5 research outputs found
Use of T2-weighted magnetic resonance imaging of the optic nerve sheath to detect raised intracranial pressure.
INTRODUCTION: The dural sheath surrounding the optic nerve communicates with the subarachnoid space, and distends when intracranial pressure is elevated. Magnetic resonance imaging (MRI) is often performed in patients at risk for raised intracranial pressure (ICP) and can be used to measure precisely the diameter of optic nerve and its sheath. The objective of this study was to assess the relationship between optic nerve sheath diameter (ONSD), as measured using MRI, and ICP. METHODS: We conducted a retrospective blinded analysis of brain MRI images in a prospective cohort of 38 patients requiring ICP monitoring after severe traumatic brain injury (TBI), and in 36 healthy volunteers. ONSD was measured on T2-weighted turbo spin-echo fat-suppressed sequence obtained at 3 Tesla MRI. ICP was measured invasively during the MRI scan via a parenchymal sensor in the TBI patients. RESULTS: Measurement of ONSD was possible in 95% of cases. The ONSD was significantly greater in TBI patients with raised ICP (>20 mmHg; 6.31 +/- 0.50 mm, 19 measures) than in those with ICP of 20 mmHg or less (5.29 +/- 0.48 mm, 26 measures; P < 0.0001) or in healthy volunteers (5.08 +/- 0.52 mm; P < 0.0001). There was a significant relationship between ONSD and ICP (r = 0.71, P < 0.0001). Enlarged ONSD was a robust predictor of raised ICP (area under the receiver operating characteristic curve = 0.94), with a best cut-off of 5.82 mm, corresponding to a negative predictive value of 92%, and to a value of 100% when ONSD was less than 5.30 mm. CONCLUSIONS: When brain MRI is indicated, ONSD measurement on images obtained using routine sequences can provide a quantitative estimate of the likelihood of significant intracranial hypertension
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Abstracts from the 44th Annual Meeting of the Society for Neuroscience in Anesthesiology and Critical Care, Chicago, IL, October 20–21, 2016
Background: Metabolic derangements are common after traumatic brain
injury (TBI) (Abate et al., Neurocrit Care, 2008), but few studies have
combined 18F-fluorodeoxyglucose (FDG) and multi-tracer oxygen-15
(15O) positron emission tomography (PET) to interrogate underlying
pathophysiological mechanisms (Hatori et al., J Nucl Med, 2004). We
examined how derangements in FDG kinetic parameters within injured
brain relate to cerebral blood flow (CBF), blood volume (CBV), oxygen
metabolism (CMRO2) and oxygen extraction fraction (OEF)
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Neurocritical Care Society 14(th) Annual Meeting.
Introduction
Metabolic derangements are common after traumatic brain injury (TBI), but few studies have used multi-tracer positron emission tomography (PET) to interrogate underlying pathophysiology. We examined relationships between glucose metabolism (measured using 18F-fluorodeoxyglucose (FDG) PET) and cerebral blood flow (CBF; measured using H215O PET).
Methods
Twenty-six TBI patients with median (range) pre-intubation Glasgow Coma Score of 6 (3-12) underwent combined 15O and FDG PET on 34 occasions; 10 and 18 healthy volunteers (controls) underwent 15O and FDG PET respectively. FDG rate constants were determined with an irreversible two-compartment model: transport across BBB (K1,k2), hexokinase activity (k3), and influx rate (Ki). Regions of interest (ROIs) were defined for haemorrhagic lesion (core), hypodense tissue (penumbra), 1 cm border zone of normal appearing tissue (peri-penumbra), and remote normal appearing tissue (normal).
Results
K1 was significantly reduced within core, but was comparable to control values in peri-penumbra and normal ROIs. While k3 and Ki were lower than control values, regional increases were found in the vicinity of lesions and some structurally normal areas. Glucose delivery (measured by K1) was unrelated to CBF when values were above 30ml/100ml/min, and was significantly below 95% confidence intervals for control values when CBF was below 25ml/100ml/min. There was a clear linear relationship between K1 and CBF in core ROIs (R²=0.75, p<0.01). Ki exhibited similar relationships to CBF, but showed more variability due to changes in k3.
Conclusion
We found impaired FDG (glucose) transport within the vicinity of lesions that was linearly related to CBF below a threshold value of 30ml/100ml/min. While a similar relationship was found for FDG influx (Ki), variability in k3 suggests different metabolic derangements are responsible. Further analyses will explore how such regional heterogeneity relates to evidence of necrosis, classical ischemia, and other metabolic derangements
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Abstracts from The 34(th) Annual National Neurotrauma Symposium June 26-29, 2016 Lexington, Kentucky.
Objectives: Glial fibrillary acidic protein (GFAP) and ubiquitin Cterminal
hydrolase-L1 (UCH-L1) have been studied as potential
biomarkers of mild traumatic brain injury (mTBI). We report the
levels of GFAP and UCH-L1 in patients with acute orthopedic injuries
without central nervous system involvement and relate them to the
levels in patients with CT-negative mTBI.
Methods: Serum UCH-L1 and GFAP were measured from 73 patients
with acute orthopedic injury. The injury types were recorded
and most of the patients underwent also a head MRI. The results were
compared to those found in patients with CT-negative mTBI (n = 93).
Results: The levels of GFAP were higher in patients with acute
orthopedic trauma than in patients with CT-negative mTBI
(p = 0.026). The levels of UCH-L1 were not significantly different
between these two groups. Those patients with orthopedic trauma,
who had levels of either or both of these biomarkers in the upper
quartile, had significantly higher levels of both biomarkers than patients
with CT-negative mTBI (p < 0.001).
Conclusions: Levels of GFAP and UCH-L1 were not able to distinguish
patients with CT negative mTBI from patients with orthopedic
trauma. Patients with orthopedic trauma and high levels of
UCH-L1 or GFAP values may be falsely diagnosed as having a
concomitant mTBI. This casts a significant doubt on their diagnostic
value in cases with mTBI.
Keywords: GFAP, UCH-L1, orthopedic injur