Brain Injury Flashcards

1
Q

What types of acquired brain injury are there?

A

TBI
Anoxic (toxic, metabolic)
Stroke
Nutritional (Wernicke’s)
Tumours
Infection

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2
Q

What are the main pathological sequelae of TBI?

A

Contusions
Diffuse axonal injury
Extradural/subdural haematoma

These can be complicated by increased ICP and anoxia

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3
Q

What is the vascular source of subdural haematoma?

A

Vein
Low pressure and will accumulate over days/weeks

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4
Q

What is the vascular source of extradural haematoma?

A

Artery
(often the middle meningeal artery)

High pressure (seen by dura forced away from bone and in concave shape)
Develops rapidly, can be dead in hours

Fracture of the temporal bone from a fall can have this happen easily

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5
Q

What is the first line treatment for extradural haematoma?

A

Trepanning

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6
Q

What is a typical presentation of a patient with extradural haematoma?

A

Had a fall in preceding few hours
Drunk or confused
Worsening GCS (should be checked every 15 mins)

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7
Q

How and when do retraction balls form in the white matter?

A

Over the course of 24h
Damage to the membrane at the point of impact causes disruption of transport through the axon.
Accumulation of products results in balls

Early intervention and delivery of oxygen to the brain can stave this.

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8
Q

What is fractional anisotropy tractography?

A

Graphical imagery of connectivity in the brain using diffusion tensor imaging

It will show differences in connectivity even when MRI looks normal

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9
Q

What are the key markers of diffuse axonal injury?

A

Microhaemorrhages (due to being stretch of white matter blood vessels at point of impact)

These have a parafalcine distribution (sagittal)

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10
Q

How are shear microhaemorrhages picked up on MRI?

A

Gradient echo
Susceptibility weighted imaging
-these images pick up the haemosiderin

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11
Q

What pathology happens in the long term after injury?

A

Cerebral atrophy
-particularly white matter atrophy
-resultant ventriculomegaly
-thinning of corpus callosum

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12
Q

What are the consequences of bleeding into the brain?

A

Blood blocks the aqueducts prevent drainage of CSF and causing hydrocephalus

Enlarged ventricles from this should be distinguished from enlargement due to cerebral atrophy.

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13
Q

What happens to the brain when intracranial pressure reduces space in the cranial cavity?

A

herniation of uncus into post fossa
herniation of cerebellar tonsils into foramen magnum

Damage to midbrain/pons
Ischaemia of brain stem
Squeezing of PCA

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14
Q

What is Duret haemorrhage?

A

Haemorrhage to the pons or midbrain caused by transtentorial herniation from high intracranial pressure.

There is very low chance of recovery and care is often withdrawn

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15
Q

How would a lumbar puncture reveal SAH?

A

Blood in CSF indicating bleed into into subarachnoid space

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16
Q

What are the side effects of craniectomy post TBI?

A

Low CSF
Syndrome of the trephined

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17
Q

What are the presentations of CTE?

A

Alcohol intolerance
Behavioural change
Concentration and memory difficulties
Movement disorder
Dementia

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18
Q

What are the pathological features of CTE?

A

Cavum septum pellucidum
Cerebellar scarring
Cerebral atrophy
Neurofibrillary tangles
Tau deposition in the depths of sulci (pathognomonic)

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19
Q

What is a postulated relation of the site of tau accumulation to CTE?

A

Possible site of shear injury

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20
Q

What are the criteria for traumatic encephalopathy syndrome?

A

Exposure to repetitive head injuries
Cognitive impairment or behavioural dysregumatiob
Progressive course
No other condition that could account for symptoms

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21
Q

How does CTE differ from TES?

A

TES is clinical and found in life
CTE is pathological diagnosis

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22
Q

How do TES and CTE overlap?

A

TES diagnosis had high sensitivity for CTE
TES did not have high specificity for CTE
70% of those with TES had CTE

23
Q

What conditions may cause metabolic injury to the brain?

A

Anoxia
Hypoglycaemia
Carbon monoxide poisoning

24
Q

Which brain areas sustain the most anoxic damage?

A

High metabolic demand areas
Grey matter more than white
Basal ganglia
Hippocampus

Aggravated by epilepsy/alcohol withdrawal

25
Q

Why do epilepsy and alcohol withdrawal aggravate anoxic brain injury?

