1/153. noonan syndrome and cavernous hemangioma of the brain.We present two patients with multiple characteristics that occur in Noonan phenotype and cavernous hemangioma of the brain. The first patient, who had been diagnosed radiographically as having a cavernous hemangioma in the left basal ganglia at age 15 years, developed massive intracerebral hemorrhage, resulting in sudden death at home at 19 years. The second patient, who was diagnosed radiographically as having a cavernous hemangioma in the left parietal lobe at age 17 years, is being followed carefully (the patient is currently 18 years old). A review disclosed four cases of structural cerebrovascular abnormalities with or without subsequent hemorrhage. Neither these four patients nor our two patients had any severe anomalies in the heart or large vessels, which are frequently seen in patients with noonan syndrome. Cerebrovascular abnormalities might have a significant influence on the prognosis of patients with noonan syndrome, especially those having no severe abnormalities in the heart or large vessels.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/153. Dural arteriovenous malformation in the anterior cranial fossa.Two cases of dural arteriovenous malformation (AVM) at the base of the anterior cranial fossa are described. In both cases an intracerebral hematoma following the rupture of the AVM was the first indication of the disease. In one case, the malformation was supplied both by the anterior ethmoidal artery and frontopolar artery draining into the superior sagittal sinus. In the second case, the right anterior ethmoidal artery with draining veins into the superior sagittal sinus and sphenoparietal sinus was the feeding vessel. Surgical evacuation of the hematoma and excision of the malformation was performed on both patients. The typical clinical signs and radiological findings are described. A review of the pertinent literature is given.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
3/153. rupture of several parasagittal bridging veins without subdural bleeding.This case reports on a fatal craniocerebral trauma involving numerous ruptured cerebral bridging veins that did not bleed subdurally, despite approximately 15 hours of survival. A 15-year-old girl was severely injured as the passenger of a car that crashed sideways into a tree. She-suffered a cerebral trauma of the "diffuse injury" type and was unconscious after the accident. Her computed tomographic scan at admission showed massive brain edema, axial herniation, and marked hypodensity of the bilateral carotid flow area. Despite intensive care measures, the clinical course was characterized by central decompensation with therapy-resistant cardiocirculatory insufficiency. The autopsy revealed ruptures of numerous parasagittal bridging veins. The injured vessels were not thrombosed, and yet there was absolutely no subdural bleeding. This unusual combination of findings is assumed to be caused by an isolated collapse of cerebral circulation occurring shortly after the accident and primarily attributed to a rapid increase of intracranial pressure.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
4/153. Hyperacute cerebral enhancement: the earliest predictor of hemorrhage by MR imaging?A test to detect very early hemorrhage in acute cerebral infarct could offer a substantial increase in the safety and success of advanced stroke therapies, particularly when the use of thrombolytic therapies is contemplated. Currently, computed tomography is the standard test for the detection of cerebral hemorrhage but is not a valid predictor of potential areas of hemorrhagic transformation. A technique to evaluate the risk of hemorrhagic transformation in infarcted cerebral tissue has been conducted with contrast-enhanced magnetic resonance imaging in various animal stroke models. Knight demonstrated gadolinium-DTPA enhancement in the territory of occluded vessels immediately in rats after reperfusion. gadolinium enhancement was thought to predict areas of hemorrhagic transformation. Yenari and associates demonstrated in rabbit models that contrast-enhanced T1-weighted scans can reveal regions of blood-brain barrier disruption, characterized as hemorrhagic transformation in ischemic tissue. The authors report a clinical example in which hyperacute contrast-enhanced magnetic resonance imaging was the first indication of hemorrhagic transformation within 24 hours of onset of an acute cerebral infarct.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
5/153. Fatal cerebral reperfusion hemorrhage after carotid stenting.BACKGROUND: The hyperperfusion syndrome is a recognized complication of carotid endarterectomy. Reports of cerebral hyperperfusion injury following internal carotid artery (ICA) angioplasty are few, and this complication has never been reported following internal carotid stenting. CASE DESCRIPTION: A 68-year-old normotensive man was referred to our hospital for assessment 5 months after experiencing a left hemispheric ischemic stroke. angiography confirmed 95% stenosis of the left ICA. Left carotid percutaneous transluminal stenting was performed without any initial complications. color Doppler ultrasound of the ICA immediately after stenting revealed an elevated peak systolic velocity of 2.3 m/s, in the absence of significant vessel stenosis or spasm on angiography. Seven hours after the procedure, the patient suddenly deteriorated. CT of the brain revealed extensive intracerebral hemorrhage (ICH), and he subsequently died 18 days later. There was no history of headache or seizure activity, and his blood pressure was only mildly elevated at the time of the deterioration. This is the first report of ICH after internal carotid stenting. CONCLUSIONS: ICH may occur as a hyperperfusion phenomenon after internal carotid stenting, in the presence of mild to moderate arterial hypertension, without being heralded by any of the typical symptoms of the hyperperfusion syndrome. patients with increased velocities on color Doppler ultrasound of the ICA after angioplasty should be monitored closely for features of cerebral hyperperfusion injury. Further studies are warranted to determine whether more aggressive treatment of mild to moderate hypertension after carotid stenting would reduce the likelihood of this potentially fatal complication.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
