Muscle pain is a common pain condition. Although physicians are well aware of its prevalence, muscle pain is often not sufficiently diagnosed. The need for experimental research in muscle pain is emphasized and has attracted a growing interest.

One of the topics of our interest has been myofascial pain from muscle trigger points (TrPs). This is a common condition and patients often report referred pain and a feeling of fatigue during use of the muscle. The diagnosis is sometimes difficult to establish. We conducted a study in patients suspected of carpal tunnel syndrome and found that approximately half of the patients with normal nerve conduction of the median nerve, had a trigger point in the infraspinatus muscle (Qerama et al 2009). 

Moreover, we have studied the underlying pathophysiology of TrPs and suggested that clusters of muscle nociceptors are possibly located in close proximity to the motor endplate regions, thus making these regions susceptible to pain and probably a source for the formation of trigger points in the muscle (Qerama et al 2004). Indeed, endplate noise and endplate spikes have been identified and significantly associated with TrPs (Simons DG 2002Fernandes de las Penas 2007). 
Weakness and complaints of fatigue often accompany musculoskeletal pain conditions (Couppé et al. 2001). Painful muscles are often unable to exert maximal isometric force and show greater fatigability than normal muscles (Jensen R et al 1994). 

We found that following experimental pain, a shift towards lower frequencies and reduction in the number of turns and amplitude of the interference pattern of the muscle was seen similar to that seen in muscle fatigue. These findings indicate that the nociceptive input exerts an inhibitory effect on motor function (Qerama et al, 2005). 

Whether this inhibitory effect is caused by peripheral or central mechanisms is still a matter of debate. By means of direct muscle stimulation we have studied the muscle fibre conduction properties during evoked pain and the ongoing analysis of the data suggests a concomitant peripheral effect of the evoked pain (Duez et al., 2015). 

On the other hand, strength training can result in dramatic increases in muscle force output, cross-sectional area and electromyographic (EMG) activity (Folland at al 2007). In a study we found that baseline interference pattern amplitude measurements of the trained subjects were higher than of untrained subjects, probably due to increased motor unit recruitment, larger motor units or increased firing frequency in the trained subjects (Duez et al 2010). 

While a lot of studies have focused on the cortical presentation of the cutaneous pain, very few have examined the representation of muscle pain in the brain. The brain regions that most frequently respond to acute muscle pain as shown by fMRI with BOLD technique are thalamus, SI and SII, Insula, cingulate and prefrontal cortices along with less involved areas such as cerebellum, basal ganglia and SMA (Niddam DM et al 2009). In clinical muscle pain, peripheral and central sensitisation act concomitantly to induce spontaneous pain, hyperalgesia or refferred pain (Niddam DM 2009), thus studies on experimental and clinical muscle pain and its cortical representation using different electro-/magnetoencelographic methods are required. 


Erisela Qerama, MD, PhD, Associate Professor,