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D. Michele Basso

D. Michele Basso

· Clinical Assistant Professor of Athletic Training

Ohio State University · Respiratory Therapy

Active 1987–2025

h-index37
Citations12.1k
Papers1006 last 5y
Funding$5.5M
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About

D. Michele Basso, Ed.D, PT, is a professor at the School of Health and Rehabilitation Sciences at The Ohio State University. Her research focuses on spinal cord injury (SCI), aiming to develop rehabilitative therapies that promote recovery of mobility. She works closely with the OSU NeuroRecovery Network clinic, which uses treadmill training to facilitate recovery after chronic, incomplete SCI, examining the rate and extent of functional and quality of life improvements. Her work involves understanding the complex process of locomotor recovery, which depends on reducing inhibitory cellular cascades and promoting neural plasticity, while also addressing neuropathic pain that can interfere with recovery. Dr. Basso combines behavioral, cellular, and physiological assessments, developing new tools to quantify motor and sensory recovery in both animals and humans with SCI. She believes that optimal therapeutic outcomes depend on tailoring treatments to the severity of neuropathology, timing of intervention, and specificity of training tasks, considering cellular factors such as inflammation and matrix biology at the synapse. Her contributions include developing assessment tools and conducting systems-based research to better understand and enhance recovery processes in SCI.

Research topics

  • Psychology
  • Neuroscience
  • Medicine
  • Radiology
  • Physical medicine and rehabilitation
  • Biology
  • Internal medicine
  • Surgery
  • Pathology
  • Anatomy

Selected publications

  • Outcome measures in rodent models for spinal cord injury and their human correlates

    Experimental Neurology · 2025-01-28 · 3 citations

    review
  • Mouse Model of Spinal Cord Hypoperfusion with Immediate Paralysis Caused by Endovascular Repair of Thoracic Aortic Aneurysm

    Anesthesiology · 2023-01-30 · 2 citations

    articleOpen access

    BACKGROUND: A clinically relevant mouse model of thoracic endovascular aortic repair-induced ischemic spinal cord injury has been lacking since the procedure was first employed in 1991. The hypothesis was that ligation of mouse intercostal arteries would simulate thoracic endovascular aortic repair-induced ischemic spinal cord injury and behavioral deficit. The aim was to create a mouse model of thoracic endovascular aortic repair-induced spinal cord hypoperfusion by ligating five pairs of mouse intercostal vessels. METHODS: Mice were divided into sham (n = 53) and ligation (n = 60) groups. The procedures called for double ligation of three pairs and single ligation of two pairs of thoracic intercostal arteries in adult C57BL/6 mice. A laser Doppler probe was used in vivo on the spinal cords and intercostal arteries to document the extent of arterial ligation and spinal cord hypoperfusion. The Basso Mouse Scale for Locomotion, histological studies, and electron microscopy demonstrated postligation locomotive and histopathological changes. RESULTS: Ligation induced a significant and instantaneous drop in blood flow in the intercostal arteries (% change; mean = -63.81; 95% CI, -72.28 to -55.34) and the thoracic spinal cord (% change; mean = -68.55; 95% CI, -80.23 to -56.87). Paralysis onset was immediate and of varying degree, with behavioral deficit stratified into three groups: 9.4% exhibited severe paralysis, 37.5% moderate paralysis, and 53.1% mild paralysis at day 1 (n = 32; P < 0.001). Mild and moderate paralysis was transient, gradually improving over time. Severe paralysis showed no improvement and exhibited a higher mortality rate (83%; n = 15 of 18) compared to moderately (33%; n = 6 of 18) and mildly (24%; n = 6 of 25) paralyzed mice (P < 0.001). The overall ligation group survival rate (84%; n = 46 of 55) was significantly lower than the sham group (100%; n = 48 of 48) with P = 0.003. CONCLUSIONS: The mouse model generates reproducible spinal cord hypoperfusion and accompanying histopathological ischemic spinal cord damage. The resulting anatomical changes and variable behavioral deficits mimic the variability in radiological and clinical findings in human patients.

  • Histological Findings After Aortic Cross-Clamping in Preclinical Animal Models

    Journal of Neuropathology & Experimental Neurology · 2021 · 9 citations

    • Medicine
    • Pathology
    • Surgery

    Spinal cord ischemic injury and paralysis are devastating complications after open surgical repair of thoracoabdominal aortic aneurysms. Preclinical models have been developed to simulate the clinical paradigm to better understand the neuropathophysiology and develop therapeutic treatment. Neuropathological findings in the preclinical models have not been comprehensively examined before. This systematic review studies the past 40 years of the histological findings after open surgical repair in preclinical models. Our main finding is that damage is predominantly in the grey matter of the spinal cord, although white matter damage in the spinal cord is also reported. Future research needs to examine the neuropathological findings in preclinical models after endovascular repair, a newer type of surgical repair used to treat aortic aneurysms.

