Offset Analgesia: Novel Pain Modulation Test in Chronic Orofacial Pain

Objectives: Offset analgesia (OA) is an endogenous pain temporal filtering mechanism characterized by a disproportionate decrease in perceived pain intensity following a small decrease in noxious stimulation. Reduced OA responses in chronic pain patients have been reported, suggesting endogenous pain modulation (EPM) dysfunction. Persistent dentoalveolar pain (PDAP) and temporomandibular disorders (TMD) are two frequently comorbid chronic orofacial pain (OFP) conditions that manifest over dentoalveolar tissues and TMJ and/or masticatory muscles respectively. To date OA has not been assessed in chronic OFP. In order to better understand EPM in this population, we measured OA responses in OFP patients (PDAP and/or TMD) and pain-free controls.
Methods: Five female OFP patients and four age/sex-matched pain-free controls underwent OA testing and completed Graded Chronic Pain Scale (GCPS) questionnaire to evaluate pain-related disability. OA was determined by applying noxious heat stimulus using a 30x30mm thermal probe to volar forearm while real-time pain ratings were collected using electronic visual analog scale (eVAS) with anchors “no pain” (0) and “most intense pain imaginable” (100). Pre-determined individualized test temperature (TT) evoked pain ratings ≥30/100 but ≤50/100. Three 30s OA trials were done in a three-step fashion, following 10s baseline(32°C): 5s(TT), 5s(TT+1°C), 20s(TT). OA response was determined as highest pain rating (peak-eVAS) minus lowest divided by peak-eVAS*100.
Results: Participants’ characteristics are described in Table 1. Mean peak-eVAS for OFP patients was 62.5±27.8(SD), while for controls was 43.0±24.1. Mean pain rating reduction during noxious heat temperature challenge for OFP patients was 73.3±35.5%, while controls experienced 96.1±5.7% decrease in pain rating.
Conclusions: This is the first study to assess OA in chronic OFP patients. These results suggest that OA is a measurable EPM mechanism in OFP with regards to pain temporal filtering. They also suggest a reduced pain inhibitory modulation capacity in OFP patients relative to painfree controls.