scholarly journals Capillary Transit Time Heterogeneity and Flow-Metabolism Coupling after Traumatic Brain Injury

2014 ◽  
Vol 34 (10) ◽  
pp. 1585-1598 ◽  
Author(s):  
Leif Østergaard ◽  
Thorbjørn S Engedal ◽  
Rasmus Aamand ◽  
Ronni Mikkelsen ◽  
Nina K Iversen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Transit Time ◽  
Capillary Flow ◽  
Biophysical Model ◽  
Therapeutic Consequences ◽  
Capillary Flows ◽  
Flow Disturbances ◽  
Show Evidence ◽  
Diffuse Brain Swelling

Most patients who die after traumatic brain injury (TBI) show evidence of ischemic brain damage. Nevertheless, it has proven difficult to demonstrate cerebral ischemia in TBI patients. After TBI, both global and localized changes in cerebral blood flow (CBF) are observed, depending on the extent of diffuse brain swelling and the size and location of contusions and hematoma. These changes vary considerably over time, with most TBI patients showing reduced CBF during the first 12hours after injury, then hyperperfusion, and in some patients vasospasms before CBF eventually normalizes. This apparent neurovascular uncoupling has been ascribed to mitochondrial dysfunction, hindered oxygen diffusion into tissue, or microthrombosis. Capillary compression by astrocytic endfeet swelling is observed in biopsies acquired from TBI patients. In animal models, elevated intracranial pressure compresses capillaries, causing redistribution of capillary flows into patterns argued to cause functional shunting of oxygenated blood through the capillary bed. We used a biophysical model of oxygen transport in tissue to examine how capillary flow disturbances may contribute to the profound changes in CBF after TBI. The analysis suggests that elevated capillary transit time heterogeneity can cause critical reductions in oxygen availability in the absence of ‘classic’ ischemia. We discuss diagnostic and therapeutic consequences of these predictions.

Pathophysiology of traumatic brain injury

2019 ◽  
pp. 483-496
Author(s):  
Geoffrey T. Manley ◽  
John K. Yue ◽  
Hansen Deng ◽  
Ethan A. Winkler ◽  
John F. Burke ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Injury Severity ◽  
Cerebral Metabolism ◽  
Classification Systems ◽  
Reactivity Index ◽  
Management Options ◽  
Diagnosis And Prognosis ◽  
Flow Disturbances

This chapter provides summative information on the biomechanics, classification, and metabolism of traumatic brain injury (TBI). Impact, impulse, static/quasistatic loading, and related biomechanical sequelae following rotational shear and strain are discussed. Morphological classifications across extradural, acute/chronic subdural, subarachnoid, and intraventricular haemorrhages, as well as cerebral contusions and axonal injuries, are characterized and correlated with injury severity. Management options and implications for penetrating TBI and mild TBI/concussion are described. Cerebral metabolism including pressure/viscosity, CO2 reactivity, and autoregulation are explained in detail to provide for in-depth exploration of a spectrum of secondary injury cascades, encompassing glutamatergic excitotoxicity, autoregulatory loss, and the pressure reactivity index, flow disturbances, elevated intracranial pressure, cortical spreading depression and seizures/epilepsy. Beta-amyloid deposition in response to TBI, and genetic susceptibilities to poor recovery are covered. Current developments to standardize TBI classification systems, establish evidentiary benchmarks for quality of care, and accelerate advances in diagnosis and prognosis are highlighted.

Epidemiology and pathophysiology of traumatic brain injury

2016 ◽  
Author(s):  
Imoigele Aisiku ◽  
Claudia S. Robertson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion ◽  
The Elderly ◽  
Bimodal Distribution ◽  
Developed Countries ◽  
Mortality And Morbidity ◽  
Initial Injury ◽  
Diffuse Brain Swelling ◽  
Mass Lesions

Although medical management of traumatic brain injury (TBI) may have improved in developed countries, TBI is still a major cause of mortality and morbidity. The demographics are skewed towards the younger patient population, and affects males more than females, but in general follow a bimodal distribution with peaks affecting young adults and the elderly. As a result, the loss of functional years is devastating. Pathology due to brain trauma is a complex two-hit phenomenon, frequently divided into ‘primary’ and ‘secondary’ injury. Hypoxia, ischaemia, and inflammation all play a role, and the importance of each component varies between patients and in an individual patient over time. The initial injury may increase intracranial pressure and reduce cerebral perfusion due to the presence of mass lesions or diffuse brain swelling. Further secondary insults, such as hypotension, reduced cerebral perfusion pressure, hypoxia, or fever may exacerbate swelling and inflammation, and further compromise cerebral perfusion. Although there are currently no specific effective treatments for TBI, an improved understanding of the pathophysiology may eventually lead to treatments that will reduce mortality and improve long-term functional outcome.

Abstract WP326: Cortical Border Zones Are More Vulnerable to Spreading Depression-Induced Capillary Flow Disturbances

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Aslihan Taskiran-Sag ◽  
Nina Kerting Iversen ◽  
Eugenio Gutiérrez-Jiménez ◽  
Leif Østergaard ◽  
Turgay Dalkara
Keyword(s):  
Transit Time ◽  
Spreading Depression ◽  
Capillary Flow ◽  
Mean Transit Time ◽  
Border Zone ◽  
Dilution Method ◽  
Cranial Window ◽  
Normal Limits ◽  
Flow Disturbances ◽  
Border Zones

