22014 Brunet | Bee ie” Bin SecrioN eorroRs Chief Editor Lorimer Moseley Pho University af Sout sala News eRe Brain Imaging Katja Wiech Pho University of Oxiore, UK Clinical applications Tasha Stanton PhO University of Sa. Australa& lence Research Clinical trials & systematic reviews Neil o‘Connell Pid Baurell Uriversty Londen, UK Multisensory processing ‘Alberto Gal University Mis Biecaca aly ce PRO Neuroimmunelogy Mick Thacker Pad scp King’s College London uk Neurophysiology of nociception Role of te halaman neuronatic pain Chronic Pain: Lost Inhibition? PART TWO In our last blog (Chronic Pain: Lost inhibition?) we talked abou e rae of the thalamus in the development maintenance of orofacial neuropathic pain. We rec that painful rgeminal neuropathic pain (PTN) is red lated with altered thalamic anatomy, function and biochemisty, which may disturb central processing and play a key role in the persistent experi pain (Henderson et al. 2013). In particular, we showed that PIN s associated with a significant reduction in thalamic Gamma-sminobutyric acid (GABA) content, ‘rey matter lood flow and ‘Ac this point in time, sn ly clear whether the revealed thalamic alterations are associated purely with © injury tsel. Because we compared individuals with PTN ta inahiduals without PTN, neuropat the injury itself was not factored out (Henderson et al. 2013). To clarify this, we recently compared brain blood emistryn 12 people win below-level ain after complete thora: flow and bio neuropat al cord Injury (SCH to 11 people with similar injuries and ne jain, and 21 age- and gender-mat healthy controls (Gustin et al. 2014), Our study revealed that she in i associated with seni acthity. More spectically the preser pain after SClis associated with significant reductions in partate (NAA), GABA con blood flow in the region of ssence of neuropathic nt changes in thalamic Biochemistry and neuronal ce of neuropathic thalamic Neacetyla thalamic reticular nucleu changes, iis neuropathic pain SCI on its owm did nat accoune for th Therefore, our findings show t d and ni that s associa ith altered thalamic biochemistry and blood perfusi the injury tse. Taken together, four research resuted in the identification of shalamic ‘olomarkers’ of neuropathic pain and we ceveloped a putative thalamoco al model for the generation of neuropathic pain (Gustin etal, 2010, Gustin et al 2011 Henderson etal, 2013, Gustin et al. 2014). This naw model implies that inhiotory brain cells (which normally block out pain) within the thalamus have reduced funcxioning in indivduals with neuropathic pain, Asa resuk, there sa reductien of bload flow in the thalamus and the amount htpihwabodyeeind.orgichreri-pir-ostntbtion-part- te! Selec Language SAVE THE DATE! 30 MARCH 2015 tes on again! The Painadelaide Steno Censor is proud to presere‘Proba best little pain meeting in the wor! Register here SAPAI seven got t’svery nn website now Come to Adelaide in November to take pain challenge, Can you tough out 8r rien There are 4 hour and 2 hour oo iets all about you pan challenge. RIDE FQR Take pain Adelaide ‘ioe on November 16th Clck onthe R Pain logo to learn move 2015 sen oS 3S a Seth Seo, Managing t BBD fom Work