Reduced basal ganglia μ-opioid receptor availability in trigeminal neuropathic pain: A pilot study
1 Headache & Orofacial Pain Effort (H.O.P.E.), Department of Biologic and Materials Sciences and MCOHR, School of Dentistry, University of Michigan, Michigan, Ann Arbor, MI 48109-5720, USA
2 Translational Neuroimaging Laboratory, Molecular and Behavioral Neuroscience Institute (MBNI), University of Michigan, Michigan, Ann Arbor, MI 48109-5720, USA
3 Faculdade de Medicina, Universidade Federal do Rio de Janeiro, Federal do Rio de Janeiro, Brazil
4 Faculdade de Odontologia, Universidade Federal do Rio de Janeiro, Federal do Rio de Janeiro, Brazil
5 UM3D Lab, Digital Media Commons/MLibrary, University of Michigan, Michigan, USA
Molecular Pain 2012, 8:74 doi:10.1186/1744-8069-8-74Published: 24 September 2012
Although neuroimaging techniques have provided insights into the function of brain regions involved in Trigeminal Neuropathic Pain (TNP) in humans, there is little understanding of the molecular mechanisms affected during the course of this disorder. Understanding these processes is crucial to determine the systems involved in the development and persistence of TNP.
In this study, we examined the regional μ-opioid receptor (μOR) availability in vivo (non-displaceable binding potential BPND) of TNP patients with positron emission tomography (PET) using the μOR selective radioligand [11C]carfentanil. Four TNP patients and eight gender and age-matched healthy controls were examined with PET. Patients with TNP showed reduced μOR BPND in the left nucleus accumbens (NAc), an area known to be involved in pain modulation and reward/aversive behaviors. In addition, the μOR BPND in the NAc was negatively correlated with the McGill sensory and total pain ratings in the TNP patients.
Our findings give preliminary evidence that the clinical pain in TNP patients can be related to alterations in the endogenous μ-opioid system, rather than only to the peripheral pathology. The decreased availability of μORs found in TNP patients, and its inverse relationship to clinical pain levels, provide insights into the central mechanisms related to this condition. The results also expand our understanding about the impact of chronic pain on the limbic system.