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.

Thursday, October 27, 2022

Lithium Biological Action Mechanisms after Ischemic Stroke

You can ask your doctor what has been done with all this earlier research. No knowledge you need to fire your doctor.

I've got 13 posts on lithium back to 2011 and I bet your stroke medical 'professionals' have not done one damn thing. You're screwed from all the incompetency out there. And this is just a lazy review article, NOT how lithium can be used to help recovery.

 

  • lithium (13 posts to September 2011)

Lithium Biological Action Mechanisms after Ischemic Stroke

Constantin Munteanu1,2, *, 
Mariana Rotariu 1, 
Marius Turnea Ligia Gabriela Tătăranu, 
Gabriela Dogaru 4,5,
Cristina Popescu, 
Aura Spî 2,3, 
Ioana Andone 2,3 
Elena Valentina Ionescu 6,7, 
Roxana Elena Țucmeanu 6,7 
Carmen Oprea 6,7, 
Alin Țucmeanu, 
Carmen Nistor Cseppento 8 *, 
Sînziana Calina Silișteanu 9 and Onose 2,3 Faculty of Medical Bioengineering, University of Medicine and Pharmacy Grigore T. Popa 700454 Iași, Romania Teaching Emergency Hospital Bagdasar Arseni”, 041915 Bucharest, Romania Faculty of Medicine, University of Medicine and Pharmacy Carol Davila 020022 Bucharest, Romania Faculty of Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 400012 Napoca, Romania Clinical Rehabilitation Hospital, 400437 Napoca, Romania Faculty of Medicine, Ovidius University of Constanta, 900470 Constanta, Romania 7 Balneal and Rehabilitation Sanatorium of Techirghiol, 906100 Techirghiol, Romania Faculty of Medicine, University of Oradea, 410073 Orade a, Romania Faculty of Medicine and Biological Sciences, University of Suceava, 720229 Suceava, Romania Correspondence: constantin.munteanu.biolog@umfiasi.ro(C.M.) delia_cseppento@yahoo.com (C.N.C.) Abstract Lithium is a source of great scientific interest because although it has such a simple structure, relatively easy analyze chemistry, and well established physical properties, the plethora of which influence numerous cellular and molecular processes through not entirely explained mechanisms of actiongenerate a mystery that modern science is still trying to decipher. Lithium has multiple effects on neurotransmitter mediated receptor signaling, ion transport, signaling cascades, hormonal regulation, circadian rhythm, and gene expression. The biochemical mechanisms of lithium action appear to be multifactorial and interrelated with the functioning of several enzymes, hormones, vitamins, and growth and transformation factors. The widespread and chaotic marketing of lithium salts in potions and mineral waters, always at inadequate concentrations for various diseases, has contributed to the general disillusionment with empirical medical hypotheses about the therapeutic role of lithium. Lithium salts were first used therapeutically in 1850 to relieve the symptoms of gout, rheumatism, and kidney stones. In 1949, Cade was credited with discovering the sedative effect of lithium salts in the state of manic agitation, but frequent cases of intoxication accompanied the therapy. In the 1960s, lithium was shown to prevent manic and also depressive recurrences. This prophylactic effect was first demonstrated in an open label study using the mirror method and was later (after 1970) confirmed by several placebo controlled double blind studies. Lithium prophylaxis was similarly effective in bipolar and also unipolar patients. In 1967, the therapeutic value of lithemia was determined, included in the range of 0.51 mEq l. Recently, new therapeutic perspectives on lithium are connected with improved neurological outcomes after ischemic stroke. The effects of lithium on the development and maintenance of neuroprotection can be divided into two categories: short term effects and longterm effects. Unfortunately, the existing studies do not fully explain the lithium biological action mechanisms after ischemic stroke. (So WHOM is going to do the further research needed?)

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