Dementia


Dementia
   Dementia, in the sense of a temporary or permanent loss of brain function that could affect people of all ages, has always been familiar to physicians. The elderly in particular have often been implicated in global deficits in personality, intelligence, and emotion. Medicine once knew many phrases for this, including "melancholia." As Robert Burton (1577–1640), an Oxford cleric, wrote in 1621 in his Anatomy of Melancholy: "After 70 years . . . all is trouble and sorrow. [The elderly] are overcome with melancholy in an instant. Or if they do continue in such courses, they dote at last (an old man is twice a boy) and are not able to manage their estates through common infirmities incident in their age. Full of ache, sorrow, and grief, children again, dizzards [fools], they carle [are gruff and snarling] many times as they sit, and talk to themselves" (p. 183). Some landmarks in the narrowing of brain pathology to our current concept of dementia as cognitive dysfunction and personality deterioration in the elderly are as follows:
   Cullen’s "amentia" (1777). In First Lines of the Practice of Physic, published in 1777 and in following years, Edinburgh’s William Cullen described "amentia" as a subclass of the "Vesaniae," or disorders of judgment. One variety of amentia was "amentia senilis, from decay of perception and memory, in old age." In 1785, Philippe Pinel translated the fourth edition (1784) of Cullen’s work into French, rendering amentia as "dementia." That represents the definitive appearance of the term on the medical stage, although it had been used occasionally before.
   Esquirol’s "senile dementia" (1814). (See Depression: Emergence: differential diagnosis of depression from dementia [1814].) Étienne Esquirol was among the first to differentiate dementia from the form of depression that he called lypemania. In his essay "On dementia" in the Dictionary of Science and Medicine (Dictionnaire des sciences médicales), he wrote that "in an illness that is frequently the end point of a large number of other illnesses, [dementia] is, so to say, the constitutional state of old age" (vol. 2, p. 237). "Senile dementia" was differentiated from the "chronic" and "acute" varieties in representing "the result of the process of aging. As the individual is imperceptibly pushed toward old age, he loses his sensibility together with the free exercise of his faculties of reasoning, yet before reaching the final stage of decreptitude. Senile dementia installs itself slowly. It begins with the weakening of memory, especially that of recent events" (p. 262).
   Bayle’s "chronic arachnitis": the first organic dementia identified (1822). See Psychosis: Emergence; Unitary Psychosis.
   Krafft-Ebing differentiates reversible "dementia" in younger patients from "senile" dementia (1872, 1879). Although a number of authors had been differentiating dementia from mental illness, or "vesanic dementia" from senile dementia, in 1872 Richard von Krafft-Ebing in his textbook drew a clear line between "primary treatable dementia," which he also called "stupidity" (Stupidität), and "Dementia senilis." Stupidity-style dementia was a "psychoneurosis" chracterized by the slowing or indeed the suspension of psychic functioning with emotional flattening (Stimmungsmangel). Stupor, hallucinations, and delusions were complications. Although stupidity was conditioned by a heavy constitutional predisposition, it was, unlike mental retardation, acquired in adult life. As causes, Krafft-Ebing hypothesized either brain "exhaustion" or "masturbatory excesses." Krafft-Ebing introduced the concept of "stupidity" in the 1872 edition, then expanded on it in subsequent editions. As he noted of "stupidity: primary treatable dementia" in the second edition in 1879, "Those affected by it are usually youthful, primarily male individuals under 30." Yet the prognosis, in contrast to that of senile dementia, was favorable: "Only in seldom cases does the functional exhaustion [of the brain] pass into irreparable dementia" (vol. II, pp. 47, 49). Here, Krafft was adumbrating a distinction between favorableoutcome psychosis and senile dementia.
