Cases reported "Brain Ischemia"

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1/37. Temporary occlusion of middle cerebral artery by macroembolism in carotid surgery.

    Two patients are presented who during carotid endarterectomy (CEA) temporarily showed an obstruction of the middle cerebral artery (MCA) mainstem by a macroembolus resulting in cerebral ischaemia. Both cases are unusual examples of CEA and selected from a cohort of more than 1,500 operations. During surgery with general anaesthesia, brain function was monitored with computerized electroencephalography (EEG) and transcranial Doppler (TCD) ultrasonography. The simultaneous use of EEG and TCD monitoring allowed us to witness the development of intraoperative cerebral ischaemia and to relate these events to a temporary occlusion of the MCA mainstem by a macroembolus. This is the first life report that describes obstruction of a cerebral artery by arterial embolism resulting in cerebral ischaemia.
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2/37. brain injuries in early foetal life: consequences for brain development.

    learning disability and cerebral palsy are often related to factors present before birth. We report three patients (two with schizencephaly, one with unilateral cerebellar agenesis) in whom the timing of an insult to the foetus was known. In the first case, the mother had a trauma at 16 weeks of pregnancy and schizencephaly was discovered in the male infant associated with a left hemiplegia. In the second child, amniocentesis performed at 16 weeks into pregnancy may have been responsible for the same cortical anomaly. In the third case, sequential foetal echographies clearly demonstrated that an apparent unilateral cerebellar agenesis was related to an haemorrhagic event secondary to cerebellar trauma that occurred at 19 weeks of pregnancy. It is suggested that these brain malformations are related to an ischemic mechanism or a traumatic event in foetal life.
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3/37. diffusion-weighted magnetic resonance imaging in two patients with polycythemia rubra vera and early ischemic stroke.

    polycythemia rubra vera (PRV) is a rare myeloproliferative disorder with a high risk of ischemic stroke. Although thrombosis of large cerebral arteries is the most frequently presumed pathomechanism, various infarct patterns have been described in patients with PRV and ischemic stroke. We report two patients with mild acute ischemic strokes and known PRV, in whom a scattered lesion pattern was detected by diffusion-weighted magnetic resonance imaging (DWI), but was not visible on computed tomography (CT) and conventional magnetic resonance imaging (MRI). Further diagnostic work-up including extra- and transcranial Doppler sonography (ECD, TCD), transesophageal echocardiography (TEE), magnetic resonance angiography and Holter monitoring revealed no obvious sources of cerebral embolism in both cases. However, TEE in one patient demonstrated spontaneous echo contrast (SEC) in the left atrium. In both patients the symptomatology resolved completely. The detection of a scattered infarct pattern by DWI in patients with PRV and acute ischemic stroke has not been reported previously. DWI findings together with the SEC in one patient emphasize the assumption that a prothrombotic state with subsequent arterial embolism rather than local arterial thrombosis may be the underlying pathomechanism of stroke in some patients with PRV. Adding DWI to the diagnostic work-up may help to clarify etiology in patients with PRV and acute ischemic stroke.
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4/37. COX-2 inhibitor for the treatment of idiopathic stabbing headache secondary to cerebrovascular diseases.

    The idiopathic stabbing headache (ISH) is characterized by a stabbing pain of short duration, variable localization and an errant evolution pattern. As its biological mechanisms are unknown and the treatment options are little effective, this disorder shows a strong impact on the patient's life. Two females and one male, aged 76, 66 and 72 years, respectively, started presenting ISH within 20 days after the onset of a stroke. All the patients were treated for the ISH with celecoxib, a COX-2 specific inhibitor, with full recovery from ISH up to 6 days after it was first administered. The interruption of the drug 60 days after the treatment with celecoxib induced again the appearance of algic symptoms in two patients. We concluded that cerebrovascular diseases (CD) can lead to ISH and that the COX-2 inhibitor can be an effective prophylactic drug for ISH after CD.
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5/37. Release of fatty acid amides in a patient with hemispheric stroke: a microdialysis study.

    BACKGROUND: Excitotoxic insults such as stroke may induce release of fatty acid ethanolamides (FAEs), contributing to the downstream events in the ischemic cascade. We therefore studied release of FAEs such as anandamide, palmitylethanolamide (PEA), and oleylethanolamide (OEA) in the brain of a patient suffering from malignant hemispheric infarction treated with hypothermia. CASE DESCRIPTION: A patient with life-threatening hemispheric stroke was treated with moderate hypothermia (33 degrees C) that was maintained for 3 days, followed by a 3-day rewarming period. microdialysis was applied to measure glutamate, lactate, and glycerol by using a microdialysis analyzer. FAEs were measured by microdialysis coupled with high-performance liquid chromatography/mass spectrometry. Release of neuroprotective fatty amides occurred within the first day after ischemia and reached high concentrations for all 3 substances in tissue surrounding the primary ischemic lesion: anandamide up to 42 pmol/mL, PEA up to 120 pmol/mL, and OEA up to 242 pmol/mL. There was a significant correlation with elevation of lactate as early marker for the hypoxic insult. CONCLUSIONS: This is the first report demonstrating release of FAEs in vivo during human stroke and may suggest contribution of the FAE signaling system to the pathophysiological events after ischemia.
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6/37. time lag to diagnosis of stroke in children.

