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, January 29, 2013

Neuro-Protection after Traumatic Brain Injury: Novel Strategies.

Nothing really new here but it does put the problem into more scientific terms than I can regarding the neuronal cascade of death.
http://www.iosrjournals.org/iosr-jdms/papers/Vol3-issue6/Q0367585.pdf
I. Introduction
Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury,
causes substantial disability and mortality. Traumatic Brain Injury is a significant public health
problem worldwide and is predicted to surpass many diseases as a major cause of death and disability
by the year 20201. The majority of TBI cases (60%) are a result of road traffic injuries (RTI),
followed by falls (20-30%), and violence (10%)2. In India it is estimated nearly 1.6 million individuals will sustain TBI and seek hospital care annually3.RTI are the leading cause of TBI in India accounting for 45-60% of TBI, and falls account for 20-30% of TBI, paralleling the findings from the Global Burden of Disease Study4. Traumatic brain injury causes mechanical tissue destruction which can be supposed to be the primary mechanism of brain injury that results in neuronal cell death causing cerebral edema and rise in intracranial tension contributing to impaired cerebral vasoregulation, cerebral ischemia/hypoxia and brain damage. Primary injury itself acts as trigger for secondary mechanism responsible for brain injury i.e. the neuronal cell death associated with cerebral ischemia is due to the lack of oxygen and glucose, and may involve the loss of ATP, excitotoxicity of glutamate, oxidative stress, reduced neurotrophic support, and multiple other metabolic stresses5. One major event taking place at the moment of TBI is the massive ionic in flux referred to as traumatic depolarization.
Excitatory amino acids may play a vital role in this depolarization. This represents one of the most
important mechanisms of diffuse neuronal cell dysfunction and damage associated with TBI. Cerebral edema and associated increased intracranial pressure are the major immediate consequences of TBI that contribute to most early deaths. There are at least two kinds of delayed and progressive pathobiological changes induced by TBI. One of these is axonal damage, which is not the direct
consequence of traumatic tissue tearing. Rather, results from complex axolemmal or cyto-skeletal
changes, or both, which lead to cyto-skeletal collapse and impairment of axoplasmic transport. The
other change in traumatized brains occurs concomitantly with compromised blood brain barrier (BBB) function. Secondary damage in TBI is influenced by changes in cerebral blood flow (CBF), cerebral metabolic dysfunction and inadequate cerebral oxygenation. Excitotoxic cell damage and inflammation may lead to apoptosis6. Furthermore, it is also becoming clear that these secondary insults are, to a significant degree, are preventable. Since multiple derangements starts simultaneously it is essential to have effective neuroprotective therapy to prevent early brain damage. Management of head injury focuses on preventing, detecting and correcting the secondary brain injury after trauma. Duration and severity of such secondary brain damage influences the possible outcome. Unfortunately, numerousneuroprotective drugs have failed to demonstrate beneficial effects in Phase II/III clinical trials, despite previous encouraging preclinical results7. However, some drugs that have been approved for use in the clinic have neuroprotective effects, and these could be used for the treatment and improvement in functional recovery in patients of traumatic brain injury.

Lots more at the link.

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