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Sarah Dominguez Project Title: Explanation of Pain and Central Sensitization Can Improve Symptoms and Restore Function in Chronic Pelvic Pain Research Mentor: Wen Liu, PhD |
| Sarah has practiced as a physical therapist clinically for 9 years, 8 of these specifically in women’s health relating to pelvic dysfunction in all phases of women’s lifespan. She has recently added lymphedema and a new found interest in oncology rehabilitation, seeing more patients with chronic pain, or movement dysfunction due to the sequeulae that follow cancer treatment. The cancer population is understudied, especially female cancers of the pelvic region. Cancer treatment can lead to nerve damage, lumbar spine and hip movement dysfunction, pelvic pain syndromes, incontinence and lymphedema. Sarah has treated pelvic pain and incontinence for years, but has recently seen an increase in referrals for women who have chronic pelvic pain as a result of surgery or radiation or both. It is well established that pelvic pain can impact a person’s life, work, interpersonal relationships as well as mental health. This population is under-represented in the literature however, regarding neurological dysfunction and how this applies to our rehabilitative approach to these patient populations. Uncovering whether the painis more centrally or peripherally mediated and whether loss of spinal inhibition plays a role in post-cancerchronic pelvic pain,will be important in devising optimal rehabilitation therapies. | |
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Natalia Loskutova, MD Project Title: Brain atrophy as a mechanism of bone loss in Alzheimer's disease Clinical Mentor: Jeffrey Burns |
Description: Epidemiologic projections indicate that the prevalence of Alzheimer’s disease (AD) will increase dramatically in the coming decades due largely to the demographics of the disease and our aging population. Associated cognitive and physical decline greatly contributes to disability in older adults and places considerable burden on the health system, patients, and caregivers. Bone health is an important issue in AD given that AD patients are at higher risk than cognitively healthy adults for osteoporosis, falls, bone fractures and poor post-fracture outcomes. Bone mineral density (BMD) is a strong predictor of bone fractures and accounts for 60-70% of bone strength. The central nervous system (CNS) plays a direct role in regulating bone remodeling, primarily through the actions of the hypothalamus. Clinical, neuropathological, and neuroimaging data together suggest that the hypothalamus is affected in AD and undergoes neuronal loss, profound plaque and tangle formation and overall atrophy. However, there have been no studies to investigate whether neurodegeneration of CNS, and the hypothalamus specifically, is associated with bone loss. Thus, the overall hypothesis of my research project is that atrophy of the hypothalamus and loss of hypothalamic neurons associated with AD may be one of the mechanisms of accelerated bone loss in AD. The aim of my study is systematic evaluation of bone health in AD and exploration of underlying neural substrate of an association between BMD and neuroimaging markers of neurodegeneration (i.e. global and regional measures of brain volume) in early AD and non-demented aging. |
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