Schizophrenia as a Toxic Encephalopathy

Neurologists have not taken much interest in schizophrenia, except for a few in India. This is unfortunate because I feel that neurologists could contribute because schizophrenia is a disease of the brain.

"In the 1970s, broad surveys again showed that catatonia was as common as before among patients with mania and depression, and as a toxic response to neuroleptic drugs. The latter recognition, that the neuroleptic malignant syndrome is the same syndrome as malignant catatonia, and is effectively treated as such, sparked a renewed interest." M. Fink (1)

Sudden Death

"People with schizophrenia show a two- to three-fold increased risk to die prematurely. Mortality is accounted for by a combination of factors (patients' life style, suicide, premature cardiovascular disease, metabolic syndromes and, not so often mentioned, sudden death). The cause of sudden death in schizophrenia is unknown, but cardiac arrhythmia plays a potential role. Patients with schizophrenia are at high risk for cardiovascular disease, and some antipsychotics may be associated with cardiovascular adverse events (e.g., electrocardiograph QT interval prolongation), suggesting that this could lead to sudden cardiac death."

Scorza FA, Cysneiros RM, Terra VC, Scorza CA, Cavalheiro EA, Ribeiro MO, Gattaz WF.

Disciplina de Neurologia Experimental, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), Rua Botucatu, 862, Edifício Leal Prado, CEP 04023-900, São Paulo, Brazil.

The Brazilian authors favor the fish oil treatment. However, there has been a problem with fish being contaminated with methylmercury.

Lethal Catatonia

Catatonia can be lethal (3). This may be due to an internal toxin produced in the disease.

Psychiatric Drugs

Unfortunately there have been terrible problems with psychiatric drugs (4, 5).

British Work

A British group (7) reported a "cytopathic effect" of an "agent" found in the cerebrospinal fluid of schizophrenics. At first they thought it was a virus, but all tests for a virus failed (8). As hard as they could to prove it to be a virus, they couldn't (9-11, 13, 14). My own view is that they found a toxin.

"Degenerated cultures show polymorphous nuclei with condensed nuclear chromatin and enlarged mitochondria with few cristae but virus particles were not identified." Tyrrell DA, Parry R, Davies H, Bloxham C, Crow TJ. (Ref. 7)

Neuropathology studies have repeatedly reported gliosis, which suggests an unknown toxic factor (12).

Cuban Research

Dr. Mesa of Havana did neuropathology studies and other studies. He found deposition of glycoprotein granules around the vessels in the amygdala in schizophrenia. He also found degenerative changes in the neurons in the amygdala and a microglial reaction around the degenerated neurons. This information is presented on the website www.wpanet.org, which is the website of the World Psychiatric Association. Go to this website and search for "Mesa".

In paranoid schizophrenia he found the deposition of lipids in degenerated neurons in the amygdala. He also found particles, nuclear bodies, and membrane proliferation using the electron microscope. Particles were seen in the nucleus.

Intranuclear filamentous inclusion bodies were seen. However, virus particles are not filamentous as a rule. They can be spherical.

Mesa also studied platelets, which he found to be abnormal in schizophrenia. He reported a biological test for schizophrenia using the platelets examined under a microscope. Morphological alterations were seen in the platelets, as in the neurons. mIn schizophrenia the platelets were increased in size up to three times the normal platelets. There were glycogen deposits and big vacuoles. This appears to suggest defective glucose metabolism. The glucose metabolism would be slow to produce the glycogen deposits.

Conclusions

Schizophrenia is caused by a toxic factor in the blood and in the cerebrospinal fluid. the nature of this factor is controversial. The diminished electron density reported by Mesa in the platelets suggests fat. Large filopodia were seen in the platelets.

Mesa has published his work in both Sanish (15) and English (16).

My interpretation is that these results could be explained if amino acids were flooding the cells. But what are the treatments?

I favor orthomolecular treatments (17, 18). However, I am also open to psychosocial rehabilitation (19).

