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.  

Personal Injury, Chronic Pain and Comorbidities

Dr. Daniel Gouws completed his medical degree at University of Stellenbosch before emigrating to work in Southland, New Zealand, and Saskatchewan before coming to British Columbia. He passed his Master of Sciences at McGill University in Occupational Health Sciences before becoming a board member of the Occupational and Environmental Medical Association of Canada. He is an extremely intelligent, lucid presenter whose clinical experience is obvious from his revealing insights into the care of patients.  His talk, "Comorbidities and Timelines - What to watch when for when your injured patient or client isn't getting better" was a most informative.
The objective was to identify the factors that could contribute to a poor outcome in patients with soft tissue injuries.
The Trial Lawyers Association of British Columbia, Essential Soft Tissue Injury Conference provided a CD with the notes of speakers and other relevant information. I made some notes during the presentation relevant to my own personal interest. It doesn't do true justice to the wealth and breadth of information that Dr. Gouws presented or give you the slides both medical and humorous that accompanied his presentation.  It does give a glimpse and for that reason alone I think it's worth including them here.

Soft Tissue Injury Conference, TSABC, Vancouver Convention Centre

March3012

Comorbidities and Timelines, What to watch for when your injured patient or client isn’t getting better

Dr. Daniel Gouws,

South Africa

Occupational Health McGill

Mechanism of Injury

• whiplash injuries occur when head accelerates relative to the body, excessive torgue and shear...damage through compression and distraction

Forces involved are considerable, at an imact speed of 20mph (32 km/hr) the human head reachs a peak acceleration of 12 g during extension

If the individual head is in slight rotation, a rear end impact will force the head further into rotation before extension occurs.

In addition to neck pain

-headache

visual disturbances

dizzines

weakness

parasthesiae

cognitive deficits

TMJ

They can often be presenting also with symptons of concussion

Clinical course

Majority of patients improve spontaneously over the first three months

don’t know which go sour

Medical Model

Diagnois

• History (subjective)
• Exam (objective)
• Ass
• Plan

Differences

Acute pain versus chronic pain

• chronic pain doesn’t get better

Role of patient with pain is different for acute versus chronic

Acute - follow treatment advice

Chronic pain - ‘partner’ relationship in care , patient responsible for daily management, very different from treatment of appendicitis

Chronic Pain

-lasts more than 3-6 months

varies in intensity from mild to excruciating

one area or multiple areas

emegence of complications

• increased sensitivity to pain
• emotional and cognitive distress
• non restorative sleep
• fatigue

What is happening in backgrown

• dogs in background of slides

Chronic Pain

• chronic co morbidities

Patients get frustrated with us

We get frustrated with them

Blame game

-There is no exact relationship among - degree of pain, extent of pathological change and extent of impairment

-We do not prove or disprove pain with special investigations.  Special investigatiosn are only considered to be appropriate if they will change the management of the patient

-It is inappropriate to request special investigaton in the abscenede of clinical findings such as nerve root entrapment or potentially surgically correctable lesions.

Comorbidities

• psychosocial
• what is the effect of the injury and comorbidities
• deconditioning
• post traumatic stress
• substance abuse
• Depression and anxiety
• Chronic pain patients who are depressed are 9x more likely to be disabled
• Untreated psychopathology is greatest likelihood for poor outcome

Loss of Control

• Regression
• Isolation

All my friends are dead

Diagnostic Dilemna

• extensive assessment by multiple physicians
• numerous investigations (included repeated diagnostic studies) without any real improvement or resolution of symptons

Drugs

• chronic pain is not an emergency, should get appropriate appointments at appropriate times
• beware of opiates
• Canada has distinction of being one of the top prescribers of opiates in the world

Cognitive Distortions

• unconscious complications of chronic pain
• non uncommon - we are all prone to cognitive distortions - ex ‘the little engine that couldn’t because he was a worthless bum like your father’
• emotional reasonling
• mind reading
• entitlement
• ‘la belle indifference’  - patient smiling while saying her pain is 9/10
• hopelessness

Kinesiophobia

limits activity

limits treatment compliance

becomes self perpetuating - less action - less activity - more pain

Catastrophizing

• research shows relationship between catastrophising and heightened pain intensity -

Relationship problems

-less interest in sex

Procrastination

-once pain is under control I’ll do more

-I have to wait for my MRI because I can do anything (like take out garbage)

Loss of control

• fundamental to ability to cope
• learned helplessness
• the ability to gain a sesnse of control is fundamental to the ability to cope - self control likened to an energy source and fatigue
• once you become disabled a lot of that which was taken for granted becomes a bid decision

Workplace Factors

• adverse outcomes in pain study
• 1)do you enjoy your job
• 2) do you get along with your supervisor

Workplace autonomy

• a factor - disability of chronic pain - less work autonomy - more pain disability

After 6 months chance of return to work drop

Discuss return to work considerations

What can be done?

-individual cognitive behavioural psychotherapy

-exercise

-work conditioning/work hardening

-ergonomic modifications

-modalities used in conjunction with active exercise

• pain self-management programs
• PDP, PGAP programs

Elements

-set personal goals

• improve sleep
• -increase physical activity
• manage stress
• etc

Loss of control

Goal therapy can be effective in helping patients regain control

Chronic Pain Self Management Program

www.selfmanagementbc.ca