In our May, 2014 post, we reported on research showing that traumatic brain injury, including mild traumatic brain injury (mTBI), can damage and cause dysfunction in the pituitary gland resulting in deficiencies in key hormones released by the pituitary gland, such as Growth Hormone (GH). As we explained in that post, the anatomy of the pituitary gland makes it particularly susceptible to the sheering injuries seen in TBI. These hormone deficiencies can produce many of the persistent symptoms seen following a TBI, such as fatigue, poor memory, depression, anxiety, emotional lability, exercise intolerance, lack of concentration and attention difficulties. (Although not always the case, these deficiencies can also produce physical symptoms, such as increased fat mass – especially in the abdominal area – and increased cholesterol.) We also noted findings showing that pituitary dysfunction can worsen over the five year period following an injury – in other words, that this is an issue that deserves to be monitored on an ongoing basis. Read More
Researchers at the University of Toronto have released the results of a study of the incidence of suicide in 236,000 concussion patients followed over a 20 year period. Read More
On January 16, 2016 the University of Pennsylvania announced the findings of a unique team studying concussion science, consisting of a professor of materials science and engineering and a professor of neurosurgery (also director of Penn Center for Brain Injury and Repair.) Read More
The University of Pennsylvania Perelman School of Medicine issued a press release on November 23, 2015 declaring “mild brain injury an oxymoron” based on newly released research. The research, performed in collaboration with the University of Glasgow, demonstrates how brain wiring can be damaged after a concussion–damage that in some cases never repairs.
The research, published online in November in Acta Neuropathologica, builds on prior studies showing that nerve fiber damage in the brain can be demonstrated by the presence of a brain protein called SNTF. Read More
Neuroinflammation as a likely cause of persistent symptoms following traumatic brain injury (TBI), as well as increased risk of neurodegenerative complications, is leading to increased attention on anti-inflammatory strategies with diet, exercise, lifestyle and medication
Our May 28, 2015 blog post discussed the evidence offered by McMasters University researchers in support of their conclusion that the body’s immune response following injury can lead to unchecked, ultimately destructive neuroinflammation and that this likely underlies persistent symptoms following TBI as well as increased risk of neurodegenerative conditions such as chronic traumatic encephalopathy (CTE) and Alzheimers. The authors observed similar neuroinflammatory processes in patients without a history of head injury, such as patients with serious infections, PTSD and Depression. They also noted that subtle genetic differences may explain differences in inflammatory responses between patients, leading to different long term outcomes. The October 2015 issue of Trends in Neuroscience includes a review by Ohio State neuroscientists with further support for this new paradigm for understanding the brain’s response to injury. See “Priming the Inflammatory Pump of the CNS after Traumatic Brain Injury.” Read More
Research from the National Institute of Health, published in the August 3, 2015 issue of JAMA Neurology, shows that a protein that was until recently linked only to acute symptoms following traumatic brain injury, may also be responsible for chronic neurological symptoms, such as headache and dizziness, found in patients diagnosed with persistent post-concussion syndrome.
Tau is a protein known to play a significant role in the development of Alzheimer’s disease and Parkinson’s disease. Using ultra-sensitive technology, the researchers measured levels of tau in the blood months and years after injury. These levels correlated with the severity of post-concussive symptoms. If these findings are further confirmed, this could be the first biomarker that is sensitive and specific to ongoing TBI symptoms. Read More
The Radiology Society of North America has published a new study that identifies particular white matter brain injury patterns in patients with persistent depression and anxiety following mild traumatic brain injury (concussion or mTBI.) Read More
The April, 2015 issue of The American Surgeonreports on a retrospective study of 395 patients admitted to the ER following concussions (MTBI, or mild traumatic brain injury). The patients had “normal” Glascow Coma scores of 15 and normal CT scans and therefore met discharge criteria. The study found that a surprisingly high percentage of these patients (27%) had persistent deficits after neurocognitive testing and benefitted from referral for ongoing therapy. The study is authored by Hartwell et. al. and entitled “You Cannot Go Home: Routine Concussion Evaluation is Not Enough.” Read More
In a study published in April 2015 in the medical journal Brain Behavior and Immunity, a team of Canadian researchers at McMaster University presents a new understanding of the cause of the wide-array of symptoms experienced by some patients following concussion, such as headaches, dizziness, sleep disturbance, fatigue, cognitive impairment and neuropsychiatric symptoms.
This new paradigm helps to explain why the same pattern of symptoms can be found in some non-head injury patients, such a patient who has experienced infections or a patient diagnosed with post-traumatic stress disorder. It also helps to explain why some patients recover and others do not and why pre-accident experience can influence the course of post-accident recovery. Read More
The latest issue of the Journal of Neuroscience (April 22, 2015) reports on animal research from the University of Kentucky which “adds to an increasing body of knowledge strongly indicating that traumatic brain injury is a contributor to increased susceptibility to Alzheimer’s Disease-relevant pathologies, including cognitive dysfunction.”
The authors begin by noting that “epidemiological studies have associated increased risk of Alzheimer’s disease-related clinical symptoms with a medical history of head injury,” but that “little is known about the pathophysiological mechanisms linked to this association.” Prior studies, as well as this study, did find that persistent neuroinflammation is one outcome observed in patients after a single head injury. Read More
