Inherited prothrombotic risk factors and cerebral venous thrombosis. (1/698)

Fifteen patients with cerebral venous thrombosis were ascertained retrospectively. Their case notes were reviewed, and stored or new blood was assayed for factor V Leiden (FVL) mutation, prothrombin gene mutation 20201A, and 5,10 methylene tetrahydrofolate reductase (MTHFR) C677T mutation. A clinical risk factor was identified in 13 patients--the oral contraceptive pill (5), puerperium (1), HRT (1), mastoiditis (1), dehydration (1), lumbar puncture and myelography (1), carcinoma (1), lupus anticoagulant (2). In addition, two patients had the FVL mutation and five (one of whom also had the FVL mutation) were homozygous for the MTHFR mutation. The latter showed a higher than expected frequency compared to 300 healthy controls from South Wales (OR 3.15.95% Cl 1.01-9.83). No patient had the prothrombin 20201A mutation. Two patients died and three had a monocular visual deficit following anticoagulation (13) or thrombolytic (2) treatment, but there was no association between the presence of a primary prothrombotic risk factor and outcome. These results confirm the importance of investigating patients for both clinical predisposing factors and primary prothrombotic states.  (+info)

Computerised axial tomography in patients with severe migraine: a preliminary report. (2/698)

Patients suffering from severe migraine, usually for many years, have been examined by the EMI scanner between attacks. Judged by criteria validated originally by comparison with pneumoencephalography, about half of the patients showed evidence of cerebral atrophy. Perhaps of more significance than generalised atrophy was the frequency of areas of focal atrophy and of evidence of infarction.  (+info)

Rupture mechanism of a thrombosed slow-growing giant aneurysm of the vertebral artery--case report. (3/698)

A 76-year-old male developed left hemiparesis in July 1991. The diagnosis was thrombosed giant vertebral artery aneurysm. He showed progressive symptoms and signs of brainstem compression, but refused surgery and was followed up without treatment. He died of rupture of the aneurysm and underwent autopsy in March 1995. Histological examination of the aneurysm revealed fresh clot in the aneurysmal lumen, old thrombus surrounding the aneurysmal lumen, and more recent hemorrhage between the old thrombus and the inner aneurysmal wall. The most important histological feature was the many clefts containing fresh blood clots in the old thrombus near the wall of the distal neck. These clefts were not lined with endothelial cells, and seemed to connect the lumen of the parent artery with the most peripheral fresh hemorrhage. However, the diameter of each of these clefts is apparently not large enough to transmit the blood pressure of the parent artery. Simple dissection of the aneurysmal wall by blood flow in the lumen through many clefts in the old thrombus of the distal neck may be involved in the growth and rupture of thrombosed giant aneurysms of the vertebral artery.  (+info)

Cerebral venous thrombosis: combined intrathrombus rtPA and intravenous heparin. (4/698)

BACKGROUND AND PURPOSE: We chose to evaluate the safety and efficacy of combined intrathrombus rtPA and intravenous heparin in cerebral venous thrombosis (CVT). METHODS: We treated 12 patients with symptoms of 1 to 40 days' duration (eg, headache, somnolence, focal deficits, seizures, and nausea and vomiting). Pretreatment MRI disclosed subtle hemorrhagic venous infarction in 4 patients, obvious hemorrhagic infarction in 2, small parenchymal hemorrhage from recent pallidotomy in 1, and no focal lesion in 5. Magnetic resonance venography and contrast venography identified thrombi in the superior sagittal sinus (SSS) in 3 patients; transverse/sigmoid sinus (TS/SS) in 2; SSS and both TS/SS in 1; SSS and 1 TS/SS in 5; and SSS, 1 TS/SS, and straight sinus in 1 patient. A loading dose of rtPA was instilled throughout the clot at 1 mg/cm, followed by continuous intrathrombus infusion at 1 to 2 mg/h. Intravenous heparin was infused concomitantly. RESULTS: Flow was restored completely in 6 patients and partially in 3, with a mean rtPA dose of 46 mg (range, 23 to 128 mg) at a mean time of 29 hours (range, 13 to 77 hours). Symptoms improved in these 9 patients concomitantly with flow restoration. Flow could not be restored in 3 patients. In 1 of them, treatment was stopped when little progress had been made, and fibrinogen level dropped to 118 mg/dL. In the other 2 patients, hemorrhagic worsening occurred, and treatment was abbreviated after initial rtPA dosing. In 1 of these, the hematoma was evacuated. CONCLUSIONS: Our experience with intrathrombus rtPA in conjunction with intravenous heparin in patients with CVT is encouraging. This therapy should probably be regarded as unsafe in patients with obvious hemorrhage. Time to restore flow may be faster than with urokinase (an average of 71 hours has been reported for 29 documented patients). Further evaluation of rtPA with heparin in CVT is warranted.  (+info)

