Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, PC301

Poster Communications

Possible nerve inflammation in patients with diffuse chronic pain syndromes

A. Dilley1, J. Greening1

1. Clinical and Laboratory Investigation, Brighton and Sussex Medical School, Falmer, Brighton, United Kingdom.


Laboratory studies suggest that inflammation of peripheral nerve trunks in the absence of gross pathology may contribute towards symptoms of chronic pain (Bove et al., 2003; Dilley et al., 2005). In these studies, inflamed nociceptive axons develop ongoing activity and axonal mechanical sensitivity. On T2-weighted magnetic resonance imaging (MRI), nerve signal intensity is increased in inflamed peripheral nerves (Filler et al., 2004; Stanisz et al., 2004). Therefore, this study has used 1.5 Tesla MRI to examine nerve signal strength in the upper limb peripheral nerves of four patients with diffuse upper limb pain. Four female patients who presented with fibromyalgia or non-specific arm pain (NSAP) without signs of tissue injury or neurological deficit and six healthy control subjects were recruited. Patients were examined prior to imaging for signs of nerve trunk mechanosensitivity. Transverse images of the median and ulnar nerve were obtained at the wrist using T1-weighted and T2-weighted proton density turbo-spin echo sequences. Coronal images of the brachial plexus were also obtained in the neck of three patients and three controls using a T1-weighted and a T2-weighted Short Tau Inversion Recovery sequence with flow suppression. On the T2-weighted sequences, mean grey scale values were determined from regions of interest drawn over the median/ulnar nerves at the proximal carpal tunnel and distal forearm, and the C6-8 roots of the brachial plexus. Signal intensity ratios were calculated from adjacent soft tissue. In the control group, there was no difference in median or ulnar nerve signal intensity ratio at the proximal carpal tunnel or distal forearm and therefore the data was pooled (median nerve = 1.21 ± 0.07 SEM; ulnar nerve = 1.40 ± 0.11). There was a significant increase in the signal intensity ratio at the proximal carpal tunnel in the patient group compared to controls for both the median (2.26 ± 0.19 SEM) and ulnar nerve (2.78 ± 0.33 SEM; p <0.05 unpaired t test). In the distal forearm, the signal intensity ratio for both the median (1.63 ± 0.36) and ulnar nerve (1.95 ± 0.34 SEM) returned to control levels (p>0.06). Compared to the controls, there was a 55% increase in signal intensity ratio in the brachial plexus on the most symptomatic side in one NSAP patient. Using validated clinical tests (Kleinrensink et al., 2000), all four patients showed signs of nerve trunk mechanosensitivity to pressure and stretch. A possible cause of the observed nerve signal hyper-intensity in the patients is inflammation, although this cannot be confirmed without histological examination. However, MRI and clinical data from this pilot study suggests that the peripheral nervous system may be involved in the pathogenesis of these diffuse chronic pain conditions.

Where applicable, experiments conform with Society ethical requirements