Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 17205 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!Just think of all thetrillions and trillions of neuronsthateach daybecause there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 493 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. My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html
Friday, July 6, 2018
Low Serum Calcium and Magnesium Levels and Rupture of Intracranial Aneurysms
Background and Purpose—Both low serum calcium and magnesium levels have been associated with the extent of bleeding in patients with intracerebral hemorrhage, suggesting hypocalcemia- and hypomagnesemia-induced coagulopathy as a possible underlying mechanism. We hypothesized that serum albumin-corrected total calcium and magnesium levels are associated with ruptured intracranial aneurysms.
Methods—The medical records of 4701 patients, including 1201 prospective patients, diagnosed at the Brigham and Women’s Hospital and Massachusetts General Hospital between 1990 and 2016 were reviewed and analyzed. One thousand two hundred seventy-five patients had available serum calcium, magnesium, and albumin values within 1 day of diagnosis. Individuals were divided into cases with ruptured aneurysms and controls with unruptured aneurysms. Univariable and multivariable logistic regression analyses were performed to determine the association between serum albumin-corrected total calcium and magnesium levels and ruptured aneurysms.
Results—In multivariable analysis, both albumin-corrected calcium (odds ratio, 0.33; 95% confidence interval, 0.27–0.40) and magnesium (odds ratio, 0.40; 95% confidence interval, 0.28–0.55) were significantly and inversely associated with ruptured intracranial aneurysms.
Conclusions—In this large case–control study, hypocalcemia and hypomagnesemia at diagnosis were significantly associated with ruptured aneurysms. Impaired hemostasis caused by hypocalcemia and hypomagnesemia may explain this association.
Recently, both hypocalcemia and hypomagnesemia have been significantly associated with extent of bleeding in patients with intracerebral hemorrhage.1–3 Because both calcium and magnesium are involved in platelet function and the coagulation cascade, impaired hemostasis caused by hypocalcemia and hypomagnesemia may explain this association.2,4–6 In addition, hypomagnesemia has been associated with severity of aneurysmal subarachnoid hemorrhage (aSAH) and related complications such as delayed cerebral ischemia,7 although conflicting results have been reported.8 However, studies investigating this association in the context of intracranial aneurysm rupture risk are lacking. Here, we present a large case–control study investigating the association between albumin-corrected total calcium and magnesium values at admission and the risk of aSAH.