Is all cognitive impairment in Parkinson’s disease “mild cognitive impairment”?
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- Martínez-Horta, S. & Kulisevsky, J. J Neural Transm (2011) 118: 1185. doi:10.1007/s00702-011-0675-9
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Cognitive impairment can be demonstrated in Parkinson’s disease (PD) from the very beginning of the disease. Clinical manifestations range from slight deficits, only demonstrable by means of neuropsychological testing, up to dementia. If a linear involution is supposed for the cognitive worsening in PD, then the relatively subtle cognitive defects should be taken as the earliest signs of dementia implying that PD-MCI concept would be thoroughly equivalent to that used for the early prediction of other dementias among healthy population. Cognitive defects in PD, however, may not follow a normal distribution. While fronto-striatal deficits, such as working memory, set-shifting and free-recall verbal memory appear altered in most patients during long periods of time, certain functions depending on more posterior-cortical regions, such as copying or naming, usually characterize patients with dementia. Fronto-striatal and posterior-cortical cognitive defects may have a different pathophysiological substrates, evolution and prognosis. While fronto-striatal defects appear more related to dopaminergic defects, posterior-cortical defects may obey multiple neurotransmitter failure. Designing criteria to accurately diagnose PD-MCI is highly relevant for clinical treatment, research, care-giving and decision-making. Besides quantitative defects, an operative definition of MCI in PD should clearly distinguish a “risky cognitive profile” among the broad cognitive defects intrinsic to PD. Thus, along with other possible biological markers, from a neuropsychological point of view, posterior-cortical defects probably represent the very syndrome of MCI in PD.