Deans' stroke musings: Trigger Factors and Their Attributable Risk for Rupture of Intracranial Aneurysms

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, May 17, 2011

Trigger Factors and Their Attributable Risk for Rupture of Intracranial Aneurysms

I haven't followed this very much because mine was ischemic and preventing these is harder.
http://stroke.ahajournals.org/cgi/content/abstract/STROKEAHA.110.606558v1
Abstract
Background and Purpose—Little is known about activities that trigger rupture of anintracranial aneurysm. Knowledge on what triggers aneurysmalrupture increases insight into the pathophysiology and facilitatesdevelopment of prevention strategies. We therefore aimed toidentify and quantify trigger factors for aneurysmal ruptureand to gain insight into the pathophysiology.
Methods—During a 3-year period, 250 patients with aneurysmal subarachnoidhemorrhage completed a structured questionnaire regarding exposureto 30 potential trigger factors in the period soon before subarachnoidhemorrhage (hazard period) and for usual frequency and intensityof exposure. We assessed relative risks (RR) of rupture afterexposure to triggers with the case-crossover design comparingexposure in the hazard period with the usual frequency of exposure.Additionally, we calculated population-attributable risks.
Results—Eight triggers increased the risk for subarachnoid hemorrhage:coffee consumption (RR, 1.7; 95% CI, 1.2–2.4), cola consumption(RR, 3.4; 95% CI,1.5–7.9), anger (RR, 6.3; 95% CI, 4.6–25),startling (RR, 23.3; 95% CI, 4.2–128), straining for defecation(RR, 7.3; 95% CI, 2.9–19), sexual intercourse (RR, 11.2;95% CI, 5.3–24), nose blowing (RR, 2.4; 95% CI, 1.3–4.5),and vigorous physical exercise (RR, 2.4; 95% CI, 1.2–4.2).The highest population-attributable risks were found for coffeeconsumption (10.6%) and vigorous physical exercise (7.9%).
Conclusions—We identified and quantified 8 trigger factors for aneurysmalrupture. All triggers induce a sudden and short increase inblood pressure, which seems a possible common cause for aneurysmalrupture. Some triggers are modifiable, and further studies shouldassess whether reduction of exposure to these factors or measurespreventing sudden increase in blood pressure decrease the riskof rupture in patients known to have an intracranial aneurysm.