Chronic musculoskeletal conditions are increasingly conceived as involving altered central nervous system processing, and impaired nociceptive flexor reflex appears to reflect altered central nervous system processing. This is supported by a meta-analysis which was performed during the literature review and it was found that the nociceptive flexion reflex threshold were significantly lower in subjects with primary headache (p = 0.005, standardized mean difference = -0.45), fibromyalgia (p < 0.001, standardized mean difference = -0.63), knee pain (p < 0.001, standardized mean difference = -1.51) and whiplash (p < 0.001, standardized mean difference = -0.73) when compared to the healthy controls.
Another painful and disabling musculoskeletal condition includes lateral epicondylalgia which significantly impacts on the individual and society. Even though manual therapy has been shown to be effective in relieving pain in lateral epicondyalalgia, an understanding of the mechanisms underlying lateral epicondylalgia and its management remains poorly understood. For example, is spinal cord hyperexcitability present in lateral epicondylalgia? Does lateral epicondylalgia exhibit deficit in conditioned pain modulation? Does manual therapy exert its effect through the central nervous system? This thesis aimed to investigate the neurophysiological mechanisms underpinning lateral epicondylalgia and its management.
There is emerging evidence of altered pain signal processing as a likely underlying neurophysiological mechanism in chronic lateral epicondylalgia. Furthermore, it has been suggested that neurodynamic tests reflect nociceptive withdrawal responses. Nociceptive flexion reflex threshold, pain-free grip, and pressure pain threshold were measured in 30 lateral epicondylalgia participants and 31 healthy controls. Test of neural tissue involvement (using upper limb neural tension, radial bias) was used to differentiate lateral epicondylalgia participants with or without positive neurodynamic tests. There were significant differences in nociceptive flexion reflex threshold between the control and lateral epicondylalgia with or without positive neurodynamic test (p = .006, standardized mean difference = 0.80 to 0.89) suggesting the presence of spinal cord hyperexcitability in lateral epicondylalgia.
By inference from previous studies which reported deficiencies in conditioned pain modulation in other forms of chronic musculoskeletal pain, it is speculative that conditioned pain modulation is likewise afflicted in chronic lateral epicondylalgia Twenty lateral epicondylalgia participants and 22 healthy controls participated in the study. Pressure pain threshold (test stimulus) was measured over the lateral epicondyles before and during noxious heat pain (conditioning stimulus) which was applied to the calf. There were significant mean differences in pressure pain threshold change between the groups (p = 0.001, standardized mean difference = 1.00). The findings from this study demonstrated that chronic lateral epicondylalgia does not exhibit mechanical pain modulation in response to noxious conditioning heat stimulus.
A randomized, double-blinded clinical trial investigated the neurophysiological effects of mobilisation with movement. Forty participants with chronic lateral epicondylalgia were randomly assigned to an elbow mobilisation with movement or manual contact intervention. Pressure pain threshold and nociceptive flexion reflex threshold were measured pre and post intervention whilst pain-free grip was measured pre, during and post intervention. There were significant mean differences in pressure pain threshold change (p = 0.046, standardized mean difference = 0.76), pain-free grip (during intervention) change (p=0.007, standardized mean difference = 1.45), pain-free grip (post-intervention) change (p= 0.049, standardized mean difference = 1.03) and nociceptive flexion reflex threshold change (p=0.046, standardized mean difference = 0.59) between the manual contact and MWM intervention group. These suggest that MWM has the capacity to modulate spinal cord hyperexcitability in lateral epicondylalgia.
Taken together, these studies improve our understanding of the neurophysiological mechanisms underlying lateral epicondylalgia and its management. The findings suggest evidence of spinal cord hyperexcitability in lateral epicondylalgia with and without positive neurodynamic test. Chronic lateral epicondylalgia also appears to have a lack of ability to engage the endogenous pain suppression system to modulate spinal cord excitability. Mobilisation with movement may have the capacity to reduce spinal cord hyperexcitability in chronic LE, at least in the short term, by stimulating the descending pain inhibitory system.