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Management of Disorders > Brain Injury Treatment > Flashcards

Brain Injury Treatment Flashcards

1
Q

What is acquired brain injury?

A

Any non-congenital, non-degenerative injury to the brain, including TBI

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2
Q

Incidence of ABI is _____________ in the developed world due to _____________ but ______________ in the developing world.

A

▪️Decreasing
▪️Better road safety
▪️Increasing

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3
Q

What are the main risk factors for ABI?

A

▪️Male gender
▪️Age 15-24 and over 75
▪️Alcohol abuse
▪️Risk-taking behaviour
▪️Lower socioeconomic status
▪️Psychiatric history

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4
Q

What are the main types of closed TBI?

A

▪️Direct impact
▪️Coup/contrecoup
▪️Acceleration/deceleration
▪️Blast injury (e.g. shockwave)

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5
Q

What are the two parts of a coup/contrecoup injury?

A
  1. Primary impact - brain hits skull on side of impact, usually front of brain
  2. Secondary impact - brain hits posterior area of the skill as it goes back (occipital pole)
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6
Q

What pathogy is commonly seen in acceleration/deceleration injuries?

A

Diffuse axonal injury - the shearing forces cause axonal tear and retraction

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7
Q

Where is cerebral oedema most commonly seen following brain injury?

A

In regions of contusions, infarcts, and haematomas

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8
Q

What are the three sectilms of the Glasgow Coma Scale?

A
  1. Eye opening response
  2. Best verbal response
  3. Best motor response
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9
Q

When should the GCS be used?

A

In acute scenarios, best straight after injury

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10
Q

What does GCS score of 13-15 suggest?

A

Mild TBI

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11
Q

What does a GCS score of 9-12 indicate?

A

Moderate TBI

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12
Q

What does a GCS score of 3-8 indicate?

A

Severe TBI - patient is unresponsive or comatose

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13
Q

What are the three main classifications of TBI according to the Mayo system?

A

▪️Definite moderate-severe TBI
▪️Probable mild TBI
▪️Possible TBI

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14
Q

What is a concussion?

A

Immediate, transient alteration/loss of consciousness after force to the head

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15
Q

What symptoms may be present in the acute stage of a mild TBI?

A

▪️Confusion/Disorientation
▪️Altered mental state (e.g. panic)
▪️Headache
▪️Transient loss of function (e.g. freezing)

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16
Q

What intervention may be required during the acute stage of mild TBI?

A

▪️Possibly analgesia or anxiolytics
▪️May not need hospital admission

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17
Q

What may be present in the acute stage of severe TBI?

A

▪️Loss of consciousness
▪️Severe autonomic disturbance
▪️Compromised vital functions
▪️Coma and death

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18
Q

What intervention may be required in the acute stage of a severe TBI?

A

▪️Ventilation
▪️Life support
▪️Neurosurgery (e.g. evacuation of haematoma)

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19
Q

What might delayed post-traumatic amnesia indicate?

A

The development of a secondary complications such as an extradural haemorrhage

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20
Q

Who is at risk of longer confusion and disorientation following TBI?

A

▪️The elderly
▪️People with cerebrovascular disease
▪️Alcohol abuse
▪️Medication withdrawal

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21
Q

What is retrograde amnesia?

A

The time between moment of injury and the last clear memory before the injury

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22
Q

What memories are more vulnerable to retrograde amnesia?

A

Emotionally salient events such as the RTA

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23
Q

How does retrograde amnesia usually compare to PTA?

A

It’s usually much shorter - typically a few seconds to minutes

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24
Q

What might longer retrograde amnesia indicate?

A

▪️More severe injuries
▪️Psychogenic origin?

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25
Q

What is anterograde amnesia?

A

A deficit in forming new memories after injury.

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26
Q

What is usually the last function to return after consciousness is regained?

A

Anterograde amnesia

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27
Q

What are considered good indicators of head injury severity?

A

▪️Depth of unconsciousness (GCS)
▪️Duration of LoC
▪️Duration of PTA
▪️Delirium immediately after injury
▪️Neurological symptoms and signs
▪️Skull fracture
▪️Imaging abnormalities
▪️Blood in CSF

28
Q

What are considered poor indicators of head injury severity?

A

▪️Duration of retrograde amnesia
▪️EEG abnormalities
▪️Facial injuries

29
Q

What chronic cognitive sequelae may be present in severe head injury?

A

Minimally conscious state (used to be persistent vegetative state)

30
Q

What chronic cognitive sequelae may be present in less severe head injury?

A

▪️Cognitive slowing
▪️Apathy
▪️Dysarthria
▪️Emotional lability
▪️Motor disability
▪️Incontinence

31
Q

What are symptoms of post-concussional syndrome?

A

▪️Headache
▪️Dizziness
▪️Fatigue
▪️Noise intolerance
▪️Irritability
▪️Emotional lability
▪️Insomnia
▪️Impaired concentration/memory

32
Q

What might chronic postconcussional syndrome indicate?

A

A psychological basis

33
Q

How long does postconcussional syndrome last?

A

50% recover by 2 month, and 99% by 12 months

34
Q

What factors may contribute to postconcussional syndrome?

A

▪️Premorbid personality
▪️Emotional factors
▪️Compensation/litigation
▪️Cognitive impairment
▪️Epilepsy

35
Q

What are symptoms of orbitofrontal damage?

A

▪️Disinhibition
▪️Euphoria
▪️Emotional lability
▪️Poor judgement
▪️Environmental dependency

36
Q

What are the symptoms of anterior cingulaye cortex damage?

