Cases reported "Brain Ischemia"

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1/56. 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.
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2/56. Continuous monitoring of cerebrospinal fluid acid-base balance and oxygen metabolism in patients with severe head injury: pathophysiology and treatments for cerebral acidosis and ischemia.

    INTRODUCTION: Continuous monitoring of cerebral acid-base balance and oxygen metabolism has been introduced in neurointensive care settings. The hypothesis of this study utilizing multimodal neuromonitoring modalities is that hyperventilation and hypothermia improve cerebral acidosis through prevention of cerebral ischemia aggravation in patients with severe head injury. patients AND methods: Continuous monitoring of cerebrospinal fluid (CSF) pH, PCO2, HCO3-, base excess (BE), PO2, SO2, temperature, lactate and pyruvate (La and Py) measurements were conducted in 8 patients with severe head injury. temperature-corrected CSF parameters were correlated with those in the jugular blood including oxygen saturation (SjO2), regional oxygen saturation (rSO2), intracranial pressure (ICP) and cerebral perfusion pressure (CPP), jugular blood temperature (Tjb), and endtidal PCO2 (PetCO2). Therapeutic significance of hyperventilation and hypothermia was evaluated. RESULTS: 1) CSF acidosis was observed in all cases (minimum pH 6.59-7.17) due to increased CSF PCO2 and/or decreased CSF HCO3- and tended to associate with abnormal ICP and/or CPP or ischemic episodes indicated by CSF PO2 and SO2, rSO2, and/or SjO2 during monitoring. 2) It was more obvious in CSF than in jugular blood that increased PCO2, La and Py, and/or decreased HCO3- resulted in decreased BE and pH. 3) Decreased CSF PO2 and SO2 only correlated with severe CSF acidosis. 4) hyperventilation: Decreased PetCO2 did not always closely correlate with CSF PCO2 decrease and CSFpH increase. 5) hypothermia: There were negative correlations of Tjb with CSF pH and SO2 in all cases, though correlation coefficients were not always high. CONCLUSIONS: CSF acidosis caused by increased CSF PCO2, La and Py, and/or decreased HCO3- tended to associate with abnormal ICP and CPP, and desaturation indicated by CSF SO2, rSO2, and/or SjO2. hypothermia rather than hyperventilation tends to improve cerebral acidosis and ischemia.
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3/56. Cerebrovascular ischemic events in wind instrument players.

    Two cases of ischemic stroke due to carotid artery dissection occurring during wind instrument playing, probably caused by increased intrathoracic and subsequent intrapharyngeal pressure, are presented. A review of the literature revealed three similar patients with other types of cerebrovascular events, such as paradoxical cerebral embolism due to a patent foramen ovale and spinal epidural hematoma during trumpet playing.
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4/56. Cerebral oximetry for the detection of cerebral ischemia during temporary carotid artery occlusion.

    The near-infrared spectroscopy cerebral oximeter was assessed as a monitoring device for detecting and/or predicting cerebral ischemia during carotid endarterectomy (CEA) and the balloon occlusion test in 24 patients, 12 males and 12 females aged 28 to 77 years (mean 59.9 years). Tolerance testing of complete internal carotid artery (ICA) occlusion by balloon inflation for 20 minutes was performed in nine patients (cerebral aneurysm 6, neck tumor 3) and CEA was performed in 15 patients. The probe of the cerebral oximeter was placed on the forehead of the affected side and regional cerebral oxygen saturation (rSO2) was monitored continuously during all procedures. Stump pressure was measured just after ICA occlusion. collateral circulation detected by digital subtraction angiography was classified into three groups: good, moderate, or poor. Stump pressure was 41-90 mmHg (mean 61.3 mmHg) in the good collateral circulation group, 40-43 mmHg (41.5 mmHg) in the moderate group, and 14-30 mmHg (23.8 mmHg) in the poor group. Change in rSO2 after ICA occlusion was 3.5(-)-4.2% (mean -1.6%) in the good collateral circulation group, -1.2(-)-6.6% (-3.2%) in the moderate group, and -2.4(-)-10.2% (-6.6%) in the poor group. Changes in rSO2 were significantly different between the good and poor collateral circulation groups (p < 0.01). A greater than 5% fall in rSO2 was observed in 0 of 15 patients in the good collateral circulation group, one of five in the moderate group, and three of four in the poor group. The cerebral oximeter is a useful, real-time, non-invasive method to measure brain oxygenation during CEA, skull base surgery, or other procedures which need to evaluate brain ischemia. A fall of greater than 10% from the rSO2 baseline value is dangerous, but less than 5% is safe.
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5/56. An adult case of congenital external carotid-jugular arteriovenous fistula with reversible circulatory insufficiency in the cerebellum and lower brain stem.

