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, December 17, 2016

Progesterone sharpens temporal response profiles of sensory cortical neurons in animals exposed to traumatic brain injury

Followup should be done since there are conflicting results for stroke and TBI, but that will never occur until our fucking failures of stroke associations are destroyed.
http://www.ingentaconnect.com/content/cog/ct/pre-prints/content-ct-1705_allitt_et_al
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Abstract:

Traumatic brain injury (TBI) initiates a cascade of pathophysiological changes that are both complex and difficult to treat. Progesterone (P4) is a neuroprotective treatment option that has shown excellent preclinical benefits in the treatment of TBI but these benefits have not translated well in the clinic. We have previously shown that P4 exacerbates the already hypoactive upper cortical responses in the short-term post-TBI and does not reduce upper cortical hyper-activity in the long-term, and we concluded that there is no tangible benefit to sensory cortex firing strength. Here we examined the effects of P4 treatment on temporal coding resolution in the rodent sensory cortex in both the short-term (4 days) and long-term (8 weeks) following impact acceleration-induced TBI. We show that; in the short-term post-injury TBI has no effect on sensory cortex temporal resolution and that P4 also sharpens the response profile in all cortical layers in the uninjured brain and all layers other than layer 2 in the injured brain. In the long-term TBI broadens the response profile in all cortical layers despite firing rate hyperactivity being localised to upper cortical layers and P4 sharpens the response profile in TBI animals in all layers other than L2 and has no long-term effect in the Sham brain. These results indicate that P4 has long-term effects on sensory coding that may translate to beneficial perceptual outcomes. The effects seen here, combined with previous beneficial pre-clinical data, emphasise that P4 is still a potential treatment option in ameliorating TBI induced disorders.
Keywords: Cortical laminae; Electrophysiology; Progesterone; Sensory cortex; Traumatic brain injury
DOI: https://doi.org/10.3727/096368916X694229
Affiliations: Department of Physiology, Monash University, Clayton VIC, Australia
Appeared or available online: December 7, 2016

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