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.

Wednesday, July 24, 2013

A COMBINATION THERAPY OF NICOTINAMIDE AND PROGESTERONE FOR FUNCTIONAL RECOVERY FOLLOWING TRAUMATIC BRAIN INJURY

So which researcher is going to follow this up and test it for stroke? Or are we going to have to tell our doctors the day after the stroke that we want this and damn the consequences? The dissertations I've seen answer better questions than standard researchers.

A COMBINATION THERAPY OF NICOTINAMIDE AND PROGESTERONE FOR FUNCTIONAL RECOVERY FOLLOWING TRAUMATIC BRAIN INJURY

Abstract

Traumatic Brain Injury (TBI) is a leading cause of death and disability in the United States for which there are no federally approved pharmacological treatments. Preclinical trials with nicotinamide (NAM) and progesterone (Prog) treatment demonstrate beneficial neuroprotection and recovery of function following TBI. The primary goal of this study was to assess both neuroprotection and recovery of function in an animal model of TBI after combination treatment of both NAM and Prog. Animals received a cortical contusion injury over the sensorimotor cortex and were treated with either nicotinamide (75 mg/kg, i.p. NAM loading dose, 12 mg/kg/hr NAM, s.c. over 72 hrs), Prog (10 mg/kg Prog, i.p. over 72 hrs), NAM and Prog(75 mg/kg, i.p. NAM loading dose, followed by continuous infusion of 12 mg/kg/hr NAM, s.c. over 72 hrs; 10 mg/kg Prog, i.p. over 72 hrs) or Vehicle (75 mg/kg, i.p. sterile saline loading dose, followed by continuous infusion 12 mg/kg/hr sterile saline, s.c. over 72 hrs; 10 mg/kg peanut oil, i.p. over 72 hrs), and compared to a craniotomy only (Sham) group. Following this regimen they were assessed in a battery of behavioral (fine and gross motor, sensory, and cognitive) tasks or a histological assessment at 24 hrs post-injury assessing lesion cavity size, degenerating neurons, and reactive astrocytes. Our results replicate the beneficial effects of treatment with either NAM or Prog demonstrating significant improvements in recovery of function, and a reduction in lesion cavitation, degenerating neurons and reactive astrocytes 24 hours post-injury. The combination treatment of NAM and Prog led to a significant improvement in both neuroprotection at 24 hrs post-injury and recovery of function in sensorimotor related tasks when compared to each individual treatment (NAM or Prog). It is suggested here that further preclinical trials using NAM and Prog as a combination treatment should be done to identify any drug interactions, pharmacokinetics, and a new window of opportunity and proper dosing of this combination treatment.

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