Hemorrhage, cerebral

Cerebral sinus thrombosis, progressing to hemorrhagic cerebral infarction, occurred in a 52-year-old woman (32). 

A 44-year-old woman was given ephedrine intravenously, to manage hypotension during spinal anesthesia. She developed intracranial hypertension and focal cerebral deficits related to multiple hemorrhagic cerebral infarcts. Angiography showed reversible beading, consistent with cerebral arteritis. 

Gore JM, Sloan M, Price TR, Randall AM, Bovill E, Collen D, Forman S, Knatterud GL, Sopko G, Terrin ML. Intracerebral hemorrhage, cerebral infarction, and subdural hematoma after acute myocardial infarction and thrombolytic therapy in the Thrombolysis in Myocardial Infarction Study. Thrombolysis in Myocardial Infarction, phase 11, pilot and clinical trial. Circulation 1991 83(2) 448-59. 

Also see CEREBRAL HEMORRHAGE CEREBRAL INFARCT and HIGH BLOOD PRESSURE.)... 

Untoward effects of both E and NE (usually to a lesser degree) are anxiety, headache, cerebral hemorrhage (from vasopressor effects), cardiac arrhythmias, especially in presence of digitaUs and certain anesthetic agents, and pulmonary edema as a result of pulmonary hypertension. The minimum subcutaneous lethal dose of E is about 4 mg, but recoveries have occurred after accidental overdosage with 16 mg subcutaneously and 30 mg intravenously, followed by immediate supportive treatment. 

Stroke. A general term commonly used to denote a sudden paralysis resulting from a cerebral hemorrhage. 

Thymic hemorrhage and congested cerebral blood vessels occurred in rats exposed to a 1-hour LC50 of methyl parathion described in Section 3.2.1.1 (EPA 1978e). These are probably nonspecific agonal lesions. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Basic aspects of the proteins of the blood coagulation system and of fibrinolysis are described in this chapter. Some fundamental aspects of platelet biology are also presented. Hemorrhagic and thrombotic states can cause serious medical emergencies, and thromboses in the coronary and cerebral arteries are major causes of death in many parts of the world. Rational management of these conditions requires a clear understanding of the bases of blood clotting and fibrinolysis. 

Del Zoppo GJ, Copeland BR, Anderchek K, Hacke W, Koziol JA. Hemorrhagic transformation following tissue plasminogen activator in experimental cerebral infarction. Stroke. 1990 21 596-601. 

Lyden PD, Zivin JA, Clark WA, Madden K, Sasse KC, Mazzarella VA, Terry RD, Press GA. Tissue plasminogen activator-mediated thrombolysis of cerebral emboli and its effect on hemorrhagic infarction in rabbits. Neurology. 1989 39 703-708. 

Fiorelli M, Bastianello S, von Kummer R, del Zoppo GJ, Larrue V, Lesaffre E, Ringleb AP, Lorenzano S, Manelfe C, Bozzao L. Hemorrhagic transformation within 36 hours of a cerebral infarct Relationships with early clinical deterioration and 3-month outcome in the european cooperative acute stroke study i (ECASS i) cohort. Stroke. 1999 30 2280-2284. 

Kase CS, Furlan AJ, Wechsler LR, Higashida RT, Rowley HA, Hart RG, Molinari GF, Frederick LS, Roberts HC, Gebel JM, Sila CA, Schulz GA, Roberts RS, Gent M. Cerebral hemorrhage after intra-arterial thrombolysis for ischemic stroke the PROACT n trial. Neurology 2001 57 1603-1610. 

Tseng MY, Czosnyka M, Richards H, Pickard JD, Kirkpatrick PJ. Effects of acute treatment with pravastatin on cerebral vasospasm, autoregulation, and delayed ischemic deficits after aneurysmal subarachnoid hemorrhage a phase II randomized placebo-controlled trial. Stroke 2005 36 1627-1632. 

Asahi M, Asahi K, Wang X, Lo EH. Reduction of tissue plasminogen activator-induced hemorrhage and brain injury by free radical spin trapping after embolic focal cerebral ischemia in rats. J Cereb Blood Flow Metab 2000 20 452 57. 

Yang Y, Li Q, Shuaib A. Enhanced neuroprotection and reduced hemorrhagic incidence in focal cerebral ischemia of rat by low dose combination therapy of urokinase and topiramate. Neuropharmacology 2000 39 881-888. 

Dissection of the internal carotid and vertebral arteries is a common cause of stroke, particularly in young patients. Although many occur due to trauma, it is estimated that over half occur spontaneously. The mechanism of stroke following arterial dissection is either by artery-to-artery embolism, by thrombosis in situ, or by dissection-induced lumenal stenosis with secondary cerebral hypoperfusion and low-flow watershed infarction. Occasionally, dissection may lead to the formation of a pseudoaneurysm as a source of thrombus formation. Vertebrobasilar dissections that extend intracranially have a higher risk of rupture leading to subarachnoid hemorrhage (SAH). ° ... 

Corticosteroids have been evaluated in several types of cerebral injury, including cerebral infarction. Corticosteroids reduce vasogenic edema, such as that associated with neoplasms, but not cytotoxic edema, the type associated with ischemic stroke. A large meta-analysis found no benefit to the use of corticosteroids in ischemic stroke (or intracerebral hemorrhage), and their use is not recommended, except to treat concomitant conditions that mandate it (e.g., COPD flare). 

Kassell, N.F., Haley, E.C., Halves, W.M., Hunsen, C.A. and Weir, B. (1993). Phase two trial of tirilazad in aneurysmal subarachnoid hemorrhage. Vth International Symposium on Cerebral Vasospasm, Edmonton and Jasper, Alberta, Canada, May 18-21. Can. J. Neurol. Sci. 20, S29. 

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