The Pathological Anatomy of Schizophrenia

Introduction  

  In 1913 A. Alzheimer wrote a brilliant paper about "dementia praecox", which is now called "schizophrenia". However, there were those before him. In 1884 Meynert published a book called "Psychiatrie". Meynert was from Vienna. Meynert found atrophy of the frontal lobes in what is now called "schizophrenia".

Alzheimer  

  In 1913  Alzheimer described pigmentary degeneration. This was confirmed by Vogt & Vogt in 1952. The Vogts studied catatonia. They found abnormal neurons in the cingulate and prefrontal cortex. They thought that the diseased cells caused schizophrenic symptoms. Also in 1952 Von Buttlar-Brentano reported similar pathology.

Uranova (1988)  

  Uranova, is a series of papers that began in 1988, reported "ultrastructural alterations of the prefrontal cortex in schizophrenia. She used the electron microscope. She found the synapses to be abnormal.

Casanova et al (1990)   

  Casanova et al  reported central chromatolysis and gliosis in the brainstem and thalamus. Cell loss, dystrophic neurons, etc. were seen in the frontal lobes, piriform cortex, and entorhinal region. Manuel Casanova, of Augusta, Georgia, suggested "disturbance of dopaminergic neurons" since these areas invlove such neurons.

International Neuropathology Research

  There have been numerous positive neuropathology reports in schizophrenia and related diseases. These reports prove Scientology to be wrong. Scientology has accused psychiatry of "junk science and bad medicine". They claim that there is no chemical imbalance. However, neuropathology data supports chemical imbalance theories. It is Scientology itself that is junk science.

South Africa        

  In 1975 Fisman of South Africa reported positive findings in the brain stem in "psychosis". He found ventricular diation, atrophy, lipofuscin, glial knots, corpora amylacea, perivascular infiltration, necrosis, cell loss, calcification, neuronophagia, gliosis, sclerosis, iron encrustation, etc.   A case with Huntington's chorea showed marked frontal atrophy and atrophy of the caudate nucleus. The patient had been suicidal. Lipofuscin was seen even though death was at 35 years of age. Gliosis and corpora amylacea were seen. Thus the neuropathology picture was similar to that seen in schizophrenia. After this study Fisman moved to Canada.

Germany         

  In 1897 and 1913 Alzheimer published articles on "dementia praecox". These articles were not about the disease that now bears his name. That was discussed in another article. Alzheimer reported cerebral lesions. The lesions and deficit were mainly in the second and third cortical layers. These were small-celled layers.   The Vogts described alveolar degeneration, lipoid sclerosis, cellular ballooning, etc. This was reported by C. Vogt and O. Vogt in 1952. 

France         

  Between 1904 and 1909 Klippel and Lhermitte published reports of cerebral lesions in "dementia praecox", which is now called "schizophrenia". They found progressive atrophy of the pyramidal cells of the fifth and sixth cortical layers with disappearance of Nissl bodies and of neurofibrils. Lipid deposits appeared in the cytoplasm. There was a marked reaction of the neuroglia. There was secondary degeneration of myelin related to the lesions of the pyramidal cells.   There were similar lesions in the subcortical nuclei.

Italy         

  Buscaino reported racemose areas formed by metachromatic bodies in the cerebral cortex of schizophrenics. The myelin did not stain with the usual colorants. He attributed this to an abnormal amine (substance X).

United States         

  Scharenberg & Brown (1954) reported marked alterations in catatonia. They found extensive necrosis with marked reactions of the three types of glia. This appears to suggest an unknown toxic factor. This supports the toxin reported by Buscaino. Although Buscaino published many reports, one appeared in 1958.

Canada         

  Elvidge & Reed reported swelling of the oligodendroglia in both schizophrenia and manic-depressive psychosis. They found hypertrophy of astrocytes. They found a chronic process which suggested a toxic factor of metabolic origin. This was reported in 1938.

Mexico         

  Nieto & Escobar used Hortega's lithium-silver carbonate stain for neuroglial impregnation. They found glial prolifation in the diencephalon and mesencephalon. Unfortunately this does not tell us exactly what is happening, but it tells us where it is happening. In particular the hypothalamus was affected. The thalamus was also affected.

United Kingdom      

  Mott found atrophic changes in the hypophysis, an endocrine gland located in the base of the brain. 

A Possible Cure for Mental Disease

  Since there is a biological cause for schizophrenia, the cure will also be biological. But, unfortunately, this is easier said than done. First one should understand the physiological basis for schizophrenia. Then one should correct the chemical errors. This is the approach of the late Linus Pauling. Unfortunately, Pauling never completely understood the chemical errors.

Buscaino  

  In 1921 Buscaino used silver nitrate in a test of the urine of schizophrenics. It seems that the urine of a schizophrenic causes a black precipitate, whereas the urine of normals causes a white precipitate. This was later called the "black reaction".   In 1922 V. M. Buscaino published his results. Buscaino had previously studied brain pathology in what is now called "schizophrenia". Buscaino reported the presence of substances of the amine type.

Autopsies  

  Autopsies by various scientists revealed neuronal damage both in the cortex and in the basal ganglia and brainstem. The glia were abnormal. There was metachromatic formations of myelin, areas of hypo and demyelinization, etc. In 1921 V. M. Buscaino reported "clods of disintegration in clusters". These were limited ovoidal or bullet-shaped swellings with a granular or amorphous content.   In 1964 Pecchiai reported confirmation of this work. The material was glyco-lipidic. This suggests deposits of carbohydrate and fat. But what could cause this? If excessive amino acids flooded the cells, some of these amino acids would be converted to fat.

Dysmetabolism  

  The cure may involve correcting the dysmetabolism. Carbohydrate deposits could occur if the cells burned amino acids instead of carbohydrates. Thus the cure, or treatment, could be a diet low in fat and low in amino acids.

Conclusions  

  The whole picture is extremely complicated, unfortunately. However, there is a great deal of data, which is good. Making sense of this data is difficult but important. Kraepelin analyzed Alzheimer's data and compared it to the work of others in 1913. Kraepelin felt that it was valid. The disappearance of the Nissl bodies, reported by French workers and German workers, could be explained if amino acids were flooding the cells. This would also explain the lipid eposits reported by Klippel & Lhermitte.  

  The gliosis reported by the Mexican workers and others supports a toxic factor theory. According to Buscaino, this toxic factor is an amine. Hopf reported lipofuscin deposits in 1952, which was a banner year for this type of research. The lipofuscin could either be a toxic factor itself or represent residue from the toxic amine or both. Amines can sometimes end up as neuromelanin (as in the case of dopamine), which looks like lipofuscin. It could be that an abnormal amine produces an abnormal type of neuromelanin. The abnormal amine could cause the cells to be flooded with amino acids, explaining much of the data.   

  If all of this is true, it would appear that a therapy could be a diet very low in amino acids. The Vogts found that the cellular structures slowly disintegrate. This probably means that the whole cell is affected. The first structure to go is the Nissl bodies, which house amino acids.   The Mexican workers felt that stress was involved. They were probably correct. Stress might cause the release of the toxin.     

  Casanova's "disturbance of dopaminergic neurons" seems to support the late Dr. Friedhoff's biochemical theory. Friedhoff found a toxin, DMPEA, which was produced from dopamine. DMPEA was found only in schizophrenics.