Hemorrhage symptomatic intracranial

OR 1.81, 95% Cl 1.46-2.24), most of which were related to symptomatic intracranial hemorrhage (OR 3.37, 95% Cl 2.68. 22). In addition, a pooled analysis of six major randomized placebo-controlled IV rt-PA stroke trials (Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS) I and II, European Cooperative Acute Stroke Study (ECASS) I and II, and NINDS I and II), including 2775 patients who were treated with IV rt-PA or placebo within 360 minutes of stroke onset, confirmed the beneht up to 3 hours and suggested a potential beneht beyond 3 hours for some patients. The pattern of a decreasing chance of a favorable 3-month outcome as the time interval from stroke onset to start of treatment increased was consistent with the findings of the original NINDS study. ... 

Stenting of an acutely occluded intracranial vessel may provide fast recanalization by entrapping the thrombus between the stent and the vessel wall. A recent study in which 19 patients with acute occlusions at the ICA terminus n = 8), M1/M2 (n = 7), or basilar artery (n = 4) were treated with balloon-expandable stents showed a TIMI 2 and 3 recanalization rate of 79% and no symptomatic intracranial hemorrhages (Fig. 4.5). ... 

Table 3.6 NCCT predictors of symptomatic intracranial hemorrhage postthrombolysis for stroke ...

Randomized Controlled Trial PSAS Prospective Single-Arm Study sICH symptomatic intracranial hemorrhage lAT number of patients treated with intra-arterial thrombolysis Primary end point (90-day mRS <2) was reached (p = 0.04)... 

Subarachnoid hemorrhage (SAH) is most commonly caused by rupture of an intracranial aneurysm. It can produce vasospasm that may cause ischemia and infarction. Currently, vasospasm has surpassed rebleeding as the most important complication after rupture of an aneurysm. Vasospasm due to SAH is thought to occur in the majority of cases of SAH (angiographic vasospasm is detectable in perhaps as many as 60-70% of patients after subarachnoid hemorrhage), but is symptomatic only in about a third of this population [81]. Symptomatic vasospasm carries a 15% to 20% risk of stroke or death. Vasospasm peaks around 1 week after SAH, but it can be seen as early as 3 days or as late as 3 weeks after the initial event [82], The underlying mechanisms are not understood, but vasospasm is clearly related to the amount of blood and its location in the subarachnoid space. Clinical symptoms generally develop slowly over a period of several hours to 1 or 2 days however, clinical evolution can be rapid in the onset with a stroke-like presentation [81, 82]. 

Autopsy data showed that only 12% of AVMs become symptomatic during life (The Arteriovenous Malformation Study Group 1999), and intracranial hemorrhage is the most common clinical presentation (Al-Shahi and Warlow 2001 Hofmeister et al. 2000 The Arteriovenous Malformation Study Group 1999). 

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