6/153. hepatopulmonary syndrome and venous emboli causing intracerebral hemorrhages after liver transplantation: a case report.Increasing experience has fostered the acceptance of liver transplantation as a treatment for patients with hepatopulmonary syndrome. morbidity and mortality is most commonly attributed to progressive arterial hypoxemia postoperatively. A cerebral hemorrhage has been reported in one patient with hepatopulmonary syndrome after transplantation. However, a postmortem examination of the brain was not performed and the pathogenesis or type of cerebral hemorrhage was undefined. We report on a patient with severe hepatopulmonary syndrome who developed multiple intracranial hemorrhages after transplantation. The intracerebral hemorrhages were most consistent with an embolic etiology on postmortem examination. We postulate that venous embolization, caused by the manipulation of a Swan Ganz catheter in a thrombosed central vein, resulted in pulmonary emboli that passed through dilated intrapulmonary vessels into the cerebral microcirculation. Special attention to central venous catheters and avoidance of manipulation may be warranted in subjects with severe hepatopulmonary syndrome after liver transplantation.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
7/153. Management of residual dysplastic vessels after cerebral arteriovenous malformation resection: implications for postoperative angiography.OBJECTIVE: The verification of surgical resection of cerebral arteriovenous malformations (AVMs) relies on angiography. Abnormal vasculature often is identified after removal of the AVM. Differentiation of dysplastic feeding vessels that resemble the neovascularity of moyamoya disease, as distinct from residual AVM, is crucial for preserving critical brain areas. We review a large experience with immediate postoperative angiography after AVM resection and discuss the implications for management of abnormal dysplastic vessels discovered after AVM resection. methods: Beginning in 1992, 86 consecutive patients with AVMs underwent operations by standard protocol for immediate postoperative angiography under the same general anesthetic. Angiographic interpretation dictated admission to the intensive care unit or return to the operating room for further resection. RESULTS: In 78 patients, the angiogram revealed complete resection. Two patients were returned to the operating room, one for residual malformation with an early draining vein, and one for resection of residual dysplastic vessels. There was one postoperative hemorrhage in a patient whose postoperative angiogram was falsely negative for AVM. Six patients with residual dysplastic vessels mimicking residual AVM, but without an early draining vein, were managed conservatively. Delayed follow-up angiography demonstrated spontaneous involution of these abnormal vessels in all of these patients. CONCLUSION: Residual dysplastic feeding vessels resembling the neovascularity of moyamoya disease but not associated with an early draining vein do not necessarily represent residual malformation after AVM resection. The abnormal vessels will proceed to complete spontaneous resolution. Given the difficulty of interpreting intraoperative angiography, immediate postoperative angiography may be a viable alternative after AVM resection.- - - - - - - - - - ranking = 5.5keywords = vessel (Clic here for more details about this article) |
8/153. Stress-related primary intracerebral hemorrhage: autopsy clues to underlying mechanism.BACKGROUND: research into the causes of small-vessel stroke has been hindered by technical constraints. Cases of intracerebral hemorrhage occurring in unusual clinical contexts suggest a causal role for sudden increases in blood pressure and/or cerebral blood flow. CASE DESCRIPTION: We describe a fatal primary thalamic/brain stem hemorrhage occurring in the context of sudden emotional upset. At autopsy, the brain harbored several perforating artery fibrinoid lesions adjacent to and remote from the hematoma as well as old lacunar infarcts and healed destructive small-vessel lesions. CONCLUSIONS: We postulate that the emotional upset caused a sudden rise in blood pressure/cerebral blood flow, mediating small-vessel fibrinoid necrosis and rupture. This or a related mechanism may underlie many small-vessel strokes.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |
9/153. Repeated hemorrhage in ciliated craniopharyngioma--case report.A 49-year-old female presented with a ciliated craniopharyngioma manifesting as repeated intratumoral hemorrhage. Histological examination suggested that the hemorrhage originated from the many thin blood vessels in the cyst wall stroma associated with inflammation. Symptomatic hemorrhage in cystic craniopharyngioma may mimic pituitary apoplexy but the etiology is quite different. Minor hemorrhage may recur unless the cyst wall is totally removed.- - - - - - - - - - ranking = 1.4434628000639keywords = blood vessel, vessel (Clic here for more details about this article) |
10/153. facial pain as a presenting feature of intracerebral haemorrhage.A literature review from 1966 using medline with keywords 'cerebral haemorrhage' and 'facial pain' failed to reveal any cases in which facial pain was the initial feature of intracranial haemorrhage. The following case describes ipsilateral facial pain which is previously undescribed as a presentation of intracranial bleeding. A 53 year old female who was previously well, with no significant history of headache, developed right facial pain from the orbit to the maxilla. Ten to 15 min later she developed nausea and vomiting with unsteadiness and confusion. She had difficulty with left-hand fine finger movements, with normal sensation and reflexes but an extensor plantar response on the left. facial pain persisted for 3 days. Initial imaging revealed a 4 x 3 cm right temporal lobe haemorrhage with mass effect and oedema extending into the subarachnoid space. Angiogram revealed a right temporal lobe arteriovenous malformation. The basis of the pain remains speculative but includes sensation from the torn vessel wall being referred to the face and subarachnoid blood irritation of the meninges in the middle cranial fossa. Another possibility is irritation of somatosensory cortex II, but why this should result in only ipsilateral pain is unclear. facial pain should be an alerting symptom to the neurologist when it appears with no apparent cause.- - - - - - - - - - ranking = 0.5keywords = vessel (Clic here for more details about this article) |
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