[Awareness of deficits and anosognosia in Alzheimer's disease].Encephale 2004 Nov-Dec; 30(6):570-7E
This article reviews studies concerning unawareness of deficits in Alzheimer's disease. Unawareness of the deficits associated with dementia has frequently been reported in clinical descriptions of the later stages of the disease. Consistent with the literature, we shall use the expressions impaired awareness, unawareness of deficits, anosognosia, and lack of insight interchangeably. Anosognosia can be defined as an impaired ability to recognize the presence or appreciate the severity of deficits in sensory, perceptual, motor, affective, or cognitive functioning. Unawareness has been operationally defined in a variety of ways. Unawareness can be measured as the discrepancy between the patient's self-report and the report of a natural caregiver or the clinical rating of a health care professional. The reports generally concern with several domains, most often memory domain. Discrepancy between subjective ratings and neuropsychological performance during clinical assessment has also been used to measure anosognosia. Advantages, limits and equivalence of these different methods are discussed. The impact of family burden has to be considered as a systematic methodological bias if the natural caregiver is implicated in the assessment. The psychometric properties of the clinical assessment have also to be discussed. The psychological nature of the discrepancy between patient's self-report and cognitive performances has to be analyzed and the necessity of ecological protocols, longitudinal assessment is discussed. The major results concerning prevalence, nature of anosognosia and the associated disorders are analyzed. In particular, the notion of heterogeneity of anosognosia and the correlates with depression, severity of dementia and executive dysfunction are developed. Prevalence is largely function of methodological choices and conceptual definition of anosognosia. Three major researches are compared and the contrast between their results (prevalence from 23% to 75% in AD) is analyzed. Particularly, the hypotheses about anosognosia play a great role in the findings. At first time of research, anosognosia was considered as a general symptom and so, studies were centered on the unawareness related to only one cognitive function. But the 90's findings suggest that patients with AD have impaired awareness for some types of deficits (affective or cognitive functions) but can more accurately appraise other deficits. Currently anosognosia cannot be considered as a unitary entity. It may be that patients with AD are unaware of some types of deficits, but are aware of others, and that nature and intensity of their anosognosia may change during the course of the dementia. It has been proposed that depression is more common when disease is mild and awareness of deficits is retained, and that depression becomes less common when disease increases and awareness declines. Depression is conceived as a psychological reaction. However, the correlations between anosognosia level and depression scores reveal either weak relationships or no relationships. Alternative hypothesis is that anosognosia is related to overall dementia severity and to memory impairment. However, correlations of unawareness of deficits, i.e. the difference between self-report and relative's -rating, with a measure of dementia and with patient's performance on objective memory tasks did not reveal strong, consistent relationships between degree of anosognosia and severity of dementia or of memory impairment. On the other hand, the best neuropsychological predictors of impaired insight are Trail Making Test or Wisconsin Card Sorting Test, i.e. tests that have been shown to be sensitive to a frontal lobe dysfunction. SPECT measures of regional cerebral blood flow have been used in the study of anosognosia. The main findings are that unawareness in AD is associated with hypoperfusion of the right dorsolateral frontal lobe. Anosognosia may result from the disruption of broader cognitive process that is subsumed by the frontal lobes. The mechanisms of unawareness are not well known and studies are essentially descriptive works and try to give information about pre-valence or clinical associated disorders of anosognosia. Several authors have proposed that unawareness is part of a defensive mechanism that would protect demented patients from depressive feelings. Other authors have proposed that anosognosia may result from dysfunction in specific brain areas. It is suggested that anosognosia in AD may result from greater impairment of a central executive system, which is a metacognitive structure that is involved in planning, cognitive resource allocation, and set shifting. The main problem with those both major hypotheses is their incapacity to explain the heterogeneous impairment of awareness. Other authors speculate that the impaired insight of Alzheimer's disease has several components, psychological and neuropsychological. This view doesn't seem convincing and new components have to be taken in account in order to propose a theoretical framework about anosognosia in AD. Environmental and dispositional components and an interactional view could be interesting. Those possible directions for future research and solutions concerning methodological and conceptual problems are outlined. In particular, a neuro-psycho-social view of unawareness is introduced.