    OBJECTIVE: Strokes occur rarely in children, and the causes are different from those in adults. Frequently, more than 1 cause is found. The consequences are lifelong significant disability in a majority of cases. Children who are younger than 18 years have not been included in therapeutic trials of thrombolytic or neuroprotective agents. We evaluated whether children who receive a diagnosis of stroke meet a major inclusion criterion for such trials, namely time to diagnosis of <3 to 6 hours. methods: Prospective documentation and retrospective chart review was conducted of children who were 0 to 18 years and carried a diagnosis of stroke during the last 2 years in the hospital database, including children who presented with either ischemic or hemorrhagic strokes. RESULTS: Forty-seven events were encountered in 41 children. Twelve neonates with stroke, diagnosed in the neonatal period, were excluded from the subsequent analysis. In the remaining 29 children, the mean age at presentation was 8.67 years. Accurate time records were available in 24 children. In this group, 28 events were recorded. time from clinical onset to first medical contact averaged 28.5 hours, and the time to diagnosis of stroke averaged 35.7 hours. We subsequently separated between children with ischemic (21 documented events) and hemorrhagic strokes (7 documented events), because the presentation and the intervention options are different. CONCLUSIONS: stroke in children is rarely diagnosed in the time frame of 3 to 6 hours. Given the causes and outcome of stroke in children, this age group might benefit from thrombolysis and from neuroprotective therapy, yet the long delay in diagnosis in this age group excludes most cases from being considered for such treatments. This situation should encourage attempts to increase public and professional awareness of stroke in children and of the potential value of early diagnosis and treatment, preferably by broadening current educational efforts to all age groups.
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7/37. death scene gas analysis in suspected methane asphyxia.

    Two cases of methane asphyxia occurring in two boys (age 11 and 12 years) who were found at the bottom of a 37-ft (11.1-m)-deep sewer shaft are described. Attempted resuscitation of the first patient was unsuccessful and achieved only temporary stabilization of the second, who died 48 h after his discovery. Autopsies revealed relatively minor multifocal traumatic injuries, with evidence of hypoxic-ischemic encephalopathy in the patient who survived for 2 days. Subsequent analysis of gas in the shaft revealed 21% oxygen at the surface, 14.3% at a depth of 5 ft (1.5 m), and only 4.8% at depths of 10 ft (3 m) and below. Other gases detected at the lower levels were methane, nitrogen, and carbon dioxide (4.3%). These cases demonstrate the value of atmospheric gas analysis in cases of possible methane asphyxia in confirming the presence of methane and in demonstrating levels of oxygen below that necessary to support life.
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8/37. Athetoid cerebral palsy with cysts in the putamen after hypoxic-ischaemic encephalopathy.

    Three cases of athetoid cerebral palsy after hypoxic-ischaemic encephalopathy (HIE) are reported. All three neonates had haemorrhagic lesions in the basal ganglia and thalami on magnetic resonance imaging (MRI). Prior cranial ultrasound had detected the lesions in only two cases. In all three children athetoid movements began within the first year of life. Follow up MRI scans showed bilateral symmetrical cystic lesions in the posterior putamen. Although haemorrhagic lesions within the basal ganglia are a common MRI finding in neonates with HIE, few of these babies develop athetoid cerebral palsy. We believe this to be the first report of discrete cystic lesions found in the basal ganglia of children with athetoid cerebral palsy.
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9/37. Acute ischemic stroke successfully treated using sequenced intravenous and intra-arterial thrombolysis and argatroban anticoagulation: a case study.

    BACKGROUND: Direct thrombin inhibitors, a class of anticoagulants distinct from heparins, have not been evaluated for immediate use after thrombolytic therapy in acute ischemic stroke. We report a case of ischemic stroke and prothrombotic state treated using sequenced intravenous and intra-arterial thrombolytic therapy and argatroban anticoagulation. CASE DESCRIPTION: A 19-year-old man with a complicated history of recurrent life-threatening thrombosis presented at the emergency department with acute ischemic stroke. The patient received standard-dose intravenous alteplase starting 2.25 hours after symptom onset without change in his global aphasia and right hemiparesis. Five hours after symptom onset, intra-arterial reteplase was administered for treatment of a left internal carotid "T" occlusion, with successful recanalization of the left internal carotid artery, A1 and M1 segments, and right middle cerebral anterior division and with improvement in symptoms. Argatroban therapy was started after completion of intra-arterial thrombolysis, i.e., 8.5 hours after symptom onset, and was maintained for 14 days. Although the patient sustained a small left basal ganglia infarct, he improved significantly over the course of therapy and was discharged to home without bleeding or further thrombotic episodes. CONCLUSIONS: Sequenced intravenous and intra-arterial thrombolytic therapy and argatroban anticoagulation was used successfully to safely treat a patient with ischemic stroke and comorbid prothrombotic state within 8.5 hours of symptom onset.
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10/37. An unusual presentation of classic polyarteritis nodosa in a child.

    Classic polyarteritis nodosa (c-PAN) is a rare disease in adults and extremely rare in children. We report a 3-year-old girl with c-PAN who presented with disturbances of consciousness and hypertension. Cranial tomography showed a subarachnoid hemorrhage. Subsequent magnetic resonance imaging and magnetic resonance angiography demonstrated subarachnoid hemorrhage and acute ischemic lesions. Renal angiography revealed bilateral multiple aneurysms. Due to her constitutional symptoms and hypertension and radiological findings she was diagnosed as having c-PAN. She was successfully treated with hydralazine followed by angiotensin-converting enzyme inhibitor, calcium channel blocker, intravenous pulse methylprednisolone, and subsequently oral prednisolone and oral cyclophosphamide. To our knowledge this is the youngest patient with c-PAN presenting with subarachnoid hemorrhage. Malign hypertension at this young age deserves a meticulous investigation of the vascular origin. Furthermore, treatment with pulse methyl prednisolone followed by oral prednisolone and oral cyclophosphamide is a successful modality of treatment in such a life-threatening presentation of c-PAN in childhood.
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