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Purpose: Concussion management is shifting away from a rest-is-best approach, as data now suggest that exercise-is-medicine for this mild brain injury. Despite this, we have limited data on habitual physical activity following concussion. Therefore, our objective was to quantify accelerometer-measured physical activity and sedentary time in children with concussion (within the first month of injury) and healthy controls. We hypothesized that children with concussion would be less active than their healthy peers. Methods: We performed a secondary analysis of prospectively collected accelerometer data. Our sample included children with concussion (n = 60, 31 females) and historical controls (n = 60) matched for age, sex, and season of accelerometer wear. Results: Children with concussion were significantly more sedentary than controls (mean difference [MD], 38.3 min/d, P =.006), and spent less time performing light physical activity (MD, −19.5 min/d, P =.008), moderate physical activity (MD, −9.8 min/d, P <.001), and vigorous physical activity (MD, −12.0 min/d, P <.001); these differences were observed from 8:00 AM to 9:00 PM. Sex-specific analyses identified that girls with concussion were less active and more sedentary than both boys with concussion (P =.010) and healthy girls (P <.010). Conclusion: There is an activity deficit observed within the first month of pediatric concussion. Physical activity guidelines should address this while considering sex effects. [ABSTRACT FROM AUTHOR]

Background: Recent scientific evidence has challenged the traditional "rest-is-best" approach for concussion management. It is now thought that "exercise-is-medicine" for concussion, owing to dozens of studies which demonstrate that sub-maximal, graded aerobic exercise can reduce symptom burden and time to symptom resolution. However, the primary neuropathology of concussion is altered functional brain activity. To date, no studies have examined the effects of sub-maximal aerobic exercise on resting state functional brain activity in pediatric concussion. In addition, although exercise is now more widely prescribed following concussion, its cardiopulmonary response is not yet well understood in this population. Our study has two main goals. The first is to understand whether there are exercise-induced resting state functional brain activity differences in children with concussion vs. healthy controls. The second is to profile the physiological response to exercise and understand whether it differs between groups. Methods: We will perform a single-center, controlled, prospective cohort study of pediatric concussion at a large, urban children's hospital and academic center. Children with sport-related concussion (aged 12–17 years) will be recruited within 4-weeks of injury by our clinical study team members. Key inclusion criteria include: medical clearance to exercise, no prior concussion or neurological history, and no implants that would preclude MRI. Age- and sex-matched healthy controls will be required to meet the same inclusion criteria and will be recruited through the community. The study will be performed over two visits separated by 24–48 h. Visit 1 involves exercise testing (following the current clinical standard for concussion) and breath-by-breath gas collection using a metabolic cart. Visit 2 involves two functional MRI (fMRI) scans interspersed by 10-minutes of treadmill walking at an intensity calibrated to Visit 1 findings. To address sub-objectives, all participants will be asked to self-report symptoms daily and wear a waist-worn tri-axial accelerometer for 28-days after Visit 2. Discussion: Our study will advance the growing exercise-concussion field by helping us understand whether exercise impacts outcomes beyond symptoms in pediatric concussion. We will also be able to profile the cardiopulmonary response to exercise, which may allow for further understanding (and eventual optimization) of exercise in concussion management. Trial registration: Not applicable. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Cerebral small vessel disease (SVD) and amyloid beta (Aβ) pathology frequently co‐exist. The impact of concurrent pathology on the pattern of hippocampal atrophy, a key substrate of memory impacted early and extensively in dementia, remains poorly understood. METHODS: In a unique cohort of mixed Alzheimer's disease and moderate–severe SVD, we examined whether total and regional neuroimaging measures of SVD, white matter hyperintensities (WMH), and Aβ, as assessed by 18F‐AV45 positron emission tomography, exert additive or synergistic effects on hippocampal volume and shape. RESULTS: Frontal WMH, occipital WMH, and Aβ were independently associated with smaller hippocampal volume. Frontal WMH had a spatially distinct impact on hippocampal shape relative to Aβ. In contrast, hippocampal shape alterations associated with occipital WMH spatially overlapped with Aβ‐vulnerable subregions. DISCUSSION: Hippocampal degeneration is differentially sensitive to SVD and Aβ pathology. The pattern of hippocampal atrophy could serve as a disease‐specific biomarker, and thus guide clinical diagnosis and individualized treatment strategies for mixed dementia. [ABSTRACT FROM AUTHOR]

Introduction: Cerebral small vessel disease (SVD) and amyloid beta (Aβ) pathology frequently co-exist. The impact of concurrent pathology on the pattern of hippocampal atrophy, a key substrate of memory impacted early and extensively in dementia, remains poorly understood., Methods: In a unique cohort of mixed Alzheimer's disease and moderate-severe SVD, we examined whether total and regional neuroimaging measures of SVD, white matter hyperintensities (WMH), and Aβ, as assessed by 18 F-AV45 positron emission tomography, exert additive or synergistic effects on hippocampal volume and shape., Results: Frontal WMH, occipital WMH, and Aβ were independently associated with smaller hippocampal volume. Frontal WMH had a spatially distinct impact on hippocampal shape relative to Aβ. In contrast, hippocampal shape alterations associated with occipital WMH spatially overlapped with Aβ-vulnerable subregions., Discussion: Hippocampal degeneration is differentially sensitive to SVD and Aβ pathology. The pattern of hippocampal atrophy could serve as a disease-specific biomarker, and thus guide clinical diagnosis and individualized treatment strategies for mixed dementia., (© 2024 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)