   Korsakoff separates amnesia from dementia (Korsakoff’s psychosis) (1887). Sergei S. Korsakoff (1853–1900) was at the time of his discovery a staff psychiatrist at a clinic for nervous disease in Moscow; in retrospect, he counts as one of the founders of Russian psychiatry. Writing in a Russian psychiatry journal, the Arkh. Psikhiat. Nevrol., in 1887, Korsakoff identified an amnestic syndrome, often involving neuritis, occurring in alcoholics that he called "cerebropathia psychica toxaemica" (today, "Korsakoff’s syndrome" or "Korsakoff’s psychosis"). "The disorder of memory manifests itself in an extraordinarily peculiar amnesia, in which the memory of recent events, those which just happened, is chiefly disturbed, whereas the remote past is remembered fairly well" (p. 398 of English translation in Neurology in 1955). In 1904, psychiatry professor Karl Bonhoeffer (1868–1948), then at Heidelberg, differentiated toxic (as in alcoholism) Korsakoff memory loss from senile memory loss in an article published in the Allgemeine Zeitschrift für Psychiatrie. He said that loss of recent memory was the distinguishing characteristic of the syndrome. Later, it was established that Korsakoff’s patients were suffering from Wernicke’s disease, a pattern of brain lesions caused by thiamine deficiency (secondary usually to alcoholism). (See WERNICKE–KORSAKOFF SYNDROME.)
   Beginning the differentiation of the organic dementias: the dementia of neurosyphilis (1894). In his laboratory at the Frankfurt asylum, Alois Alzheimer began his careful delineation of dementia caused by "progressive paralysis," or "general paralysis of the insane" (later, neurosyphilis). His 1894 article in the Neurological Central Journal (Neurologisches Centralblatt) marked the beginning of his work in this area, which culminated in a 1902 contribution in the General Journal of Psychiatry (Allgemeine Zeitschrift für Psychiatrie).
   Alzheimer’s presenile dementia (1906, 1910). In November 1906, Alois Alzheimer reported at a meeting the case of a 51-year-old woman who was fully psychotic, lacking in short-term memory, and had localized neurological signs and progressive dementia. At autopsy, he identified various pathological brain changes, some of which were already known in the literature, namely brain atrophy, arteriosclerosis, and senile plaques. A fourth finding, neurofibrillary tangles, Alzheimer himself had already described. Plaques and tangles had not been previously noted in dementia cases in younger patients. Alzheimer’s paper for that meeting was summarized in the General Journal of Psychiatry (Allgemeine Zeitschrift für Psychiatrie) in 1907; in no way did he claim that he had identified a new disease, but rather that this case represented "such a divergent pattern that it is not to be classified among any of the known diseases; anatomically there are findings that deviate from all of the disease processes presently known." He said that in recent years there had been an increasing number of such cases, and that "at some point we should be able to delineate them clinically in a more precise manner." The title of the article was "On a Distinctive Illness of the Cerebral Cortex" ("Über eine eigenartige Erkrankung der Hirnrinde"). (There was no discussion following the presentation.)
   Alzheimer did not use the term "presenile dementia." (Indeed, an early use of the expression "presenile dementia" occurs in 1898 in Jena psychiatry professor Otto Binswanger’s [1852–1929] brief research note without postmortem histology in the Munich Medical Weekly [Münchener Medizinische Wochenschrift].) In the eighth edition of his textbook in 1910, Kraepelin argued that these cases of early psychosis that progressed rapidly to dementia probably represented a separate category of illness sui generis. He noted that in the three cases that had come to autopsy, Alzheimer had discovered identical pathology. Kraepelin made these patients part of the larger group of "presenile insanity" (praeseniles Irresein) and said, "The area of the presenile psychoses is currently perhaps the most baffling in psychiatry" (Psychiatrie, 8th ed., II(1), p. 534).
   "Pick’s" disease (1892 and after). As early as 1892, Arnold Pick (1851–1924), professor of psychiatry at the German university in Prague, began reporting cases of cerebral atrophy resulting in dementia with focal symptoms, meaning symptoms localizable to a certain area of the brain; these were of interest at the time because Carl Wernicke believed that the symptoms of senile dementia were always nonfocal. (See Wernicke–Kleist–Leonhard Pathway.) Pick articulated these views in 1892 in the Prague Medical Weekly (Prager Medicinische Wochenschrift) in the article "On the Relationship of Senile Brain Atrophy to Aphasia" ("Über die Beziehungen der senilen Hirnatrophie zur Aphasie"). This case is often cited as the locus classicus for "Pick’s disease." Yet, it is not. A 60-year-old man whose case Pick reported in 1906 did have severe frontal- and temporal-lobe wasting at autopsy (in the Monthly Review of Psychiatry and Neurology (Monatsschrift für Psychiatrie und Neurologie), the kind of pathology that was evident in the disease later named after him and that is really the first reported case of "Pick’s disease."
