Bradykinesia in Alzheimer's disease and its neurophysiological substrates. Issue 4 (April 2020)

• Record Type: Journal Article
• Authors: Bologna, Matteo; Guerra, Andrea; Colella, Donato; Cioffi, Ettore; Paparella, Giulia; Di Vita, Antonella; D'Antonio, Fabrizia; Trebbastoni, Alessandro; Berardelli, Alfredo
• Is Part Of: Clinical neurophysiology. Volume 131:Issue 4(2020:Apr.)
• Page Start: 850
• Page End: 858
• Publication Date: 2020-04
• Subjects: Alzheimer's disease -- Bradykinesia -- Cholinergic system -- Kinematic analysis -- Primary motor cortex -- Motor control; AMT active motor threshold -- AD Alzheimer's Disease -- ANOVA analysis of variance -- BDI Beck Depression Inventory -- CV coefficient of variation -- EMG electromyography -- FAB Frontal Assessment Battery -- FSS Fatigue Severity Scale -- HC healthy controls -- I/O input-output -- ISI inter-stimulus interval -- LTP long-term potentiation -- MEP motor-evoked potentials -- MDS-UPDRS Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale -- M1 primary motor cortex -- MMSE Mini Mental State Examination -- PAS paired associative stimulation -- PD Parkinson's disease -- RMT resting motor threshold -- SAI short-latency afferent inhibition -- SICI short-interval intracortical inhibition -- iTBS intermittent theta burst stimulation -- TMS transcranial magnetic stimulation; Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2019.12.413
• Languages: English
• ISSNs: 1388-2457

Abstract

Highlights: Clinical observations indicate that bradykinesia can be observed in Alzheimer's disease (AD). We here found that movement slowness in AD correlates with measures of cholinergic dysfunction. This study provides information on the pathophysiology of altered voluntary motor control in AD. Abstract: Objective: Alzheimer's disease is primarily characterized by cognitive decline; recent studies, however, emphasize the occurrence of motor impairment in this condition. Here, we investigate whether motor impairment, objectively evaluated with kinematic techniques, correlates with neurophysiological measures of the primary motor cortex in Alzheimer's disease. Methods: Twenty patients and 20 healthy subjects were enrolled. Repetitive finger tapping was assessed by means of a motion analysis system. Primary motor cortex excitability was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and short-latency afferent inhibition. Plasticity-like mechanisms were indexed according to changes in motor-evoked potential amplitude induced by the intermittent theta-burst stimulation. Results: Patients displayed slowness and altered rhythm during finger tapping. Movement slowness correlated with reduced short-latency afferent inhibition in patients, thus suggesting that degeneration of the cholinergic system may also be involved in motor impairment in Alzheimer's disease. Moreover, altered movement rhythm in patients correlated with worse scores in the Frontal Assessment Battery. Conclusion: This study provides new information on the pathophysiology of altered voluntary movements in Alzheimer's disease. Significance: The study results suggest that a cortical cholinergic deficit may underlie movement slowness in Alzheimer's disease.