Vascular tunnel creation to improve the efficacy of decompressive craniotomy in post-traumatic cerebral edema and ischemic stroke

2002 ◽  
Vol 57 (2) ◽  
pp. 126-129 ◽  
Author(s):  
András Csókay ◽  
László Együd ◽  
László Nagy ◽  
Gergely Pataki
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Edema ◽  
Decompressive Craniotomy ◽  
Post Traumatic

Bifrontal decompressive craniotomy for massive cerebral edema

1971 ◽  
Vol 34 (4) ◽  
pp. 488-493 ◽  
Author(s):  
Raymond N. Kjellberg ◽  
Alberto Prieto
Keyword(s):  
Cerebral Edema ◽  
Massachusetts General Hospital ◽  
Pseudotumor Cerebri ◽  
Toxic Encephalopathy ◽  
Brain Swelling ◽  
High Mortality Risk ◽  
Content Type ◽  
Decompressive Craniotomy ◽  
Post Traumatic ◽  
Mass Lesions

✓ A large bifrontal craniotomy was used in selected patients judged to carry an unusually high mortality risk due to brain swelling secondary to brain trauma. The procedure enabled exploration of both hemisphere convexities, evacuation of accumulated blood and necrotic brain, and decompression of swollen brain. This report reviews 73 cases operated on at the Massachusetts General Hospital since March, 1962; 18% of these patients survived. The largest experience was with post-traumatic cerebral edema, although intractable edema secondary to mass lesions, hemorrhage, toxic encephalopathy, and pseudotumor cerebri was also treated.

scholarly journals Pure Motor Stroke Secondary to Cerebral Infarction of Recurrent Artery of Heubner after Mild Head Trauma: A Case Report

2016 ◽  
Vol 4 (1) ◽  
pp. 139-141
Author(s):  
Ali Yilmaz ◽  
Zahir Kizilay ◽  
Ayca Ozkul ◽  
Bayram Çirak
Keyword(s):  
Ischemic Stroke ◽  
Head Trauma ◽  
Distal Part ◽  
Brain Mri ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Post Traumatic ◽  
The Brain ◽  
Perforating Arteries ◽  
Pure Motor

BACKGROUND: The recurrent Heubner's artery is the distal part of the medial striate artery. Occlusion of the recurrent artery of Heubner, classically contralateral hemiparesis with fasciobrachiocrural predominance, is attributed to the occlusion of the recurrent artery of Heubner and is widely known as a stroke syndrome in adults. However, isolated occlusion of the deep perforating arteries following mild head trauma also occurs extremely rarely in childhood.CASE REPORT: Here we report the case of an 11-year-old boy with pure motor stroke. The brain MRI showed an acute ischemia in the recurrent artery of Heubner supply area following mild head trauma. His fasciobrachial hemiparesis and dysarthria were thought to be secondary to the stretching of deep perforating arteries leading to occlusion of the recurrent artery of Heubner.CONCLUSION: Post-traumatic pure motor ischemic stroke can be secondary to stretching of the deep perforating arteries especially in childhood.

scholarly journals Decompressive craniotomy: prognostic factors and complications in 89 patients

2008 ◽  
Vol 66 (2b) ◽  
pp. 369-373 ◽  
Author(s):  
Rodrigo Moreira Faleiro ◽  
Luiz Carlos Mendes Faleiro ◽  
Elisa Caetano ◽  
Isabella Gomide ◽  
Cristina Pita ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Head Injury ◽  
Severe Head Injury ◽  
Traffic Accidents ◽  
Acute Subdural Hematoma ◽  
Brain Swelling ◽  
Decompressive Craniotomy ◽  
Independent Test ◽  
Post Traumatic ◽  
Subdural Effusions

Decompressive craniotomy (DC) is applied to treat post-traumatic intracranial hypertension (ICH). The purpose of this study is to identify prognostic factors and complications of unilateral DC. Eighty-nine patients submited to unilateral DC were retrospectively analyzed over a period of 30 months. Qui square independent test and Fisher test were used to identify prognostic factors. The majority of patients were male (87%). Traffic accidents had occurred in 47% of the cases. 64% of the patients had suffered severe head injury, while pupillary abnormalities were already present in 34%. Brain swelling plus acute subdural hematoma were the most common tomographic findings (64%). Complications occurred in 34.8% of the patients: subdural effusions in 10 (11.2%), hydrocephalus in 7 (7.9%) and infection in 14 (15.7%). The admittance Glasgow coma scale was a statistically significant predictor of outcome ( p=0.0309).

