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, February 21, 2012

Melatonin ameliorates neural function by promoting endogenous neurogenesis through MT2 melatonin receptor in ischemic stroke mice.

Another hyperacute possibility, but it doesn't say how it was administered.
http://www.ncbi.nlm.nih.gov/pubmed/22330064

Abstract

Melatonin has many protective effects against ischemic stroke, but the underlying neuroprotective mechanisms are not fully understood. Our aim was to explore the relationship between melatonin's neuroprotective effects and activation of the MT2 melatonin receptor in a murine ischemic stroke model. Male ICR mice were subjected to a transient middle cerebral ischemic/reperfusional injury and melatonin (5 and 10mg/kg, i.p.) was administrated once daily starting 2h after ischemia. More than 80% of the mice died within 5days after stroke without treatment. Melatonin treatment significantly improved the survival rates and neural functioning with modestly prolonged lifespan of the stroke mice by preserving blood-brain barrier (BBB) integrity via a reduction in the enormous amount of stroke-induced free radical production and significant gp91(phox) cell infiltration. These protective effects of melatonin were reversed by pretreatment with MT2 melatonin receptor antagonists (4-phenyl-2-propionamidotetralin (4P-PDOT) and luzindole). Moreover, treatment with melatonin after stroke dramatically enhanced endogenous neurogenesis (doublecortin-positive) and cell proliferation (ki67-positive) in the peri-infarct regions. Most ki67-positive cells were nestin-positive and NG2-positive neural stem/progenitor cells that co-expressed two neurodevelopmental proteins (adam11 and adamts20) and MT2 melatonin receptor. RT-PCR revealed that the gene expression level of doublecortin, ki67, adamts20 and adam11 are markedly reduced by stroke, but are restored by melatonin treatment; furthermore, pretreatment with 4P-PDOT and luzindole antagonized melatonin's restorative effect. Our results support the hypothesis that melatonin is able to protect mice against stroke by activating MT2 melatonin receptors, which reduces oxidative/inflammatory stress. This results in the preservation of BBB integrity and enhances endogenous neurogenesis by up-regulating neurodevelopmental gene/protein expression.

Higher magnesium intake associated with reduced ischemic stroke risk

You will notice they say dietary not supplements.
http://www.prohealth.com/library/showarticle.cfm?libid=16832
Abstract:
Background: Prospective studies of dietary magnesium intake in relation to risk of stroke have yielded inconsistent results.

Objective: We conducted a dose-response meta-analysis to summarize the evidence regarding the association between magnesium intake and stroke risk.

Design: Relevant studies were identified by searching PubMed and EMBASE from January 1966 through September 2011 and reviewing reference lists of retrieved articles. We included prospective studies that reported RRs with 95% CIs of stroke for 3 or more categories of magnesium intake. Results from individual studies were combined by using a random-effects model.

Results: Seven prospective studies, with 6,477 cases of stroke and 241,378 participants, were eligible for inclusion in the meta-analysis.

We observed a modest but statistically significant inverse association between magnesium intake and risk of stroke.

An intake increment of 100mg per day was associated with an 8% reduction in risk of total stroke (combined RR: 0.92; 95% CI: 0.88, 0.97), without heterogeneity among studies (P = 0.66, I2 = 0%).

Magnesium intake was inversely associated with risk of ischemic stroke [100mg more daily intake, 9% less incidence of blockage-caused stroke] (RR: 0.91; 95% CI: 0.87, 0.96) but not intracerebral hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10) or subarachnoid hemorrhage (RR: 1.01; 95% CI: 0.90, 1.14).

Conclusion: Dietary magnesium intake is inversely associated with risk of stroke, specifically ischemic stroke.

Sunday, February 19, 2012

Deadly carbon monoxide prevents miscarriage

One line for our perusal. We do want to stop apoptosis as a result of our stroke keeping more brain cells alive.
Deadly carbon monoxide prevents miscarriage

Heme oxygenase-1 is essential for the growth of blood vessels in the placenta and in establishing blood flow in the umbilical cord. Too little HO-1 can lead to a restriction in the growth of the fetus and even in fetal death and miscarriage. New research published in BioMed Central's open access journal Medical Gas Research has shown that low dose carbon monoxide therapy is able to restore placental function and prevent fetal death in mice, without any detrimental effects.
Intrauterine growth restriction due to problems in placental function and blood flow can result in a 'small for gestational age' baby, miscarriage or perinatal death. Both miscarriage and pre-eclampsia are associated with low levels of HO-1 in the placenta, however research suggests that carbon monoxide can mimic the effects of HO-1. Researchers from the Otto-von-Guericke University, Germany tested carbon monoxide therapy on intrauterine growth restriction in mice. They found that an extended course of low dose (50ppm) carbon monoxide was able to reduce fetal loss from 30% to zero – all the babies survived.
Prof Ana Claudia Zenclussen, who led the research explained, "At the levels used to prevent fetal death we found that inhaled low dose carbon monoxide was anti-inflammatory. It reduced the amount of cell death (apoptosis), and increased levels of the anti-apoptotic molecule BAG-1, in the placenta and additionally increased the level of vascular endothelial growth factor (VEGF), which is associated with angiogenesis and blood vessel repair."
Intrauterine growth restriction is a serious complication of pregnancy. Surviving babies have a lifelong increased risk of hypertension, cardiovascular disease and renal disease. In the face of these fears carbon monoxide therapy may provide a lifeline to mothers at risk. However there is a cautionary note - higher doses of carbon monoxide were able to improve placental function but were damaging to the fetus, shorter treatment at low dose was not enough to prevent fetal death. Prof Zenclussen warned, "It is very important, given the inherent dangers in using carbon monoxide, that the dose and length of treatment are tightly controlled."

Eating Fewer Calories May Lower Risk of Asthma, Other Diseases

A couple lines in here may be for us.
http://www.myhealthnewsdaily.com/2258-caloric-restriction-medical-therapy-alzheimers-disease.html
Research on animals also suggests caloric restriction reduces neurological damage after a stroke, but only on young or middle-aged animals. Older animals do not appear to benefit, indicating that caloric restriction may offer stroke benefits only at certain points in life, Mattson said.
Caloric restriction may also help prevent Alzheimer's disease. Just as exercising benefits your muscles, "exercising your nerve cells does the same thing," Mattson said. Reducing daily calories puts stress on the brain cells that, in a sense, exercises them, Mattson said.
In mice designed to develop Alzheimer's disease, those fed a calorie-restricted diet performed better on memory tests, and had reduced levels of amyloid beta protein in their brain compared with mice not fed a restricted diet. Amyloid beta aggregates in the brains of patients with Alzheimer's disease, and is thought contribute to disease onset.
Caloric restriction has been showed to increase levels of a protein in the brain called BDNF. This protein is thought to be involved in the generation of new brain cells, Mattson said.

Saturday, February 18, 2012

Nude stroke rehab

Got your attention didn't I. I'm up in northern Minnesota at the Maplelag resort. XC skiing went ok, about 4k today, only fell once going down a slight hill when the groomed tracks disappeared and I no longer can jump around on my skiis to catch myself before falling. The owner collects signs and this one is on the wall. On Sunday I skied 8k, fell three times, twice because the temperature hit 43 softening the snow in the sun, going down hills switching from shade to sun caused me to lose control plowing face forward into the snow. The third time I was skiing on Luckys' Loype, a single track trail, you need to be able to do step turns on this one, the groomed tracks disappear quickly. I sat down and plowed into the woods. Still a lot of fun.