Abstract
Non-surgical treatment of knee osteoarthritis (KOA) is often focused on the motor component of KOA even though there is evidence that sensory dysfunctions play an important role in the impaired control of the affected joint. Excitation of sensory afferents can increase motor function by exploiting the nervous system’s ability to adapt to changing environments (i.e., neuronal plasticity). Therefore, the aim of this study was to explore the acute effects of a single session (30 min) of sensory intervention targeting neuronal plasticity using low-frequency (10 Hz) somatosensory electrical stimulation (SES) of the femoral nerve. We evaluated the effects of SES on the position and force control of the affected knee and self-reported pain in KOA patients (n = 14) in a sham-controlled randomized trial. The results showed that SES did not improve measures of lower-limb motor coordination compared to sham stimulation in KOA patients, nor did it improve self-reported knee function and pain (all p > 0.05). In conclusion, despite sensory involvement in KOA, the sensory intervention used in the present explorative study did not relieve self-reported pain, which may underlie the absence of an effect on measures of motor coordination. In sum, the present explorative study showed that SES alone does not improve motor coordination in KOA patients.
Highlights
Knee osteoarthritis (KOA) is a chronic joint disease affecting 10 and 18% of men and women (WHO)
Since the same sensory structures are involved in the processing of both types of sensory information, there is a continuous performer–environment interaction that is required for accurate motor behavior
We aim to increase sensory function, and in particular, the processing of proprioceptive information that is impaired but often underappreciated [3] in KOA patients, despite evidence that KOA-related sensory dysfunction is a major contributor to motor impairments including, but not limited to, locomotor activities [6]
Summary
Knee osteoarthritis (KOA) is a chronic joint disease affecting 10 and 18% of men and women (WHO). Sensory dysfunctions impairs the control of the affected joint [3,4]. Since the same sensory structures are involved in the processing of both types of sensory information, there is a continuous performer–environment interaction that is required for accurate motor behavior. We do not aim to provide evidence for one particular theoretical framework but rather capitalize on increasing the effectiveness of the sensorimotor system, focusing on its functionality. We aim to increase sensory function, and in particular, the processing of proprioceptive information that is impaired but often underappreciated [3] in KOA patients, despite evidence that KOA-related sensory dysfunction is a major contributor to motor impairments including, but not limited to, locomotor activities [6]
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