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, December 29, 2016

The late effects of stress: New insights into how the brain responds to trauma

My stroke was probably the most stressful event in my life. What protocol needs to be created to stop these damaging stress effects from the stroke? It looks like we might have days to treat this so possibly no need to get this done in the first hours. But never mind, NOTHING will get done on this because we have NO strategy to update and NO leadership to execute that strategy.
http://www.neuroscientistnews.com/research-news/late-effects-stress-new-insights-how-brain-responds-trauma
Mrs. M would never forget that day. She was walking along a busy road next to the vegetable market when two goons zipped past on a bike. One man's hand shot out and grabbed the chain around her neck. The next instant, she had stumbled to her knees, and was dragged along in the wake of the bike. Thankfully, the chain snapped, and she got away with a mildly bruised neck. Though dazed by the incident, Mrs. M was fine until a week after the incident.
Then, the nightmares began.
She would struggle and yell and fight in her sleep every night with phantom chain snatchers. Every bout left her charged with anger and often left her depressed. The episodes continued for several months until they finally stopped. How could a single stressful event have such extended consequences?
A new study by Indian scientists has gained insights into how a single instance of severe stress can lead to delayed and long-term psychological trauma. The work pinpoints key molecular and physiological processes that could be driving changes in brain architecture.
The team, led by Sumantra Chattarji from the National Centre for Biological Sciences (NCBS, India) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), Bangalore, India, has shown that a single stressful incident can lead to increased electrical activity in the brain's amygdala. This activity sets in late, occurring ten days after a single stressful episode, and is dependent on a molecule known as the N-methyl-D-aspartate receptor (NMDA-R), an ion channel protein on nerve cells known to be crucial for memory functions.
The amygdala, a small, almond-shaped groups of nerve cells, is located deep within the temporal lobe of the brain where it is known to play key roles in emotional reactions, memory and making decisions. Changes in the amygdala are linked to the development of post-traumatic stress disorder (PTSD), a mental condition that develops in a delayed fashion after a harrowing experience.
Previously, Chattarji's group had shown that a single instance of acute stress had no immediate effects on the amygdala of rats. But ten days later, these animals began to show increased anxiety, and delayed changes in the architecture of their brains, especially the amygdala. "We showed that our study system is applicable to PTSD. This delayed effect after a single episode of stress was reminiscent of what happens in PTSD patients," says Chattarji. "We know that the amygdala is hyperactive in PTSD patients. But no one knows as of now, what is going on in there," he adds.
Investigations revealed major changes in the microscopic structure of the nerve cells in the amygdala. Stress seems to have caused the formation of new synapse connections in this region of the brain. However, until now, the physiological effects of these new connections were unknown.

No comments:

Post a Comment