Brain injury management Flashcards

1
Q

What are the risk factors for TBI?

A

Male (1.5-2.5x)
Age 15-24 or 75+
Alcohol
Risk taking behaviour
Lower socioeconomic status
Psychiatric history

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2
Q

What are the types of TBI?

A

Direct impact - damage to tissue underlying the impact area

Coup-contre coup - usually after hitting stationary object (generally contre coup is worse)

Acceleration-deceleration - shearing forces cause diffuse axonal injury (road accidents)

Blast injury - damage from shockwave

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3
Q

What are the two types of cerebral hypoxia?

A

Hypoxic brain injury - due to loss of oxygen supply

Hypoxic-ischaemic injury - due to compromise of blood supply (cardiac arrest/respiratory depression)

Brain scans may look normal in the first few days, over time damage will arise

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4
Q

What areas of the brain are affected most by hypoxia?

A

Basal ganglia
Thalami
Highly metabolic areas

Worsened by antipsychotics or alcohol withdrawal

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5
Q

What factors affect the recovery in hypoxia?

A

Duration of hypoxia
Speed of emergency care delivery
Pre existing health status

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6
Q

What is a contusion?

A

Mix of cortical necrosis and haemorrhage

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7
Q

Where are contusions most common?

A

Orbital PFC
Medial PFC
temporal pole
Occipital contre coup

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8
Q

What are the pathological outcomes of DAI?

A

Axonal tear
Myelin resorption
Retraction ball formation

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9
Q

What GCS score indicates severe TBI?

A

8 or less (comatose)

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10
Q

What is the application of GCS?

A

Useful in acute scenario
Not a reliable indicator of prognosis

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11
Q

What are symptoms of mild TBI?

A

Confusion, disorientation
Altered mental state
Headache
Transient loss of function

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12
Q

What is the definition of mild TBI/concussion?

A

Immediate transient alteration or loss of consciousness after force to the head

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13
Q

How might mild TBI be treated acutely?

A

Anxiolytics or analgesics
May not need hospital admission

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14
Q

How might severe TBI be treated acutely?

A

Ventilation and life support
Neurosurgical intervention (eg evacuation of haematoma)

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15
Q

What are the psychiatric consequences of moderate to severe TBI?

A

25-50% of survivors

Confusion and disorientation
Memory impairment
Dysexecutive syndrome
Affective outbursts: emotional lability
Chronic irritability
Epileptic episodes
Hallucinatory episodes
Paranoia
Intellectual impairment

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16
Q

How long might post traumatic amnesia last?

A

Minutes to weeks
(Onset might be delayed, such as in extradural haemorrhage)

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17
Q

What is the watershed for PTA and memory improvement?

A

6 weeks

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18
Q

How does PTA link to long term outcome?

A

1hr - return to work within a month
More than 2 weeks - residual cognitive impairments
PTA explains 25-50% of outcome

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19
Q

What is the last function to return usually in patients that fully recover?

A

Anterograde amnesia

20
Q

What are indicators of severity of head injury?

A

GVS
Duration of loss of consciousness
Duration of PTA
Delirium
Neurological signs and symptoms
Skull fracture or imaging abnormalities
Blood in CSF

21
Q

What percentage of people suffer mood and anxiety disorders after brain injury?

A

20-30% in the first year (particularly in left frontal lobe damage)

Anxiety - 10-15%

PTSD - 10-30% (less common if PTA was 1hr+)

22
Q

How does psychosis typically present post-TBI?

A

Much less common
Occurs in predisposed individuals
May interact with cognitive deficits (losing things may fuel persecutory delusions)

Confusional states and confabulation are not strictly psychosis

23
Q

What are the risk factors for suicide?

A

3-4x more common than general population

Risk factors for TBI
Alcohol
Substance use
Male
Risk taking behaviour
Lower socioeconomic status

24
Q

What is the prognosis for postconcussional syndrome?

A

50% better at 2 months
90% better at 12 months

25
What is the possible aetiology for postconcussional syndrome?
Pre morbid personality Emotional factors Possible damage to white matter tracts (diffusion tensor imaging) Compensation/litigation?
26
How common is personality change/behavioural disturbance post brain injury?
~50% (10-70%) Associated with long term changes, particularly with frontal lobe damage
27
What factors affect personality change?
Pre morbid Cognitive status Psychiatric illness Personality disorder Substance use Post injury Care/support Neuro rehabilitation Complicating effects of legal proceedings
28
How does personality change progress?
Seen in 30-60% of moderate- severe brain injury survivors Fluctuates but persists over time May need to be moved to specialist care
29
What are the pharmacological considerations in brain injury?
Start low go slow Titrate cautiously and monitor for adverse effects Sedating drugs may compromise cognitive/physical gains over time Wean down meds over time and liaise with other services
30
What are early pharmacological interventions?
Reduction of agitation Propranolol, amantadine, valproate, carbamazepine, antipsychotics Don’t use: benzodiazepines, opiates, phenytoin, psychostimulants
31
What are longer term pharmacological interventions for brain injury?
Valproate and carbamazepine Propranolol Antidepressants may have use even outside of mood disorder (Antipsychotics only for those with psychosis)
32
What non-pharmacological treatment is used post BI?
Physiotherapy Psychology Occupational therapy Speech and language therapy Social care and placement
33
What would be the work of a psychologist post brain injury?
Neuropsychological assessment CBT Cognitive training Relaxation Mindfulness Anger management Social skills training
34
What would be the work of OT post brain injury?
Real world skills Task oriented Shopping, cooking, household Managing demands of life
35
What would be the work of a SaLT post brain injury?
Dysphasia Dysphagia Dysarthria Communication problems, including style
36
What is the most extreme form of apathy?
Rare Akinetic mutism Associated with damage to ACC
37
How common is apathy in BI survivors?
10%
38
What treatments are used for apathy post BI?
Dopamine agonists (amantadine) Psychostimulants (methylphenidate) Some use of antidepressants but for depressed patients
39
What is cognition?
Mental process of knowing, including perception awareness reasoning and judgement
40
How do frontal lobe syndromes present?
Personality change Orbitofrontal: Disinhibition Euphoria Emotional lability Poor judgement Dorsolateral: Loss of initiative, apathy Slowing of thought and action Inattention Distractibility Poor planning and judgement Reduced verbal fluency Brocas
41
How might parietal lobe syndromes present?
Cortical sensory loss Astereognosis (recognition by touch) Disorders of body schema Anosognosia Gerstmann syndrome
42
What are the features of Gerstmann syndrome?
Dyscalculia Dysgraphia Finger agnosia R-L disorientation
43
How might temporal lobe syndromes present?
Auditory deficits Sensory dysphasia (Wernicke’s) Visual impairments (prosopagnosia) Memory impairments Personality change/psychosis (superstition/schizotypal)
44
How might occipital lobe syndromes present?
Cortical blindness Homonymous hemianopia Scotomata Visual agnosia Alexia without agraphia
45
What is the underlying mechanism of cerebellar cognitive affective syndrome?
Reciprocal connections between the cerebellum and cortical regions are disturbed by cerebellar damage