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Subarachnoid hemorrhage stroke

Drug-associated cerebrovascular events and fatalities Cerebral hemorrhage, subarachnoid hemorrhage, stroke, and other cerebrovascular events have been reported in patients treated with dihydroergotamine some have resulted in fatalities. Other vasospasm-related events Dihydroergotamine, like other ergot alkaloids, may cause vasospastic reactions other than coronary artery vasospasm. Myocardial and peripheral vascular ischemia have been reported with dihydroergotamine. [Pg.970]

Conway JE, Tamargo RJ. Cocaine use is an independent risk factor for cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2001 32(10) 2338-43. [Pg.530]

Hellingman CA, van den Bergh WM, Beijer IS et al. (2007). Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal subarachnoid hemorrhage. Stroke 38 96-99... [Pg.359]

Initial loss of consciousness and risk of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Stroke 30 2268-2271... [Pg.359]

Biller J, Godersky JC, Adams HP Jr (1988) Management of aneurysmal subarachnoid hemorrhage. Stroke 19 1300-1305... [Pg.271]

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. [Pg.116]

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). ° ... [Pg.152]

Hemorrhagic stroke is a result of bleeding into the brain and other spaces within the central nervous system and includes subarachnoid hemorrhage, intracerebral hemorrhage, and subdural hematomas. [Pg.161]

Hemorrhagic strokes account for 12% of strokes and include subarachnoid hemorrhage, intracerebral hemorrhage, and subdural hematomas. Subarachnoid hemorrhage may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation. Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain parenchyma causes formation of a hematoma. Subdural hematomas are most often caused by trauma. [Pg.169]

Antithrombin HI (ATHI). There are only a few references concerning the evaluation of antithrombin III (AT III) in cerebrospinal fluid. Extension of evaluated groups of patients is not sufficient a comparison with other CSF protein fractions and with CSF cytological findings was not done. Some experimental works describe the vasorelaxant effect of AT III on brain arteries, and the inhibitory influence of AT III in subarachnoid hemorrhage on onset of vasospasms is expected (W2). AT III also plays a possible role in etiopathogenesis of ischemic stroke (A19, W2). [Pg.20]

Nimodipine, a member of the dihydropyridine group of calcium channel blockers, has a high affinity for cerebral blood vessels and appears to reduce morbidity after a subarachnoid hemorrhage. Nimodipine was approved for use in patients who have had a hemorrhagic stroke, but it has recently been withdrawn. Nicardipine has similar effects and is used by intravenous and intracerebral arterial infusion to prevent cerebral vasospasm associated with stroke. Verapamil as well, despite its lack of vasoselectivity, is used by the intra-arterial route in stroke. Some evidence suggests that calcium channel blockers may also reduce cerebral damage after thromboembolic stroke. [Pg.262]

The risk of stroke is concentrated in women over age 35. It is increased in current users of oral contraceptives but not in past users. However, subarachnoid hemorrhages have been found to be increased among both current and past users and may increase with time. [Pg.910]

Kiiker W, Thiex R, Block F (1999) Hyperacute perimesencephalic subarachnoid hemorrhage demonstration of blood extravasation with MRI. J Comput Assist Tomogr 23 521-523 Kwa VH, Franke CL, Verbeeten B Jr et al (1998) Silent intracerebral microhemorrhages in patients with ischemic stroke. Ann Neurol 44 372-377... [Pg.170]

Rosenberg GA, Mun-Bryce S, Wesley M et al (1990) Collagenase-induced intracerebral hemorrhage in rats. Stroke 21 801-807 Rumboldt Z, Kalousek M, Castillo M (2003) Hyperacute subarachnoid hemorrhage on T2-weighted MR images. AJNR Am J Neuroradiol 24 472-475... [Pg.170]

Komatsu Y., Fujita K., and Iguchi M. (2000) Mild hypothermia as a protective therapy for severe subarachnoid hemorrhage. Surg. Cereb. Stroke 29,16-20. [Pg.12]


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See also in sourсe #XX -- [ Pg.415 , Pg.416 , Pg.423 ]




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