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PATHOLOGY CAM304 > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

How do we grade TBI?

A

Mild: transient lossof consciousness/confusion
Moderate:loss of consciousness (15 min-6hour)
Severe: >6 hour :LOC

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2
Q

What are some long term consequences of MILD HEAD INJURY?

A

15% of mild TBI will experience

  • nausea, diziness
  • subtle but potentially disabling changes- memory problems, impaired concentration, extreme tiredness, other minor cognitive deficits, emotional lability/disinhibition
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3
Q

What are the outcomes of MODERATE HEAD INJURY?

A

On going dysfunction in consequence

  • physical: headaches, diziness, extreme tiredness
  • Cognitive: deficits in memory, functions, attention, concentration and language (word finding). Will depend on cortical area damaged
  • Behavioural: irritability, anxiety, disinhibition, emotional lability
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4
Q

What are the outcomes of severe head injury?

A

– Persistent vegetative state
– Severe physical, cognitive and behavioural problems
– Typically require constant care

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5
Q

What are the 3 types of head injury?

A

I. Penetrative Head Injury - penetration of the skull and/or brain by an external object (e.g. missile).
II. Closed Head Injury - acceleration, deceleration and rotational forces to the head that cause movement of the brain within the skull.
III. Crushing Head Injury - caught between two hard objects

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6
Q

What is the most common form of TBI?

A 
Closed head injury
- Relates to forces that affect the brain
 •  Acceleration/deceleration
•  Rotational/angular
•  Propagation of shock wave
 Head impact may or may not occur
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7
Q

Fixed surface closed head injury- where will damage be?

A

Coup: area first impacted, then contracoup-= where brain bounces back to other side of skull going to be damaged
Shearing forces throughout entire brain
Subdural veins torn as the brain rotates
Damage to temporal bone from rough bones at the base & damage to brain stem - causing swelling etc.

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8
Q

Lesions can be focal or diffuse- explain

A 
•  Focal
–  contusions 
–  lacerations
 – skull fracture
•  Diffuse (occur immedialtey or develop over time)
– axonal injury
 – neuron degeneration
 –  micro-haemorrhages
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9
Q

wht are FOCAL CONTUSIONS

A

Pattern of superficial bruises on outside surface of brain.
Largely about brain moving within skull cavity and impacting within the skull.
Contusions can become haemorrhagic, contributing towards swelling of brain, ICP

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10
Q

What are FOCAL lacerations?

A

Tearing of brain (typically frontal and temporal lobes) as brain rotates across ridges inside the skull.
• May also lead to significant tearing of blood vessels.

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11
Q

Explain some sensory damage which can occur secondary to TBI? (9)

A
  • Brain swelling/edema
  • Haemmorhage
  • Increased intracranial pressure
  • Mass effects/ herniation
  • Excitotoxicity due to excess neurotransmitters • Infection
  • Epilepsy
  • Ischemia/hypoxia/free radicals
  • Diffuse axonal injury
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12
Q

what is an intra cranial haemorrhage? what can it cause? what are the types?

A

Bleeding in and/or around the brain. May lead to ‘mass effect’ = cerebral compression and herniation

• Epidural hematoma
– torn vessels under the skull
• Subdural hematoma
– usually tearing of veins in subdural space
• Subarachnoid haemorrhage
• Intra-cerebral or cerebellar hematomas
– Tearing of vessels in brain parenchyma

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13
Q

When would you get an epidural haematoma?

A

Almost always result of skull fracture
• Typically rupture of middle meningeal artery (under temporal bone) or damage to a sinus
• Hematoma may cause increased ICP, compression/herniation of brain
• Often a ‘lucid’ period between initial injury and subsequent deterioration due to accumulation of blood

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14
Q

What is a subdural haematoma?

A

Tearing of veins where they penetrate the dura • Acute and chronic forms

  • > Acute usually follows severe head injury, involves rapid functional deterioration
  • > Chronic forms may involve minimal injury - slowly increasing size of hematoma and consequent increased ICP
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15
Q

What is battered child Syndrome?

What would you see pathologically?

A

Clinical manifestations
– Irritable, refuse eating, vomiting, seizures
• Common pathological changes
– Subdural haemorrhage, shearing changes, diffuse cerebral edema
(+mass effect), retinal haemorrhage

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16
Q

Diffuse Axonal Injury -

A

Widespread damage to axons within the CNS that results from severe acceleration/deceleration, rotation or shock wave forces on those long axons.
Associations with shearing/stretching forces on axons due to linear or rotational movement of the brain- this is not enough to damage them- the initial form of damage sets a biochemical change within axon which means eventual damage
More obvious in WHITE MATTER TRACTS with most susceptible being long connecting axons.
There are varying degrees of severity, with likely most substantial cause of ongoing disability in brain injury survivors.

