UVM Theses and Dissertations
Format:
Print
Author:
Corey, Sarah
Dept./Program:
Neuroscience Graduate Program
Year:
2011
Degree:
Ph. D.
Abstract:
Non-specific, chronic low back pain is a condition that affects individuals worldwide. Although there have been many research investigations on the topic of chronic low back pain, the underlying cause has yet to be determined, and an effective treatment has not been established. Interestingly, body-based (manual and movement) therapies using tissue stretch (physical therapy, yoga, massage) have been shown in some clinical research studies to reduce lumbar pain and/or inflammation. Although the mechanism of action of these treatments remains mostly unknown, therapeutically relevant tissue stretch applied in in vitro studies has been shown to reduce inflammatory mediators.
The overall hypothesis of this dissertation is that the nonspecialized connective tissues of the low back could playa role in both the persistence of low back pain and as a target of body-based therapies. Aims of this dissertation project include 1) characterization of the innervation of the nonspecialized connective tissues in the low back of a rodent and 2) evaluation of behavioral and lumbar tissue changes inresponse to in vivo stretching of the back in a novel connective tissue inflammation model. The long term goal of this work is to better understand the role of connective tissues in the development of persistent low back pain and how body-based therapies can ameliorate symptoms.
Evidence from the literature demonstrates that innervated connective tissues throughout the body are involved in the persistence of pain. To better understand the role of connective tissues in the pathophysiology of low back pain we had to first establish its normal sensory innervation. We hypothesized that sensory nerve fiber terminals were present within the connective tissues of the low back. Using retrograde tracing, immunohistochemical, and confocal microscopy methods, we identified and quantified the calcitonin gene-related peptide expression of the nonspecialized connective tissues in the low back of the rodent.
We then hypothesized that application of in vivo tissue stretch to a model of nonspecialized connective tissue inflammation would decrease pain and inflammation. First, we developed a model of inflammation of the nonspecialized connective tissues of the low back in a rodent. Next, we applied an in vivo tissue stretch intervention and measured changes in mechanical sensitivity with Von Frey filaments, gait measurements, an open field test, ultrasound and immunohistochemistry. Overall, in rodents with inflamed lumbar tissue we found that stretching of the back in vivo twice a day for two weeks decreased responsiveness to mechanical stimuli of the low back, improved overall movement, and decreased macrophage expression in the connective tissues of the low back.
This dissertation project represents a first step toward investigating the interface between the nervous system and local inflammatory responses in the nonspecialized connective tissues of the low back. These studies highlight the importance of gaining a greater understanding of the role of connective tissue in the pathophysiology and the treatment of low back pain.
The overall hypothesis of this dissertation is that the nonspecialized connective tissues of the low back could playa role in both the persistence of low back pain and as a target of body-based therapies. Aims of this dissertation project include 1) characterization of the innervation of the nonspecialized connective tissues in the low back of a rodent and 2) evaluation of behavioral and lumbar tissue changes inresponse to in vivo stretching of the back in a novel connective tissue inflammation model. The long term goal of this work is to better understand the role of connective tissues in the development of persistent low back pain and how body-based therapies can ameliorate symptoms.
Evidence from the literature demonstrates that innervated connective tissues throughout the body are involved in the persistence of pain. To better understand the role of connective tissues in the pathophysiology of low back pain we had to first establish its normal sensory innervation. We hypothesized that sensory nerve fiber terminals were present within the connective tissues of the low back. Using retrograde tracing, immunohistochemical, and confocal microscopy methods, we identified and quantified the calcitonin gene-related peptide expression of the nonspecialized connective tissues in the low back of the rodent.
We then hypothesized that application of in vivo tissue stretch to a model of nonspecialized connective tissue inflammation would decrease pain and inflammation. First, we developed a model of inflammation of the nonspecialized connective tissues of the low back in a rodent. Next, we applied an in vivo tissue stretch intervention and measured changes in mechanical sensitivity with Von Frey filaments, gait measurements, an open field test, ultrasound and immunohistochemistry. Overall, in rodents with inflamed lumbar tissue we found that stretching of the back in vivo twice a day for two weeks decreased responsiveness to mechanical stimuli of the low back, improved overall movement, and decreased macrophage expression in the connective tissues of the low back.
This dissertation project represents a first step toward investigating the interface between the nervous system and local inflammatory responses in the nonspecialized connective tissues of the low back. These studies highlight the importance of gaining a greater understanding of the role of connective tissue in the pathophysiology and the treatment of low back pain.