Past Students

Sarah Dominguez Pic

Sarah Dominguez
Grad Student, Department of Anatomy and Cell Biology

Project Title: Explanation of Pain and Central Sensitization Can Improve Symptoms and Restore Function in Chronic Pelvic Pain

Research Mentor: Wen Liu, PhD
Co-Mentor: TBA

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.


Natalia Loskutova Pic

Natalia Loskutova, MD
Grad Student, Department of Physical Therapy and Rehabilitation Sciences

Project Title: Brain atrophy as a mechanism of bone loss in Alzheimer's disease

Clinical Mentor: Jeffrey Burns
Research Mentor: John Stanford

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.

 

William Messamore Pic

William Messamore
Grad Student, Department of Molecular and Integrative Physiology

Project Title: Cortical Control of Hindlimb Muscles

Research Mentor: Paul Cheney
Co-Mentor: Jules Nazzaro

Description: Cortical organization relates directly to aspects of movement disorders, making understanding normal cortical organization and control of movement a topic of clinical and rehabilitative importance. The cortical control of the arm and hand in primates has been studied extensively; however, there have been only a handful of studies focusing on the control of the lower limb. Recent research in our lab has elucidated the basic features of the M1 cortical hindlimb map along with the strength and nature of the synaptic linkages. I plan to determine the characteristics of M1 cortical output effects on ipsilateral hindlimb muscles, in comparison to effects on the contralateral side. In addition I plan on using electrophysiological recording techniques to determine the organization of output effects from single M1 cortical neurons to hindlimb muscles including fast and slow ankle extensor muscles. The data collected from these experiments will form the foundation for interpreting data from future experiments designed to investigate recovery of lower extremity function following brain injury.

 
Kristin Russell Picture

Kristin Russell
Grad Student, Department of Pharmacology, Toxicology, & Therapeutics

Project Title: Functional and biochemical effects of brain fatty acid content on recovery from juvenile TBI

Research Mentor: Beth Levant
Co-Mentor: Russell Swerdlow

Description: Children under 5 years of age are at high risk for sustaining traumatic brain injuries (TBI) and tend to have poorer outcomes despite the greater neuroplasticity in children. Omega-3 polyunsaturated fatty acids (PUFA), a major component of neural membranes, accumulate in the brain during late gestation and early childhood. Low dietary content of these essential fatty acids results in decreased omega-3 PUFA accumulation in the developing brain. Omega-3 PUFAs have multiple neuroprotective and anti-inflammatory activities, thus low dietary omega-3 PUFA content may put children at risk for poorer outcomes after TBI. Therefore, my research focuses on how the functional and biochemical outcomes of juvenile TBI are influenced by the fatty acid composition of the brain. Additionally, I am researching the possibility of using omega-3 fatty acids as a therapeutic after TBI to decrease inflammation and apoptosis and improve outcomes. Knowing the full relationship between omega-3 PUFAs and brain injuries could lead to novel therapeutic strategies to improve the outcomes of TBI.

 

 Jessica Witherspoon Picture

Jessica Witherspoon
Grad Student, Physical Therapy and Rehabilitation Service

Project Title: Glenohumeral Joint Laxity: A Neural Contribution

Research Mentor: Terence McIff
Co-Mentor: Irina Smirnova

Description: The purpose of this study is to assess neural density and collagen composition of the glenoid labrum and capsule as they relate to anterior and posterior shoulder laxity. When reduced glenohumeral joint (GHJ) stiffness occurs, GHJ laxity increases resulting in shoulder instability, which can progress to subluxation and dislocation. According to research, the occurrence and reoccurrence of subluxations and dislocations become career ending for the workforce as well as for athletes. Rehabilitation and surgery protocols have been established to address instability related to GHJ dynamic stabilizers (musculature); however, there is a 14-94% reoccurrence post rehabilitation and/or surgery. This study will investigate the properties of the glenoid labrum and capsule, which are static stabilizers, as they relate to GHJ laxity and stiffness. It is hypothesized that the shoulders with a larger laxity zone and less tissue stiffness will present with lower neural densities as well as lower type I (providing tensile strength) to type III (sustaining elasticity) collagen ratios. The specific aims of this study are: 1) to define anterior and posterior GHJ instability based on the analysis of stiffness and zone of laxity in cadaveric models without muscular involvement; 2) to identify neural density in the labrum and capsule and determine whether it correlates with GHJ laxity; and 3) to determine whether the ratio of type I to type III collagen in the glenoid labrum and capsule correlates with GHJ stiffness. The clinical load and shift stability test will be performed on fifteen cadaveric shoulder pairs in the sagittal plane by a physical therapist and the Instron material testing machine to establish the zone of laxity and stiffness. Samples will then be collected from the anterior, anteroinferior, posterior and posteroinferior aspects of the labrum and capsule to evaluate the neural density of pacini and ruffini corpuscles as well as golgi tendon organs. In addition, the type I to type III collagen ratio will be determined. From these data, labral and capsular proprioceptive properties and stiffness will be correlated with available anterior and posterior joint movement for each shoulder. Determining the neural density, using immunofluorescence, will allow recognition of proprioceptive contribution to GHJ stability. Evaluating type I to type III collagen protein ratio, using enzyme-linked immunoassay (ELISA) will implicate the extent of tensile strength available to limit joint movement. We expect the shoulders with larger laxity zones and less stiffness will exhibit reduced neural density and type I to type III collagen ratio. Due to the high reoccurrence rate and career ending consequences of shoulder instability, it is vital to understand all the components that maintain shoulder stability, especially neural signaling that may be affected by changes in neural density . This study will aide in the development of specific treatment approaches for preventing or treating shoulder instability.

Last modified: Jan 30, 2014
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