Abstract T P45: Automated CSF Segmentation to Quantify Cerebral Edema Following Large Hemispheric Ischemic Stroke

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yasheng Chen ◽  
Qingyang Yuan ◽  
Raj Dhar ◽  
Kristin Guilliams ◽  
Laura Heitsch ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Edema ◽  
Large Population ◽  
False Negative ◽  
Hounsfield Unit ◽  
Ground Truth ◽  
Mass Effect ◽  
Stroke Patients ◽  
Segmentation Strategy ◽  
Combined Strategy

Introduction: Cerebral edema with resultant mass effect is a potentially fatal consequence of ischemic stroke, but early and sensitive biomarkers of brain tissue compression are lacking. To quantify brain mass effect, we developed a novel, automated segmentation method to delineate CSF spaces in CT images from ischemic stroke patients. Methods: CTs from sixteen acute ischemic stroke patients (median NIHSS 16.5, median age 61.5 yrs, 14-92 hrs after stroke onset) were included after informed consent was obtained. After infarction, conventional CSF segmentation using Hounsfield unit (HU) thresholding is suboptimal due to infarct hypodensity. Utilizing manually delineated infarct and CSF spaces as training samples, we augmented conventional HU threshold segmentation with level sets, sparse regression and random forest segmentation methods. Using leave-one-out cross-validation, the combined approach was compared to HU thresholding using Dice ratios (a measure of the overlap between the segmented and the ground-truth CSF spaces). Results: Shown is an example of a CT brain slice segmented by HU thresholding and the combined strategy: false negative (red), false positive (green), and true positive (yellow). The Dice ratios for HU thresholding and the combined approaches were 58.2±16.3% and 68.9±14.6%, respectively, demonstrating the significantly improved performance for the combined strategy (p=0.0014). Conclusions: We have developed an advanced image segmentation strategy to delineate CSF spaces which outperforms conventional HU thresholding. An automated CSF segmentation strategy will permit quantification of cerebral edema in a large population of stroke patients, as required for genetic studies, for example.

Decompressive Hemicraniectomy in Children With Severe Ischemic Stroke and Life-Threatening Cerebral Edema

2008 ◽  
Vol 23 (8) ◽  
pp. 889-894 ◽  
Author(s):  
Vijay Ramaswamy ◽  
Vivek Mehta ◽  
Mary Bauman ◽  
Lawrence Richer ◽  
Patti Massicotte ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Edema ◽  
Decompressive Hemicraniectomy ◽  
Life Threatening

scholarly journals Effects of estradiol on ischemic factor-induced astrocyte swelling and AQP4 protein abundance

2011 ◽  
Vol 301 (1) ◽  
pp. C204-C212 ◽  
Author(s):  
Jennifer M. Rutkowsky ◽  
Breanna K. Wallace ◽  
Phyllis M. Wise ◽  
Martha E. O'Donnell
Keyword(s):  
Ischemic Stroke ◽  
Cell Volume ◽  
Cerebral Edema ◽  
Glucose Deprivation ◽  
Aquaporin 4 ◽  
Oxygen Glucose Deprivation ◽  
Protein Abundance ◽  
Astrocyte Swelling ◽  
Aqp4 Protein ◽  
Stimulation Of

