Sensory axons excitability changes in carpal tunnel syndrome after neural mobilization

Abstract

Increased mechanosensitivity of the median nerve in carpal tunnel syndrome (CTS) has been demonstrated during upper limb tension test 1 (ULTT1) when the nerve is passively elongated. However, the neurophysiological changes of the sensory axons during stressing activities are unknown. The aim of present study was to verify possible changes in the excitability of median nerve afferent axons following nerve stress in elongation, in subjects with and without CTS. Eight CTS hands and eight controls were selected. Recruitment properties of the median nerve were studied by analyzing the relationship between the intensity of electrical stimulation and the size of motor response, before and after intermittent-repetitive neural mobilization. Only in CTS hands, after the intervention, the stimulus-response curve was strikingly abnormal: both plateau and slope values were significantly lower. During anatomical stress across the median nerve in elongation, compressive forces may exert mechanical traction on the median nerve, since it is 'tethered' at the carpal tunnel, resulting inactivation of Na(+) channels at the wrist, or impairment of energy-dependent processes which affect axonal conduction block. We conclude that in entrapment neuropathies, neural mobilization during nerve elongation may generate conduction failure in peripheral nerve. Our study supports specific considerations for patient education and therapeutic approaches.

Diagnostic Value of Virtual Touch Tissue Imaging Quantification for Evaluating Median Nerve Stiffness in Carpal Tunnel Syndrome

“…Prior studies have demonstrated that most clinical anatomic characteristics of the median nerve stiffness in patients with carpal tunnel syndrome showed a flat median nerve at the hook of the hamate bone (the thickest flexor retinaculum) and a dilated median nerve at the proximal pisiform bone. The carpal tunnel inlet and boundary of the flexor retinaculum are located at the pisiform bone near the hook of the hamate bone, which is where the front median nerve wall of most patients with carpal tunnel syndrome was relatively weak.…”

The effect of nerve mobilization exercise in patients with rheumatoid arthritis: a pilot study

“…The mobilization was shown to redistribute the sodium ion channels of sensory axons (25), increase neural growth factor and myelin protein zero in injured nerves (38,39). Overall, the therapeutic effects of the nerve mobilization could be accounted for by reduction of physical stress through the movements of the nerves (17,18) and intraneural fluid dispersion (19,20), normalization of sensory axons excitability (25), and promotion of nerve regeneration by stimulating expression of neural growth factor and myelin protein zero (38,39).…”

“…Overall, the therapeutic effects of the nerve mobilization could be accounted for by reduction of physical stress through the movements of the nerves (17,18) and intraneural fluid dispersion (19,20), normalization of sensory axons excitability (25), and promotion of nerve regeneration by stimulating expression of neural growth factor and myelin protein zero (38,39). As a pilot study, the methodology had several limitations such as sample size, subjects' homogeneity and the length of the follow-up period.…”

“…The rationale for performing nerve mobilization exercises is to remove or mobilize the pressure points on the neural tissues, reduce nerve adherence, increase neural vascularity, disperse noxious fluids and improve axoplasmic flow (17,19,21,23,24). In addition, the mobilization of entrapped nerves could significantly normalize the excitability of sensory axons by the redistribution of sodium ion (Na + ) channels (25). This kind of nerve mobilization has been demonstrated to have both localised and systemic hypoalgesic effects (23,24).…”

Advances in clinical neurology through the journal “Neurological Sciences” (2015–2016)

“…Facial onset sensory and motor neuronopathy (FOSMN) is a recently defined slowly progressive motor neuron disorder [145]. Brachial plexus injury (BPI) causes functional changes in the brain, but the structural changes resulting from BPI remain unknown [146]. Neuromyotoxicity due to therapy with hydroxychloroquine has been reported in a case [147].…”