Cerebral injury after cardiac surgery: identification of a group at extraordinary risk. Multicenter Study of Perioperative Ischemia Research Group (McSPI) and the Ischemia Research Education Foundation (IREF) Investigators. (5/698)

BACKGROUND AND PURPOSE: Cerebral injury after cardiac surgery is now recognized as a serious and costly healthcare problem mandating immediate attention. To effect solution, those subgroups of patients at greatest risk must be identified, thereby allowing efficient implementation of new clinical strategies. No such subgroup has been identified; however, patients undergoing intracardiac surgery are thought to be at high risk, but comprehensive data regarding specific risk, impact on cost, and discharge disposition are not available. METHODS: We prospectively studied 273 patients enrolled from 24 diverse US medical centers, who were undergoing intracardiac and coronary artery surgery. Patient data were collected using standardized methods and included clinical, historical, specialized testing, neurological outcome and autopsy data, and measures of resource utilization. Adverse outcomes were defined a priori and determined after database closure by a blinded independent panel. Stepwise logistic regression models were developed to estimate the relative risks associated with clinical history and intraoperative and postoperative events. RESULTS: Adverse cerebral outcomes occurred in 16% of patients (43/273), being nearly equally divided between type I outcomes (8.4%; 5 cerebral deaths, 16 nonfatal strokes, and 2 new TIAs) and type II outcomes (7.3%; 17 new intellectual deterioration persisting at hospital discharge and 3 newly diagnosed seizures). Associated resource utilization was significantly increased--prolonging median intensive care unit stay from 3 days (no adverse cerebral outcome) to 8 days (type I; P<0.001) and from 3 to 6 days (type II; P<0.001), and increasing hospitalization by 50% (type II, P=0.04) to 100% (type I, P<0.001). Furthermore, specialized care after hospital discharge was frequently necessary in those with type I outcomes, in that only 31% returned home compared with 85% of patients without cerebral complications (P<0.001). Significant risk factors for type I outcomes related primarily to embolic phenomena, including proximal aortic atherosclerosis, intracardiac thrombus, and intermittent clamping of the aorta during surgery. For type II outcomes, risk factors again included proximal aortic atherosclerosis, as well as a preoperative history of endocarditis, alcohol abuse, perioperative dysrhythmia or poorly controlled hypertension, and the development of a low-output state after cardiopulmonary bypass. CONCLUSIONS: These prospective multicenter findings demonstrate that patients undergoing intracardiac surgery combined with coronary revascularization are at formidable risk, in that 1 in 6 will develop cerebral complications that are frequently costly and devastating. Thus, new strategies for perioperative management--including technical and pharmacological interventions--are now mandated for this subgroup of cardiac surgery patients.  (+info)

Thrombolysis with tissue plasminogen activator alters adhesion molecule expression in the ischemic rat brain. (6/698)