17
Q

What is the pathogenesis of diffuse axonal injury?

A

• Primary axotomy
– Tearing of axons - relatively rare in
less than severe injuries
• Secondary axotomy
– Slower change within the axon. Axonal swelling may be followed by degeneration
– May be due to increased permeability of axonal membrane for calcium, or effect of mechanical force on intracellular components (e.g. cytoskeleton)
– Even mild brain trauma can result in evolving axonal injury
– Slower evolution of axonal damage may indicate a therapeutic window

18
Q

What is a primary cause of diffuse axonal injury?

A

Inhibition of a Ca2+-activated phosphatase, calcineurin, inhibits progression to secondary axotomy

19
Q

who gets chronic traumatic encephalopathy?

A

Form of progressive brain degeneration linked to repeated head injury

  • Pathology includes brain atrophy, presence of neurofibrillary tangles
  • Clinical symptoms include dementia, depression, aggression and confusion ->also potential link with ALS
20
Q

What are some impacts of TBI?

A

Recovry outcomes are expected for the first months following injury
Many patients will experience limited and incomplete recoveries, causing financial burden to the individual and the community

21
Q

What occurs in post concussion syndrome?

A 
irritability
mood change
restlessness
anger and aggression
impulsivity
headaches
diziness
sensitivity to light and noise
22
Q

How do you make the prognosis of recover?

A

Patterns of recovery are highly variable.
Most cognitive recovery occurs within the first three months following injury
Symptoms of PCS can take years to resolve
NEED accurate prognosis

23
Q

Current Prognosis for predicting outcome and impaired recovery:

A

USE GCS, LOC, PTA (duration of post traumatic amnesia) - > this is poor accuracy for prognosing an individuals outcome
very low false positive rate

24
Q

What do accurate clinical prognostics include?

A

Effective referrals for rehab
Flagging for overnight admission
WILL REDUCE time and expenses assoc. with follow up sessions
Prevention of conditions becoming chronic

25
Q

How do we PREDICT OUTCOME?

A

OUtcome is poorly predicted by current diagnostic measures.

by using an IPSATIVE RECOVERY MODEL- can improve accuracy of prediction

26
Q

Outcome versus recovery = normative versus Ipsative

A

Outcome (normative) assumes a regression to a standard of population, and not a recovery to the individuals premorbid functioning (ipsative).

27
Q

How do we define IMPAIRED

A

Impairment is a semntic/operational issue. Following injury, a patient may be considered impaired across three definitions

  1. NORMATIVELY imaired: individual performance compared with the pop
  2. IPSITAVILY IMPAIRED: individual performance compared with pre morbid ability
  3. IMPAIRED RECOVERY: individual erformance compared with expectations (given the predicted trajectory of their recovery)
28
Q

Psychological involvement- REHAB

A

There has been a shift in the clinical emphasis of rehabilitation.
From ameliorating impairments and disabilities
to re establising life roles, and promotion of participation.
Rewind, retrace, redo, regrow, restate ETC!
CBT, mood regulation strategies, problem solving
Managment involves serial assessment across a range of cognitive domains, with specific emphasis on those that are more sensitive to the effects of TBI.
- speed of processing; attention and concentration, fluid reasoning, verbal fluency

29
Q

Explain a typical neuropsychological assessment

A
  • global assessment of current cognitive functioning -eg. IQ
  • Comprehensive memory assessment
  • Clinical comparison to premorbid functioning
  • Base- rate analyses for any discrepancies
  • Functional implications for discrepancies of a clinical magnitude
  • Evidence for the abscence of malingering
30
Q

In summary how do we assess TBI

A

HOW DISCREPANT ARE THE PERSONS ABILITIES NOW comparied with HOW THEY WERE
How rare is a discrepancy of this magnitude, and WHAT are the FUNCTIONAL IMPLICATIONS of these discrepancies?

31
Q

How would we test for a malingerer

A

Rigorous evidentary standards: testing is often harder than it sounds, a misleading domain, pathologically inconsistent, or requires heirarchical consistency according to difficulty.
Such evidence opines that a variable other than (or in addition to) genuine impairment has influenced the test performance.

PATHOLOGY CAM304 (16 decks)

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