In the early hours of ischemic stroke, cerebral edema forms as Na, Cl, and water are secreted across the blood-brain barrier (BBB) and astrocytes swell. We have shown previously that ischemic factors, including hypoxia, aglycemia, and arginine vasopressin (AVP), stimulate BBB Na-K-Cl cotransporter (NKCC) and Na/H exchanger (NHE) activities and that inhibiting NKCC and/or NHE by intravenous bumetanide and/or HOE-642 reduces edema and infarct in a rat model of ischemic stroke. Estradiol also reduces edema and infarct in this model and abolishes ischemic factor stimulation of BBB NKCC and NHE. There is evidence that NKCC and NHE also participate in ischemia-induced swelling of astrocytes. However, little is known about estradiol effects on astrocyte cell volume. In this study, we evaluated the effects of AVP (100 nM), hypoxia (7.5% O2), aglycemia, hypoxia (2%)/aglycemia [oxygen glucose deprivation (OGD)], and estradiol (1–100 nM) on astrocyte cell volume using 3- O-methyl-d-[3H]glucose equilibration methods. We found that AVP, hypoxia, aglycemia, and OGD (30 min to 5 h) each significantly increased astrocyte cell volume, and that estradiol (30–180 min) abolished swelling induced by AVP or hypoxia, but not by aglycemia or OGD. Bumetanide and/or HOE-642 also abolished swelling induced by AVP but not aglycemia. Abundance of aquaporin-4, known to participate in ischemia-induced astrocyte swelling, was significantly reduced following 7-day but not 2- or 3-h estradiol exposures. Our findings suggest that hypoxia, aglycemia, and AVP each contribute to ischemia-induced astrocyte swelling, and that the edema-attenuating effects of estradiol include reduction of hypoxia- and AVP-induced astrocyte swelling and also reduction of aquaporin-4 abundance.

scholarly journals Cerebral edema and its treatment

Medicina ◽  
2007 ◽  
Vol 43 (2) ◽  
pp. 170 ◽  
Author(s):  
Dalia Adukauskienė ◽  
Asta Bivainytė ◽  
Edita Radavičiūtė
Keyword(s):  
Cerebral Perfusion Pressure ◽  
Cerebral Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Energy Potential ◽  
Antiinflammatory Drugs ◽  
Antihypertensive Medications ◽  
Cerebral Tumor ◽  
Decompressive Craniotomy

Cerebral edema is a life-threatening condition that develops as a result of an inflammatory reaction. Most frequently, this is the consequence of cerebral trauma, massive cerebral infarction, hemorrhages, abscess, tumor, allergy, sepsis, hypoxia, and other toxic or metabolic factors. At present, the following types of cerebral edema are differentiated: the vasogenic cerebral edema resulting from an increased permeability of the endothelium of cerebral capillaries to albumin and other plasma proteins; the cytotoxic cerebral edema resulting from the exhaustion of the energy potential of cell membranes without damage to the barrier; the hydrostatic cerebral edema resulting from disturbance of the autoregulation of cerebral blood circulation; the osmotic cerebral edema resulting from dilution of blood; and the interstitial cerebral edema resulting from acute hydrocephaly. Some authors also differentiate ischemic cerebral edema. At present, when various traumas and traumatic cerebral injuries are frequent causes of death in young people, treatment strategy for cerebral edema is of utmost importance. Monitoring of the patient’s condition in the intensive care unit is a necessity. It is important to ensure proper positioning of the patient – the head should be tilted at 30o in order to optimize the cerebral perfusion pressure and control of the increase in intracranial pressure. Hyperventilation should be applied. Controlled hypothermia decreases the rate of metabolism in the brain. Slightly positive fluid balance should be maintained using crystalloid or colloid (hypertonic–hyperoncotic) solutions, at the same time maintaining cerebral perfusion pressure exceeding 70 mmHg. The treatment includes administration of antihypertensive medications, nonsteroidal antiinflammatory drugs, and barbiturates. Steroids decrease the permeability of capillaries and the hemato-encephalic barrier, promoting the movement of Na+/K+ ions and water through the main endothelial membrane, and therefore they are used in the treatment of vasogenic cerebral edema as well as edema caused by a cerebral tumor. Glutamate and N-methyl-D-aspartate receptor antagonists improve cerebral microcirculation and metabolism. Trometamol corrects cerebral acidosis. Extended cerebral edema is treated surgically via a bilateral decompressive craniotomy, sometimes including craniotomy of lateral and posterior fossae. The treatment of cerebral edema is complex, and positive results may be expected only if the diagnosis and the provision of assistance are timely.

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