  • Eccentric rehabilitation induces white matter plasticity and sensorimotor recovery in chronic spinal cord injury

    Experimental Neurology · 2021 · 28 citations

    Senior authorCorresponding
    • Medicine
    • Neuroscience
    • Physical medicine and rehabilitation
  • Behavioral testing in animal models of spinal cord injury

    Experimental Neurology · 2020 · 32 citations

    Senior authorCorresponding
    • Neuroscience
    • Medicine
    • Psychology
  • Eccentric-focused rehabilitation promotes myelin plasticity in individuals with chronic, incomplete spinal cord injury

    medRxiv · 2020-04-29 · 1 citations

    preprintOpen accessSenior authorCorresponding

    Abstract Background Myelin plasticity has emerged as a novel mechanism by which the nervous system can change with experience, offering new potential for rehabilitation-induced recovery after neurotrauma. This first-in-human study investigated whether innovative, downhill locomotor rehabilitation promotes myelin plasticity in individuals with chronic, incomplete spinal cord injury (SCI). Methods Of 20 individuals with SCI that enrolled, 4 passed the imaging screen and had myelin water imaging (MWI) before and after a 12-week (3 times/week) downhill locomotor treadmill training program (SCI+DH). One individual was excluded for imaging artifacts. Uninjured control participants (n=7) had two MWI sessions within the same day. Changes in myelin water fraction (MWF), a histopathologically-validated myelin biomarker, were analyzed in a priori motor learning and non-motor learning brain regions and the cervical spinal cord using statistical approaches appropriate for small sample sizes. Results Within SCI+DH individuals, significantly more motor learning regions showed increased MWF than non-motor learning regions (p&lt;.05). Compared to Control, MWF in the SCI+DH group increased in white matter underlying postcentral and precuneus cortices, combined motor learning brain regions, and ventral spinal cord (p&lt;.05). To account for small sample size, an estimation-based approach showed the pattern of MWF increase was specific to training and region. Conclusion Downhill training increased MWF in brain regions specifically associated with motor learning and in the ventral spinal cord. Trial Registration ClincialTrials.gov ( NCT02498548 , NCT02821845 ) Funding National Institutes of Health [F31NS096921 (TDF), R21HD082808 (DMB)], Craig H. Neilsen Foundation [316282 (DMB)], Foundation for Physical Therapy Research [Promotion of Doctoral Studies Level II Scholarship (TDF)]

  • [The role of nurses in health education about vaccines: analysis of style and communication models of institutional vaccination campaigns].

    PubMed · 2020-01-28 · 5 citations

    article

    Vaccine hesitancy represents an increasingly important global health issue. Nurses, together with other healthcare professionals, can play a key role in increasing vaccination uptake. The aim of this article is to analyze the main elements of positive communication styles used in vaccination campaigns and initiatives. The most important components in style, construction and contents used in several vaccination campaigns were evaluated through an original instrument, specifically developed for the present study. The most relevant aspects of nursing expertise and competencies were mixed with foundations of mass communication theory, in order to develop a framework made by 13 items, useful to evaluate different aspects of immunization campaigns. A multi-professional project was developed, to obtain a deep integration between nurse expertise in health promotion and other groups with similar public health orientation. The Authors further evaluated sociological instruments and theories from other fields, as mass communication theory and the social/behavioral approach. An integrative review was performed, about the following main themes: vaccination adherence basis; nurse role in health promotion; health education competences; multi-professionals integration in public health; positive communication style; efficacy evaluation. Key elements were collected, to prepare an original instrument to be used in evaluating several communication campaigns. The evaluation framework (13 items) was prepared and applied to vaccine communication in different institutional settings in the last five years. Main components are: elements taken from main communication models (persuasive communication models); nurse competencies in health education; public health expertise (from an expert panel). The main findings of this study regard the usefulness of evaluating main aspects of communication in the vaccine field. Nurses' knowledge and competencies in health promotion and health education add relevant meanings and cues to act against the causes for not vaccinating. It shows that is worth analyzing the main aspects of communication techniques and evaluating innovative methods to increase population confidence levels in public health.

