Our aim was to describe the differences in the presence of trigger points (TrPs) in the shoulder muscles and to investigate the presence of mechanical hypersensitivity in patients with unilateral shoulder impingement and healthy controls. Twelve patients with strictly unilateral shoulder impingement and 10 matched controls were recruited. TrPs in the levator scapula, supraspinatus, infraspinatus, subscapularis, pectoralis major, and biceps brachii muscles were explored. TrPs were considered active if the local and referred pain reproduced the pain symptoms and the patient recognized the pain as a familiar pain. Pressure pain thresholds (PPT) were assessed over the levator scapulae, supraspinatus, infraspinatus, pectoralis major, biceps brachii, and tibialis anterior muscles. Both explorations were randomly done by an assessor blinded to the subjects' condition. Patients with shoulder impingement have a greater number of active (mean +/- SD: 2.5 +/- 1; P < 0.001) and latent (mean +/- SD: 2 +/- 1; P = 0.003) TrPs when compared to controls (only latent TrPs, mean +/- SD: 1 +/- 1). Active TrPs in the supraspinatus (67%), infraspinatus (42%), and subscapularis (42%) muscles were the most prevalent in the patient group. Patients showed a significant lower PPT in all muscles when compared to controls (P < 0.001). Within the patient group a significant positive correlation between the number of TrPs and pain intensity (r (s) = 0.578; P = 0.045) was found. Active TrPs in some muscles were associated to greater pain intensity and lower PPTs when compared to those with latent TrPs in the same muscles (P < 0.05). Significant negative correlations between pain intensity and PPT levels were found. Patients with shoulder impingement showed widespread pressure hypersensitivity and active TrPs in the shoulder muscles, which reproduce their clinical pain symptoms. Our results suggest both peripheral and central sensitisation mechanisms in patients with shoulder impingement syndrome.

A latent myofascial trigger point (MTP) is defined as a focus of hyperirritability in a muscle taut band that is clinically associated with local twitch response and tenderness and/or referred pain upon manual examination. Current evidence suggests that the temporal profile of the spontaneous electrical activity at an MTP is similar to focal muscle fiber contraction and/or muscle cramp potentials, which contribute significantly to the induction of local tenderness and pain and motor dysfunctions. This review highlights the potential mechanisms underlying the sensory-motor dysfunctions associated with latent MTPs and discusses the contribution of central sensitization associated with latent MTPs and the MTP network to the spatial propagation of pain and motor dysfunctions. Treating latent MTPs in patients with musculoskeletal pain may not only decrease pain sensitivity and improve motor functions, but also prevent latent MTPs from transforming into active MTPs, and hence, prevent the development of myofascial pain syndrome.

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A latent MTP is associated with an accelerated development of muscle fatigue and simultaneously overloading active motor units close to an MTP. Elimination of latent MTPs and inactivation of active MTPs may effectively reduce accelerated muscle fatigue and prevent overload spreading within a muscle.

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