    A 27-year-old man with congenital external carotid-jugular arteriovenous fistula presented with a diminished level of consciousness and an ataxic gait. Axial fluid-attenuated inversion-recovery (FLAIR) MR imaging revealed venous congestion, a dilated right jugular vein, and an area of high signal intensity in the brain stem and cerebellum. angiography showed a dilated right external carotid artery and jugular vein and the presence of a fistula. After coil embolization of the fistula, axial MR FLAIR images showed only a few areas of high signal intensity in the brain stem and cerebellum. The causal factor was venous congestion in the inferior petrosal sinus and basilar plexus due to high blood pressure in the jugular vein. This case is presented for its unusual clinical and radiologic findings.
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6/56. Brain tissue PO(2), PCO(2), and pH during cerebral vasospasm.

    BACKGROUND: The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients. methods: After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. Brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies. RESULTS: Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO(2)) remained above 20 mmHg, carbon dioxide pressure (PCO(2)) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO(2) was not different from the control group. However, PCO(2) increased to 60 mmHg and pH decreased to 6.7 (p < 0.001). CONCLUSION: In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO(2) compared to controls. However, there was no significant change in PO(2) levels associated with vasospasm. Brain tissue monitoring can provide an indication of ischemia during vasospasm.
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7/56. blood pressure manipulation during awake carotid surgery to reverse neurological deficit after carotid cross-clamping.

    We describe the management of three patients undergoing awake carotid surgery who developed signs of cerebral ischaemia after carotid cross-clamping. Drug treatment to increase arterial blood pressure above baseline reversed the neurological deficit and an internal carotid artery shunt was not needed. Shunt insertion is less frequent with regional rather than general anaesthesia, and blood pressure control can reduce this even more. Coincidentally, one of the patients, who gave a history of angina of effort after walking 100 m, complained of chest pain after cross-clamp release. This was treated successfully with sublingual nitroglycerin before ST segment changes became apparent on the ECG. These reports suggest that regional anaesthesia for carotid surgery allows potential complications to be identified earlier than under general anaesthesia using reports from the patient, so that treatment may be modified to prevent morbidity and even mortality.
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8/56. Simultaneous onset of haemorrhagic and ischaemic strokes in a haemodialysis patient.

    Primary brain haemorrhage and infarction only very rarely occur simultaneously. A patient with end stage renal disease from diabetic nephropathy suddenly had motor aphasia and horizontal nystagmus soon after finishing haemodialysis. Neuroradiological studies showed a haematoma on the right side of the pons and an infarct in the left frontal lobe with occlusion of the left internal carotid artery. Specific conditions of the haemodialysis--including anticoagulant use, relative hypovolaemia and hypertension just before haemodialysis, and an abrupt decrease in blood pressure during haemodialysis--seemed to be the major reason for the simultaneous onset of dual strokes.
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9/56. Noninvasive monitoring of hypertensive breakthrough of cerebral autoregulation in a patient with acute ischemic stroke.

    BACKGROUND AND PURPOSE: We describe the first documentation of hypertensive breakthrough of cerebral autoregulation in a patient with acute stroke with transcranial Doppler sonography. CASE DESCRIPTION: A 55-year-old patient with acute left hemispheric stroke was treated with moderate hypothermia. He died of transtentorial herniation 4 days after admission. Static cerebral autoregulation (sCA) of the unaffected hemisphere was evaluated 6 times during this period and always found to be intact. A bolus application of epinephrine resulted in a hypertensive episode (mean arterial pressure (MAP) 135 mm Hg); hypertensive breakthrough of cerebral autoregulation was evident when MAP exceeded approximately 110 mm Hg. Interestingly, no such breakthrough was evident during testing of sCA, even when MAP reached 120 mm Hg. CONCLUSIONS: Our observation suggests that (1) the pace of the MAP increase is crucial for the occurrence of a hypertensive breakthrough of the cerebral autoregulation and (2) the disturbance of cerebral autoregulation is potentially longer as previously assumed.
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10/56. Large cerebral arteriovenous malformation presenting with venous ischemia in the contralateral hemisphere. Case report.

    The authors report a rare case in which a large cerebral arteriovenous malformation (AVM) located in the left parietooccipital region presented with venous ischemia in the contralateral hemisphere. A 74-year-old man was admitted to the hospital because he was experiencing a loss of appetite, disorientation, and left hemiparesis. Computerized tomography scans revealed a low-density area in the right temporal lobe. angiography demonstrated a large AVM in the left parietooccipital lobe and dilation, stagnation, and meanders of cortical veins in the contralateral hemisphere. The authors speculated that the elevated sinus pressure caused by a huge venous return of blood from the AVM produced venous ischemia in the contralateral hemisphere.
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