Neurotrauma Prevention Review: Improving Helmet Design and Implementation

Goutnik, Michael; Goeckeritz, Joel; Sabetta, Zackary; Curry, Tala; Willman, Matthew; Willman, Jonathan; Thomas, Theresa Currier; Lucke‐Wold, Brandon

doi:10.3390/biomechanics2040039

Cited by 8 publications

(4 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, connective tissue disorders such as Ehlers-Danlos syndrome have been implicated in increased vulnerability to neurological insult such as traumatic brain injury and higher rates of complication and mortality after neuroendovascular procedures 58 – 60 . Decreased cerebral blood flow velocity correlated with the function of age, increases risks for severity after neurological insult, neuropathology, and cognitive impairment 61 – 65 . Due to recent findings and the overlapping characteristics displayed with aging, it is plausible that the cerebral vasculature and brain could be affected in MFS patients.…”

Section: Discussionmentioning

confidence: 99%

In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation

Curry,

Barrameda,

Thomas

et al. 2024

Sci Rep

View full text Add to dashboard Cite

In individuals with Marfan Syndrome (MFS), fibrillin-1 gene (FBN1) mutations can lead to vascular wall weakening and dysfunction. The experimental mouse model of MFS (Fbn1C1041G/+) has been advantageous in investigating MFS-associated life-threatening aortic aneurysms. It is well established that the MFS mouse model exhibits an accelerated-aging phenotype in elastic organs like the aorta, lung, and skin. However, the impact of Fbn1 mutations on the in vivo function and structure of various artery types with the consideration of sex and age, has not been adequately explored in real-time and a clinically relevant context. In this study, we investigate if Fbn1 mutation contributes to sex-dependent alterations in central and cerebral vascular function similar to phenotypic changes associated with normal aging in healthy control mice. In vivo ultrasound imaging of central and cerebral vasculature was performed in 6-month-old male and female MFS and C57BL/6 mice and sex-matched 12-month-old (middle-aged) healthy control mice. Our findings confirm aortic enlargement (aneurysm) and wall stiffness in MFS mice, but with exacerbation in male diameters. Coronary artery blood flow velocity (BFV) in diastole was not different but left pulmonary artery BFV was decreased in MFS and 12-month-old control mice regardless of sex. At 6 months of age, MFS male mice show decreased posterior cerebral artery BFV as compared to age-matched control males, with no difference observed between female cohorts. Reduced mitral valve early-filling velocities were indicated in MFS mice regardless of sex. Male MFS mice also demonstrated left ventricular hypertrophy. Overall, these results underscore the significance of biological sex in vascular function and structure in MFS mice, while highlighting a trend of pre-mature vascular aging phenotype in MFS mice that is comparable to phenotypes observed in older healthy controls. Furthermore, this research is a vital step in understanding MFS's broader implications and sets the stage for more in-depth future analyses, while providing data-driven preclinical justification for re-evaluating diagnostic approaches and therapeutic efficacy.

show abstract

Section: Discussionmentioning

confidence: 99%

In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation

Curry,

Barrameda,

Thomas

et al. 2024

Sci Rep

View full text Add to dashboard Cite

show abstract

“…[49][50][51] Decreased cerebral blood flow velocity correlated with the function of age, increases risks for severity after neurological insult, neuropathology, and cognitive impairment. [52][53][54][55][56] Due to recent findings and the overlapping characteristics displayed with aging, it is plausible that the cerebral vasculature and brain could be affected in MFS patients. Together with the increased risk for cerebral aneurysms and stroke (hemorrhagic and ischemic) in MFS patients, further research is needed to understand the magnitude of risk, the potential discovery of novel targets for prevention and treatment, and the impact of current treatments on neurological concerns.…”

Section: Discussionmentioning

confidence: 99%

In VivoPhenotypic Vascular Dysfunction Extends Beyond the Aorta in a Mouse Model for Fibrillin-1 (FBN1) Mutation

Curry,

Barrameda,

Currier Thomas

et al. 2023

Preprint

View full text Add to dashboard Cite

In individuals with Marfan Syndrome (MFS), fibrillin-1 gene (FBN1) mutations can lead to vascular wall weakening and dysfunction. The experimental mouse model of MFS (FBN1C1041G/+) has been advantageous in investigating MFS-associated life-threatening aortic aneurysms. Although the MFS mouse model presents an accelerated-aging phenotype in elastic organs (e.g., lung, skin), the impact ofFBN1mutations on other central and peripheral arteries function and structure with the consideration of the impact of sex remains underexplored. In this study, we investigate ifFBN1mutation contributes to sex-dependent alterations in central and cerebral vascular function similar to phenotypic changes associated with normal aging in healthy control mice.In vivoultrasound imaging of central and cerebral vasculature was performed in 6-month-old male and female MFS and C57BL/6 mice and sex-matched 12-month-old (middle-aged) healthy control mice. Our findings confirm aortic enlargement (aneurysm) and wall stiffness in MFS mice, but with exacerbation in male diameters. Coronary artery blood flow velocity (BFV) in diastole was not different but left pulmonary artery BFV was decreased in MFS and 12-month-old control mice regardless of sex. At 6 months of age, MFS male mice show decreased posterior cerebral artery BFV as compared to age-matched control males, with no difference observed between female cohorts. Reduced mitral valve early-filling velocities were indicated in MFS mice regardless of sex. Male MFS mice also demonstrated left ventricular hypertrophy. Overall, these results underscore the significance of biological sex in vascular function and structure in MFS mice, while highlighting a trend of pre-mature vascular aging phenotype in MFS mice that is comparable to phenotypes observed in older healthy controls.

show abstract

“…These findings also contribute to the pathology seen in a diffuse axonal injury TBI. 22 Thus, some propose further testing is required to better prevent neck injury in all scenarios. 23 A few papers have demonstrated the potential effectiveness of neck protection devices in minimizing the severity of neck injuries in motorcycle accidents.…”

Section: Protective Gearmentioning

confidence: 99%

Unveiling the Vital Role of Critical Neck Protection Devices for Motorcycle Riders: A Review

Sabetta,

Shore,

McCarter

et al. 2024

Preprint

View full text Add to dashboard Cite

Fatal motorcycle accidents on- and off-road continue to be overlooked in the literature. Research is scant on morbidity and mortality due to neck injury, which leaves patients and their families debilitated chronically. Great Lakes EMS Inc. conducted a 10-year retrospective case study, which highlighted that motocross riders who do not wear a neck brace are at an 89% higher risk of a critical cervical spine injury; highly unstable cervical spinal fractures have a sustainably higher risk of morbidity and mortality. Proposed mechanisms of motocross neck braces displace the forces on the neck onto the helmet of the rider to provide a smooth distribution of forces, whereas lack of neck brace use places riders at risk for upper cervical spine fractures such as Jefferson fractures, Hangman's fractures, and Odontoid fractures. Further, evidence suggests the use of back protectors may increase the risk of thoracic and upper spine injuries during a motorcycle crash. The limited data on this topic continues to be a challenge, as there is a lack of understanding of the nature of these injuries, which are likely preventable with proper neck protection.

show abstract

Neurotrauma Prevention Review: Improving Helmet Design and Implementation

Cited by 8 publications

References 98 publications

In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation

In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation

In VivoPhenotypic Vascular Dysfunction Extends Beyond the Aorta in a Mouse Model for Fibrillin-1 (FBN1) Mutation

Unveiling the Vital Role of Critical Neck Protection Devices for Motorcycle Riders: A Review

Contact Info

Product

Resources

About