Human Studies

Neuropathic pain (NP) remains a major debilitating condition affecting more than 26% of breast cancer survivors worldwide. NP is diagnosed using a validated 10-items Douleur Neuropathique – 4 screening questionnaire which is administered 3 months after surgery and requires patient-doctor interaction. To develop an effective prognosis model admissible soon after surgery, without the need for patient-doctor interaction, we sought to [1] identify specific pain characteristics that can help determine which patients may be susceptible to NP after BC surgery, and 2) assess the utility of machine learning models developed in objective [1] as a knowledge discovery tool for downstream analysis.

PTSD symptoms and other negative psychosocial factors have been implicated in the transition from acute to persistent pain. Women (N = 375) who presented to an inner-city Emergency Department (ED) with complaints of acute pain were followed for 3 months. They completed a comprehensive battery of questionnaires at an initial visit, and provided ratings of pain intensity at the site of pain presented in the ED during 3 monthly phone calls. Latent class growth analyses were used to detect possible trajectories of change in pain intensity from initial visit to 3 months later. A 3-trajectory solution was found which identified three groups of participants. One group (early recovery; n = 93) had recovered to virtually no pain by the initial visit, whereas a second group (delayed recovery; n = 120) recovered to no pain only after one month. A third group (no recovery; n = 162) still reported elevated pain at 3-months post ED visit. The no recovery group reported significantly greater PTSD symptoms, anger and sleep disturbance, as well as lower social support, at initial visit than both the early recovery and delayed recovery groups. Results suggest that women with high levels of PTSD symptoms, anger, sleep disturbance and low social support who experience an acute pain episode serious enough to prompt an ED visit may maintain elevated pain at this pain site for at least three months. Such an array of factors may place women at increased risk of developing persistent pain following acute pain.

Burning mouth syndrome (BMS) is a chronic pain disorder affecting the oral cavity. Previous work has shown promising analgesic results of bodily illusions in other chronic pain conditions. The aim of this proof-of-concept, pilot study was to investigate whether bodily illusions reduce pain in BMS patients.

To describe the core elements of a Whole Health Primary Care Pain Education and Opioid Monitoring Program (PC-POP) and examine its effectiveness at increasing adherence to six of the Veteran Affairs/Department of Defense (VA/DoD) recommended guidelines for long-term opioid therapy (LOT) among chronic noncancer patients seen in primary care (i.e., urine drug screens [UDS], prescription drug monitoring program [PDMP] queries, informed consent, naloxone education/prescriptions, morphine equivalent daily dose [MEDD], and referrals to nonpharmacological pain interventions).

We previously reported that neuropathic pain was associated with smaller posterior cingulate cortical (PCC) volumes, suggesting that a smaller/dysfunctional PCC may contribute to development of pain via impaired mind wandering. A gap in our previous report was lack of evidence for a mechanism for the genesis of PCC atrophy in HIV peripheral neuropathy. Here we investigate if volumetric differences in the subcortex for those with neuropathic paresthesia may contribute to smaller PCC volumes, potentially through deafferentation of ascending white matter tracts resulting from peripheral nerve damage in HIV neuropathy. Since neuropathic pain and paresthesia are highly correlated, statistical decomposition was used to separate pain and paresthesia symptoms to determine which regions of brain atrophy are associated with both pain and paresthesia and which are associated separately with pain or paresthesia. HIV+ individuals (N = 233) with and without paresthesia in a multisite study underwent structural brain magnetic resonance imaging. Voxel-based morphometry and a segmentation/registration tool were used to investigate regional brain volume changes associated with paresthesia. Analysis of decomposed variables found that smaller midbrain and thalamus volumes were associated with paresthesia rather than pain. However, atrophy in the PCC was related to both pain and paresthesia. Peak thalamic atrophy (p = 0.004; MNI x = - 14, y = - 24, z = - 2) for more severe paresthesia was in a region with reciprocal connections with the PCC. This provides initial evidence that smaller PCC volumes in HIV peripheral neuropathy are related to ascending white matter deafferentation caused by small fiber damage observed in HIV peripheral neuropathy.