Physiologic and functional outcome correlates of brain tissue hypoxia in traumatic brain injury*

Chang, Jason J.; Youn, Teddy S.; Benson, Dan; Mattick, Heather; Andrade, Nicholas S.; Harper, Caryn R.; Moore, Carol; Madden, Christopher J.; Diaz‐Arrastia, Ramon

doi:10.1097/ccm.0b013e318192fbd7

Cited by 156 publications

(90 citation statements)

References 37 publications

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“…Adequate function of mitochondria is pivotal for the survival and activity of all brain cells, and even brief periods of oxygen or glucose deprivation could shut down brain functions within seconds, damaging neurons within minutes. 4 Abundant data from retrospective studies and prospective clinical trials have shown brain hypoxia to be an early predictor of adverse outcomes after TBI, [5][6][7] because efficient ATP production by the mitochondrial respiratory chain relies on continuous oxygen supply.…”

Section: Traumatic Brain Injury (Tbi)mentioning

confidence: 99%

Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

Dong

Zhang

Hamblin

et al. 2015

J Cereb Blood Flow Metab

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Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memory function, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energyproducing insufficient tissue-like injured brain.

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Section: Traumatic Brain Injury (Tbi)mentioning

confidence: 99%

Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

Dong

Zhang

Hamblin

et al. 2015

J Cereb Blood Flow Metab

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show abstract

“…16 Common causes of elevated ICP include development of mass lesions such as subdural hematoma, epidural hematoma, and intracerebral contusions. Additionally, cerebral edema and communicating and noncommunicating hydrocephalus are treatable causes of increased ICP.…”

Section: Physiology Of Icp and Cppmentioning

confidence: 99%

Traumatic Brain Injury: Advanced Multimodal Neuromonitoring From Theory to Clinical Practice

Cecil¹,

Chen²,

Callaway³

et al. 2010

Critical Care Nurse

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“…The correlation between clinical deterioration and ICP is not a robust one: because the brain is anatomically compartmentalized, fatal herniation syndromes may occur without associated changes in ICP, for example, after posterior fossa hemorrhage or infarction. Studies conducted in TBI patients with parenchymal oxygen or microdialysis probes demonstrate that brain tissue hypoxia and metabolic distress can occur independently of ICP or CPP [9,10], perhaps superseding the latter in terms of prognostic significance [11]. Evidence that cerebral pressure autoregulation is globally or regionally impaired following severe TBI means that ischemia can occur at apparently adequate CPP levels [12,13]-a serious challenge to the current recommendation of a single CPP target in all patients [14].…”

mentioning

confidence: 99%

Intracranial pressure and its surrogates

Frattalone

Stevens

2011

Intensive Care Med

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Intracranial hypertension [intracranial pressure (ICP) [20 mmHg] is a life-threatening complication seen in a significant proportion of patients following severe traumatic and nontraumatic brain insults [1][2][3]. Sustained elevations in ICP generally signal secondary injury processes such as cerebral edema, hemorrhage, hydrocephalus and ischemia, and as a consequence the management of ICP has become a keystone in neurocritical care. Especially in unresponsive patients when the diagnostic yield of physical examination is limited, temporal trends in ICP can help identify critical changes in intracranial compliance and responses to therapy. Many studies indicate an independent association between the magnitude and duration of ICP elevation and unfavorable outcomes following severe brain injury [2][3][4]. The difference of ICP and mean arterial pressure, cerebral perfusion pressure (CPP), is widely used to infer relationships between systemic circulatory function and cerebral blood flow. Many interventions in brain resuscitation, such as hyperosmolar therapy, sedation, controlled ventilation, and use of vasopressor or inotropic agents, are targeted to ICP and CPP goals. Current guidelines recommend ICP monitoring in patients with severe traumatic brain injury (TBI) who are comatose after resuscitation and who either have abnormalities on cranial computed tomography (CT) scan or meet at least two of the following three criteria: age[40 years; systolic blood pressure \90 mmHg; or motor posturing [5].The gold standard for measuring ICP is via devices placed inside the brain (intraventricular and intraparenchymal monitors). These devices are resource-intensive, carry small but significant risks of infection and hemorrhage, and in the case of intraparenchymal monitors are prone to drift with accuracy declining over time. Alternative methods have been proposed that noninvasively assess ICP through the measurement of a surrogate variable: these include neuroimaging (cranial CT and brain MRI), transcranial Doppler, tympanic membrane displacement, intraocular pressure, venous ophtalmodynanometry, and changes in the optic nerve sheath diameter (ONSD). In this issue of Intensive Care Medicine, Dubourg et al.[6] present a meta-analysis of studies

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Physiologic and functional outcome correlates of brain tissue hypoxia in traumatic brain injury*

Cited by 156 publications

References 37 publications

Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

Low-Level Light in Combination with Metabolic Modulators for Effective Therapy of Injured Brain

Traumatic Brain Injury: Advanced Multimodal Neuromonitoring From Theory to Clinical Practice

Intracranial pressure and its surrogates

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