Rigidity in Parkinson’s disease: evidence from biomechanical and neurophysiological measures

Author:

Asci Francesco12ORCID,Falletti Marco1,Zampogna Alessandro1,Patera Martina1,Hallett Mark3ORCID,Rothwell John4,Suppa Antonio12

Affiliation:

1. Department of Human Neurosciences, Sapienza University of Rome , 00185 Rome , Italy

2. IRCCS Neuromed Institute , 86077 Pozzilli (IS) , Italy

3. Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health , Bethesda, MD 20814 , USA

4. UCL Queen Square Institute of Neurology , London WC1N 3BG , UK

Abstract

Abstract Although rigidity is a cardinal motor sign in patients with Parkinson’s disease (PD), the instrumental measurement of this clinical phenomenon is largely lacking, and its pathophysiological underpinning remains still unclear. Further advances in the field would require innovative methodological approaches able to measure parkinsonian rigidity objectively, discriminate the different biomechanical sources of muscle tone (neural or visco-elastic components), and finally clarify the contribution to ‘objective rigidity’ exerted by neurophysiological responses, which have previously been associated with this clinical sign (i.e. the long-latency stretch-induced reflex). Twenty patients with PD (67.3 ± 6.9 years) and 25 age- and sex-matched controls (66.9 ± 7.4 years) were recruited. Rigidity was measured clinically and through a robotic device. Participants underwent robot-assisted wrist extensions at seven different angular velocities randomly applied, when ON therapy. For each value of angular velocity, several biomechanical (i.e. elastic, viscous and neural components) and neurophysiological measures (i.e. short and long-latency reflex and shortening reaction) were synchronously assessed and correlated with the clinical score of rigidity (i.e. Unified Parkinson’s Disease Rating Scale—part III, subitems for the upper limb). The biomechanical investigation allowed us to measure ‘objective rigidity’ in PD and estimate the neuronal source of this phenomenon. In patients, ‘objective rigidity’ progressively increased along with the rise of angular velocities during robot-assisted wrist extensions. The neurophysiological examination disclosed increased long-latency reflexes, but not short-latency reflexes nor shortening reaction, in PD compared with control subjects. Long-latency reflexes progressively increased according to angular velocities only in patients with PD. Lastly, specific biomechanical and neurophysiological abnormalities correlated with the clinical score of rigidity. ‘Objective rigidity’ in PD correlates with velocity-dependent abnormal neuronal activity. The observations overall (i.e. the velocity-dependent feature of biomechanical and neurophysiological measures of objective rigidity) would point to a putative subcortical network responsible for ‘objective rigidity’ in PD, which requires further investigation.

Funder

NIH

Publisher

Oxford University Press (OUP)

Subject

Neurology (clinical)

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