No coin nor oath required. For personal study only.
Objective: To evaluate the impact of cognitive impairment on disease severity and motor function in idiopathic Parkinson's disease (PD) patients.
Background: Parkinson's disease is very commonly complicated by cognitive impairment. Although the characteristics of cognitive impairment in PD have been widely studied, its effect on the clinical phenotype of the disease has never been investigated.
Method: Forty-one patients were retrieved from Parkinson's Disease registry of the University Department of Neurology, Patras, Greece, with Mini Mental State Examination (MMSE) score Յ24 (PD-CI). Each PD-CI patient was matched for disease onset (Ϯ2 years) and duration (Ϯ2 years) with a PD patient with MMSE score Ͼ24 (PD-Control). Diagnosis of PD was made according to the UK brain bank criteria. Cases considered as atypical parkinsonism and cases who presented memory loss, dementia, psychosis, major depression or receiving anti-psychotic or antidepressive medication before the motor manifestations of PD were excluded during patient selection. Psychiatric disorders were diagnosed by psychiatrist, using standard criteria. The Unified Parkinson's Disease Rating Scale (UPDRS) was completed during clinical examination. In the comparisons between PD-CI patients and their controls were also used items of the UPDRS for tremor (item 20; score: 0 -16), for rigidity (item 22; score: 0 -16), for bradykinesia (items 23-26; score: 0 -32), and for axial impairment (items 18, 19, 27-31; score: 0 -28).
Results: The total UPDRS and all UPDRS subscores, apart of UPDRS IV, and the mean Hoehn&Yahr and Swab & England scores were significantly higher in the PD-CI patients compared with their controls. The UPDRS items for rigidity, bradykinesia and axial impairment were also significantly higher in the PD-CI patients compared with PD-Control patients, whilst the prevalence of tremor (rest tremor, not action tremor which can be influenced by anxiety) did not differ between groups.
Significantly more PD-CI patients were receiving higher doses of levodopa than their controls, but there was not statistically significant difference in the intake of the other antiparkinsonian medications. Twenty-three (56%) of the 41 PD-CI patients were receiving acetyl-cholinesterase inhibitor therapy (either rivastigmine or donepezil). Eleven (26.8%) PD-CI patients (5 (12.2%), and 6 (14.6%) PD-Control patients were receiving or have received atypical neuroleptics in the course of their disease. The UPDRS items for rigidity, bradykinesia and axial impairment, as well as UPDRS I, II, and III remained significantly associated with cognitive impairment after adjusting each of them for sex and antiparkinsonian drugs in the multivariate logistic regression.
Conclusion: PD patients with cognitive impairment had poorer motor function, worse rigidity (both axial and limb) and bradykinesia, as well as worse performance in activities of daily living compared with matched PD patients without cognitive impairment. This could either be attributed to a direct effect of cognitive impairment on parkinsonian symptoms or to decreased compliance of patients during clinical examination.
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