Objective: To characterize degenerative cerebellar ataxia by measuring quantitative electrophysiology, upper limb kinematics and gait.

Background: Loss of cerebellar brain inhibition (CBI) in ataxia leads to increased excitability of the motor cortex and can lead to network dysfunction [1,2]. Current studies have shown that impaired cerebellar control of cortical excitability results in abnormalities in movement-related sensory data acquisition, visuo-kinesthetic perception of hand movement, control of grip forces, timing and sensorimotor synchronization of voluntary limb movements [3]. In this study, detailed characterization is performed in ataxia using resting quantitative EEG (qEEG), spatio-temporal gait parameter measurement and upper limb spatiotemporal kinematic manipulations.

Method: Twenty-three patients with degenerative cerebellar ataxia of various etiologies were assessed using:
1. Quantitative EEG: Resting condition eyes-closed EEG data were recorded using 32 channels g. Nautilus g.tec wireless bio-signal acquisition system. Fast Fourier transform (FFT)-based spectral power analysis was performed for the frequency bands.
2. KinArm: Ten features were extracted using MATLAB from the kinematic data pertaining upper-limb movements during a variety of manipulations (e.g., force variations).
3. Gait: ProtoKinetics Zeno Gait Walkway was used to capture footfalls in real-time using the ProtoKinetics software (PKMAS).

Results: In qEEG, ataxia patients displayed significantly lower (p = 0.005) alpha activity globally compared to healthy control subjects. Performance of the ataxia and control groups were compared using the features extracted from the KINARM. Compared to the controls, the ataxia patients hit 8.3% lesser targets, exhibited an increase of 13% in endpoint error, 16% in mean perpendicular error and 19% in the direction errors. The mean and peak speed for the ataxia patients were 12% and 5% lower compared to controls and ataxia patients took 3% more time to reach the target. Spatio-temporal gait parameters were compared between age-matched controls and the ataxic patients. Normalized velocity and walk ratio was a mean -1.9 Z-score deviations worse than controls. Variability in normalized velocity and walk ratio was a mean +4.5 Z-score deviations higher than controls.

Conclusion: The study reveals that ataxia results in overall dysfunction across many domains that involve different aspects of motor control.

References: [1] Caligiore D, Pezzulo G, Baldassarre G, et al. Consensus Paper: Towards a Systems-Level View of Cerebellar Function: the Interplay Between Cerebellum, Basal Ganglia, and Cortex. Cerebellum. 2017;16(1):203-229. doi:10.1007/s12311-016-0763-3.
[2] Bodranghien F, Bastian A, Casali C, et al. Consensus Paper: Revisiting the Symptoms and Signs of Cerebellar Syndrome. Cerebellum. 2016;15(3):369-391. doi:10.1007/s12311-015-0687-3.
[3] Manto M, Bower JM, Conforto AB, et al. Consensus paper: roles of the cerebellum in motor control–the diversity of ideas on cerebellar involvement in movement. Cerebellum. 2012;11(2):457-487. doi:10.1007/s12311-011-0331-9.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/electrophysiologic-and-kinematic-characterization-of-degenerative-cerebellar-ataxia/