KLKelly A. Larkin-Kaiser

Kelly A. Larkin-Kaiser

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

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Previous Organizations / Institutes

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Kelly A. Larkin-Kaiser has a total of 19 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Open Access

    Robot-Assisted Gait Training with Trexo Home: Users, Usage and Initial Impacts

    by Christa M. Diot, Jessica L. Youngblood, Anya H. Friesen, Tammy Wong, Tyler A. Santos, Benjamin M. Norman, Kelly A. Larkin-Kaiser, Elizabeth G. Condliffe

    Robotic gait training has the potential to improve secondary health conditions for people with severe neurological impairment. The purpose of this study was to describe who is using the Trexo robotic gait trainer, how much training is achieved in the home and community, and what impacts are observed after the initial month of use. In this prospective observational single-cohort study, parent-reported questionnaires were collected pre- and post-training. Of the 70 participants, the median age was 7 years (range 2 to 24), 83% had CP, and 95% did not walk for mobility. Users trained 2–5 times/week. After the initial month, families reported a significant reduction in sleep disturbance (p = 0.0066). Changes in bowel function, positive affect, and physical activity were not statistically significant. These findings suggest that families with children who have significant mobility impairments can use a robotic gait trainer frequently in a community setting and that sleep significantly improves within the first month of use. This intervention holds promise as a novel strategy to impact multi-modal impairments for this population. Future work should include an experimental study design over a longer training period to begin to understand the relationship between training volume and its full potential.


  • Open Access

    Relationship of muscle morphology to hip displacement in cerebral palsy: a pilot study investigating changes intrinsic to the sarcomere

    by Kelly A. Larkin-Kaiser, Jason J. Howard, Timothy Leonard, Venus Joumaa, Luke Gauthier, Karl Logan, Benjamin Orlik, Ron El-Hawary, Walter Herzog

    Cerebral palsy (CP) is the most common cause of childhood disability, typified by a static encephalopathy with peripheral musculoskeletal manifestations—most commonly related to spasticity—that are progressive with age. Hip displacement is one of the most common manifestations, observed to lead to painful degenerative arthritis over time. Despite the key role that spasticity-related adductor muscle contractures are thought to play in the development of hip displacement in CP, basic science research in this area to date has been limited. This study was initiated to correlate hip adductor muscle changes intrinsic to the sarcomere—specifically, titin isoforms and sarcomere length—to the severity of hip displacement in children with spastic cerebral palsy. Single gracilis muscle biopsies were obtained from children with CP (Gross Motor Function Classification System (GMFCS) III-V; n = 10) who underwent adductor muscle release surgery for the treatment of hip displacement. Gel electrophoresis was used to estimate titin molecular weight. Sarcomere lengths were measured from muscle fascicles using laser diffraction. The severity of hip displacement was determined by measuring by Reimers migration percentage (MP) from anteroposterior pelvic x-rays. Correlation analyses between titin, sarcomere lengths, and MP were performed. The mean molecular weight of titin was 3588 kDa. The mean sarcomere length was 3.51 μm. Increased MP was found to be associated with heavier isoforms of titin (R2 = 0.65, p < 0.05) and with increased sarcomere lengths (R2 = 0.65, p < 0.05). Heavier isoforms of titin were also associated with increased sarcomere lengths (R2 = 0.80, p < 0.05). Our results suggest that both larger titin isoforms and sarcomere lengths are positively correlated with increased severity of hip displacement and may represent adaptations in response to concomitant increases in spasticity and muscle shortening. As this study does not report the results of a health care intervention on human participants, it has not been registered.


  • Range of Motion as a Predictor of Clinical Shoulder Pain During Recovery From Delayed-Onset Muscle Soreness

    by Kelly A. Larkin-Kaiser, Jeffrey J. Parr, Paul A. Borsa, Steven Z. George

    Context: Athletic trainers use clinical pain and range of motion (ROM) to gauge recovery after musculoskeletal injury. Limited evidence to date suggests which shoulder ROM measures can predict symptomatic relief and functional recovery after delayed-onset muscle soreness (DOMS). Objective: To determine whether shoulder passive internal rotation, passive external rotation, active abduction, and active flexion and evoked pain with abduction are associated with resting pain experienced after exercise-induced DOMS. Design: Descriptive laboratory study. Setting: Controlled research laboratory. Patients or Other Participants: A total of 110 healthy, right-hand–dominant participants (44 men: age = 25.39 ± 7.00 years, height = 178.93 ± 7.01 cm, weight = 78.59 ± 14.04 kg; 66 women: age = 22.98 ± 6.11 years, height = 164.64 ± 6.94 cm, weight = 61.86 ± 11.67 kg). Intervention(s): Participants completed an exercise-induced DOMS protocol for the external rotators of the dominant shoulder to replicate muscle injury. Main Outcome Measure(s): Current resting pain was assessed daily for 96 hours using the Brief Pain Inventory. We evaluated functional recovery with measures of ROM in abduction, internal rotation, external rotation, and flexion. Evoked pain with active abduction was reported, and the pain rating served as the dependent variable in the regression model. Results: Impairment measures explained resting pain at 48 (R2 = 0.392) and 96 hours (R2 = 0.164). Abduction and internal-rotation ROM and evoked pain with abduction predicted resting pain at 48 hours (P < .001). At 96 hours, evoked pain with abduction of the injured arm (P < .001) was the significant contributor to resting pain. Conclusions: These models suggest that resting pain after experimentally induced DOMS occurs at 48 hours and is associated with specific ranges of motion and evoked pain with abduction.