Neuropathic pain: human: Cerebral representation of mechanical allodynia in neuropathic pain patients during ongoing background pain

Abstract

Using fMRI (functional Magnetic Resonance Imaging) we studied the cerebral representation of allodynic pain in patients with neuropathic pain. By altering the individual pain medication we were able to investigate the impacts of altered pain intensity on the neurophysiological response to allodynic pain in neuropathic pain patients. Prior to imaging, patients were thoroughly characterised using Quantitative Sensory Testing (QST), as well as depression and anxiety questionnaires. Subjects underwent a first imaging session in which their typical pain, being either dynamic or punctuate allodynia, was provoked using a soft brush and von Frey filaments, respectively. Pain ratings were obtained for the ongoing background pain as well as the provoked pain after each functional scan. Patients were imaged a second time using the same experimental protocol after having either increased or decreased their pain medication. FMR Imaging was carried out at 1.5 Tesla using a standard gradient echo EPI sequence. Image analysis was done using FEAT (FMRIB Expert Analysis Tool). Patients with mechanical allodynia presented typically accompanying cold allodynia or aggravation of their ongoing pain by cold as revealed by QST. Alteration of the analgesic medication led either to a perceived decrease or increase in pain intensity of the ongoing background pain whereas the allodynic pain remained unchanged in the majority of the cases. Preliminary data analysis shows that the fMRI signal during allodynic pain seems to be attenuated when a high level of background pain is present despite the behavioural report not changing. We are currently analysing which brain regions show this characteristic because these could be regions which are not particularly involved in the processing of pain intensity perception but process other characteristics of pain. Alternatively the BOLD fMRI response might have reached saturation because of the high ongoing pain. Using fMRI (functional Magnetic Resonance Imaging) we studied the cerebral representation of allodynic pain in patients with neuropathic pain. By altering the individual pain medication we were able to investigate the impacts of altered pain intensity on the neurophysiological response to allodynic pain in neuropathic pain patients. Prior to imaging, patients were thoroughly characterised using Quantitative Sensory Testing (QST), as well as depression and anxiety questionnaires. Subjects underwent a first imaging session in which their typical pain, being either dynamic or punctuate allodynia, was provoked using a soft brush and von Frey filaments, respectively. Pain ratings were obtained for the ongoing background pain as well as the provoked pain after each functional scan. Patients were imaged a second time using the same experimental protocol after having either increased or decreased their pain medication. FMR Imaging was carried out at 1.5 Tesla using a standard gradient echo EPI sequence. Image analysis was done using FEAT (FMRIB Expert Analysis Tool). Patients with mechanical allodynia presented typically accompanying cold allodynia or aggravation of their ongoing pain by cold as revealed by QST. Alteration of the analgesic medication led either to a perceived decrease or increase in pain intensity of the ongoing background pain whereas the allodynic pain remained unchanged in the majority of the cases. Preliminary data analysis shows that the fMRI signal during allodynic pain seems to be attenuated when a high level of background pain is present despite the behavioural report not changing. We are currently analysing which brain regions show this characteristic because these could be regions which are not particularly involved in the processing of pain intensity perception but process other characteristics of pain. Alternatively the BOLD fMRI response might have reached saturation because of the high ongoing pain.