Research

Interactions between peripheral and central pain networks

There are no clear biological and/or experiential factors that predict the development of pain after SCI. These studies assess whether aberrant noxious stimulation, biological processes such as stress, anxiety and inflammatory responses at the time of SCI can influence the onset and expression of long-term pain hypersensitivity after SCI.

Plasticity of ‘touch’ afferent populations

Only few studies have assessed potential mechanisms of at-level allodynia after SCI. Two sub-populations of low threshold mechanoreceptors (LTMRs) known as C- and Ad-LTMRs are found in hairy skin and normally encode distinct modalities of touch. These studies investigate whether these C- and Ad-LTMRs are transformed into pain-encoding afferents after SCI. The studies are undertaken in transgenic mice that allow us to selectively target these individual populations of primary afferents.  These studies will also examine whether functional and/or anatomical plasticity of C- and Ad-LTMRs is a potential mechanical of at-level allodynia.

Interactions between autonomic dysfunction and neuropathic pain

Like pain, autonomic dysfunction is a major occurrence after SCI and dysfunction in autonomic signaling may significantly associate with sensory dysfunction after SCI. We undertake studies that use remote monitoring of heart rate (HR) and respiratory rate (RR) as measurable indices of sympathetic arousal that may also be indicative of pain after SCI.

BDNF-TrkB plasticity after SCI

Research examining the role BDNF plays in spinal nociception and pain overwhelmingly suggests that BDNF promotes pronociceptive effects. However, it is still unclear whether BDNF similarly contributes to neuropathic pain after SCI, although it has been shown to promote adaptive plasticity. Studies are done to examine the role peripheral and central BDNF-TrkB signaling plays in pain hypersensitivity after SCI. 

Cellular mediators of neuropathic pain after SCI

These studies focus on temporal and spatial expression patterns of several cytokines and kinases that are involved in inflammatory and neuropathic pain. These include TNFa, IL-6, ERK and pERK.