References

1. Catatonia: a syndrome appears, disappears, and is rediscovered. Fink M. Can J Psychiatry. 2009 Jul;54(7):437-45.

2. Omega-3 consumption and sudden cardiac death in schizophrenia. Scorza FA, Cysneiros RM, Terra VC, Scorza CA, Cavalheiro EA, Ribeiro MO, Gattaz WF. Prostaglandins Leukot Essent Fatty Acids. 2009 Jul 21. [Epub ahead of print]

3. Catatonia Is not Schizophrenia: Kraepelin's Error and the Need to Recognize Catatonia as an Independent Syndrome in Medical Nomenclature. Fink M, Shorter E, Taylor MA. Schizophr Bull. 2009 Jul 8. [Epub ahead of print]

4. Clozapine-induced fatal fulminant hepatic failure: a case report. Chang A, Krygier DS, Chatur N, Yoshida EM. Can J Gastroenterol. 2009 May;23(5):376-8.

5. Successful treatment of tardive lingual dystonia with botulinum toxin: case report and review of the literature. Hennings JM, Krause E, Bötzel K, Wetter TC. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jul 1;32(5):1167-71. Epub 2007 Sep 18. Review.

6. Clozapine-induced hypersalivation: a review of treatment strategies. Sockalingam S, Shammi C, Remington G. Can J Psychiatry. 2007 Jun;52(6):377-84. Review.

7. Further studies of the cytopathic effect in tissue cultures inoculated with CSF from patients with schizophrenia and other nervous system diseases. Tyrrell DA, Parry R, Davies H, Bloxham C, Crow TJ. Br J Exp Pathol. 1983 Aug;64(4):445-50.

8. Virus-like agent in CSF in schizophrenia and some neurological disorders. Taylor GR, Crow TJ, Ferrier IN, Johnstone EC, Parry RP, Tyrrell DA. Lancet. 1982 Nov 20;2(8308):1166-7.

9. Virus-like particles in CSF in schizophrenia. Grow TJ, Tyrrell DA, Ferrier IN, Johnstone EC, Macmillan JF, Owens DG, Parry RP. Lancet. 1979 Jul 7;2(8132):35.

10. Characteristics of patients with schizophrenia or neurological disorder and virus-like agent in cerebrospinal fluid. Crow TJ, Ferrier IN, Johnstone EC, Macmillan JF, Owens DG, Parry RP, Tyrrell DA. Lancet. 1979 Apr 21;1(8121):842-4.

11. Possible virus in schizophrenia and some neurological disorders. Tyrrell DA, Parry RP, Crow TJ, Johnstone E, Ferrier IN. Lancet. 1979 Apr 21;1(8121):839-41.

12. Harrison PJ : The neuropathology of schizophrenia. A critical review of the data and their interpretation. Brain 1999; 122 :593-624.

13. J Neurol Neurosurg Psychiatry. 1985 Mar;48(3):281. The cytopathogenic agent in CSF: evidence for a relationship with enolase levels.Taylor GR, Roberts GW, Crow TJ, Royds JA, Gamble SJ, Taylor CB, Carter GI, Timperley WR.

14. Exp Mol Pathol. 1985 Apr;42(2):271-7. Cytopathogenic cerebrospinal fluid from neurological and psychiatric patients. Taylor GR, Crow TJ, Carter GI, Gamble SJ.

15. Mesa CS, Niubó CE, González NL. Características histopatológicas de una reacción de aglutinación observada en pacientes psicóticos. IV Congreso Ibero-Americano de Anatomía Patológica. IV-CVHAP 2001 Comunicación-E-001; 2001.

16. Mesa CS. Schizophrenia: cytopathological diagnosis valuation scale. Carib Med J 1998; 60: 29-32.

17. www.associatedcontent.com/article/2215925/the_glutamateglutamine_theory_for_schizophrenia.html

18. www.associatedcontent.com/article/2205997/excessive_amino_acids_in_the_brain.html

19. http://www.associatedcontent.com/article/141020/the_fountain_house_standards_are_they.html