Early Cerebral Circulation Disturbance in Patients Suffering from Different Types of Severe Traumatic Brain Injury: A Xenon CT and Perfusion CT Study

Honda, Masashi; Sase, Sadanori; Yokota, Kyosuke; Ichibayashi, Ryo; Masuda, Hiroyuki; Uekusa, Hiroyuki; Nomoto, Jun; Sugo, Nobuo; Kishi, Taichi; Seiki, Yoshikatsu

doi:10.1007/978-3-7091-1434-6_49

Cited by 11 publications

(8 citation statements)

References 11 publications

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“…Identifying cases of TBI where the use of hypothermia is warranted is vital. In agreement with previously mentioned data, xenon- and perfusion-CT analyses demonstrated disturbances in cerebral blood flow (CBF) in TBI patients [53]. In that study, Honda et al .…”

Section: Prophylactic Hypothermia and Hyperbaric Oxygen Therapy (Hbot)supporting

confidence: 89%

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Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

Algattas

Huang

2013

IJMS

227

178

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Traumatic Brain Injury (TBI) affects a large proportion and extensive array of individuals in the population. While precise pathological mechanisms are lacking, the growing base of knowledge concerning TBI has put increased emphasis on its understanding and treatment. Most treatments of TBI are aimed at ameliorating secondary insults arising from the injury; these insults can be characterized with respect to time post-injury, including early, intermediate, and late pathological changes. Early pathological responses are due to energy depletion and cell death secondary to excitotoxicity, the intermediate phase is characterized by neuroinflammation and the late stage by increased susceptibility to seizures and epilepsy. Current treatments of TBI have been tailored to these distinct pathological stages with some overlap. Many prophylactic, pharmacologic, and surgical treatments are used post-TBI to halt the progression of these pathologic reactions. In the present review, we discuss the mechanisms of the pathological hallmarks of TBI and both current and novel treatments which target the respective pathways.

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Section: Prophylactic Hypothermia and Hyperbaric Oxygen Therapy (Hbot)supporting

confidence: 89%

“…In that study, Honda et al . (2013) found CBF in focal TBI patients to be more perturbed than in diffuse TBI [53]. The research group suggested moderate hypothermia should be used in managing cases of TBI involving larger CBF changes.…”

Section: Prophylactic Hypothermia and Hyperbaric Oxygen Therapy (Hbot)mentioning

confidence: 99%

Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

Algattas

Huang

2013

IJMS

227

178

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“…that do not reach ischemic levels. 225,226 However, after TBI, metabolic/hemodynamic requirements of the tissue may differ from normal tissues and could potentially participate in both the acute and more chronic consequences of neurotrauma. 227 In addition to alterations in blood flow, changes in vascular reactivity to various stimuli, including vasodilators, have also been emphasized in the literature.…”

Section: Cerebral Blood Flow Alterationsmentioning

confidence: 99%

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Bramlett

Dietrich

2015

Journal of Neurotrauma

372

257

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Traumatic brain injury (TBI) is a significant clinical problem with few therapeutic interventions successfully translated to the clinic. Increased importance on the progressive, long-term consequences of TBI have been emphasized, both in the experimental and clinical literature. Thus, there is a need for a better understanding of the chronic consequences of TBI, with the ultimate goal of developing novel therapeutic interventions to treat the devastating consequences of brain injury. In models of mild, moderate, and severe TBI, histopathological and behavioral studies have emphasized the progressive nature of the initial traumatic insult and the involvement of multiple pathophysiological mechanisms, including sustained injury cascades leading to prolonged motor and cognitive deficits. Recently, the increased incidence in age-dependent neurodegenerative diseases in this patient population has also been emphasized. Pathomechanisms felt to be active in the acute and long-term consequences of TBI include excitotoxicity, apoptosis, inflammatory events, seizures, demyelination, white matter pathology, as well as decreased neurogenesis. The current article will review many of these pathophysiological mechanisms that may be important targets for limiting the chronic consequences of TBI.

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“…Furthermore, CBF can be calculated either by a non-deconvolution or a deconvolution algorithm, of which the latter is less prone to error and was preferred (229). There are several studies validating and standardising the results of CTP based measurements of CBV and CBF (229) and showing adequate correlation between CBF calculations derived from CTP and Xe-CT (230,231), thus the CBF data was pooled before statistical analysis.…”

Section: Perfusion Computed Tomographymentioning

confidence: 99%

“…Although above ischemic thresholds, CBF was lower than normal, plausibly due to an effect of sedation used in the majority of patients (11/12) at time of CBF evaluation. The use of two different methods for determining CBF can be criticised, although there are studies showing reliable translation of CBF between Xe-CT and CTP (230,231,262). Failure to utilise CTP would exclude all extubated patients from the study protocol, since Xe-CT requires sedation and mechanical ventilation.…”

Section: Metabolic Crisis In Perihaemorrhagic Zone (Paper I)mentioning

confidence: 99%

Surgically Treated Intracerebral Haemorrhage : Pathophysiology and Clinical Aspects

Tobieson

2019

Linköping University Medical Dissertations

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To Ester!If it doesn't challenge you it doesn't change you! /the inside of my Ironman cap  Abstract i ABSTRACT Mortality and morbidity of intracerebral haemorrhage (ICH) is excessively high, and the case fatality rate has not improved in the last decades. Although surgery for ICH can be life-saving, no positive effect on functional outcome has been found in large cohorts of ICH patients. Increased understanding of the pathophysiology of ICH is needed to develop improved treatment strategies. Svensk sammanfattningiii KIRURGISK BEHANDLING AV HJÄRN-BLÖDNINGAR Spontan primär hjärnblödning (ICH), som inte beror på pulsåderbråck, utgör ca 12.5% av alla strokeinsjuknanden per år i Sverige, och står för en ansenlig del av den årliga stroke-relaterade dödligheten och förlusten av funktion. Endast en liten del av patienterna kan rehabiliteras åter till ett självständigt liv. I dagsläget saknas effektiv behandling utöver att förebygga att blödningen ökar i storlek genom snabb korrigering av koagulationsrubbningar och blodtryckssänkande behandling. Ca 5 % av alla ICH i Sverige opereras, men det saknas tydlig evidens för nyttan av kirurgi utöver som livräddande åtgärd.(ii-iii) Mikrodialys är en användbar metod för att studera hjärnskada efter ICH och kan kombineras med proteomik analys men det finns fallgropar och svårigheter med tekniken att ta hänsyn till, såsom att proteiner fastnar på mikrodialysmembranet.(iv) Den nationsövergripande genomgången av kirurgiskt behandlade ICH patienter påvisar likheter avseende patienternas ålder och medvetandegrad, men skillnader i volym och lokalisation av opererade blödningar, samt i den postoperativa vården. Dessa skillnader bör vara fokus för framtida forskningsstudier för att möjliggöra utformningen av bättre riktlinjer för klinisk praxis.

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Early Cerebral Circulation Disturbance in Patients Suffering from Different Types of Severe Traumatic Brain Injury: A Xenon CT and Perfusion CT Study

Cited by 11 publications

References 11 publications

Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

Traumatic Brain Injury Pathophysiology and Treatments: Early, Intermediate, and Late Phases Post-Injury

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes

Surgically Treated Intracerebral Haemorrhage : Pathophysiology and Clinical Aspects

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