BACKGROUND AND PURPOSE: We tested the hypothesis that treatment of embolic stroke with recombinant human tissue plasminogen activator (rhtPA) alters cerebral expression of adhesion molecules. METHODS: Male Wistar rats were subjected to middle cerebral artery occlusion by a single fibrin-rich clot. P-selectin, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) immunoreactivity was measured at 6 or 24 hours after embolic stroke in control rats and in rats treated with rhtPA at 1 or 4 hours after stroke. To examine the therapeutic efficacy of combined rhtPA and anti-ICAM-1 antibody treatment at 4 hours after embolization, ischemic lesion volumes were measured in rats treated with rhtPA alone, rats treated with rhtPA and anti-ICAM-1 antibody, and nontreated rats. RESULTS: Administration of rhtPA at 1 hour after embolization resulted in a significant reduction of adhesion molecule vascular immunoreactivity after embolization in the ipsilateral hemisphere compared with corresponding control rats. However, when rhtPA was administered to rats at 4 hours after embolization, significant increases of adhesion molecule immunoreactivity in the ipsilateral hemisphere were detected. A significant increase of ICAM-1 immunoreactivity was also detected in the contralateral hemisphere at 24 hours after ischemia. A significant reduction in lesion volume was found in rats treated with the combination of rhtPA and anti-ICAM-1 antibody compared with rats treated only with rhtPA. CONCLUSIONS: The present study suggests that the time of initiation of thrombolytic therapy alters vascular immunoreactivity of inflammatory adhesion molecules in the ischemic brain and that therapeutic benefit can be obtained by combining rhtPA and anti-ICAM-1 antibody treatment 4 hours after stroke.  (+info)

EEG surveillance as a means of extending operability in high risk carotid endarterectomy. (7/698)

Some patients who have transient ischemic attacks are denied operation because severe occlusive lesions in other extra-cranial arteries may be inappropriately interpreted as constituting an unacceptable surgical risk, or because the lesion is so distal as to make its removal hazardous. Failure of endarterectomy is usually due to incomplete removal of the lesion or to thrombosis upon the frayed intima. Such lesions require excellent visualization and meticulous surgical technique -- not always possible with a shunt. Among 130 consecutive carotid endarterectomies performed under general anesthesia, EEG changes consistent with cerebral ischemia appeared in only nine (7%). These patients required a shunt. In 11 patients normal EEG tracings were obtained during endarterectomy despite contralateral carotid occlusion. None of these patients had a neurological deficit. Continuous EEG monitoring is a reliable method of detecting changes in cerebral perfusion, permits a more meticulous endarterectomy in high-lying lesions without a shunt, and extends operability in high risk patients. Angiographical findings may be an unreliable predictor concerning risk of endarterectomy.  (+info)

A prospective study of cerebrovascular disease in Japanese rural communities, Akabane and Asahi. Part 1: evaluation of risk factors in the occurrence of cerebral hemorrhage and thrombosis. (8/698)

An epidemiological study of cerebrovascular disease in Akabane and Asahi, Japan, was made. (These cities are located near Nagoy, Japan.) The study population included 4,737 men and women aged 40 to 79 at the time of entry into the study. There were 4,186 persons who were examined and, of these, 264 cases of cerebrovascular attacks were observed between 1964 and 1970. The incidence rate of stroke in those persons not responding to the survey was 15.9 times higher than in those persons examined according to person-year observation in Akabane. The risk factors for cerebral hemorrhage and thrombosis were evaluated by age-adjusted and sex-adjusted relative risks. The predisposing factors to cerebral hemorrhage appeared to be high blood pressure, high left R wave, ST depression, T abnormality, capillary fragility counts, previous medical history of stroke and albuminuria. For cerebral thrombosis, the predisposing factors appeared to be high blood pressure, ST depression and funduscopic sclerotic findings, and those factors assumed to be significant were glycosuria and smoking habits. Ocular funduscopic abnormality was the most prominent risk factor for cerebral thrombosis, while high blood pressure and ECG abnormalities were highly related to cerebral hemorrhage. It was suggested that those subjects with a relatively higher blood pressure may have a higher relative risk of cerebral hemorrhage than those with a lower (normal range) blood pressure. A previous or family history of stroke also appeared significantly related to cerebral hemorrhage.  (+info)