Abstract

ObjectiveTo investigate prevalence of EMG patterns underlying hypertonia in multiple sclerosis (MS) and whether these patterns indicate different levels of spinal excitability. MethodsWe investigated the EMG activity recorded from 108 hypertonic muscles of 59 consecutive MS patients. To investigate spastic dystonia (SD), we looked for the presence of EMG activity in muscles in a resting position. To investigate dynamic stretch reflex (DSR) and static stretch reflex (SSR), we looked for the presence of EMG activity in response to a manually performed passive stretch of the muscle. ResultsDSR was evoked in 104 muscles. In 51 muscles, DSR was the sole EMG activity. This pattern corresponds to the classical notion of spasticity, and was predominant in extensors. In contrast, SSR was detected in 48 muscles – predominantly in flexors. SD was observed in 28 muscles, showing even distribution in flexor and extensor muscles. Only in the flexors, SSR was associated with a larger DSR compared to spasticity. ConclusionsThese findings likely depend on the central effects of both flexor and extensor spindle afferents on the homonymous spinal motor neurons. SignificanceImproving our capacity to assess spinal excitability in MS patients.

Highlights

  • To investigate dynamic stretch reflex (DSR) and static stretch reflex (SSR), we looked for the presence of EMG activity in response to a manually performed passive stretch of the muscle

  • These findings likely depend on the central effects of both flexor and extensor spindle afferents on the homonymous spinal motor neurons

  • In patients affected by chronic upper motor neuron syndrome (UMNS), one common clinical sign is muscle hypertonia, which is often velocity-dependent, i.e. greater resistance is experienced with fast stretches

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Summary

Introduction

In patients affected by chronic upper motor neuron syndrome (UMNS), one common clinical sign is muscle hypertonia, which is often velocity-dependent, i.e. greater resistance is experienced with fast stretches. Muscle hypertonia can hinder function, and result in pain and complications, limiting the potential benefit of rehabilitation. Compelling evidence shows that in the overwhelming majority of UMNS patients, muscle hypertonia is due to increased stretch reflex activity (Thilmann et al, 1991) - a condition that can be called reflex hypertonia. Only reflex hypertonia is reported to be velocity-dependent, intrinsic hypertonia and reflex hypertonia often co-exist within the same muscle (Sheean, 1998a), and it can be difficult to distinguish between the two forms in a clinical setting (Malhotra et al, 2008; O’Dwyer and Ada, 1996)

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