Sensorimotor Function in Progressive Multiple Sclerosis

Background: A sensitive test reflecting subtle sensorimotor changes throughout disease progression independent of mobility impairment is currently lacking in progressive multiple sclerosis. Objectives: We examined non-ambulatory measures of upper and lower extremity sensorimotor function that may reveal differences between relapsing–remitting and progressive forms of multiple sclerosis. Methods: Cutaneous sensitivity, proprioception, central motor function and mobility were assessed in 32 relapsing–remitting and 31 progressive multiple sclerosis patients and 30 non-multiple sclerosis controls. Results: Cutaneous sensation differed between relapsing–remitting and progressive multiple sclerosis at the foot and to a lesser extent the hand. Proprioception function in the upper but not the lower extremity differed between relapsing–remitting and progressive multiple sclerosis, but was different for both upper and lower extremities between multiple sclerosis patients and non-multiple sclerosis controls. Foot-tap but not hand-tap speed was slower in progressive compared to relapsing–remitting multiple sclerosis, suggestive of greater central motor function impairment in the lower extremity in progressive multiple sclerosis. In addition, the non-ambulatory sensorimotor measures were more sensitive in detecting differences between relapsing–remitting and progressive multiple sclerosis than mobility assessed with the 25-foot walk test. Conclusion: This study provides novel information about changes in sensorimotor function in progressive compared with relapsing–remitting forms of multiple sclerosis, and in particular the importance of assessing both upper and lower extremity function. Importantly, our findings showed loss of proprioceptive function in multiple sclerosis but also in progressive compared to relapsing–remitting multiple sclerosis

History of forest insect investigations in British Columbia III. The Vernon Laboratory and federal entomology in British Columbia

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Activating germline mutations in STAT3 cause early-onset multi-organ autoimmune disease.

Monogenic causes of autoimmunity provide key insights into the complex regulation of the immune system. We report a new monogenic cause of autoimmunity resulting from de novo germline activating STAT3 mutations in five individuals with a spectrum of early-onset autoimmune disease, including type 1 diabetes. These findings emphasize the critical role of STAT3 in autoimmune disease and contrast with the germline inactivating STAT3 mutations that result in hyper IgE syndrome.This article is freely available via PubMed Central. Click on the 'Additional Link' above to access the full-text