Comprehensive evaluation of spasticity and other sensorimotor dysfunctions after lesions to the central or peripheral nervous system

Abstract: Background: Understanding how sensorimotor impairments may contribute to changes in body structure and function, and also to activity and participation limitations is an important challenge in neurorehabilitation research, of high clinical relevance. Available assessment methods include mainly clinical scales, often with inadequate psychometric properties, such as the Modified Ashworth scale for assessment of spasticity. Novel tools, incorporating kinetic or kinematic aspects, are therefore needed to improve the diagnostic accuracy and management of sensorimotor impairments in neurological disorders. Aim: The overall aim of this thesis was to improve methods of assessment of sensorimotor impairments after central or peripheral nervous system lesions by the use of standardized and valid objective measurement tools. This thesis examined the validity and reliability of the novel NeuroFlexor foot module, a method designed to distinguish the contribution of reflex hyperexcitability from secondary changes of passive muscle properties to muscle tone. Moreover, it aimed to provide reference data of the NeuroFlexor method for the upper and lower extremities from a representative sample of healthy adult subjects and to establish cut-off values to differentiate the contributors to passive stretch resistance between patients in different phases after stroke and individuals with muscle-related effects of poliomyelitis infection. Methods: A total of 93 patients (64 patients in different phases after stroke and 19 patients with prior polio) and 180 healthy subjects were examined with the NeuroFlexor hand and/or foot module. Neural, elastic and viscous components of passive movement resistance were quantified (in Newton, N) using a biomechanical model, during passive wrist extension and/or ankle flexion at controlled slow and fast velocities. In Study II the measured neural component, reflecting stretch reflex mediated resistance, was validated against electromyography activity of calf muscles recorded during NeuroFlexor assessment. A test-retest design with a two-way random effects model studied intra-rater reliability. Cut-off values for the NeuroFlexor components were established for the upper extremity (Study I) and lower extremity (Study II) by adding 3 SD to the mean. Additionally, specific limits were determined for the elastic component in the upper limb, which is significantly affected by age and gender. In the lower extremity, the pathological neural component was verified against electromyography amplitude using a Receiver Operating Characteristic (ROC) curve analysis. In Study III, the NeuroFlexor method in conjunction with electromyography evaluated the effectiveness of one session of electrical stimulation with the EXOPULSE Mollii suit at different stimulation frequencies on objective signs of spasticity. The response to passive muscle stretch with the NeuroFlexor instrument was characterized in patients in the sub-acute phase (Study I) or chronic phase (Study II) after stroke, and in subjects with prior paralytic poliomyelitis, with or without a diagnosis of progressive post-polio syndrome (Study IV). Finally, the Modified Ashworth scale of spasticity, the Medical Research Council scale, Jamar dynamometer and Biodex Multi-Joint System for muscle strength, the Fatigue Severity Scale and the Multidimensional Fatigue Inventory (MFI-20) for the severity of fatigue, and the Visual Analogue Scale for pain were used as complementary tests of neurological impairment. Results: The neural component measured with the NeuroFlexor foot module revealed a velocity dependent response correlating with the increase in electromyography amplitude (p ≤ 0.005). Reliability was good for the neural component (ICC2,1 ≥ 0.899) and high for the elastic component (ICC2,1 ≥ 0.909). In the upper extremity, the cut-off value (mean + 3 SD) identified for the neural component was 3.4 N. In the lower limb, the neural component cut-off value (according to ROC analysis) for 40 degree stretch was 31.5 N and for 30 degree stretch was 18.9 N. Sixteen out of 39 patients (41%) early after stroke had a pathologically high neural component of the upper extremity and 11 out of 15 chronic stroke patients (73%) in the lower extremity. A limited correspondence between clinical evaluation of spasticity and NeuroFlexor measurement was observed. The NeuroFlexor was sufficiently sensitive to detect variations in neural and mechanical contributions to the muscle resistance induced by the electrical stimulation with the EXOPULSE Mollii suit at different frequencies at the individual level. However, at group level no significant reduction in spasticity was observed during or immediately after 60 minutes of electrical stimulation at any frequency (p > 0.35), and there were no significant differences between OFF settings and active frequencies (20 and 30 Hz) of stimulation. Both NeuroFlexor neural and mechanical components differed significantly in subjects with prior polio compared to healthy subjects (p < 0.001), with the elastic component contributing most to passive resistance. Low values of neural component were observed, especially in individuals with severe muscle atrophy. Finally, significant correlations were found between NeuroFlexor components, severity of fatigue and perceived pain (p < 0.05). Conclusions: The NeuroFlexor may offer a clinically feasible and non-invasive way to objectively quantify post-stroke spasticity and polio-related neuromuscular alterations in the upper and lower extremities. The method may assess changes in spasticity after treatment with, for example, electrical stimulation, and elucidate potential associations between altered neural and passive muscle properties and clinical issues. Finally, it may guide new therapeutic approaches. However, further evaluation of the NeuroFlexor foot module is needed.