Pathophysiology of Brain Injury and Dr. Cheryl Wellington

The University of British Columbia Department of Psychiatry hosts one of the best learning experiences in the city weekly. These are the Neuropsychiatry Rounds in the Deitweiller Pavillion.  They are telebroadcast around the city, province and even to other provinces given the demand for them.  I have attended many over the years with the utmost appreciation for the excellence of presentation and the integrity of the researchers.  Unfortunately being in private clinical practice, it often costs a couple of hours of time getting to the university through city traffic on Wednesday morning at 11 am when I have dual addiction medicine and psychiatry clinic obligations.
This week it was a must to hear Dr. Cheryl Wellington present on the Pathophysiology of Brain Injury.  She is a professor in the Department of Pathology and Laboratory Medicine at UBC, having done her phd in Microbiology there before doing her post graduate training at Harvard Medical School.  Dr. Wellington's research investigates lipid and lipoprotein metabolism in the brain and her group has made key contributions to the understanding of Alzheimer's Disease and Traumatic Brain Injury.
A dynamic presenter she began with an overview of the risk of the field, discussing clinical matters before honing into the underlying pathology.  "Traumatic Brain Injury is the leading cause of death in persons under 40 in the developed world," she said.  Motor Vehicle Accidents were the principal cause. In the elderly though falls became the principal cause instead.
Brain Injuries have been considered as mild, moderate and severe based on Glasgow Scores. However she quoted a colleague who questioned this nomenclature by saying, "Can you imagine us describing cancer as mild, moderate or severe.'  Certainly those who have had brain injuries and know their potential  devastation would appreciate that concern.  Dr. Cheryl Wellington demonstrated her sensitivity and empathy throughout her presentation something much appreciated from someone working principally in the academic laboratory research world. It was so apparent she appreciated patients as people first.
Much of her talk was focused on the Mild Traumatic Brain Injury which has a Glasgow score of 13 to15, often as not, normally according to this rather gross scale originally developed with an emphasis on the acutely severest of cases.
MTBI accounted for 80% of presentations and could be sub categorized as 'Concussive', "Subconcussive" and "Repetitive" as well as "Focal", "Diffuse"and "Mixed".
Discussing Concussions she emphasized the range of symptons that patients presented with including headaches and neck pain that didn't resolve', 'slowness in thinking', 'confusion', 'aggressiveness or irritability', and even olfactory and sensory deficits.
When brains of patients who have died after concussions have been studied they have showned 'Diffuse axonal damage".  Axons are the electrical chords of the brains neuroelectrochemical communication and storage system.  Synapses are like the 'connectors' in the system by comparison.
What has been of significance in the news recently has been the sports injuries and those athletes who have died especially by suicide after once being so celebrated for their performances. Now this concern has been directed specifically to children and adolescences where the risks and consequences of early concussions are being recognised as having more serious potential for long term negative consequence than previously understood.  Indeed Dr. Wellington's team are doing life saving research in this area of community concern.
The term for this specific condition has been "Chronic Traumatic Encephalopathy".  It was previously recognised in boxers who having had multiple knockouts in the ring developed a condition once term "Dementia pugilistica".
Chronic Traumatic Encephalopathy is the consequence of long term repeated trauma.  It's significant in that there is memory impairment, emotional lability, aggression and gait abnormalities. Indeed the picture suggests a process of dementia similiar in ways to Alzheimers coupled with a movement disorder in a way like Parkinson's.  There is this triad of cognitive, personality and movement pathology clinically.
Autopsies have shown the following structures are involved - cerebrum, medial temporal lobe, thalamus, mammillary bodies, and brainstem. The ventricles are dilated as well.
In CTE (Chronic Traumatic Encephalopathy) there is a pattern of tau pathology  and amyloid disorder that is distinct from Alzheimers. In alzheimers the distribution of tau and amyloid is distinct in that with CTE there is significantly more tau.   Further Perivascular tau pathololgy, suggesting vessel trauma, occurrs early. CTE pathology is more in the frontal and temporal lobes where as Alzheimer's begins in the entorrhins and spreads to the limbic system and later the cortex.
An amyloid precurser protein is increased after atonal damage and interstitial ab level correlatess with neurological status
Significant for clinical medicine is the recognition that edema is the major concern and that anything that helps clear away the debris will likely help recover. Thanks to the learning from pathology this is the direction that present clinical research is taking.
Dr. Cheryl Wellington went on to discuss bio markers and the potential for development of neuropsychological scales that might clinically measure the changes caused by tau post injury.  She had some very innovative ideas to share indeed.
To hear more about this we were all invited to the July 12, 2012 UBC Conference on "Pathophysiology of TBI".  She described the work of some of the world's leading researchers and contributors who would be coming to that conference and celebrated their achievements.  It will be worth it just to hear more from Dr. Wellington's and her group.