Facilitatory and inhibitory pain mechanisms are altered in patients with carpal tunnel syndrome

Abstract

Preliminary evidence from studies using quantitative sensory testing suggests the presence of central mechanisms in patients with carpal tunnel syndrome (CTS) as apparent by widespread hyperalgesia. Hallmarks of central mechanisms after nerve injuries include nociceptive facilitation and reduced endogenous pain inhibition. Methods to study nociceptive facilitation in CTS so far have been limited to quantitative sensory testing and the integrity of endogenous inhibition remains unexamined. The aim of this study was therefore to investigate changes in facilitatory and inhibitory processing in patients with CTS by studying hypersensitivity following experimentally induced pain (facilitatory mechanisms) and the efficacy of conditioned pain modulation (CPM, inhibitory mechanisms). Twenty-five patients with mild to moderate CTS and 25 age and sex matched control participants without CTS were recruited. Increased pain facilitation was evaluated via injection of hypertonic saline into the upper trapezius. Altered pain inhibition through CPM was investigated through cold water immersion of the foot as the conditioning stimulus and pressure pain threshold over the thenar and hypothenar eminence bilaterally as the test stimulus. The results demonstrated that patients with CTS showed a greater duration (p = 0.047), intensity (p = 0.044) and area (p = 0.012) of pain in response to experimentally induced pain in the upper trapezius and impaired CPM compared to the control participants (p = 0.006). Although typically considered to be driven by peripheral mechanisms, these findings indicate that CTS demonstrates characteristics of altered central processing with increased pain facilitation and reduced endogenous pain inhibition.

Perceived Pain Extent Is Not Associated with Physical, Psychological, or Psychophysical Outcomes in Women with Carpal Tunnel Syndrome

“…These sensory deficits are not associated with electrodiagnostic findings suggesting that sensitization is not related to the damage of the median nerve but rather can be present from the onset of the condition (9). A recent study confirming the hypothesis of altered central pain processing in CTS has shown that patients not only exhibit increased pain facilitation but that they also have reduced endogenous pain inhibition (10). Nevertheless, other studies have not found widespread sensory changes in patients with CTS without concomitant neck pain suggesting that there might be subgroups of subjects with CTS with varying levels of sensitivity (11).…”

Pain Modulation: From Conditioned Pain Modulation to Placebo and Nocebo Effects in Experimental and Clinical Pain

“…A pro-nociceptive pattern of amplified pain facilitation (central sensitization) and reduced endogenous pain inhibition is also common in carpal tunnel syndrome, chronic pancreatitis (Soon, Vicenzino, Schmid, & Coppieters, 2017), whiplash-associated disorders (Daenen et al, 2013; Ng, Pedler, Vicenzino, & Sterling, 2014; Yarnitsky, 2015) and in primary headaches such as migraine, chronic tension-type headache and chronic post-traumatic headache following mild traumatic brain injury (Sandrini et al, 2006). In patients with acute and chronic low back pain, CPM effect is triggered following counter-irritation, but its duration is significantly reduced compared to healthy individuals (Mlekusch et al, 2016).…”

Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management

“…Central changes after severe experimental nerve injury include, but are not limited to, central immune-inflammatory mechanisms, 81 , 101 , 122 , 123 central sensitisation, 80 and changes to cortical representations. 43 , 104 , 105 , 150 Clinical hallmarks of central mechanisms including bilateral sensory deficits in unilateral painful entrapment neuropathies, 29 , 37 , 59 , 142 widespread hypersensitivity, 37 , 53 , 142 , 171 , 172 and impaired conditioned pain modulation 138 have been described in patients with entrapment neuropathies. Furthermore, cortical changes have been reported including functional and structural changes of the somatosensory cortex in patients with CTS 43 , 93 , 104 , 150 and changes in cortical morphometry in patients with lumbar radicular pain.…”