Brain atrophy

A thromboembolic diathesis is not unusual and strokes have been reported. Other pathological changes have included microgyri, demyelination, gliosis and brain atrophy. Lipid-laden macrophages have been described. 

Muuronen, A., Bergman, H., Hindmarsh, T, and Telakivi, T. (1989) Influence of improved drinking habits on brain atrophy and cognitive performance in alcoholic patients a 5-year follow-up study. Alcohol Clin Exp Res 13 137—141. 

Fox, N.C., Freeborough. P.A. Brain atrophy progression measured from registered serial MRI validation and application to Alzheimer s disease. J. Magn. Res. Imag. 7, 1069-1075, 1997. 

Yoshii, F., Barker, W.W., Chang, J.Y., Loewenstein, D.. Apicella, A., Smith, D.. et al. Sensitivity of cerebral glucose metabolism to age, gender, brain volume, brain atrophy, and cerebrovascular risk factors. J. Cerebr. Blood Flow Metab. 8(5), 654-661, 1988. 

In 14-week studies, male and female Fischer 344/N rats and BbCSF, mice were exposed to 100-1600 ppm [446-1780 mg/m ] bromoethane by inhalation for 6 h per day on five days per week. In rats, tremors, paresis, mineralization and degeneration in the brain, atrophy of the testes, haemosiderosis of the spleen and some depletion of haematopoietic cells in the bone marrow were observed. Involution of the ovary was observed in mice in the 800 and 1600 ppm dose groups (lARC, 1991). 

As stated above, the main pathological features of Alzheimer s disease are the amyloid deposits around blood vessels and in many brain areas, intraneuronal neurofibrillary tangles, neuronal cell loss and brain atrophy. Recently four genes have been linked to Alzheimer s disease. Most of the cases of the familial, early onset, form are associated with mutations in genes on chromosomes 1,14 and 21. The late onset and most common form of the disease which occurs in those of 55+ years, whether of the familial or sporadic type, is linked to a gene on chromosome 19. 

Two studies that evaluated relatively young and relatively untreated patients diagnosed with schizophrenia found enlarged ventricles, a marker for brain atrophy (Schulz et al., 1983 Weinberger et al., 1982 reviewed in detail in Breggin, 1990). However, very small numbers of patients were involved, and other studies have not confirmed their findings (Benes et al., 1982 Iacono et al., 1988 Jernigan et al., 1982 Tanaka et al., 1981). 

Mounting radiological evidence from PET, MRI, and CT scans confirms the presence of chronic brain dysfunction (PET scans) and brain atrophy (MRI and CT scans) in neuroleptic-treated patients diagnosed with schizophrenia. It also confirms the brain-disabling concept. 

There is a very cogent reason to believe that the atrophy found on CT scans cannot be the product of schizophrenia. Brain atrophy is far more accurately and definitively evaluated by a direct postmortem pathological examination than on a CT or MRI brain scan. The actual pathology, if it exists, can more easily be identified and accurately measured by direct observation and microscopic analyses. 

Despite the infinitely greater sensitivity, usefulness, and relevance of autopsy examinations and microscopic pathology studies, no consistent finding of brain atrophy or any other pathology has been made despite hundreds of these studies performed on thousands of patients diagnosed... 

In summary, there is little or no reason to believe that findings of brain atrophy and dementia are caused by so-called schizophrenia, while there is overwhelming evidence to indict neuroleptic therapy. 

Severity of white matter change, brain atrophy and the presence of infarction are associated with decline in information-processing speed and executive function (Prins et al. 2005). Presence of subcortical hyperintensities is associated with cognitive impairment following clinical stroke secondary to lacunar infarction (Mok et al. 2005 Grau-Olivares et al. 2007). 

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