Dementia

Introduction

Dementia is currently defined as ‘a syndrome consisting of progressive impairment in both memory and at least one of the following cognitive deficits: aphasia, apraxia, agnosia or disturbance in executive abilities, sufficient to interfere with social or occupational functioning, in the absence of delirium or major non-organic psychiatric disorders’ (American Psychiatric Association, 1994). This narrow definition is a remnant of the ‘cognitive paradigm’ of dementia (Berrios, 1989). According to the latter view (developed during the late 19th century), cognitive deficits are the only pathognomonic features of dementia and psychiatric and behavioural [Page 298]symptoms are just coincidental encumbrances. Due to the work of Ebbinghaus, memory became the first measurable cognitive deficit and this introduced a lasting bias in that ever since memory impairment has tended to be considered as the main cognitive deficit of the dementias.

Up to the 1970s, the cognitive paradigm seriously emasculated clinical research, particularly into the diagnosis of ‘early dementia’ and the identification of varieties and subtypes of dementia. The realization that neuropsychological assessment alone was not going to resolve these problems led during the 1980s to the acceptance that psychiatric symptoms were, after all, central to dementia (Berrios, 1992). In due course, this allowed for a better understanding of the disease and the identification of subtypes such as, for example, Lewy body Dementia.

The problem of what is ‘early dementia’ and how it can be identified has not yet been resolved in spite of the desperation of the pharmaceutical industry which would like to have a reason to start pro-cholinergic ‘treatment’ early. Likewise, little is known about ‘symptom-sequencing’, namely the finding that psychiatric and personality changes may precede or follow the cognitive deficits. The central questions in this regard are whether the sequencing is random or reflects the influence of clinical and genetic factors. The development of neuroimaging and genetics (inter alia) has of late led to important advances in the classification of the dementias.

The dementias are complex neuropsychiatric disorders with a clinical profile that includes disorders of personality, emotions, mood, and will; conventional mental symptoms (hallucinations, delusions, agitation, sadness, anxiety, etc.); disorders of awareness and consciousness; psychosocial incompetence; and the full gamut of neuropsychological deficits. It follows from this that subjects suffering from dementia should be clinically looked after by multidisciplinary teams and that it should be considered unethical for neurologists, psychiatrists or psychologists alone to monopolize their diagnosis and/or care (Berrios & Hodges, 2000).

It also follows from the symptomatic complexity of the dementias that their assessment must be exhaustive and longitudinal. Together with the finding of specific markers such as volumetric changes in the medial temporal lobes, analysis of these clinical data should contribute to resolve the problems of symptom-sequencing and ‘early dementia’. In this latter case, it is expected that the old concept of early dementia as a ‘minidementia’ (i.e. one dependent upon instrument sensitivity) will change to one with a broader symptom profile which may include personality and behavioural changes as markers of early dementia.

It has been said that the assessment of dementia should be carried out by a multi-disciplinary process involving the neurologist, neuropsychiatrist, neuropsychologist and occupational therapist. In terms of the objectives of assessment, as important as determining a ‘diagnosis’ is the profiling of deficits and assets. Outcome measures, developed on the basis of this knowledge, will have the adequate sensitivity and specificity to help select the right treatments for the right patients and also to take other hard therapeutic decisions (e.g. rationing of expensive treatments such as pro-cholinergic medication).

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