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.

Saturday, September 24, 2011

Is Lithium a Potential Aid in Traumatic Brain Injury?

I'm not sure I would want to try this one.
http://brainposts.blogspot.com/2011/09/is-lithium-potential-aid-in-traumatic.html
Lithium carbonate serves as a primary treatment option in the treatment of mania and bipolar affective disorder. An elemental metal, lithium has atomic number 3 in the periodic table of elements.

The mechanism of action for lithium carbonate in bipolar disorder is unclear. Some of the proposed mechanisms for lithium in the central nervous system include:

  • alteration of the neurotransmitter glutamate (affected by other drugs linked to therapeutic effect in bipolar disorder, i.e. sodium valproate and lamotrigine)
  • alteration in gene expression
  • inactivation of the GSK-3B (glycogen synthase kinase) enzyme known to be involved in circadian clock regulation
  • interaction with the NO (nitrous oxide) signalling pathway
Inhibition of the GSK-3B enzyme has been shown to have potential beneficial effects in stimulating neuroplasticity as it is associated with enhanced expression of brain-derived neurotrophic factor (BDNF). Fengshan Yu and colleagues at NIH and the University of Health Sciences have recently explored the effect of lithium on traumatic brain injury using a mouse model.

In their experiment, mice received doses of lithium chloride ranging form 1.0 to 5.0 mEq/kg dose of lithium or placebo following a controlled episode of brain trauma under anesthesia. Doses were repeated daily for three days.

Brain injury response to lithium treatment was monitoring using neuropathological techniques as well as behavior and motor coordination tests. The key results of the study include:
  • Lithium chloride at 1.5 to 3.0 mEq/kg reduced brain lesion volume compared to control
  • Lithium chloride reduced post-trauma related anxiety behavior during the outcome monitoring
  • Lithium chloride reduced breakdown of the blood-brain barrior
  • Short-term and long-term motor coordination was better in the lithium group

The authors note that their study suggests the neuroprotective effect of lithium administration following traumatic brain injury in the mouse model appears related to a GSK-3B mechanism. The study timed lithium administration to 3 hours after the trauma providing a realistic model for a trial in human clinical scenarios. They conclude "Our results that demonstrate its (lithium chloride) benefits in the mouse model pave the way for early clinical trials as potential treatment for TBI (traumatic brain injury) patients.

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