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Cognitive function in Parkinson's disease: from description to theory.

R G Brown1, C D Marsden

  • 1MRC Human Movement, National Hospital, London, UK.

Trends in Neurosciences
|January 1, 1990
PubMed
Summary

This review examines cognitive deficits in Parkinson's disease (PD), exploring specific impairments and theoretical frameworks. It discusses psychological and neurobiological models to explain the observed behavioral and cognitive changes in PD patients.

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Area of Science:

  • Neuroscience
  • Cognitive Psychology
  • Neurology

Background:

  • Parkinson's disease (PD) is associated with significant cognitive dysfunction.
  • Previous research has identified various cognitive deficits in PD patients.
  • Understanding these deficits is crucial for managing the disease.

Purpose of the Study:

  • To review and characterize the cognitive deficits observed in Parkinson's disease.
  • To explore theoretical frameworks explaining these cognitive impairments.
  • To integrate psychological and neurobiological perspectives on PD-related cognitive changes.

Main Methods:

  • Literature review of empirical evidence on cognitive function in Parkinson's disease.
  • Analysis of descriptions of specific cognitive domains (visuospatial, memory, frontal functions).

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  • Examination of general cognitive descriptions (set-shifting, sequencing, bradyphrenia).

    • Main Results:

    • Cognitive deficits in Parkinson's disease span multiple domains, including visuospatial, memory, and executive functions.
    • General descriptions encompass issues with set-shifting, sequencing, temporal ordering, and bradyphrenia.
    • Two theoretical frameworks are proposed: a psychological model of depleted processing resources and a neurobiological model.

    Conclusions:

    • Cognitive impairments in Parkinson's disease are multifaceted and require comprehensive theoretical explanations.
    • A combination of psychological and neurobiological approaches offers a more complete understanding of PD-related cognitive deficits.
    • Further research integrating these models can elucidate the neuroanatomical and neurochemical underpinnings of these deficits.