Temporal and Spatial Profile of Brain Diffusion-Weighted MRI After Cardiac Arrest

Mlynash, Michael; Campbell, Dennis; LeProust, Emily; Fischbein, Nancy J.; Bammer, Roland; Eyngorn, Irina; Hsia, Amie W.; Moseley, Michael E.; Wijman, Christine A.C.

doi:10.1161/strokeaha.110.582452

Cited by 147 publications

(129 citation statements)

References 21 publications

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“…In a small study subpopulation 292 (12 patients; verylow-quality evidence), presence of diffuse DWI abnormalities in cortex or brainstem at a median of 80 hours from ROSC predicted poor outcome, with 0 (0-35)% FPR. In another small study 337 (12 patients; very-low-quality evidence), presence of extensive (cortex, basal ganglia, and cerebellum) DWI changes predicted poor outcome, with 0 (0-45)% FPR.…”

Section: Mrimentioning

confidence: 98%

“…241,279,289 For the critical outcome of survival with unfavorable neurologic status or death at 180 days, we identified 6 studies on CT or magnetic resonance imaging (MRI; 246 subjects; very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision). 251,287,[290][291][292][293] CT Scan. The main CT finding of global anoxic-ischemic cerebral insult after cardiac arrest is cerebral edema, 294 which appears as a reduction in the depth of cerebral sulci (sulcal effacement) and an attenuation of the gray matter/white matter (GM/WM) interface, due to a decreased density of the GM.…”

Section: Imagingmentioning

confidence: 99%

See 1 more Smart Citation

Part 4: Advanced Life Support

Nolan¹,

Hazinski²,

Aickin³

et al. 2015

Circulation

551

125

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Questions to be addressed (using the PICO [population, intervention, comparator, outcome] format) 3 were prioritized by ALS Task Force members (by voting). Prioritization criteria included awareness of significant new data and new controversies or questions about practice. Questions about topics no longer relevant to contemporary practice or where little new research has occurred were given lower priority. The ALS Task Force prioritized 42 PICO questions for review. With the assistance of information specialists, a detailed search for relevant articles was performed in each of 3 online databases (PubMed, Embase, and the Cochrane Library).By using detailed inclusion and exclusion criteria, articles were screened for further evaluation. The reviewers for each question created a reconciled risk of bias assessment for each of the included studies, using state-of-the-art tools: Cochrane for randomized controlled trials (RCTs), 4 Quality Assessment of Diagnostic Accuracy Studies (QUADAS)-2 for studies of diagnostic accuracy, 5 and GRADE for observational studies that inform both therapy and prognosis questions. 6 GRADE evidence profile tables 7 were then created to facilitate an evaluation of the evidence in support of each of the critical and important outcomes. The quality of the evidence (or confidence in the estimate of the effect) was categorized as high, moderate, low, or very low, 8 based on the study methodologies and the 5 core GRADE domains of risk of bias, inconsistency, indirectness, imprecision, and other considerations (including publication bias). 9 These evidence profile tables were then used to create a written summary of evidence for each outcome (the consensus on science statements). Whenever possible, consensus-based treatment recommendations were then created. These recommendations (designated as strong or weak) were accompanied by an overall assessment of the evidence and a statement from the task force about the values, preferences, and task force insights that underlie the recommendations. Further details of the methodology that underpinned the evidence evaluation process are found in "Part 2: Evidence Evaluation and Management of Conflicts of Interest."The task force preselected and ranked outcome measures that were used as consistently as possible for all PICO questions. Longer-term, patient-centered outcomes were considered more important than process variables and shorter-term outcomes. For most questions, we used the following hierarchy starting with the most important: long-term survival with neurologically favorable survival, long-term survival, short-term survival, and process variable. In general, longterm was defined as from hospital discharge to 180 days or longer, and short-term was defined as shorter than to hospital discharge. For certain questions (eg, related to defibrillation or confirmation of tracheal tube position), process variables such as termination of fibrillation and correct tube placement were important. A few questions (eg, organ donation) required unique outcomes....

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Section: Mrimentioning

confidence: 98%

Section: Imagingmentioning

confidence: 99%

Part 4: Advanced Life Support

Nolan¹,

Hazinski²,

Aickin³

et al. 2015

Circulation

551

125

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“…In a recent prospective cohort study in patients with global cerebral ischemia after cardiac arrest, 3 out of 15 patients with poor neurological outcome had no DWI abnormalities at all after 2, 7, and 14 hours, respectively. 126 In another patient with severe global ischemic brain injury affirmed by autopsy findings, no DWI abnormalities were found 6 hours after the onset of ischemia. 124 Similar findings have been reported in patients with focal ischemia.…”