A

They are metabolically demanding conditions and increase oxygen demand. This speeds up anoxic damage.

26
Q

What are recognised potential causes of diffuse axonal injury?

A

Trauma (rotational, acceleration/deceleration)
Anoxia

27
Q

what are the neuropsychiatric sequelae of falcine meningioma?

A

personality change
global cognitive impairment

28
Q

What is the role of thiamine in metabolism?

A

Co-enzyme in aerobic respiration

29
Q

Which parts of the brain are particularly affected by Wernicke’s encephalopathy?

A

Periaqueductal grey
Mammillary bodies (memory)
Medial thalamus (memory)

30
Q

Which neuropsychiatric sequelae are common to all brain injury?

A

Cognitive
-slowed information processing
-concentration and memory impairment
-dysexecutive problems

Behavioural
-poor organisation, chaotic
-sled-centred, impulsive, suspicious
-inflexible

Emotional
-labile, anxious, depressed, irritable

31
Q

What is a particular neuropsychiatric sequela of subarachnoid haemorrhage from the anterior communicating artery?

A

Spontaneous confabulation

32
Q

What is the neuropsychiatric quadrad of Korsakoff syndrome?

A

Disorientation
Anosognosia
Amnesia
Confabulation

33
Q

What are particular neurological sequelae of anoxia?

A

Parkinsonism
myoclonus
dyskinesia

34
Q

What are particular neuropsychiatric sequelae of anoxia?

A

Severe cognitive impairment
Significant behavioural problems

These tend to have a much poorer prognosis than traumatic brain injury

35
Q

What are the causes of anoxia that might reflect deliberate self harm?

A

Insulin overdose
Hanging
Drowning

36
Q

What are questions to ask interpreting brain injury symptoms?

A

Are the symptoms misattributed to the injury?
Symptoms common in general population or associated with another disorders

Is reverse causality at play?

Are the symptoms a psychological response to the situation of being injured?

37
Q

What factors exist in those most likely to get a head injury?

A

Psychiatric disorder
Alcohol/drug abuse
Deliberate self harm
Previous head injury
Young males
Those at risk of schizophrenia
Lower IQ
Low SE status
Unemployment
Life events

38
Q

What are the criteria of mild TBI?

A

GCS 13-15
LoC <30 mins
PTA <24h

39
Q

What percentage of TBI is mild?

A

80%

40
Q

What percentage of mild TBI shows abnormality when imaged?

A

20-40%

41
Q

What are the criteria of severe TBI?

A

GCS <9
LoC >24h
PTA > 1 week

42
Q

What is the PTA watershed for full recovery (returning to work)?

A

1 month
(PTA longer than this likely to have long term disability)

43
Q

After mild TBI, after what amount of time is it likely someone will have fully recovered?

A

3 months

44
Q

What are typical symptoms after mTBI/concussion?

A

Blurred/double vision
Nausea
Dizziness/fatigue
Headache
Poor concentration/memory
Noise/light sensitivity

45
Q

What percentage of patients are troubled by post consssion symptoms after 12 months?

A

12.5%
(3 months -50%, 6 months 25%)

46
Q

What are post concussion symptoms?

A

Fatigue/dizziness
Blurred/double vision
Nausea
Fatigue/insomnia
Headache
Noise/light sensitivity
Concentration/memory problems
Irritability

47
Q

What did Tator find in concussion in sports injury?

A

50% had symptoms after 9 months
The greater the number of symptoms the worse the prognosis

48
Q

What do longstanding symptoms after a mild head injury suggest?

A

Somatisaton disorder

49
Q

What methods might be used for management of behavioural symptoms post TBI?

A

Psychotropic medication
Behavioural interventions

50
Q

How does craniectomy lead to syndrome of the trephined?

A

Low csf causes brain to change position in skull and the brain stem isn’t well situated.

51
Q

Why might medial orbotofromtal lesions be missed on CT?

A

Artefacts from bone interference

52
Q

What is Capgras delusion?

A

Delusional misidentification of people you know as identical impostors

53
Q

What is Fregoli delusion?

A

Delusional misidentification of strangers as people you know in disguise

54
Q

What would be the outcome of brain swelling squeezing the PCA?

A

Effective stroke from lack of blood supply
Damage to occipital lobe - primary cortical blindness
Could also affect brain stem cerebellum thalamus