Traumatic brain injury

Ghajar, Jamshid

doi:10.1016/s0140-6736(00)02689-1

Cited by 1,101 publications

(545 citation statements)

References 83 publications

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“…Therefore, we determined IL-8 levels in central venous blood plasma and cerebrospinal fluid (CSF) of patients with isolated TBI at admittance to Intensive Care Unit and analyzed their potential relevance as prognostic indicators of mortality. The age of patients as well as clinical scoring systems Acute Physiologic and Chronic Health Evaluation (APACHE II) and Glasgow Coma Scale (GCS) known to be reliable predictive parameters in TBI patients (Ghajar 2000;Boto et al 2006) were also analyzed in respect to the mortality.…”

mentioning

confidence: 99%

Plasma Interleukin-8 as a Potential Predictor of Mortality in Adult Patients with Severe Traumatic Brain Injury

Gopčević

Mazul-Sunko

Marout

et al. 2007

Tohoku J. Exp. Med.

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mentioning

confidence: 99%

Plasma Interleukin-8 as a Potential Predictor of Mortality in Adult Patients with Severe Traumatic Brain Injury

Gopčević

Mazul-Sunko

Marout

et al. 2007

Tohoku J. Exp. Med.

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“…This primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, occurring within seconds to minutes after the trauma and lasting for days, months or years [40]. The ongoing brain damage characteristic of secondary injury culminates in notable cell death [24,40,41]. Typically, initial neuronal death following acute brain injury occurs by necrosis, on a time scale of minutes, then, a second wave of delayed cell death occurs mostly by apoptosis [13,[42][43][44][45].…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Understanding the pathophysiology of TBI is crucial for the development of more effective therapeutic strategies. At the moment of the traumatic impact, transfer of kinetic forces causes neurologic damage; this primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, called secondary neural injury. These areas of ongoing secondary injury, or areas of "traumatic penumbra," represent crucial targets for therapeutic interventions. This chapter is focused on the interplay between progression of parenchymal injury and the neuroprotective and neurorestorative processes that are emerging and developing subsequently to traumatic impact. Thus, we emphasized the role of traumatic penumbra in TBI pathogenesis and suggested a crucial contribution of the neurovascular units (NVUs) and paracrine effects of exosomes and miRNAs in promoting neurological recovery.

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“…Распространенность ЧМТ в последние десятилетия резко возросла, главным образом из-за увеличивающегося использования ав-тотранспортных средств в развивающихся странах [12,15,18]. ЧМТ уже начали называть «тихой эпи-демией» [23] из-за роста масштабов этой проблемы, низкой общественной осведомленности о ее зна-чимости и неполных эпидемиологических данных.…”

Section: Introductionunclassified