Pain influences somatosensory perception : an experimental and clinical study

Abstract

The underlying mechanisms maintaining long-term pain localised to musculoskeletal structures and joints are not infrequently unknown. In routine clinical work with such patients insufficient attention has been paid to phenomena indicating altered excitability of the central nervous system (CNS). In subgroups of patients with pain localised to musculoskeletal structures spread of pain outside the primarily painful area (including referred pain) and sometimes even generalisation of pain in conjunction with signs of altered somatosensory function in painful as well as non-painful areas have been reported, which indicate excitability changes of the CNS.

Several mechanisms such as central sensitisation and/or altered function of endogenous systems modulating somatosensory processing could account for increased pain intensity, spread of pain outside the primary pain focus as well as changes in sensibility at examination. The general purpose of the present thesis, studying experimental and clinical pain, was to examine the influence of ongoing or recurrent pain on somatosensory processing from the local pain area, an area of referred pain as well as from a pain-free area. In addition, the potential influence of a temporary increase or decrease in spontaneous pain intensity on somatosensory function was studied as well as the function of an endogenous pain modulatory system, i.e., diffuse noxious inhibitory controls (DNIC). Pressure pain sensitivity, low threshold mechanoreceptive function and thermal sensitivity, including thermal pain and suprathreshold heat pain were assessed in the area of experimentally induced referred pain in healthy subjects, in the local pain area and the area of referred pain in patients with subacute/chronic unilateral lateral epicondylalgia (ULE) and in patients with trapezius myalgia (TM) as well as in the area overlying a painful and inflamed joint in patients with rheumatoid arthritis (RA) with two different disease durations.

To study if patients with TM and patients with RA demonstrated a generalised increased pain sensitivity and to study DNIC-related mechanisms, somatosensory function was examined at a pain-free site, i.e., the thigh before, during and following heterotopic noxious conditioning stimulation (HNCS) (tourniquet test and cold-pressor test, respectively). No significant difference in sensibility was found at baseline in the local pain area in patients with ULE or in patients with M In the area of referred pain, allodynia to heat was found in patients with ULE, whereas patients with TM exhibited an increased sensitivity to pressure pain compared to contralaterally as well as to the corresponding area in controls in conjunction with a bilaterally decreased sensitivity to light touch compared to controls.

Experimentally induced pain in healthy subjects and increased pain intensity in patients with ULE resulted in hypoaesthesia to light touch in the area of referred pain. Allodynia to pressure was found over the joint in both RA groups, in conjunction with hypoaesthesia to light touch and hyperaesthesia to innocuous cold in RA with longer disease duration. At the thigh, allodynia to pressure was found in patients with TM and in RA patients with longer disease duration. During HNCS, the sensitivity to pressure pain decreased in patients with TM and in patients with RA as well as in their respective controls alike. In all study groups, hypoaesthesia to light touch was demonstrated in the area of referred pain during ongoing/stimulus- evoked pain, suggesting altered central processing of somatosensory input from the area of referred pain. The response to HNCS was similar in patients with TM, RA and their respective controls, indicating preserved function of DNIC-related mechanisms.

Allodynia to pressure in a painfree area suggests a disorder of some other inhibitory system and/or overactivity in pain facilitatory pathways in patients with TM and in RA patients with longer disease duration. Whether altered central somatosensory processing may indicate a predisposition for further spread of pain is at present unclear. To increase the knowledge about CNS plasticity in pain conditions localised to musculoskeletal structures and joints is an important research task and may improve the diagnostic work-up and treatment for the future. It is unlikely that a continuous main focus on the periphery will be of benefit to the numerous patients suffering from long-term pain.