   In 1906, it occurred to no one that Pick was describing a new disease, as this kind of neuropathological work was becoming common in the literature. Yet in 1926, Hugo Spatz (1888–1969), head of neuropathology in the Munich Psychiatric Clinic, together with a co-worker, in the Journal of Combined Neurology and Psychiatry (Zeitschrift für die gesamte Neurologie und Psychiatrie), wrote that the regional wasting of neurons in the frontal and temporal zones represented a specific disease for which they proposed the name "Pick’s Disease." The authors acknowledged that this coinage was not exactly what Pick, who had just died, would have had in mind because he was interested in local, not regional, lesions. Throughout Pick’s histopathological work ran an important general point: that there were a variety of dementias, each corresponding to a different pattern of local changes in the brain.
   "Lewy-body" dementia (1912). In 1912, in volume 2 of Max Lewandowsky’s (1876–1918) textbook, Practical Neurology for Physicians (Praktische Neurologie für Ärzte), Friedrich (Fritz) Heinrich Lewy (1885–1950), who had just graduated in medicine in Berlin in 1910, described intracytoplasmic inclusions, later called "Lewy bodies," in the brain stem in Parkinsonism. These inclusions were later discovered to be characteristic of a common form of dementia, called "senile dementia of the Lewy body type," involving fluctuating cognitive impairment and psychosis or depression. Lewy subsequently became an important neurologist and psychiatrist and emigrated to the United States in 1934. (In 1962 neuropathologist John S. Woodard [1923–] at the Camarillo State Hospital in Camarillo, California, proposed Lewy-body mental illness in late-adulthood as a separate disease. He argued in the Journal of Neuropathology and Experimental Neurology that, "The cases seemed to represent a discrete clinicopathologic entity in relation to mental disease," and were characterized by paranoid or affective disorders in addition to "unprovoked violence and assaultiveness" [pp. 448–449].)
   Bleuler’s "organic syndrome" (1916). In his Textbook of Psychiatry (Lehrbuch der Psychiatrie), Eugen Bleuler argued that a range of diffuse disturbances of the cerebral cortex, referred to as "organic syndrome," could cause a "weakening of intelligence," especially affecting memory. "The various intellectual abilities do not disappear uniformly . . . and practiced abilities escape the general deterioration the longest. The senile bookkeeper can be markedly demented in all other directions and yet surpass many a healthy person in addition" (p. 232). As examples of the organic brain syndrome, Bleuler mentioned the "senile psychoses," of which there were three: arteriosclerotic insanity, simple brain atrophy ("dementia senilis") and "presbyophrenia" (pp. 276–277 of the English translation, 1924). The feature common to the three was "the diffuse reduction of the brain substance and symptomatologically the complex of the ‘organic psychic’ symptoms." Bleuler’s "organic syndrome" greatly influenced European thinking on dementia.
   Alzheimer’s disease and senile dementia are the same disease (1948). Although German histopathologists had long believed that Alzheimer’s pre-senile dementia and the dementia of senescence represented a single pathological process, Robert Denis Newton, a London Harley-Street psychiatrist (1904–1985), clearly articulated this notion in 1948 for a psychiatric readership in the Journal of Mental Science (later British Journal of Psychiatry). Alzheimer’s disease thus soared from a pathological curiosity affecting a small number of individuals in mid-life to the commonest disease of the elderly. "There can be no justifiable grounds for speaking of Alzheimer’s disease and senile dementia as separate entities," he wrote. "The term Alzheimer’s dementia is suggested to describe this organic syndrome" (pp. 235, 248).
