Schizophrenia Cause Dementia

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. 

The CT scan and the MRI scan capture images in the range of the human eye. The MRI scan, for example, examines a slice of brain approximately 1-3 mm thick (Innis et al., 1995). That is the width of one to three pencil leads. Furthermore, the images are limited to black and white. The best MRI resolution only begins to approximate what can be seen with the naked eye on autopsy (Innis et al., 1995). 

An autopsy can also obtain tissue slices for examination with a light microscope or an electron microscope. Furthermore, on gross examination of the brain, instead of estimating tissue loss from MRI pictures, an autopsy can actually weigh and measure the brain and examine cell density under the microscope. As a result, many diseases of the brain, such as Alzheimer s, require an autopsy rather than an MRI or CT scan to make the definitive diagnosis (Caine et al., 1995). 

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, the failure to obtain consistent findings of cerebral pathology on postmortem examination prior to the drug era strongly indicates that more recent findings of atrophy on brain scans are the result 

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The differential diagnosis of depression is organized along both symptomatic and causative lines. Symptomatically, major depression is differentiated from other disorders by its clinical presentation or its long-term history. This is, of course, the primary means of distinguishing psychiatric disorders in DSM-1V. The symptomatic differential of major depression includes other mood disorders such as dysthymic disorder and bipolar disorder, other disorders that frequently manifest depressed mood including schizoaffective disorder, schizophrenia, dementia, adjustment disorder, and post-traumatic stress disorder, and, finally, other nonpsychiatric conditions that resemble depression such as bereavement and medical illnesses like cancer or AIDS. 

Our understanding of the clinical cause of schizophrenia has evolved considerably in the last 20 years. Until the 1980s, Emil Kraepelin s notion that schizophrenia is a neurodegenerative disease basically went unquestioned. What we now call schizophrenia, Kraepelin called dementia praecox, literally precocious dementia. He believed that the illness followed a progressive downhill course and culminated in dementia. It later became clear that not all schizophrenia patients follow this deteriorating course, but the neurodegenerative concept of the illness continued for years to hold sway. 

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. 

Ketamine causes memory deficits reproduces with impressive accuracy the symptoms of schizophrenia is widely abused and induces vacuoles in neurons at moderate concentrations and cell death at higher concentrations. Memantine, on the other hand, is well tolerated although instances of psychotic side effects have been reported, in placebo-controlled chnical studies the incidence of side effects is remarkably low. Memantine improves memory in Alzheimer dementia patients and in some (but not all) studies in animals [1]. 

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