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The Long-Term Effects of Brain Injury

posted by SK Brain Injury    |   March 2, 2013 13:56

Researchers from the University of South Florida and colleagues at the James A. Haley Veterans' Hospital studying the long-term consequences of traumatic brain injury (TBI) using rat models, have found that, overtime, TBI results in progressive brain deterioration characterized by elevated inflammation and suppressed cell regeneration. However, therapeutic intervention, even in the chronic stage of TBI, may still help prevent cell death. 

Their study is published in the current issue of the journal PLOS ONE.

"In the U.S., an estimated 1.7 million people suffer from traumatic brain injury," said Dr. Cesar V. Borlongan, professor and vice chair of the department of Neurosurgery and Brain Repair at the University of South Florida (USF). "In addition, TBI is responsible for 52,000 early deaths, accounts for 30 percent of all injury-related deaths, and costs approximately $52 billion yearly to treat."

While TBI is generally considered an acute injury, secondary cell death caused by neuroinflammation and an impaired repair mechanism accompany the injury over time, said the authors. Long-term neurological deficits from TBI related to inflammation may cause more severe secondary injuries and predispose long-term survivors to age-related neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease and post-traumatic dementia. 

Since the U.S. military has been involved in conflicts in Iraq and Afghanistan, the incidence of traumatic brain injury suffered by troops has increased dramatically, primarily from improvised explosive devices (IEDs), according to Martin Steele, Lieutenant General, U.S. Marine Corps (retired), USF associate vice president for veterans research, and executive director of Military Partnerships. In response, the U.S. Veterans Administration has increasingly focused on TBI research and treatment. 

"Progressive injury to hippocampal, cortical and thalamic regions contributes to long-term cognitive damage post-TBI," said study co-author Dr. Paul R. Sanberg, USF senior vice president for research and innovation. "Both military and civilian patients have shown functional and cognitive deficits resulting from TBI." 

Because TBI involves both acute and chronic stages, the researchers noted that animal model research on the chronic stages of TBI could provide insight into identifying therapeutic targets for treatment in the post-acute stage. 

"Using animal models of TBI, our study investigated the prolonged pathological outcomes of TBI in different parts of the brain, such as the dorsal striatum, thalamus, corpus callosum white matter, hippocampus and cerebral peduncle," explained Borlongan, the study's lead author. "We found that a massive neuroinflammation after TBI causes a second wave of cell death that impairs cell proliferation and impedes the brain's regenerative capabilities." 

Upon examining the rat brains eight weeks post-trauma, the researchers found "a significant up-regulation of activated microglia cells, not only in the area of direct trauma, but also in adjacent as well as distant areas." The location of inflammation correlated with the cell loss and impaired cell proliferation researchers observed.

Microglia cells act as the first and main form of immune defense in the central nervous system and make up 20 percent of the total glial cell population within the brain. They are distributed across large regions throughout the brain and spinal cord.

"Our study found that cell proliferation was significantly affected by a cascade of neuroinflammatory events in chronic TBI and we identified the susceptibility of newly formed cells within neurologic niches and suppression of neurological repair," wrote the authors.

The researchers concluded that, while the progressive deterioration of the TBI-affected brain over time suppressed efforts of repair, intervention, even in the chronic stage of TBI injury, could help further deterioration.

 

Article from Science Daily 

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The Effects After a Brain Injury

posted by SK Brain Injury    |   January 2, 2012 12:00

The events that occur with major brain injuries and head trauma may be very similar to a rare but devastating ocean-related disaster. The initial trauma is the first insult to the brain, but what happens in the hours and days afterward may be even worse.

Neurological events called "brain tsunamis" occur several days after severe head trauma and may be responsible for inducing brain damage, according to a new study. Preventing these tsunamis or "killer waves" could help patients with severe head trauma avoid further brain damage and possibly retain most of their brain function.

The "brain tsunamis" are actually large population of brain cells that undergo massive depolarizations. Much like the weather-related tsunamis, these large waves of depolarizations spread slowly but persistently throughout the brain, causing widespread brain dysfunction.

These wave-like depolarizations have been studied in brain trauma patients for decades. But the new research showed for the first time that brain tsunamis are responsible for causing further brain damage in afflicted patients. The brain tsunamis drew the attention of the U.S. military as head injuries became a very common injury among veterans of the Iraq and Afghanistan wars.

The study is a collaboration between Kings College Hospital in London and the University of Cincinnati School of Medicine in Ohio. The researchers followed 103 people across seven different centers worldwide who underwent neurosurgery following major head trauma. Fifty-eight of those patients experienced the "brain tsunami" event, leading to a spread of cell depolarizations within the cortex.

The researchers measured the extent of the depolarizations by placing a linear strip of electrodes on the surface of the brain as the patient underwent neurosurgery. The patients were then followed for the duration of their post-operative care, to see whether the outcome of the neurosurgery was favorable.

The investigators hope that their results may alter the long-term treatment of brain trauma patients in a way that could possibly lead to better outcomes. Previous studies have identified other ways to improve outcomes in humans with brain injury.

In this case, the researchers hope that the spreading cortical depolarizations could somehow be stopped before they start in trauma patients undergoing surgery. So far, however, the investigators have not speculated how that could be achieved.

"Our ability to monitor and understand what happens in the brain after a severe injury hasn't advanced significantly in decades. The brain is like a black box, but the process of spreading depolarizations now gives us a window into that box," said principal investigator, Jed Hartings, of the University of Cincinnati College of Medicine.

The study was published in the journal Lancet Neurology.

This article found at www.theatlantic.com

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An Injured Alcoholic Brain

posted by SK Brain Injury    |   November 20, 2011 16:02

Alcoholic brains work harder to accomplish even simple tasks as compared to their sober counterparts, a new study has found.

Chronic drinking is associated with abnormalities in the structure, metabolism and function of the brain, and one of the consequences of these deficits is impairment of motor functioning.

Researchers from Vanderbilt University, using functional magnetic resonance imaging (fMRI) during a finger-tapping exercise, found that the frontal lobe and cerebellum activities were less integrated in alcoholic individuals.

“The relationship was weaker in alcoholic people, even a week after they had stopped drinking,” Baxter Rogers, the lead author said.

Rogers and his colleagues used fMRI to examine 10 uncomplicated chronic alcoholic patients after five to seven days of abstinence and once signs of withdrawal were no longer present, as well as 10 matched healthy controls.

Finger tapping recruits portions of both the cerebellum and frontal cortex, Rogers said, and previous research strongly suggested that both are affected in alcoholism, especially the cerebellum.

“We used fMRI because it measures the function of the entire brain painlessly and non-invasively.

“And it can identify specific brain regions that are involved in tasks, and that are affected in disease,” he said.

The researchers found that alcoholic patients could produce the same number of finger taps per minute as did the normal controls, but employed different parts of the brain to do it.

“This suggests that alcoholics needed to compensate for their brain injury.

“They may need to expend more effort, or at least a different brain response, to produce a normal outcome on simple tasks because they are unable to utilize the brain regions needed in an integrated fashion,” he added.

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