Abstract

Multiple cognitive deficits have been recognized in many neurological disorders but the specificity of the findings and the relationship to the underlying neuropathology remain obscure. Definitions of dementia have been proposed based on symptom profiles of the cognitive disorder and qualitative differences have been claimed between dementias of different aetiology. Some conditions have been claimed to show patterns of cognitive deficit that are distinguished from dementia and related to specific neuropathology or psychological processes, e.g. frontal lobe deficits in Parkinson's disease. Sometimes, a relationship has been established between certain cognitive deficits and particular neurochemical deficits which has led to the notion of specific drug treatment, e.g. cholinergic deficits and memory failure in Alzheimer's disease. However, these conclusions are often potentially flawed by methodological inadequacies. This critique presents some methodological issues relevant to the study of brain-behaviour and drug-behaviour relationships in syndromes of multiple cognitive deficit, using Parkinson's disease as the model. The following recommendations are made: rigid diagnostic criteria; representative patient groups; avoidance of arbitrary quantitative criteria to limit definitions of dementia; matching of groups for overall level of cognitive impairment in the search for qualitative cognitive differences related to neuropathology or effects of particular drugs; the use of suitable controls in patient groups, neuropsychological tests and treatment regimes; the use of specific quantitative tests of cognition, affect and motor disability; and longitudinal, compared with cross-sectional, study design.

Highlights

  • Dementia is recognized in Parkinson's disease (PD) but the reported prevalence varies widely and frontal-lobe deficits are described as specific changes, even in early cases

  • The neuropathological basis of the cognitive changes is unclear; interest has centered on the role of co-existent Alzheimer's disease or diffuse cortical Lewy body disease in the pathogenesis of the dementia, and of both dopaminergic and nondopaminergic neurochemical lesions in early cognitive change and possibly dementia (Agid et at., 1987)

  • Chronic levodopa therapy has been thought to induce greater cognitive impairment in PD (Rajput et at., 1984) and anticholinergic therapy may exacerbate memory loss and confusion in demented patients with PD. Observations such as these have led to numerous hypotheses concerning the psychological and pathological processes underlying the cognitive impairment in PD

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Summary

Introduction

Dementia is recognized in Parkinson's disease (PD) but the reported prevalence varies widely (reviewed Mortimer et at., 1985) and frontal-lobe deficits are described as specific changes, even in early cases (reviewed Sagar and Sullivan, 1988; Brown and Marsden, 1988, 1990). Chronic levodopa therapy has been thought to induce greater cognitive impairment in PD (Rajput et at., 1984) and anticholinergic therapy may exacerbate memory loss and confusion in demented patients with PD (de Smet et at., 1982) Observations such as these have led to numerous hypotheses concerning the psychological and pathological processes underlying the cognitive impairment in PD. No study has undertaken a detailed, comprehensive evaluation of cognitive dysfunction in PD and related it to motor deficits, effects of pharmacologically specific drugs, duration of disease and underlying neuropathology. Such studies are required but precautions must be taken in the methods that are used to evaluate the cognitive dysfunction and the factors that may be responsible for it.

Study population
Test measures: qualitative differences among dementias of different aetiology
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Findings
Conclusion
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