  • Abstract # 3205 The Role of Microglia in the Development and Exacerbation of Stress-Induced Pain Behavior

    Brain Behavior and Immunity · 2019-02-01

    article
  • 2282 Targeted eccentric motor control to improve locomotion after incomplete spinal cord injury

    Journal of Clinical and Translational Science · 2018-06-01

    articleOpen access

    OBJECTIVES/SPECIFIC AIMS: Incomplete spinal cord injury typically results in life-long disability, often in the form of profound loss of locomotion capability. Individuals who have experienced incomplete spinal cord injury exhibit persistent eccentric motor deficits, which are particularly prevalent in the weight acceptance phase of gait and emphasized in sagittal plane knee motion and frontal plane hip motion. METHODS/STUDY POPULATION: Motion analysis can capture the kinematic and joint-level deficits of these individuals, but it is impossible to directly calculate the contributions of individual muscles to weight acceptance due to the complexity of the musculoskeletal system. Instead, those muscle contributions must be simulated in order to approximate muscle power during locomotion. RESULTS/ANTICIPATED RESULTS: The traditional method for driving these simulations with electromyography readings is unavailable for individuals who have neuromuscular deficits (e.g., spasticity or paralysis), due to the need to generate reliable maximum voluntary isometric contractions for baseline purposes. Instead, this research develops a novel method for using resting electromyography data to drive musculoskeletal simulations using a muscle activation threshold paradigm. DISCUSSION/SIGNIFICANCE OF IMPACT: The simulation results of this method more closely resemble experimental results, but further simulation refinement is needed to fully capture the true muscle activity.

  • Microglia Promote Increased Pain Behavior through Enhanced Inflammation in the Spinal Cord during Repeated Social Defeat Stress

    Journal of Neuroscience · 2018-12-17 · 72 citations

    articleOpen access

    Clinical studies indicate that psychosocial stress contributes to adverse chronic pain outcomes in patients, but it is unclear how this is initiated or amplified by stress. Repeated social defeat (RSD) is a mouse model of psychosocial stress that activates microglia, increases neuroinflammatory signaling, and augments pain and anxiety-like behaviors. We hypothesized that activated microglia within the spinal cord facilitate increased pain sensitivity following RSD. Here we show that mechanical allodynia in male mice was increased with exposure to RSD. This stress-induced behavior corresponded with increased mRNA expression of several inflammatory genes, including IL-1β, TNF-α, CCL2, and TLR4 in the lumbar spinal cord. While there were several adhesion and chemokine-related genes increased in the lumbar spinal cord after RSD, there was no accumulation of monocytes or neutrophils. Notably, there was evidence of microglial activation selectively within the nociceptive neurocircuitry of the dorsal horn of the lumbar cord. Elimination of microglia using the colony stimulating factor 1 receptor antagonist PLX5622 from the brain and spinal cord prevented the development of mechanical allodynia in RSD-exposed mice. Microglial elimination also attenuated RSD-induced IL-1β, CCR2, and TLR4 mRNA expression in the lumbar spinal cord. Together, RSD-induced allodynia was associated with microglia-mediated inflammation within the dorsal horn of the lumbar spinal cord. SIGNIFICANCE STATEMENT Mounting evidence indicates that psychological stress contributes to the onset and progression of adverse nociceptive conditions. We show here that repeated social defeat stress causes increased pain sensitivity due to inflammatory signaling within the nociceptive circuits of the spinal cord. Studies here mechanistically tested the role of microglia in the development of pain by stress. Pharmacological ablation of microglia prevented stress-induced pain sensitivity. These findings demonstrate that microglia are critical mediators in the induction of pain conditions by stress. Moreover, these studies provide a proof of principle that microglia can be targeted as a therapeutic strategy to mitigate adverse pain conditions.

Recent grants

Frequent coauthors

  • Lesley C. Fisher

    The Ohio State University

    26 shared
  • James P. Schmiedeler

    University of Notre Dame

    15 shared
  • Lyn B. Jakeman

    13 shared
  • Charlotte Rosso

    Pitié-Salpêtrière Hospital

    12 shared
  • Phillip G. Popovich

    Institute for Behavioral Medicine

    12 shared
  • Karen J. Hutchinson

    Boston University

    11 shared
  • Linda J. Noble‐Haeusslein

    University of Queensland

    10 shared
  • Timothy D. Faw

    Duke University

    10 shared

Awards & honors

  • Helen J. Hislop Award for Outstanding Contributions to Profe…
  • National Research Award, Neurology Section, American Physica…
  • US Patent (Pending) Assessing Active Sensation after CNS Inj…
  • Who’s Who Among America’s Teachers (2004, 2005)
  • Outstanding Faculty Research Award, School of Allied Medical…
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