Short summary

The purpose of this study is to investigate the phenomena that stimulation with one kind of pain can inhibit the perception of stimulation with another kind of pain, also known as Conditioned Pain Modulation (CPM). 

Our hypothesis is that CPM can be affected when you are suffering from chronic neuropathic pain. We want to investigate this by comparing different test paradigms in patients and healthy subjects. 

Rationale

Endogenous modulation of pain is of great significance for our perception of pain. This perception can both be suppressed and enhanced. The endogenous pain modulation is a system involving activity in the neuronal network represented in the brainstem, spinal cord and brain. The activity in the system is regulated by different neurotransmitters, including endogenous opioids, monoamines (noradrenaline, serotonin, dopamine) and gamma-amino-butyrat (GABA). The anatomy and physiology of this system has primarily been uncovered by animal experiments. Modulation of pain through this system is often called ''diffuse noxious inhibitory control (DNIC)'' and different test paradigms, which test the effect of the system, have been suggested and is called conditioned pain modulation (CPM). 

The suggested test paradigms for CPM generally comprises two painful stimuli, one stimulus inhibiting the perception of pain from the other stimulus. Several test paradigms have been used, however a generally accepted paradigm which triggers pain modulation reliably and reproducibly is yet to be found. Furthermore, it is unclear how great a change in pain perception which is necessary for concluding whether or not a subject has a well-functioning DNIC-system. 

CPM has been found less effective in several idiopathic pain conditions compared to healthy subjects. No valid data has been found for patients with chronic neuropathic pain in regards to the function of CPM. Degeneration of parts of the endogenous pain modulation system has been suggested as one of many mechanisms for neuropathic pain.  

The purpose of this project is to investigate different CPM test paradigms in healthy subjects and in patients with peripheral neuropathic pain in order to document presence and stability of this phenomenon. Our goal is to achieve a test paradigm that is both sensitive and specific, so it can be used in clinical trials and clinical practice as a predictor of the effect of antidepressants for treatment of peripheral neuropathic pain. 

Our hypothesis is that different test paradigms for determining CPM vary in regards to sensitivity and specificity, and that poor or lacking CPM is more prevalent in patients with peripheral neuropathic pain compared to healthy subjects. 

Description of the cohort

The cohort consists of two groups, patients with peripheral neuropathic pain and healthy subjects. All subjects are between the age of 30 and 80 and must have no other known pain condition, neurological disorder or serious medical ilness. Patients must have an average pain intensity of at least 4 on a numeric scale from 0 to 10 (NRS). 

Data and biological material

Measurements from the test and demographic data. 

Collaborating researchers and departments

Department of Neurology, Odense University Hospital

• Professor, Søren Sindrup
• MD, Melissa Kreutzfeldt
• MD, Jakob Holbech

Danish Pain Research Center and Department of Neurology, Aarhus University Hospital

• Professor, Nanna B. Finnerup
• MD, Malin Carmland