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Background: Subconcussion, a mild traumatic brain injury, is best defined and identified by a lack of observable symptoms after axonal injury from minor head impacts. Subconcussive impacts are believed to accumulate with increased exposure over time, and are likely prodromal in the manifestation of a full-blown concussion. As evidenced by changes to changes in cerebral neurochemistry and structure, it is apparent that although individuals who have accumulated subconcussion may present as asymptomatic for motor and/or cognitive impairment using current clinical assessment tools, there is indication of long-term neurological damage which is presently going unrecognized. Objective: For the reasons stated above, a more sensitive and objective assessment tool is required to assess and recognize prodromal concussion manifestation in at risk populations with the intention of preventing further chronic sequelae. Design: Multiple baseline, time-series with repeated measures. Methods: Balance and bilateral reflex variability was assessed at pre-season and at post-season. Results: The current study identified significant changes to static balance postures (taken from the Balance Error Scoring System) through an objective postural assessment of centre of pressure (COP) and Area of Ellipse (AoE) calculations using a low-cost balance board and basic software interface after a season of accumulated subconcussion in female varsity rugby athletes. Specifically, double stance on the floor worsened by 31% in COPAP (p=.025) and by 26% in COPT (p=.038) and tandem stance on an unstable foam surface worsened by 180% in COPML (p=.014), 175% in COPAP (p=.025) and 141% in COPT (p=.005) between pre-and post-season. Our results indicate that these outcome measures are sensitive and can discriminate underlying balance deficits associated with accumulated subconcussive impacts. An objective measurement of spinal cord excitability through bilateral fluctuations of the Hoffman (H-) reflex in the tibial nerve found significantly elevated pre-season Cross Covariance (CCV) values which were 3x higher than those of a neurologically intact control population, suggesting prior neurological damage in study participants. Conclusion: The current study provides a platform for future research investigating bilateral fluctuation in spinal cord excitability after accumulated subconcussion and confirms balance decrements related to subconcussion can be identified through sensitive and specific measurement tools. / Graduate

Objective: Establish and validate an experimental pain model that will create pain for at least 20-minutes and then use the model to determine if: 1) cryotherapy decreases experimentally induced pain, 2) experimentally induced pain contributes to arthrogenic muscle inhibition, and 3) cold application influences pain or arthrogenic muscle inhibition. To answer these questions we conducted two experiments, the results of which are presented in two manuscripts. Methods: Seventy (n = 30 for experiment I and n = 40 for experiment II), physically active healthy male subjects participated. Interventions: Independent variables used for experiment I were condition (5% hypertonic saline infusion/cryotherapy, no-saline infusion/cryotherapy, 5% hypertonic saline infusion/sham) and time (precondition, every minute during a condition, and 10 minutes following each condition). For experiment II, independent variables were treatment (saline infusion, saline infusion/cryotherapy, saline infusion/sham, and no-saline infusion) and time (pretreatment, posttreatment, and 30-minutes posttreatment). Dependent variables measured were pain perception, knee surface and ambient temperatures, and Hmax, and Mmax measures (experiment II only). Results: Saline caused more pain than no-saline at minutes 3, 4, and 5 during infusion. Pain caused by saline and sham application remained constant from 4 minutes during application through 1 minute following application. Cold application decreased pain for 16 minutes. Pain resulted in arthrogenic muscle inhibition following and 30 minutes following saline infusion. Cryotherapy removed inhibition following but not 30 minutes following application. Pain for the saline groups increased following infusion as measured with the pain rating index and visual analogue scale. According to pain rating index, cryotherapy did not decrease pain; however, cryotherapy decreased pain as measured with the visual analogue scales. No change in temperature occurred during the non-cooling conditions. Ambient temperatures fluctuated less than 1°C. Conclusion: Saline infusion caused anterior knee pain for over 20 minutes and resulted in arthrogenic muscle inhibition. Cryotherapy disinhibited the quadriceps motoneuron pool and reduced pain as measured with visual analogue scales. Cryotherapy did not decrease pain as measured with the McGill pain questionnaire.