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Presbyophrenia and confabulation

  • - Dementia: general aspects
  • Jun 20, 2011
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Tags: | amnesia | confabulation | confabulatory euphoria | delirium tremens |

The word ‘presbyophrenia’ was coined by Kahlbaum (1863) to name a subtype of the paraphrenias (insanities occurring during periods of biological change). Presbyophrenia was a form of paraphrenia senilis characterized by amnesia, disorientation, delusional misidentification and confabulation.

Ignored for more than 30 years, the term reappeared in the work of Wernicke, Fischer and Kraepelin. Wernicke’s classification of mental disorders was based on his theory of the three-partite relational structure consciousness (outside world, body and self)  (Lanczik, 1988). Impairment of the link between consciousness and outside world led to presbyophrenia, delirium tremens, Korsakoff’s psychosis, and hallucinoses. Amongst the features of presbyophrenia, Wernicke included confabulations, disorientation, hyperactivity, euphoria, and a fluctuating course;  acute forms resolved without trace,  chronic ones merged with senile dementia (Berrios, 1986).

In France, Rouby (1911) conceived of presbyophrenia as a final common pathway for cases suffering from Korsakoff ‘s psychosis, senile dementia or acute confusion. Truelle and Bessiere (1911) suggested, in turn, that it might result from a toxic state caused by liver or kidney failure. Kraepelin (1910) lumped presbyophrenia together with the senile and presenile insanities, and (as compared with Korsakoff ‘s patients) believed presbyophrenic patients to be older,  free from polyneuritis and history of alcoholism, and showing hyperactivity and elevated mood. Ziehen (1911) wrote that ‘their marked memory impairment contrasts with the relative sparing of thinking’. Fischer (1912) suggested that disseminated cerebral lesions were the essential anatomical substratum of presbyophrenia.

During the 1930s, two new hypotheses emerged. Bostroem (1933) concluded on phenomenological grounds that presbyophrenia could be identified with mania, suggesting an interplay between two factors:  cerebral arteriosclerosis and cyclothymic premorbid personality. Lafora (1935) emphasized the role of cerebrovascular pathology, and claimed that disinhibition and presbyophrenic behaviour were caused by a combination of senile and atherosclerotic changes. Burger-Prinz and Jacob (1938), however, questioned the view that cyclothymic features were a necessary precondition. Bessiere (1948) claimed that presbyophrenia was a syndrome found in conditions such as senile dementia, brain tumours, traumatic psychoses and confusional states. More recently, it has been suggested that presbyophrenia may be a subform of AD characterized by a severe atrophy of locus caeruleus (Berrios, 1985b).

One of the features of presbyophrenia was confabulation.

This complex symptom has not quite found a place in psychopathology (Berrios, 2000b). Two phenomena are included under the name ‘confabulation’.  The first type concerns ‘untrue’ utterances of subjects with memory impairment; often provoked or elicited by the interviewer, these confabulations are accompanied by little conviction and are believed by most clinicians to be caused by the (conscious or unconscious) need to ‘cover up’ for some memory deficit. Researchers wanting to escape the ‘intentionality’ dilemma have made use of additional factors such as presence of frontal lobe pathology, dysexecutive syndrome, difficulty with the temporal dating of memories leading to an inability temporally to string out memory data, etc.

The second type concerns confabulations with fantastic content and great conviction as seen in subjects with functional psychoses and little or no memory deficit. Less is said in the neuropsychological literature about this group, although (at least in the case of schizophrenics) it has been correlated with a bad performance on frontal lobe tests. It is our belief that this group remains of crucial importance to psychiatrists. Little is known about the epidemiology of either type of confabulation.

In clinical practice,  these two ‘types’  can be found in combination. It remains unclear why so many patients with Korsakoff ‘s psychosis or frontal lobe disorder, in spite of the fact that they do meet the putative conditions for confabulation (amnesia, frontal lobe damage, difficulty with the dating of memories, etc.) do not confabulate. Furthermore, confabulations have also been reported in subjects with lesions in the non-dominant hemisphere and in the thalamus.

Under different disguises, the ‘covering up’ or ‘gap filling’ hypothesis is still going strong. Although superficially plausible, it poses a serious conceptual problem in regard to the issue of ‘awareness of purpose’: if full awareness is presumed, then it is difficult to differentiate confabulations from lying; if no awareness is presumed, then the semantics of the concept of ‘purpose’  is severely stretched and confabulations cannot be differentiated from delusions.

The received view of confabulations also neglects the clinical observation that confabulations (particularly provoked ones!) do occur in dialogical situations: for example, the way in which the patient is asked questions may increase the probability of producing a confabulation. This suggests that the view that confabulations are a disorder of a putative narrative function found in normal human subjects must be taken seriously.  It is hypothesized here that this trait is normally distributed in the population. In the absence of adequate epidemiological information, research efforts should be directed at mapping the distribution of this narrative (or confabulatory)  capacity in the community at large.  Only then will it be possible to understand the significance of its disorders. In the long term, this approach will prove more heuristic than unwarranted speculation based on a few anecdotal cases.

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