A

▪️Impaired motivation
▪️Akinetic mutism
▪️Apathy

37
Q

What are the symptoms of dorsolateral prefrontal cortex damage?

A

▪️Apathy
▪️Loss of initiative
▪️Slowing of thought and action
▪️Inattention
▪️Distract ability
▪️Poor planning and judgement

38
Q

Cortical sensory loss, astereognosis, body schema disturbance, and anosognosia might indicate damage to which area?

A

Parietal lobe

39
Q

What is Gerstmann syndrome and lesions in which area is it associated with?

A

▪️Dyscalculia
▪️Dysgraphia
▪️Finger agnosia
▪️R-L Disorientation

Indicative of dominant parietal lesion

40
Q

Patients with lesions to which brain area may present with auditory deficits, sensory dysphasia, prosopagnosia, memory impairments and psychosis?

A

Temporal lobe

41
Q

What is associated with post-TBI personality change?

A

▪️Moderate/severe injury
▪️Longer period of PTA
▪️Confabulations
▪️Behavioural disturbance
▪️Frontal and temporal damage

42
Q

What premorbid factors may increase risk of post injury personality change?

A

▪️Cognitive status
▪️Psychiatric illness
▪️Personality disorder
▪️Premorbid personality
▪️Substance misuse

43
Q

What post injury factors may increase risk of post injury personality change?

A

▪️Poor care/supprt
▪️Poor access to neurorehabiliation
▪️Complicating effects of legal proceedings

44
Q

How does personality change post injury present over time?

A

It usually fluctuates, but tends to persist

45
Q

What does cortical blindness indicate?

A

Bilateral occipital damage

46
Q

What does homonymous hemianopsia indicate?

A

Unilateral occipital damage

47
Q

What are the anatomical correlates of post injury personality change?

A

Mostly the frontal lobe, particularly the orbitofrontal cortex.

BUT not always - damage to connections to frontal lobe?

48
Q

What are the main principles of pharmacological interventions for brain injury?

A

▪️Wait for spontaneous recovery
▪️One med at a time
▪️Start low and titrate slowly
▪️Avoid anything which may cause symptoms or confusion
▪️Stop it if it doesn’t work
▪️Avoid length prescriptions in the community

49
Q

What medication shows good evidence for reducing early agitatoom following injury?

A

Propranolol (a beta blocker)

▪️Requires ECG monitoring!

50
Q

What classes of medication show negative evidence for their use in early post-injury agitation?

A

▪️Benzodiazepines
▪️Opiates
▪️Psychostimulants
▪️Phenytoin

51
Q

What are the best medications for the longer term management of agitation, aggression and impulsivity post injury?

A

▪️Anticonvulsants, particularly carbamazepine and valproate
▪️Propanolol
▪️Antipsychotics, particularly olanzapine
▪️Potentially antidepressants, such as sertraline and amitriptyline

52
Q

When is olanzapine most useful and why should you be cautious?

A

In acute crisis

Some evidence that it impairs neuronal plasticity

53
Q

What should you consider when choosing a medication for long term management of TBI sequelae, particularly agitation and aggression?

A

▪️Comorbidities, such as depression, mood disturbance, epilepsy, paranoia, or psychotic symptoms
▪️PTA - danger of increasing confusion
▪️Other medical problems and medications
▪️Tolerability

54
Q

What are the main roles of psychology in the multidisciplinary treatment of TBI?

A

▪️Neuropsychological assessment
▪️CBT and other therapies
▪️Cognitive training
▪️Relaxation training and mindfulness
▪️Anger management
▪️Social skills training

55
Q

What is the role of occupational therapy in brain injury treatment?

A

Helping the individual to maintain ‘real world’ skills such as:
▪️Self care
▪️Shopping
▪️Cooking
▪️Household tasks
▪️Planning and managing life demands

56
Q

What symptoms can be helped by a speech and language therapist?

A

▪️Dysphasia
▪️Dysphagia
▪️Dysarthria
▪️Communication problems (e.g. conversational style)

57
Q

What is akinetic mutism?

A

Intact consciousness and sensorimotor capacity but with a significant decrease in goal-directed behaviour and emotions.

Extreme apathy with slowed or nearly absent movement and speech.

58
Q

Lesions in which area is associated with akinetic mutism?

A

Anterior cingulate cortex

59
Q

Damage to which structures is associated with apathy following brain injury?

A

▪️Medial prefrontal cortex
▪️ACC
▪️Insula
▪️Subcortical structures, such as thalamus and basal ganglia

60
Q

What roles do the insula and ACC supposedly play in apathy?

A

Form a system for registering internal and external events and selecting response

Insula = input
ACC = output

61
Q

What pharmacological interventions show evidence for the management of post injury apathy?

A

▪️Dopamine agonists (particularly amantadine)
▪️Psychostimulants (particularly methylphenidate)
▪️Antidepressants (particularly if comorbid depression)

62
Q

What class of medication may be particularly helpful for cognitive apathy?

A

Psychostimulants - may improve alertness and sustain attention

63
Q

What are the main symptoms of cerebellar cognitive-affective syndrome?

A

▪️Emotional dysregulation
▪️Impaired use of language
▪️Executive dysfunction
▪️Visuospatial deficits

(similar clinically to prefrontal cortex lesions)

64
Q

Damage to which brain region is associated with cerebellar cognitive-affective syndrome?

A

Posterior lobe of the cerebellum

65
Q

Why is cerebellar damage thought to mimic frontal damage?

A

Reciprocal connections between the cerebellum and cortical regions

Management of Disorders (28 decks)

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