Dementia and Alzheimer Disease

Eugen Bleuler (1924), in a discussion of the organic psychoses, defined an organic psychosyndrome as a set of behavioral manifestations of chronic, diffuse damage to the cerebral cortex that could be due to a variety of causes, including trauma, infection (specifically, syphilis), toxins, arteriosclerosis, and senility. Its manifestations were impairments in memory, judgment, perceptual discrimination, orientation, emotional stability, and impulse control.

Bleuler recognized that all cognitive functions were not equally affected, that long-practiced abilities were the most resistant to deterioration, and that some causes of the organic psychosyndrome were still to be discovered.

He also noted that variations in the form of the psychosyndrome could be related to genetic factors such as a tendency toward complicating mood disorder in demented persons with a family history of mood disorder. Finally, he pointed out that the course of the organic psychosyndrome was related to the underlying illness, that, for example, the Korsakoff syndrome might improve slightly and remain stable, and that episodes of apparent remission might occur in neurosyphilis and arteriosclerotic brain disease.

Bleuler’s textbook contains descriptions of the senile and presenile insanities. Classed under dementia senilis are arteriosclerotic insanity and simple atrophy of the brain. Simple dementia senilis is described as a product of “the normal regression of the brain that begins in the 50s, but is not usually notable until the last decade of the normal life span” (Bleuler 1924, p. 286) (the actual length of the normal life span is not indicated). The brain shrinks, the ventricles enlarge, and there is disappearance of ganglion (pyramidal) cells. The clinical signs, in order of appearance, are 1) inability to assimilate the ideas of others, 2) increased egocentricity and stubbornness, and 3) confabulation. Bleuler (1924) also set forth the category of presbyophrenia (a term he attributed to Kahlbaum), a dementing disorder of old age characterized by constant motor activity, with pacing and repeated performance of meaningless activities. Here, the pathology was said to be senile plaques surrounded by degenerating fibrils (the neuritic plaques of today), whereas in Alzheimer disease, the pathology was said to be more intense, with rapid development of aphasia, agnosia, and apraxia.

At mid-twentieth century, Roth and Morrissey (1952) wrote that resulting from the work of Alzheimer, Kraepelin, Binswanger, Pick, and others, the mental diseases peculiar to old age had, since the beginning of the century, been subdivided into the senile, arteriosclerotic, and presenile psychoses (psychosis in this case meaning a mental disorder of sufficient severity to interfere with meeting the demands of everyday life). They regarded Alzheimer and Pick diseases as rare presenile illnesses. Roth and Morrissey described the core syndrome of senile psychosis as beginning with selective impairment of recent memory and attention and faulty location of recent events in time, followed by euphoria, confabulation, and an illsystematized paranoid element deriving from failure of memory. They recognized that this symptom complex could be the clinical manifestation of a number of underlying brain diseases. In the same paper, Roth and Morrissey reported on the 3-year survival of 150 consecutive persons age 60 years or older who had been admitted to Graylingwell Hospital in 1948. Of those with affective diagnoses, less than 25% were dead; however, 90% of those diagnosed with senile psychosis had died. Despite the fact that the modal patient with an affective disorder diagnosis was in the age range 60-65 years and the modal patient with senile psychosis was in the age range 75-79 years, this finding was probably the first statistical proof of the lethality of senile psychosis.

It has long been recognized that there is an indistinct border between what Ferrara (1959) termed psychological/ physiological senescence (the effects of normal social/brain aging) and pathological senescence (dementia). Ferrara stated that as physiological and psychological senescence gradually drifts into pathological senescence, perceptual and memory impairments are often encountered, and that impaired perception, impaired registration, and decreased impressionability often mark the onset of a senile dementia. “From a practical standpoint, one may speak of dementia when the disturbance of memory is such as to render fragmentary or falsify entirely the relationship of the patient to his surroundings” (Ferrara 1959, p. 1025).

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