Chronic traumatic encephalopathy (CTE) was found in 110 of 111 (99 percent) brains of deceased former National Football League players that were donated to scientific research, according to a study published in the medical journal JAMA. CTE, a neurodegenerative brain disease, was also neuropathologically diagnosed in 177 of the 202 players studied across all levels of play (87 percent). It was found in three of the 14 high school players and 48 of the 53 college players.
CTE is typically found in individuals who have been exposed to repeated head trauma, including veterans and football players. CTE can only be diagnosed with an autopsy. The JAMA study focused on football as the primary exposure to head trauma, whether or not the individual had exhibited symptoms while living. The study acknowledged the lack of a comparison group without which the study cannot offer an estimate on the overall risk of brain injury due to participation in football.
Four Kessler Foundation researchers were awarded two-year grants to fund studies of functional and cognitive deficits in individuals who have experienced traumatic brain injury (TBI). The grants, totaling $713,000, were awarded by the New Jersey Commission on Brain Injury Research (NJCBIR).
Researchers will study functional and cognitive deficits in individuals with moderate to severe traumatic brain injury (TBI), including learning and memory, and limb mobility.
One grant, valued at $179,000, will fund a two-phase trial testing the “modified Story Memory Technique (mSMT)” in school-aged children. The mSMT trial will compare healthy controls with children who have cognitive deficits caused by TBI. The grant awardee, Dr. Nancy Chiaravalloti, previously conducted a study involving multiple sclerosis and mSMT which found that mSMT is effective for improving learning and memory in MS patients. Dr. Chiaravalloti is the director of neuropsychology, neuroscience and TBI research at Kessler Foundation, and director of the Northern New Jersey TBI Model System.
A recent review examined clinical and experimental literature for information on the long-term cognitive impact of traumatic brain injury (TBI) in the context of cognitive aging.
Neurobiological changes take place as part of the normal aging process. The issue evaluated through the literature is whether those individuals who experience cognitive problems as a result of TBI are at risk of accelerated and premature aging, and dementia.
Much of the recent research concerning mild traumatic brain injury (mTBI) has focused on professional athletes and military veterans. This research may not apply to individuals with mTBI whose injuries result from other causes, including motor vehicle collisions and falls.
Autopsies of individuals with these types of injuries indicate that mTBI causes diffuse axonal injury and micro hemorrhages. Until recently, however, it was not possible to examine microstructural pathology in living persons because of the insufficient sensitivity of computed tomography and conventional magnetic resonance imaging (MRI). Thus, researchers were not able to explore any relationship between mTBI-related structural neuropathology and mTBI-related dysfunction, specifically cognitive impairment.
Traumatic brain injury (TBI) occurs when an external force, usually a blow or jolt to the head, disrupts the normal functions of the brain. Even a mild TBI or concussion can cause cognitive, emotional, behavioral, and physical impairments.
Often, changes in sleep patterns occur after a concussion. In fact, 30 to 70 percent of patients who have experienced a TBI experience sleep problems. The seriousness of the brain injury is not a predictor of the severity of sleep-related symptoms. Such symptoms include insomnia, increased sleep need, and excessive daytime sleepiness. For some TBI patients, although they are sleeping more than usual each night, they still experience excessive daytime sleepiness. Other sleep disorders, such as sleep-related breathing disorder, post-traumatic hypersomnia, and movement disorders may also result from a TBI. Repetitive TBIs may increase the risk of symptoms.
Researchers at Ohio State University (OSU) examined the effects of concussions on “sub-cellular levels,” possibly pointing the way for new treatments to be developed for concussions.
According to Science Daily, the OSU researchers discovered that blows to the head cause numerous small swellings along the length of neuronal axons. The study, published in The Journal of Cell Biology, observes the swelling process in live cultured neurons and could lead to new ways of limiting the symptoms associated with concussive brain injuries.
The researchers induced “mild traumatic brain injury” (mTBI) on rodents and found that part of a nerve cell swells within a matter of seconds, much faster than previously believed. The injury activated a protein that caused a chain reaction. Suppressing the protein prevented swelling. Such a finding is highly relevant to mild traumatic brain injury (mTBI), or concussion as it is more commonly known, researcher Chen Gu reports.
According to a recent study, children who sustained concussions or traumatic brain injuries (TBI) may experience anxiety, phobias, and depression years later.
Lead author Michelle Albicini, a researcher at Monash University School of Psychological Sciences in Melbourne, Australia, says that the study suggests that brain injury is related to long-term anxiety symptoms. The anxiety may be caused by actual brain damage or the result of living in an anxious family environment after the injury, said Albicini.
Albicini’s team found that children with moderately severe brain injuries and females in general were at greater risk for long-term psychological effects compared with males and those children who sustained milder brain injuries.
When brain injuries stimulate the infiltration of immune cells, it may cause inflammation and tissue damage in the brain and impair patient recovery. Thus, the brain’s recruiting of immune system cells to the brain may cause more harm than good. Johns Hopkins researchers report that they have identified how brain cells trigger a response in immune cells when the brain is injured.
As described in Science Signaling, in a new study using mice, researchers described how after a brain injury, immune cells in the brain called astrocytes released vesicles (fat-like virus-size molecules) carrying proteins, RNAs, and microRNAs into the circulation. When these vesicles reached the liver, they stimulated the secretion of cytokines that mobilized peripheral immune cells to infiltrate the brain. Researchers examined what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly considering the blood-brain barrier.
According to the Centers for Disease Control and Prevention (CDC), from 2005-2014, an average of 3,536 fatal unintentional drownings occurred per year in the United States. Approximately one in five people who die from drowning are children 14 years old or younger; children one to four years old have the highest drowning rates.
For every death caused by drowning, five children receive emergency room care for nonfatal drowning injuries. Nonfatal drowning can cause hypoxic-ischemic brain injury that may result in long-term disabilities ranging from memory problems and learning disabilities to total loss of basic functioning (persistent vegetative state).
Increasing evidence suggests that professional athletes in contact sports are suffering brain damage as a result of concussions. For many years, doctors believed that chronic traumatic encephalopathy (CTE) was limited to boxers. In that context, it was referred to as “punch-drunk syndrome.” However, pathologists are reporting similar brain damage among other athletes.
The biological processes leading to CTE may start many years before recognizable symptoms appear; however, there is no reliable test to detect CTE in its earliest stages. Often an athlete’s confusion or memory loss that is related to CTE is only confirmed following an autopsy.