Presentation on theme: "Traumatic Brain Injury Dr John O’Donovan. Go on, floor it!"— Presentation transcript:
Traumatic Brain Injury Dr John O’Donovan
Go on, floor it!
Head injury in contact sports
“I’ve been in a treatment centre for drinking, I stayed two days then escaped” The great Evil K
Traumatic brain injury 80% of patients are under 65 with TBI Both stroke and TBI have 1-3/1000 admissions to hospital PA Only 10% of TBI patients stay in hospital over 3 days Disability post stroke is 5-8/1000 and head injury is 1/1000
TBI Risks male sex 8:2 Younger men from late teens to mid 20s and older age (risk takers and falls) Impulsivity including ADHD, axis 2 disorders Alcohol and drugs Prior head injury Risky behaviors
Focal brain injury Penetrating injury Focal damage producing local haematoma, bleeding, lacerations and meningeal damage. Acceleration:deceleration injury commonly produces damage at frontal and temporal poles, somewhat consistent picture. Focal damage with contusion under the direct trauma
Anterior poles of frontal and temporal lobes in closed head injury
Diffuse brain injury Severe acceleration/decceleration and or rotation Causes axonal stretching The damage goes from cortical to deeper structures as the impact in energy terms increases “centripetal model” of head injury.
Grading as per axon stretch Stage 1, axon stretch 5%, increase ionic permeability, rapid recovery. Stage 2, axon stretch 5-10% which causes ionic shifts and swelling, recovery in days to weeks: most concussions in stage 1 and stage 2. Stage 3, axon stretch 20%, does not tear axon but impairs all functions, can cause secondary axonal loss from damage. Stage 4, excess of 20% stretch, axon damaged immediately and may tear.
Physiology 2 Remember brain autoregulation is subtle and needs BBB, cerebral circulation autoregulation, ionic flux, neurochemistry, axonal transport can all be impaired and at sites downstream from the torn axons. This means that a recovering brain from one injury is at risk from another injury which may cause catastrophic disruption, so called “second injury syndrome”
Clinically Depends on severity and whether the head injury is closed or open. Focal head injury behaves in a similar fashion to stroke with the proviso that the population are completely different. Closed head injury has a more uniform pattern.
Recovery from severe TBI Alexander’s stages 1 coma 2 unresponsive vigilance 3 mute responsivness 4 confusional state 5 independent self-care 6 intellectual independence 7 complete social recovery Ranchos Los Amigos Scale 1 generalized 2 generalized resoponse 3 local response 4 confused, agitated 5 confused, inappropriate 6 confused appropriate 7 automatic appropriate 8 purposeful and appropriate
Post Traumatic Amnesia Common exam question Refers to the period of time during which the patient remains amnestic from the injury. In essence how long post injury does the patient have an inability to form and retain memories. Do not confuse with pre TBI retrograde memory loss.
Memory in TBI In general the level of memory loss for events pre TBI as measured chronologically coincides with severity of damage. With recovery this reduces to become shorter and shorter, in moderate and severe head injury patients who recover may be a couple of days/hours. Severe retrograde autobiographical memory predating injury should not occur. Amnesia for the period of post traumatic amnesia is normal and expected.
TBI Anterograde amnesia refers to the inability to learn new information post injury. Retrograde amnesia equates to loss of memory going backwards from event. PTA: length of time from injury to regaining memory, varies depending on injury.
Chronic state Memory and learning tend to remain impaired. High end subtle functions. Frontal lobe problems Personality alteration Poor frustration tolerance Fatigue is very common Recovery is relatively rapid for first 6 months and much slower for next 18 months.
Grading severity Biomarkers GCS on admission PTA probably most useful and simplest. A PTA of under 24 hours suggests mild injury. A PTA of a week or more suggests a severe injury.
Imaging Acute setting CT blood and bone, very gross. Within 48 hours on, MRI, small contusions, haemosiderin deposition, white matter/axonal tract integrity. Imaging sequences, DTI which maps out tracts shows promise and current sequences can identity subtle contusions and haemosiderin deposition.
Recovery and prognosis In general high, IQ, good social adjustment etc are all positive factors in recovery. Age is crucial, under 40 do much better. Prior head injury is also crucial. One head injury increases the risk threefold for a further injury and having two injuries increases the risk 8 fold.
During the period of recovery Prolonged periods of agitation are common. Sleep wake cycle problems Poor attention Aggression Need for specialist psychiatric care Fatigue NB Recovery can continue for up to 2 years
Outcome predictors GCS Best eye response (E) No eye opening Eye opening in response to pain. Eye opening to speech. (Not to be confused with an awaking of a sleeping person; such patients receive a score of 4, not 3.) Eyes opening spontaneously Best verbal response (V) No verbal response Incomprehensible sounds. (Moaning but no words.) Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange) Confused. (The patient responds to questions coherently but there is some disorientation and confusion.) Oriented. (Patient responds coherently and appropriately to questions such as the patient’s name and age, where they are and why, the year etc. Best motor response (M) No motor response Extension to pain Abnormal flexion to pain Flexion/Withdrawal to pain Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets above Obeys commands. (The patient does simple things as asked.)
GCS 2 Severe, with GCS ≤ 8 Moderate, GCS 9–12 Minor, GCS ≥ 13. Good correlation with GCS as predictor of outcome. Severe injuries do not do as well. One would expect complete recovery from 13 Only 1/3 of those with post resus GCS of 3-8 will be able to complete neuropsychological testing at one year. About 40% of GCS 3-5 may die.
PTA PTA of 2/52 plus is associated with a poor outcome. In general the longer the PTA the worse the outcome in diffuse axonal brain injury.
Persistent vegetative state Sleep wake cycle and basic vegetative functions but no awareness of self or environment Can be stage in recovery from coma. If in PVS 3 months or more, then unlikely to come out of it.
Mild Traumatic Brain Injury PTA of less then 24 hours LOC of less then 30 minutes GCS of In general sequelae should mirror impact of injury, in mild TBI long term disability probably has a greater amount of psychological factors at play.