Cortical spreading depression (SD) is a major metabolic challenge to the brain and is followed by a unique hemodynamic response. It has been suggested that the oligemic phase of this response is accompanied by a mild to moderate capillary dysfunction. To test this hypothesis, we directly investigated microcirculatory flow changes during and after SD at the territory of major arteries as well as their hemodynamically vulnerable watershed zones. Swiss mice (n=6) under isoflurane anesthesia were tracheotomized, mechanically ventilated, and imaged under two-photon microscopy through a closed cranial window. Mean transit time (MTT), capillary transit time heterogeneity (CTH) and relative transit time heterogeneity (RTH) were calculated based on an indicator-dilution method using intravenous boluses of Texas-red dextran fluorescent dye (70,000 MW; 0.5%). Boluses were performed at the steady-state and 1 min, 5 min and 30 minutes after potassium chloride-induced SD. MTT, CTH, and RTH were estimated within the territory and border zone of major arteries to reveal any regional differences. Physiological parameters were monitored and kept within normal limits throughout the experiments. Both MTT and CTH increased following SD in the territorial zone from 1.07±0.03 to 1.67±0.15 s (mean±SEM;p<0.01) and from 0.51±0.03 to 0.94±0.07 s (mean±SEM;p<0.01), respectively. However, RTH was only mildly increased in this region from 0.49±0.04 to 0.59±0.06 (p=0.03). In the watershed area, all three parameters showed a more prominent increase following SD and RTH rose from 0.64±0.06 to 1.25±0.22 at 30 minutes (p=0.04). These findings provide direct experimental evidence for prolonged capillary flow disturbances induced by cortical SD, which may account for some lasting neurological symptoms after aura. The particular vulnerability of border zones to SD-induced flow disturbances may be involved in the pathogenesis of some of the white matter MRI lesions observed in migraineurs.

scholarly journals POINT/COUNTER-POINT—Beyond the headlines: the actual evidence that traumatic brain injury is a risk factor for later-in-life dementia

2019 ◽  
Vol 35 (2) ◽  
pp. 123-127 ◽  
Author(s):  
Christian LoBue ◽  
C Munro Cullum
Keyword(s):  
Traumatic Brain Injury ◽  
Risk Factor ◽  
Brain Injury ◽  
Normal Aging ◽  
Older Individuals ◽  
Pathological Changes ◽  
Increased Risk ◽  
Show Evidence ◽  
Rate Of Decline ◽  
Serious Injuries

Abstract Traumatic brain injury (TBI) as a risk factor for developing dementia later in life has been a subject of debate and controversy. TBI has been found to be associated with an increased likelihood for developing dementia 10–30 years later in several retrospective studies using population records. However, understanding the link between TBI and dementia requires looking beyond calculated risk estimates and delving into the association TBI has with pathological changes seen in Alzheimer’s disease and related conditions, as well as those seen in normal aging. Some individuals with TBI, notably those with more serious injuries, show evidence of AD-related pathological changes, such as tau aggregates, at a much earlier age than healthy older individuals without a history of TBI. This would suggest that some people may be more susceptible to the effects of TBI, accumulating additional pathological changes seen in Alzheimer disease and related conditions, which may synergistically and/or cumulatively interact with factors associated with aging. The strongest support to date suggests that TBI may confer an increased risk for earlier onset of neurodegenerative changes in some individuals, possibly as a function of an accumulation of additional pathological changes. While there appears to be a link between TBI and the development of dementia in group studies, the evidence to date does not suggest an association between TBI and progressive cognitive decline during normal aging nor a greater rate of decline in those with dementia. Thus, there remains much to be learned about the pathophysiology of this apparent relationship.

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

The Speech-Language Pathologists' Role in Mild Traumatic Brain Injury for Middle and High School–Age Children: Viewpoints on Guidelines From the Centers for Disease Control and Prevention

2019 ◽  
Vol 28 (3) ◽  
pp. 1363-1370 ◽  
Author(s):  
Jessica Brown ◽  
Katy O'Brien ◽  
Kelly Knollman-Porter ◽  
Tracey Wallace
Keyword(s):  
High School ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Disease Control ◽  
Mild Traumatic Brain Injury ◽  
School Age Children ◽  
School Age ◽  
Speech Language Pathologists ◽  
Control And Prevention ◽  
Centers For Disease Control

Purpose The Centers for Disease Control and Prevention (CDC) recently released guidelines for rehabilitation professionals regarding the care of children with mild traumatic brain injury (mTBI). Given that mTBI impacts millions of children each year and can be particularly detrimental to children in middle and high school age groups, access to universal recommendations for management of postinjury symptoms is ideal. Method This viewpoint article examines the CDC guidelines and applies these recommendations directly to speech-language pathology practices. In particular, education, assessment, treatment, team management, and ongoing monitoring are discussed. In addition, suggested timelines regarding implementation of services by speech-language pathologists (SLPs) are provided. Specific focus is placed on adolescents (i.e., middle and high school–age children). Results SLPs are critical members of the rehabilitation team working with children with mTBI and should be involved in education, symptom monitoring, and assessment early in the recovery process. SLPs can also provide unique insight into the cognitive and linguistic challenges of these students and can serve to bridge the gap among rehabilitation and school-based professionals, the adolescent with brain injury, and their parents. Conclusion The guidelines provided by the CDC, along with evidence from the field of speech pathology, can guide SLPs to advocate for involvement in the care of adolescents with mTBI. More research is needed to enhance the evidence base for direct assessment and treatment with this population; however, SLPs can use their extensive knowledge and experience working with individuals with traumatic brain injury as a starting point for post-mTBI care.

Traumatic Brain Injury: The Day My World Changed

ASHA Leader ◽  
2010 ◽  
Vol 15 (13) ◽  
pp. 38-38
Author(s):  
G. Gayle Kelley
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury
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