A new study published in the Journal of the American Medical Association adds to a growing body of evidence pointing to traumatic brain injuries, of all levels of severity, as an important risk factor for suicide.
Research scientists at the Center for Brain Health at the University of Texas at Dallas have just published a study, funded by the US Department of Defense, supporting the effectiveness of “strategy-based” cognitive training at reducing symptoms of depression commonly found in patients with chronic (greater than 6 months) traumatic brain injury (TBI) symptoms.
The training was an integrative program designed to improve cognitive control by exerting more efficient thinking strategies for selective attention and abstract reasoning. The training did not directly target psychiatric symptoms such as depression, but was nonetheless effective at reducing those symptoms. Read More
Canadian researchers assessed 236 individuals diagnosed with traumatic brain injury at 4, 8 and 12 months following injury. The results confirm prior studies showing that depression in very prevalent following TBI. Read More
As discussed in prior posts on this blog, sleep alterations are commonly found after a concussion or other traumatic brain injury, both short term and in some cases long term. One of the most well documented impacts of concussion, also discussed in prior posts, is an increased risk of mood disturbances, including depression, increased anxiety and increased risk of suicide. In recent years researchers have turned to sleep studies to explore the connection between these symptoms.
There is substantial evidence in the literature of the role healthy sleep plays in the “consolidation” of emotional memories. At first blush, this research is counter-intuitive. If sleep “consolidates” emotional memories, doesn’t this have the potential to increase rather than decrease mood disturbance? The answer appears to be that, although sleep preserves memory of events associated with emotional experience, at the same time it weakens the emotional “charge” coating the experience (referred to in the literature as “valence”) in a process called “habituation.” As one researcher hypothesized, “we sleep to forget the emotional tone, yet sleep to remember the tagged information.”Read More
The open source journal Brain Science has just published a survey of literature demonstrating that a mild traumatic brain injury (mTBI) , otherwise known as concussion, is a complex pathophysiological process that can have a systemic effect on the body aside from solely impairing cognitive function. According to the article, “dysfunction in the autonomic nervous system (ANS) has been found to be a major factor in the symptomatology in TBI, including in mTBI” and can “induce abnormalities in organ systems throughout the body.” Read More
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
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
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
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