Can an old head injury suddenly cause detrimental effects much later in life?
—Anonymous, via e-mail
Douglas Smith, professor of neurosurgery and director of the Center for Brain Injury and Repair at the University of Pennsylvania, answers:
although a brain injury from a car accident or a collision during a football game often seems to cause a sudden change to cognitive ability years later, this change does not just appear out of the blue—the damage has been building up slowly, unnoticed, over time.
Postinjury, the progressive brain deterioration that may occur likely reaches a tipping point, after which the loss of function “suddenly” becomes obvious. Depending on the type and severity of the traumatic brain injury (TBI), it can accelerate memory loss or increase a person’s chance of succumbing to Alzheimer’s disease.
TBI commonly damages nerve fibers in the brain called axons. These thin, tubelike structures transmit electrical and chemical signals that are vital for carrying information among different regions of the brain. For unknown reasons, these fragile structures not only disconnect shortly after injury but can continue to disconnect even for decades later in some patients. Once disconnected, the blunt end of an axon seals itself off, swells with fluids, enzymes and proteins and eventually bursts. When axons burst open, they often distribute amyloid proteins through the neighboring brain tissue. These sticky proteins are a hallmark of Alzheimer’s, and in fact many TBI patients exhibit signs of dementia later in life that mimic the deterioration observed in Alzheimer’s patients.
In addition, with axons disappearing or not functioning well after TBI, a person’s ability to process new information may slow down. Surviving axons may compensate for the damage by increasing electrical signaling and thus restoring the normal speed of information processing in the brain. This temporary fix, however, can cause these axons to become even more sensitive to damage if a second concussion occurs.
Most people with TBI will have progressive axonal damage, but it is difficult to predict who will suffer from cognitive changes years later. TBIs have a devastating effect on society, with more than 1.5 million cases documented in the U.S. every year. Currently no therapies exist for either short- or long-term damage, which means for now the best treatment is protection and prevention.
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8 Comments
Add CommentWho is the WE group that, " 'knows' that doctors like to cut the umbilical cord too soon." Wishful Explainers? Worthless Expostulators? Wingnuts Especial?
Reply | Report Abuse | Link to thisstew6302 - At least some of us have no idea what is too soon, or too late. To best assess this, perhaps current methods should be compared to those that worked for at least many tens of thousands of years before doctors or scalpels.
Reply | Report Abuse | Link to thisIt is pretty simple. When one is smacked in the head blood is spilled / somewhat like a 'bruise'. WHEN blood IS spilled the contents of said red blood cells RELEASE and the iron inside the red blood cell SPILLS out. This iron NORMALLY would be mopped up by the body . WHEN there is already too much iron in the body this iron is NEVER actually removed but SEQUESTERED and later becomes a problem.
Reply | Report Abuse | Link to thisBelieve it or not.
"A likely mechanism of seizure development post-TBI is
decompartmentalization of iron from extravasated hemoglobin (Hb)."
It is pretty simple. When one is smacked in the head blood is spilled / somewhat like a 'bruise'. WHEN blood IS spilled the contents of said red blood cells RELEASE and the iron inside the red blood cell SPILLS out. This iron NORMALLY would be mopped up by the body . WHEN there is already too much iron in the body this iron is NEVER actually removed but SEQUESTERED and later becomes a problem.
Reply | Report Abuse | Link to thisBelieve it or not.
"A likely mechanism of seizure development post-TBI is
decompartmentalization of iron from extravasated hemoglobin (Hb)."
In a National Geographic documentary, it was speculated that Howard Hughes' schizophrenia later in life was caused by his head injuries in plane crashes when he was young. He probably also had OCD though it was unknown during his lifetime.
Reply | Report Abuse | Link to thisI played basketball for almost 30 years and was known for crashing the boards. Consequently I was knocked out 3, maybe 4 times over that period.....wait....sorry...can't remember where I was going with this....what was the article about?
Reply | Report Abuse | Link to thisI am more than 13 years post severe brain stem and frontal lobe TBI. I am 4 years post-diagnosis with consequential Parkinson's Disease. Dr. Smith's description of a "tipping point" and subsequent reference to Alzheimer's, unfortunately, sounds too familiar and makes me acutely aware of the unpredictability of post-TBI life. Post-TBI or pre-TBI...it doesn't seem to matter. Life is as unpredictable as it is fragile. Prevention is the surest, easiest and most efficient response to the epidemic of catastrophic injury.
Reply | Report Abuse | Link to thisYou'll never convince a friend of mine that "Medicine is trying to heal & protect the brains of millions ..." For, it was "Medicine" that caused her head injury that arose years later.
Reply | Report Abuse | Link to thisJane was given "ECT"(Electroshock Therapy)years ago. When she suddenly experienced double-vision recently,the diagnosis said: "a large mass" growing behind both eyes. When she gave me the bad news, I did research,& learned an ECT session delivers 7 jolts of electricity to the brain to cause a GrandMal seizure.
It also said each jolt given is the equivalent to a 'severe closed head injury'. So,if 7 jolts are given, then the brain receives 7 traumatic blows that are equivalent to sustaining seven severe closed head injuries!
Then, I switched to researching about the large mass. It was located in the Meninges, the inner linings around the brain. The data revealed that there were only several causes for a "Meningioma" ....one of them being a 'severe blow to the head,' or a 'closed head injury' sometime in the patient's past. Jane had not received just one closed head injury to her head, but many of them; during the times she was administered ECT.
So, in this case, the medical 'treatment' of ECT actually was the causation for the growth of the mass called "Meningioma"; years down the road. Since a Meningioma is a very slow-growing tissue, Jane has probably had it growing in her head for quite some time - and only became aware of it when the size of it crossed a threshold by infiltrating to the optic nerve, and pressing on it - thus; causing the first noticeable symptom: sudden double vision. Jane's Meningioma has also attached itself to her inner facial bone structure; where it clings onto the bone structure - that, she was told (and my research showed) places her case in a most perilous situation. Because once the abnormal mass has attached itself onto the facial bone structure, there is almost no way they can remove that because of it's clingy nature and the level of infiltration it suggests. Meningiomas are not always malignant - but in Jane's case, it doesn't really matter - because the growth itself has grown so large and infiltrated into the optic nerve area, and clings to the bone structure to the point where it is almost untreatable, they said. They have not done anything to treat her. They said they're "keeping an eye on it." My common sense tells me that it can only get worse & larger-it won't get smaller by waiting and "keeping as eye on it."
Her doctors don't admit the ECT is to blame, but I say it is.