented was positive (showing positive findings). Refs. 17-29 provide more information on this complex subject. Gliosis has been repeatedly reported, indicating that a toxic factor causes schizophrenia. The toxic factor is in the bodily fluids and in the brain tissues. It may be created in the brain tissues so it does not have to cross the blood-brain barrier. This makes research difficult because researchers would have to inject the proposed toxin directly into the cerebrospinal fluid to see any effect if it couldn't cross the blood-brain barrier.
Clearly schizophrenia is organic. It is not "functional". The neurodevelopmental theory is false. Since the cells appear to be overeating some macronutrients (because of the neurotxin), a diet is suggested as a treatment. For example, if the macronutrients are amino acids, the diet would be low in protein.
References
1. The neuropathology of schizophrenia. A critical review of the data and their interpretation.
Harrison PJ.
Brain. 1999 Apr;122 ( Pt 4):593-624. Review.
2. Miyakawa T, Sumiyoshi S, Deshimaru M, Suzuki T, Tomonari H. Electron microscopic study on schizophrenia. Mechanism of pathological changes. Acta Neuropathol (Berl) 1972; 20: 67-77.
3. Plum F. Prospects for research on schizophrenia. 3. Neurophysiology. Neuropathological findings. Neurosci Res Program Bull 1972; 10: 384-8.
4. Soustek Z. Ultrastructure of cortical synapses in the brain of schizophrenics. Zentralbl Allg Pathol 1989; 135: 25-32.
5. Stevens JR. Neuropathology of schizophrenia. Arch Gen Psychiatry 1982; 39: 1131-9.
6. Stevens JR. Anatomy of schizophrenia revisited. [Review]. Schizophr Bull 1997; 23: 373-83.
7. Stevens JR, Casanova M, Poltorak M, Germain L, Buchan GC. Comparison of immunocytochemical and Holzer's methods for detection of acute and chronic gliosis in human postmortem material [see comments]. J Neuropsychiatry Clin Neurosci 1992; 4: 168-73. Comment in: J Neuropsychiatry Clin Neurosci 1993; 5: 225-7.
8. Alzheimer A: Beiträge zur pathologischen Anatomie der Hirnrinde und zur anatomischen Grundlage einiger Psychosen. Monatsschr Psychiatr Neurol 1897;2:82-119.
9. Kraepelin E: Dementia Praecox and Paraphrenia. Edinburgh, E & S Livingstone, 1919.
10. Buscaino VM: Le cause anatomo-patologiche della manifestazione schizofrenica nella demenza precoce. Riv Patol Nerv Ment 1920;25:197-226.
11. Josephy H: Dementia praecox (Schizophrenie), in Bumke O (ed): Die Anatomie der Psychosen. Berlin, Springer Verlag, 1930, p 763.
12. Spielmeyer W: The problem of the anatomy of schizophrenia. Res Publ Assoc Res Nerv Ment Dis 1931;10:105-110.
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15. Vogt C, Vogt O: Alterations anatomiques de la schizophrenia et d'autres psychoses dites fonctionelles, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 1, pp 515-532.
16. Von Buttlar-Brentano K: Pathohistologische Feststellungen am basalkern Schizophrener. J Nerv Ment Dis 1952;116:646-653.
17. Fungfeld EW:: Pathologisch-anatomische Untersuchungen im Nucleus anterior thalami bei Schizophrenie, in Proceedings of the International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 3, pp 648-659.
18. Hopf A: Über histopathologische Veränderungen im Pallidum und Striatum bei Schizophrenie, in Proceedings of the International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 3, pp 629-635.
19. Meyer A: Critical evaluation of histopathological findings in schizophrenia, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 1, pp 649-666.
20. Bruetsch WL: Specific structural neuropathology of the central nervous system (rheumatic, demyelinating, vasofunctional, etc) in schizophrenia, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 1, pp 487-499.
21. Van der Horst L: Histopathology of clinically diagnosed schizophrenic psychoses or schizophrenia-like psychoses of unknown origin, in Proceedings of the International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 3, pp 648-659. 22. Hyden H: Nerve cell chemistry and neuropathological problems studied by means of quantitative methods, in Proceedings of the First International Congress of Neuropathology. Turin, Italy, Rosenberg & Sellier, 1952, vol 3, pp 570-594.
23. Tatetsu S: On histologie findings in schizophrenia and schizophrenic state, in Mitsuda H, Fukuda T (eds): Biological Mechanisms of Schizophrenia and Schizophrenia-like Psychoses. Tokyo, Igaku-Shoin Ltd, 1974, pp 288-289.
24. Nieto D, Escobar A: Major psychoses, in Minckler J (ed):Pathology of the Nervous System. New York, McGraw-Hill Book Co, 1972, vol 3, pp 2654-2665.
25. Fisman M: The brain stem in psychosis. Br J Psychiatry 1975;126:414-422.
26. Jacobi W, Winkler H: Encephalographische Studien au chronisch Schizophrenen. Arch Psychiatr Nervenkr 1927;81:299-332.
27. Heath RG, Franklin DE, Shraberg D: Gross pathology of the cerebellum in patients diagnosed and treated as functional psychiatric disorders. J Nerv Ment Dis 1979;167:585-592.
28. Stevens JR: Pathological changes in schizophrenia: Search for a virus, in Proceedings of the Symposium on Psychobiology of Schizophrenia, Eighth International Congress of Pharmacology, Gifu, Japan, 1981. Elmsford, NY, Pergamon Press Inc.
29. Liedeman RR, Prilipko LL: The behavior of T-lymphocytes in schizophrenia, in Bergsma D, Goldstein AL (eds): Neurochemical and Immunologie Components in Schizophrenia. New York, Alan R Liss Inc, 1978, pp 339-364.
30. Tyrrell DAJ, Parry RP, Crow TJ, et al: Possible virus in schizophrenia and some neurological disorders. Lancet 1979;2:839-841.
31. Wisniewski HM, Constantinidis J, Wegiel J, Bobinski M, Tarnawski M. Neurofibrillary pathology in brains of elderly schizophrenics treated with neuroleptics. Alzheimer Dis Assoc Disord 1994; 8: 211-27.
32. Progressive Brain Volume Changes and the Clinical Course of Schizophrenia in Men: A Longitudinal Magnetic Resonance Imaging Study
Mathalon et al.
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33. Jacobsen LK, Giedd JN, Castellanos FX, Vaituzis AC, Hamburger SD, Kumra S, et al. Progressive reduction of temporal lobe structures in childhood-onset schizophrenia. Am J Psychiatry 1998; 155: 678-85.
Published by Craig Olson
I have worked at many different jobs including as a scientist, a mental health worker, a physical health worker, etc. I am an advocate for better health care and an advocate for the disabled. View profile
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