   Martin Roth says dementia is only one of several psychogeriatric outcomes (1955). In his paper "The Natural History of Mental Disorder in Old Age," published in the Journal of Mental Science in 1955, Martin Roth (1917–), at Graylingwell Hospital in Chichester, England, laid the basis of modern psychogeriatric classification by subdividing the mental disorders of later life into five groups: "affective psychosis," "late paraphrenia," "arteriosclerotic psychosis," "acute confusion," and, finally, "senile psychosis," the only member of the group that was unrecoverable. As psychogeriatrician Jeremia Heinik at Ichilov Hospital in Tel-Aviv, Israel, remarks, Roth’s classification "shed a spirit of optimism in a field considered to deal only with irreversibility (e.g. dementia)." (On Martin Roth, see also Paraphrenia.)
   Separating benign and progressive memory dysfunction (1958). Psychiatrist Vojtech Adalbert Kral (1903–1988), of the Gerontological Unit at McGill University, distinguished in the Journal of Gerontology between the "impaired recall of specific remote memories" and "progressive impairment of recent memory . . . leading to a senile amnestic syndrome" (p. 175). The following year, in Geriatrics, he and psychologist Blossom Temkin Wigdor (1924–) administered the oral androgen Halotestin to one group of elderly patients with "mild" memory dysfunction and to another with senile amnestic syndrome. The former group responded well, the latter did not, indicating that memory loss in dementia is qualitatively different from the normal forgetfulness of the elderly. Based on this research, benign senescent forgetfulness (BSF) became considered physiological, meaning a normal accompaniment of aging, whereas mild cognitive impairment (MCI) was thought of as a preliminary stage of Alzheimer’s disease.
   Associating the degree of dementia with the amount of pathological change in the brain (1967). Martin Roth (1917–) and co-workers in Newcastle upon Tyne in England demonstrated in the Proceedings of the Royal Society of Medicine in 1967 that the quantitative degree of dementia was associated with the extent of neuritic plaques in the cerebral gray matter. The severely demented probably represent a separate group, the authors said. Yet otherwise: "There is a highly significant correlation between mean plaque counts and scores given for dementia and performance in psychological tests. The findings suggest that psychological and pathological indices are closely related to one another" (p. 258). (On Martin Roth, see Paraphrenia.)
   Alzheimer’s disease is not just an acceleration of the natural aging process but an acquired age-linked disease (1977). Rejecting Martin Roth’s argument (see above), Raymond Adams (1911–), a neurology professor at Harvard, and Maurice Victor (1920–), professor of neurology at Case Western University in Cleveland, argued in their Principles of Neurology that the disease was a pathological eruption into old age, not an accelerated extension of it. They pointed out, among other arguments, that "Homo sapiens is the only animal species in which Alzheimer fibrillary changes and senile plaques are found in the aging brain. . . . It seems to us unbiologic that human aging should differ from that of all other animal species" (quotation from 2nd ed., 1981, p. 421).
   Linking familial Alzheimer’s disease to a specific chromosomal locus (1987). An international team of researchers led by Peter H. St George-Hyslop (1953–), then at the Neurogenetics Laboratory of Massachusetts General Hospital (later at the University of Toronto), suggested in an article in Science in February 1987 that a defective gene on chromosome 21 might be the cause of Alzheimer’s disease. The authors said of the significance of this discovery, "The existence of DNA markers linked to the FAD [familial Alzheimer’s disease] gene raises the possibility that they might be of use for presymptomatic or prenatal diagnosis of FAD in appropriate families" (p. 889).
   Linking early-onset Alzheimer’s disease to a specific chromosomal locus (1992). In an article in Nature Genetics, Mike Mullan and co-workers at the psychiatry center of the University of South Florida in Tampa, together with a group based in the departments of biochemistry and neurology at St. Mary’s Hospital Medical School in London, found evidence in 10 "early-onset" families that the precursor protein gene in Alzheimer’s disease was situated on the middle long-arm of chromosome 14. This suggested that a significant subset of Alzheimer’s cases—the early-onset type—were genetically caused.

Edward Shorter. 2014.

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