The cascade of damage is based on the need for the brain tissue to stop trying to use damaged cells. The damaged cells release a message, either by tRNA (transmitting RNA) or some other system of messenger that causes the surrounding cells that show any signs of stress to shut down (die). Think of it as cutting out a piece of electrical wire that is shorting out to ground, if you understand electrical principles.

There are two natural ways the brain can lessen this cascade of damage or cell death. In women, the body releases higher levels of progesterone so that the development of a fetus can tolerate the stresses of development. This same system appears to be helpful in head injury patients. Research is being completed that suggests an IV infusion of progesterone immediately after a head injury or stroke can drastically reduce this cascade of cell death.

The protocol for use of progesterone in emergency rooms is being currently investigated. The last I read, it sounds like a daily infusion of progesterone for the first 8 days to 2 weeks then decreasing the frequency for a few weeks. It sounds very promising.

A key point that makes it available is the fact that they have not found any negatives, even when used with males. The FDA may decide it is an exempt therapy because of this lack of negative risk. The question will be the availability of bio-identical progesterone. The patented progesterones used by women would not likely pass this 'no negative risk' criteria. Plus, I would personally be very hesitant to use a modified progesterone.

There is also those who suggest a specially modified magnesium can help with this cascade of damage and death. It sounds like this is targeted at the failure of magnesium in the synapse to allow correct ion exchanges to happen. This modified magnesium is promoted as able to restore this function. I posted an article last week about the magnesium being considered.

There is a hope that stem cell therapies can help the damaged and stressed brain cells based on early studies. It sounds like the stems cells can present a message that over-rides the "shut down and die" message sent out by the damaged cells. This is likely a few years or more in the future. There was a post about this research last week too under neural cell rescue.

For the time being, my wife knows to ask if I can get an infusion of progesterone if I suffer another brain injury.

I just did a search on the progesterone issue and found this article;

http://www.sciencedaily.com/releases...0219204407.htm

hi guys and gurls

this one really humming, there have been study's done but hey lets not get into self for filling proficiency here , or crystal ball gazing as to our long term prognosis I have looked into this some time ago, and found conflicting reports, but what they all tend to point to is the younger you are pre morbidity the better the long term out look , but I think we could draw that analogy with many illnesses

please see below

Longitudinal cognitive changes in traumatic brain injury
A 30-year follow-up study L. Himanen, PhLic, R. Portin, PhD, H. Isoniemi, MD, H. Helenius, PhLic, T. Kurki, MD, PhD and O. Tenovuo, MD, PhD

From the Departments of Neurology (L.H., R.P., H.I., O.T.), Biostatistics (H.H.), and Radiology (T.K.), Turku University and Turku University Hospital, Finland.

Address correspondence and reprint requests to Dr. L. Himanen, Department of Neurology, Turku University Hospital, P.O. Box 52, FIN-20521 Turku, Finland; e-mail: ls.himanen@kolumbus.fi

Objective: To evaluate longitudinal cognitive changes in patients over three decades following traumatic brain injury (TBI).

Method: Two hundred ten patients with substantial TBI of variable severity were initially assessed between 1966 and 1972 at Turku University Hospital (Finland). Of these, 61 patients could be studied using the same assessments in the follow-up examination, on average 30 years after the TBI. The results of the follow-up assessment were also compared with an age- and education-matched control group. During each examination, patients were assessed with five subtests of the Wechsler Adult Intelligence Scale, three tests for episodic memory, and the general cognitive decline was determined.

Results: The general pattern of slight cognitive decline during a 30-year follow-up contrasted with improvement in semantic memory. Women maintained their cognitive level, but men showed a decline during the follow-up, especially in visuospatial ability and visual memory. Younger patients were likely to maintain or even improve their cognitive functioning.

Conclusions: Most of the patients had mild cognitive decline during the follow-up, but this decline was influenced by gender and age at injury. Unlike the long-term course in the other domains of cognition, semantic memory showed good recovery potential after traumatic brain injury (TBI). The profile of long-term cognitive decline after TBI seems to be qualitatively different from the early signs of dementia of the Alzheimer type.