The term ‘vesanic dementia’ began to be used after the 1840s to refer to the clinical states of cognitive disorganization following insanity (Berrios, 1987); its meaning has changed with equal speed alongside psychiatric theory. According to the unitary insanity notion, vesanic dementia was a terminal stage (after mania and melancholia); according to degeneration theory, it was the final expression of a corrupted pedigree; and according to post-1880s’ nosology, a final common pathway to some insanities. Vesanic dementias were reversible, and could occur at any age; risk factors such as old age, lack of education, low social class, bad nutrition etc., accelerated the progression of the dementia or impeded recovery (p. 597) (Ball and Chambard, 1881).
The vesanic dementias included cases suffering from cognitive impairment associated with melancholia. Under the term demence melancolique Mairet (1883) reported a series of cases of depressed patients with cognitive impairment who on post mortem showed changes in the temporal lobe; this led Mairet to hypothesize that the affected sites were related to feelings, and to suggest that nihilistic delusions appeared when the lesion spread to the cortex (Berrios, 1985a). Mairet’s cases (some of which would now be called ‘Cotard’s syndrome’) showed psychomotor retardation, refused food and died in stupor (Cotard, 1882; Berrios and Luque, 1995). Others, however, got better and these cases are redolent of what nowadays might be called ‘depressive pseudodementia’.
Another contributor to the understanding of cognitive impairment in the affective disorders was George Dumas (1894) who suggested that it was ‘mental fatigue that explained the psychological poverty and monotony of melancholic depressions’ and that the problem was not ‘an absence but a stagnation of ideas’; he was, therefore, the first to explain the disorder as a failure in performance.
The word ‘pseudodementia’, however, originated in a different clinical tradition. It was first used by Carl Wernicke to refer to ‘a chronic hysterical state mimicking mental weakness’ (Bulbena and Berrios, 1986). Not used until the 1950s, it was given a lease of life by writers such as Madden et al.(1952), Anderson et al. (1959) and Kiloh (1961). Current usage is ambiguous in that it relates to three clinical situations: a real (albeit reversible) cognitive impairment accompanying some psychoses, a parody of such impairment, and the cognitive deficit of delirium (Bulbena and Berrios, 1986).
1.5.3 Brain changes and ageing
Since the beginning of the nineteenth century, cases had been described of brain ‘softening’ followed by cognitive failure.
Rostan (1823) reported 98 subjects thus affected, thought to be scorbutic in origin, and divided them into simple, abnormal and complicated (the latter two groups being accompanied by psychiatric changes). Mental symptoms might occur before, during and after the softening itself; thus, senile dementia and insanity might precede the brain changes. When it accompanied stroke, Rostan described cognitive failure and attacks of insanity suggesting that these symptoms were ‘a general feature … not a positive sign of localisation’ (pp. 214-215).
Durand-Fardel (1843) provided an account of the relationship between softening and insanity, warning that softening was used to refer both to a disease (stroke) and to a state of the brain. Psychiatric complications were acute and long term, the former including confusion, depression, irritability, acute insanity and loss of mental faculties (p. 139); the latter had gradual onset, and exhibited an impairment of memory, poverty of thinking, and a regression to infantile forms of behaviour, features which led to ‘true dementia’ (pp. 327-328).
Years later, Jackson (1875) reviewed the problem: ‘softening … as a category for a rude clinical grouping was to be deprecated’ (p. 335); he nonetheless, followed Durand-Fardel’s classification, and suggested that, after stroke, mental symptoms might be immediate or occurring after a few hours or months; he recognized that major cognitive failure may ensue, and saw this as an instance of ‘dissolution’: emotional symptoms being release phenomena (for an analysis of this concept see Berrios, 1991). He believed that anxiety, stress and irritability might be harbingers of stroke.
Alistair Burns MPhil, MD, FRCP, FRCPsych
Professor of Old Age Psychiatry,
John O’Brien MA, DM, FRCPsych
Professor of Old Age Psychiatry,
Institute for Ageing and Health,
University of Newcastle upon Tyne,
Newcastle upon Tyne, UK
David Ames BA, MD, FRCPsych, FRANZCP
Professor of Psychiatry of Old Age,
University of Melbourne, St George’s Hospital, Melbourne,
German Berrios BA (OXFORD), MD, DM H.C. HEIDELBERG, FRCPsych, FBPSS
University of Cambridge Department of Psychiatry,
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