mentioning

confidence: 90%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

215

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Abstract-In the human brain, Ϸ30% of the energy is spent on synaptic transmission. Disappearance of synaptic activity is the earliest consequence of cerebral ischemia. The changes of synaptic function are generally assumed to be reversible and persistent damage is associated with membrane failure and neuronal death. However, there is overwhelming experimental evidence of isolated, but persistent, synaptic failure resulting from mild or moderate cerebral ischemia. Early failure results from presynaptic damage with impaired transmitter release. Proposed mechanisms include dysfunction of adenosine triphosphate-dependent calcium channels and a disturbed docking of glutamate-containing vesicles resulting from impaired phosphorylation. We review energy distribution among neuronal functions, focusing on energy usage of synaptic transmission. We summarize the effect of ischemia on neurotransmission and the evidence of long-lasting synaptic failure as a cause of persistent symptoms in patients with cerebral ischemia. Finally, we discuss the implications of synaptic failure in the diagnosis of cerebral ischemia, including the limited sensitivity of diffusion-weighted MRI in those cases in which damage is presumably limited to the synapses. (Stroke. 2012;43:607-615.)Key Words: brain metabolism Ⅲ cerebral ischemia Ⅲ synaptic failure T he human brain is metabolically expensive. Although it represents only 2% of the body weight, it accounts for 20% of oxygen consumption and 25% of glucose utilization. 1,2 Cerebral ischemia is a pathological condition in which blood flow to the brain is insufficient to meet these metabolic demands, causing a loss of neuronal function and viability. Ischemia may be focal if a brain artery is occluded or global, for example, after cardiac arrest.In the 1950s, the concept of perfusion thresholds was introduced. 3 It was shown that functional activity became impaired with moderately reduced perfusion (14 -35 mL/100 g/min), along with electroencephalographic and evoked potential disturbances, whereas loss of ion gradients across the plasma membrane and subsequent cell swelling occur at lower perfusion levels Ϸ4.8 to 8.4 mL/100 g/min (Figure 1). [3][4][5] In focal brain ischemia, the brain tissue that is perfused in the flow range between these 2 levels is now called the penumbra. 6 The penumbra is considered structurally intact and viable, but functionally silent. The dysfunction is, in principle, reversible by restoration of blood flow. However, if oxygen and glucose are not resupplied in time, irreversible damage occurs.Knowledge on the distribution of energy usage among different neuronal activities may contribute to understanding the successive loss of cell function and cell damage in cerebral ischemia. In the human brain, Ϸ30% of the energy is spent on synaptic transmission. 7 Disappearance of synaptic activity is the earliest consequence of cerebral ischemia 8 and failure of synaptic transmission has been proposed to account for electric silence in the penumbra. 3,6,8 -10 The changes of syna...

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“…In hypoxic‐ischemic/reperfusion, it is the ADC but not FA values that correlate with water transport in and out of the cells (Wang, Wang, & Guo, 2012). Compared with changes in FA, quantitative changes in the ADC may be more specific for the prognostication of subtle MRI changes (Mlynash et al., 2010). In addition, technically, ADC values can be directly obtained from ADC maps.…”

Section: Introductionmentioning

confidence: 99%

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

et al. 2018

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IntroductionThe aim of this study was to explore whether patients with chronic obstructive pulmonary disease (COPD) develop vasogenic cerebral edema, and whether this edema contributes to the COPD‐related disability.MethodsEighteen stable patients with COPD and 17 matched healthy volunteers were enrolled. Apparent diffusion coefficient (ADC) values were calculated by voxel‐based analysis using DTI‐Studio software based on diffusion tensor imaging. COPD‐related disability was calculated using activities of daily living (ADL) scale.ResultsIn patients with COPD, ADC increased in the white matter fiber tracts including the bilateral anterior cingulum and posterior corpus callosum and in the white matter fibers connecting the bilateral insular cortices, sub‐lobar cortices, and pars triangularis cortices and the left rectus and olfactory gyrus. However, after further controlling for cigarette smoking, the difference in ADC values in the posterior corpus callosum between groups disappeared. Patients with COPD had significantly higher scores in ADL than that in controls. Moreover, ADL scores were positively correlated with the increased regional ADC values.ConclusionVasogenic cerebral edema occurs in patients with COPD. Cigarette smoking may be a risk factor for COPD‐related vasogenic edema. Vasogenic cerebral edema may be related to the COPD‐related ADL impairment.

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Temporal and Spatial Profile of Brain Diffusion-Weighted MRI After Cardiac Arrest

Cited by 147 publications

References 21 publications

Part 4: Advanced Life Support

Part 4: Advanced Life Support

Ischemic Cerebral Damage

Vasogenic cerebral edema associated with the disability in activities of daily living in patients with chronic obstructive pulmonary disease

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