Chronic cerebrovascular dysfunction after traumatic brain injury

Jullienne, A.; Obenaus, André; Ichkova, Aleksandra; Savona‐Baron, Catherine; Pearce, William J.; Badaut, Jérôme

doi:10.1002/jnr.23732

Cited by 98 publications

(85 citation statements)

References 185 publications

(238 reference statements)

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“…Animal experiments have reported an increase in carotid blood flow in septic shock models because of the hyperdynamic state and a loss of autoregulation of cerebral blood flow, which may have contributed to the fair agreement between carotid and TTE cardiac output. In patients with multiple trauma, 50% of whom also had traumatic brain injury in our study, the unstable hemodynamics, cerebral blood flow alterations, and autoregulation impairments also contributed to the slight agreement. In patients with respiratory failure, the huge inspiratory effort and increased negative pressure in the thoracic cavity changed the proportion of carotid blood flow from the cardiac output, thus influencing the agreement between carotid and TTE cardiac output.…”

Section: Discussionsupporting

confidence: 49%

Common Carotid Artery Sonography Versus Transthoracic Echocardiography for Cardiac Output Measurements in Intensive Care Unit Patients

Peng

Zhang

et al. 2017

J of Ultrasound Medicine

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Section: Discussionsupporting

confidence: 49%

Common Carotid Artery Sonography Versus Transthoracic Echocardiography for Cardiac Output Measurements in Intensive Care Unit Patients

Peng

Zhang

et al. 2017

J of Ultrasound Medicine

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“…Vascular disruptions figure prominently in both humans and animal models (23, 56, 57), but their extent and duration can vary widely with injury type and severity. Importantly, CBF changes have largely been examined in open-skull injury models that generate moderate to severe TBI.…”

Section: Discussionmentioning

confidence: 99%

“…Functional CBF measurements in vivo will be crucial for establishing the vascular contributions to mild injury. Reduced flow has been seen in a wide variety of animal models (18–21) and human studies (22, 23), but has largely been examined in more severe forms of injury.…”

Section: Introductionmentioning

confidence: 99%

Rapid disruption of the cortical microcirculation after mild traumatic brain injury

Witkowski¹,

Erdener²,

Kılıç³

et al. 2019

Preprint

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Keywords: traumatic brain injury, mouse, weight drop injury, cerebral blood flow, capillary, in 21 vivo, laser speckle contrast imaging, optical coherence tomography, two-photon imaging 22 23 24 Acknowledgments: We thank Tim Otchy, Jennifer Morgan, and members of the Davison and 25 Boas laboratories for comments and discussion. This work was supported by Boston University 26 startup funds.Abstract 30 Traumatic brain injury (TBI) is a major source of cognitive deficits affecting millions annually. The 31 bulk of human injuries are mild, causing little or no macroscopic damage to neural tissue, yet can 32 still lead to long-term neuropathology manifesting months or years later. Although the cellular 33 stressors that ultimately lead to chronic pathology are poorly defined, one notable candidate is 34 metabolic stress due to reduced cerebral blood flow (CBF), which is common to many forms of 35 TBI. Here we used high-resolution in vivo intracranial imaging in a rodent injury model to 36 characterize deficits in the cortical microcirculation during both acute and chronic phases after 37 mild TBI. We found that CBF dropped precipitously during immediate post-injury periods, 38 decreasing to less than half of baseline levels within minutes and remaining suppressed for 1.5-39 2 hours. Repeated time-lapse imaging of the cortical microvasculature revealed further striking 40 flow deficits in the capillary network, where 18% of vessels were completely occluded for 41 extended periods after injury, and an additional >50% showed substantial stoppages. Decreased 42 CBF was paralleled by extensive vasoconstriction that is likely to contribute to loss of flow. Our 43 data indicate a major role for vascular dysfunction in even mild forms of TBI, and suggest that 44 acute post-injury periods may be key therapeutic windows for interventions that restore flow 45 and mitigate metabolic stress. 46 47 88 dysfunction across the cortical microvasculature, where a large fraction of individual capillaries 89were occluded for periods of minutes or longer, leading to localized regions with complete loss 90 5 of perfusion. CBF largely returned to normal by 3 hours after injury and showed no measurable 91 deficits when tracked until 3 weeks. Reduced CBF was paralleled by pronounced 92 vasoconstriction, identifying a potential mechanism contributing to disrupted flow. This rapid 93 and extensive vascular dysfunction highlights the importance of immediate post-injury periods 94 for delivering interventions, and suggests that relieving vasoconstriction will be a promising 95 avenue for countering the effects of mild injury. 96 97 Methods 98 99 Animals and surgical procedures 100 All experiments were performed in 2-5 month-old male and female C57BL6/J mice in accordance 101 with guidelines of the Boston University Institutional Animal Care and Use Committee. Animals 102 were group housed on a 12-hour light/dark cycle with ad libitum access to food and water. 103 Chronic cranial windows were implanted using standard procedures (30, 31). Brie...

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“…Traumatic brain injury (TBI) accounts for more than 30% of all injury related deaths mostly from mechanical impact or blast waves and results in disruption of the structure and function of the brain, including cerebral blood vessels (Jullienne and others 2016). Disruption of blood vessels by TBI, which can present as intracranial hemorrhages, cerebral blood flow deficits, BBB disruption and/or edema could interfere with glymphatic function.…”

Section: Clinical Relevance Of the Glymphatic Systemmentioning

confidence: 99%

The Glymphatic Pathway: Waste Removal from the CNS via Cerebrospinal Fluid Transport

2017

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The overall premise of this review is that cerebrospinal fluid (CSF) is transported within a dedicated peri-vascular network facilitating metabolic waste clearance from the central nervous system while we sleep. The anatomical profile of the network is complex and has been defined as a peri-arterial CSF influx pathway and peri-venous clearance routes, which are functionally coupled by interstitial bulk flow supported by astrocytic aquaporin 4 water channels. The role of the newly discovered system in the brain is equivalent to the lymphatic system present in other body organs and has been termed the “glymphatic pathway” or “(g)lymphatics” because of its dependence on glial cells. We will discuss and review the general anatomy and physiology of CSF from the perspective of the glymphatic pathway, a discovery which has greatly improved our understanding of key factors that control removal of metabolic waste products from the central nervous system in health and disease and identifies an additional purpose for sleep. A brief historical and factual description of CSF production and transport will precede the ensuing discussion of the glymphatic system along with a discussion of its clinical implications.

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Chronic cerebrovascular dysfunction after traumatic brain injury

Cited by 98 publications

References 185 publications

Common Carotid Artery Sonography Versus Transthoracic Echocardiography for Cardiac Output Measurements in Intensive Care Unit Patients

Common Carotid Artery Sonography Versus Transthoracic Echocardiography for Cardiac Output Measurements in Intensive Care Unit Patients

Rapid disruption of the cortical microcirculation after mild traumatic brain injury

The Glymphatic Pathway: Waste Removal from the CNS via Cerebrospinal Fluid Transport

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