Contributions
Abstract: P1012
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - MS symptoms
Background: About a third of patients with multiple sclerosis (MS) suffer from chronic and excruciating central neuropathic pain (CNP). The mechanism of CNP in MS is not clear.
Objective: To study the sensory profile of MS patients with CNP and shed light on its pathophysiology.
Methods: 35 MS patients with CNP (age 45.6±13), 38 MS patients with musculoskeletal pain (53.1±11) 32 pain-free MS patients (38.7±9) and 34 healthy controls (43.7±12) underwent sensory pain evaluation by measurements of temperature and touch thresholds, temporal summation of pain (TSP) and Offset Analgesia (OA), paradigms assessing pain enhancement and pain inhibition of tonic noxious stimuli, respectively. Patients also completed the McGill pain questionnaire. A sample of MS patients with and without CNP were analyzed for volume and anatomical localization of brain MS lesions, using quantitative matlab-based software for MS lesions, and an anatomical brain MRI atlas (www.headneckbrainspine.com).
Results: MS patients with CNP did not differ in Expanded Disability Status Scale from MS patients with musculoskeletal pain and pain-free patients yet they were younger and had shorter disease duration than those with musculoskeletal pain. Whereas touch thresholds were similar across groups, the CNP group had higher cold (p< 0.01) and heat-pain thresholds (p=0.05) than the musculoskeletal pain group and both groups had higher warm and cold thresholds compared to pain free patients and healthy controls (p< 0.01). Among the CNP group, painful body regions had higher temperature thresholds than pain-free regions. In addition, TSP was increased compared to the other groups (p< 0.05). MRI analysis revealed increased prevalence and volume of MS lesions in the brain stem (p< 0.05) and thalamus (p< 0.01) among the CNP group, that correlated with CNP severity (r=0.42-0.62).
Conclusions: CNP in MS is associated with damage to the spinothalamic-thalamocortical pathways, enhanced pain excitability and damage to structures involved in pain processing and pain modulation.
Disclosure: The study was supported by a grant from the National MS Society
Abstract: P1012
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - MS symptoms
Background: About a third of patients with multiple sclerosis (MS) suffer from chronic and excruciating central neuropathic pain (CNP). The mechanism of CNP in MS is not clear.
Objective: To study the sensory profile of MS patients with CNP and shed light on its pathophysiology.
Methods: 35 MS patients with CNP (age 45.6±13), 38 MS patients with musculoskeletal pain (53.1±11) 32 pain-free MS patients (38.7±9) and 34 healthy controls (43.7±12) underwent sensory pain evaluation by measurements of temperature and touch thresholds, temporal summation of pain (TSP) and Offset Analgesia (OA), paradigms assessing pain enhancement and pain inhibition of tonic noxious stimuli, respectively. Patients also completed the McGill pain questionnaire. A sample of MS patients with and without CNP were analyzed for volume and anatomical localization of brain MS lesions, using quantitative matlab-based software for MS lesions, and an anatomical brain MRI atlas (www.headneckbrainspine.com).
Results: MS patients with CNP did not differ in Expanded Disability Status Scale from MS patients with musculoskeletal pain and pain-free patients yet they were younger and had shorter disease duration than those with musculoskeletal pain. Whereas touch thresholds were similar across groups, the CNP group had higher cold (p< 0.01) and heat-pain thresholds (p=0.05) than the musculoskeletal pain group and both groups had higher warm and cold thresholds compared to pain free patients and healthy controls (p< 0.01). Among the CNP group, painful body regions had higher temperature thresholds than pain-free regions. In addition, TSP was increased compared to the other groups (p< 0.05). MRI analysis revealed increased prevalence and volume of MS lesions in the brain stem (p< 0.05) and thalamus (p< 0.01) among the CNP group, that correlated with CNP severity (r=0.42-0.62).
Conclusions: CNP in MS is associated with damage to the spinothalamic-thalamocortical pathways, enhanced pain excitability and damage to structures involved in pain processing and pain modulation.
Disclosure: The study was supported by a grant from the National MS Society