Chronic pain is a leading cause of disability globally and associated with enormous health-care costs. The discrepancy between the extent of tissue damage and the magnitude of pain, disability, and associated symptoms represents a diagnostic challenge for rheumatology specialists. Central sensitisation, defined as an amplification of neural signalling within the CNS that elicits pain hypersensitivity, has been investigated as a reason for this discrepancy. Features of central sensitisation have been documented in various pain conditions common in rheumatology practice, including fibromyalgia, osteoarthritis, rheumatoid arthritis, Ehlers-Danlos syndrome, upper extremity tendinopathies, headache, and spinal pain. Within individual pain conditions, there is substantial variation among patients in terms of presence and magnitude of central sensitisation, stressing the importance of individual assessment. Central sensitisation predicts poor treatment outcomes in multiple patient populations. The available evidence supports various pharmacological and non-pharmacological strategies to reduce central sensitisation and to improve patient outcomes in several conditions commonly seen in rheumatology practice. These data open up new treatment perspectives, with the possibility for precision pain medicine treatment according to pain phenotyping as a logical next step. With this view, studies suggest the possibility of matching non-pharmacological approaches, or medications, or both to the central sensitisation pain phenotypes.

This study provided preliminary evidence of a short-term hypoalgesic effect of APUCM on craniofacial and cervical regions of patients with cervico-craniofacial pain of myofascial origin, suggesting that APUCM may cause an immediate nociceptive modulation in the trigeminocervical complex. We also observed a sympathoexcitatory response, which could be related to the hypoalgesic effect induced by the technique, but this aspect should be confirmed in future studies.

The aim of this study was to investigate whether bilateral widespread pressure hypersensitivity exists in patients with unilateral carpal tunnel syndrome. A total of 20 females with carpal tunnel syndrome (aged 22-60 years), and 20 healthy matched females (aged 21-60 years old) were recruited. Pressure pain thresholds were assessed bilaterally over median, ulnar, and radial nerve trunks, the C5-C6 zygapophyseal joint, the carpal tunnel and the tibialis anterior muscle in a blinded design. The results showed that pressure pain threshold levels were significantly decreased bilaterally over the median, ulnar, and radial nerve trunks, the carpal tunnel, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in patients with unilateral carpal tunnel syndrome as compared to healthy controls (all, P < 0.001). Pressure pain threshold was negatively correlated to both hand pain intensity and duration of symptoms (all, P < 0.001). Our findings revealed bilateral widespread pressure hypersensitivity in subjects with carpal tunnel syndrome, which suggest that widespread central sensitization is involved in patients with unilateral carpal tunnel syndrome. The generalized decrease in pressure pain thresholds associated with pain intensity and duration of symptoms supports a role of the peripheral drive to initiate and maintain central sensitization. Nevertheless, both central and peripheral sensitization mechanisms are probably involved at the same time in carpal tunnel syndrome.

No studies have investigated the effects of the treatments directed at the cervical spine in patients with temporomandibular disorders (TMD). Our aim was to investigate the effects of joint mobilization and exercise directed at the cervical spine on pain intensity and pressure pain sensitivity in the muscles of mastication in patients with TMD. Nineteen patients (14 females), aged 19-57 years, with myofascial TMD were included. All patients received a total of 10 treatment session over a 5-week period (twice per week). Treatment included manual therapy techniques and exercise directed at the cervical spine. Outcome measures included bilateral pressure pain threshold (PPT) levels over the masseter and temporalis muscles, active pain-free mouth opening (mm) and pain (Visual Analogue Scale) and were all assessed pre-intervention, 48 h after the last treatment (post-intervention) and at 12-week follow-up period. Mixed-model anovas were used to examine the effects of the intervention on each outcome measure. Within-group effect sizes were calculated in order to assess clinical effect. The 2 x 3 mixed model anova revealed significant effect for time (F = 77.8; P < 0.001) but not for side (F = 0.2; P = 0.7) for changes in PPT over the masseter muscle and over the temporalis muscle (time: F = 66.8; P < 0.001; side: F = 0.07; P = 0.8). Post hoc revealed significant differences between pre-intervention and both post-intervention and follow-up periods (P < 0.001) but not between post-intervention and follow-up period (P = 0.9) for both muscles. Within-group effect sizes were large (d > 1.0) for both follow-up periods in both muscles. The anova found a significant effect for time (F = 78.6; P < 0.001) for changes in pain intensity and active pain-free mouth opening (F = 17.1; P < 0.001). Significant differences were found between pre-intervention and both post-intervention and follow-up periods (P < 0.001) but not between the post-intervention and follow-up period (P > 0.7). Within-group effect sizes were large (d > 0.8) for both post-intervention and follow-up periods. The application of treatment directed at the cervical spine may be beneficial in decreasing pain intensity, increasing PPTs over the masticatory muscles and an increasing pain-free mouth opening in patients with myofascial TMD.