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Neuropsychiatric Disorders > Brain Injury > Flashcards

Brain Injury Flashcards

1
Q

What are the two main types of traumatic brain injury?

A
  1. Open (e.g. shrapnal, knife, bullet)
  2. Closed (e.g. acceleration and deceleration forced in RTA)
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2
Q

What are the main mechanisms of closed TBI damage?

A

▪️Contusions
▪️Diffuse axonal injury
▪️Cerebral atrophy
▪️Intracranial bleeding (haematoma)
▪️Chronic traumatic encephalopathy

May be complicated by
▪️Raised intracranial pressure
▪️Anoxia

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3
Q

What are contusions?

A

Areas of cerebral bruising, particularly in the grey matter, where blood leaks into the extravascular space

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4
Q

Which brain areas are most vulnerable to contusions?

A

The orbitofrontal lobe and anterior temporal lobe

(social function, decision making and memory)

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5
Q

What brain areas are least vulnerable to contusions?

A

Primary motor, somatosensory, and visual cortices

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6
Q

What is diffuse axonal injury?

A

The shearing of the brains long connecting nerve fibres (white matter) as the brain shifts and rotates in the skull

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7
Q

How does diffuse axonal injury occur?

A
  1. Damage to the soma
  2. Ca2+ influx
  3. Membrane damage
  4. Disruption of normal transport
  5. Swelling
  6. Axon snaps forming retraction balls
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8
Q

When does diffuse axonal injury occur?

A

Usually 24 hours post injury

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9
Q

How does diffuse axonal injury show on T2 MRI?

A

High signal patches (light)

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10
Q

What other issues may follow diffuse axonal injury?

A

Generalised atrophy and ventricular enlargement

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11
Q

What is diffusion tensor imaging fractional anisotropy?

A

A measure of connectivity in the brain, scored from 0-1, with a lower score representing less restricted movement, indicated disrupted fibre tracts and/or demyelination

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12
Q

What DTI-FA findings have been observed in those with brain injury?

A

Reduced FA and increased mean diffusivity, particularly in those with mood disorder

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13
Q

Which brain areas show particular disruption connectivity and reduced FA in brain injury?

A

The corpus callosum and long white matter tracts of the cerebral hemisphere (e.g. frontooccipital fasciculus)

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14
Q

What other populations show reduced FA?

A

▪️Individuals with lower IQ
▪️Individuals with depression and ADHD

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15
Q

What symptoms might you see in someone with DAI in the brain stem?

A

Slurred speech and severe ataxia

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16
Q

What are the key neuroimaging markers of DAI?

A

▪️Shear haemorrhages
▪️Often due to microhaemorrhages at the grey/white matter interface
▪️Often parafalcine (fold of dura mater between hemispheres)

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17
Q

What are the best imaging techniques for detecting DAI haemorrhages and why?

A
  1. Susceptibility weighted imaging
  2. Gradient echo

Haemoglobin turns into haemosiderin which stays in the brain tissue. This contains iron which is magnetic and shows up as dark patches.

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18
Q

When does cerebral atrophy occur in brain injury?

A

Over the course of weeks/months post-injury, particularly in the white matter if affected by DAI

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19
Q

What are the main neuroimaging signs of cerebral atrophy?

A

▪️Ventriculomegaly
▪️Thinning of corpus callosum
▪️Whole brain volume decrease

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20
Q

Which type of brain matter is particularly affected by cerebral atrophy and why?

A

White matter due to diffuse axonal injury

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21
Q

What is important you differentiate cerebral atrophy from and why?

A

The development of hydrocephalus due to raised CSF pressure. This is much more serious process.

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22
Q

What are the three main causes of raised intracranial pressure?

A

▪️Extradural haemorrhage
▪️Subdural haemorrhage
▪️Intraparenchymal haemorrhage

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23
Q

What are the two key types of herniation?

A

▪️Uncal (transtentorial)
▪️Tonsilar (coning)

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24
Q

What happens in uncal herniation?

A

Rising intracranial pressure causes the uncus to slide down into the posterior fossa, compressing the brainstem and posterior cerebral artery.

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25
Q

What happens in tonsillar herniation?

A

Raised intracranial pressure causes the cerebellar tonsils to move through the foramen magnum, pushing the cerebellum onto the brain stem.

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26
Q

What happens when damage occurs to the brainstem, through ischaemia or compression?

A

Nausea, headache, loss of consciousness, cardiorespiratory failure, death

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27
Q

How do you treat raised intracranial pressure?

A

▪️Management to alleviate pressure (e.g. elevation of head)
▪️Surgical intervention (e.g. decompressing craniectomy, Burr holes)

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28
Q

What are secondary complications of TBI?

A

▪️Hydrocephalus (particularly with subarachnoid bleeding)
▪️Low CSF pressure states
▪️Intracranial infection
▪️CSF leak
▪️Epilepsy
▪️Long term neurodegeneration?

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29
Q

What is CTE?

A

Chronic traumatic encephalopathy - multiple small head impacts (concussions), often seen in sport, which may lead to later onset of progressive neurological deterioration

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30
Q

What is dementia pugilistica?

A

A form of chronic traumatic encephalopathy, well documented in boxers, presenting with characteristics of dementia.

aka punch drunk syndrome

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31
Q

What are the main symptoms of CTE?

A

▪️Parkinsonism, e.g. dysarthria, movement difficulties, tremor
▪️Dementia, particularly memory problems
▪️Alcohol sensitivity
▪️Behavioural change

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32
Q

What are the main pathological findings of CTE?

A

▪️Cerebellar scarring
▪️Cerebral atrophy
▪️Tau deposition and NFTs
▪️Cavum septum pellucidum
▪️Acute axonal damage

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33
Q

What is the main pathognomonic feature of CTE?

A

Tau deposition in the grey matter depths of sulci

BUT is this really the primary dementia-causing pathology or a comorbidity?

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34
Q

What is the proposed mechanism for tau-protein deposition in CTE?

A
  1. Post-injury myelination
  2. Cytoskeletal damage
  3. Chronic accumulation and spread of highly phosphorylated tau
  4. Formation of NFTs
  5. Microglia activation perpetuating it
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35
Q

What is metabolic injury?

A

The disruption of the maintenance of metabolism, such a anoxia, hypoglycaemia, or carbon monoxide poisoning

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36
Q

Which brain areas are most vulnerable to anoxic brain injury?

A

Areas with high metabolic demand such as:

▪️Grey matter
▪️Basal ganglia, particularly if on antipsychotics
▪️Hippocampal formation
▪️Cerebellum (loss of Purkinje cells)
▪️Association cortices

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37
Q

In what situations is the brain particularly vulnerable to anoxia?

A

Periods of increased metabolism/overactivity such as during an epileptic seizure, or alcohol withdrawal.

Les vulnerable when cold!

38
Q

What are watershed infarcts?

A

Ischaemia lesions along the border of 2 major arteries, usually caused by a sharp drop in blood pressure

39
Q

What are the main neuroimaging signs of anoxic brain injury?

A

▪️Basal ganglia ‘lit up’, especially globus pallidus
▪️Hippocampal atrophy
▪️Global cerebral atrophy

BUT might not show anything despite clear deficits

40
Q

What are the two main causes of DAI?

A

Trauma and anoxia

41
Q

What is Wernicke’s encephalopathy?

A

A degenerative brain disorder caused by thiamine (B1) deficiency, most commonly seen in alcohol abuse

42
Q

What is the role of thiamine?

A

It acts as a co-enzyme in aerobic respiration and the breakdown of glucose, playing an important role in metabolism

43
Q

Which brain areas are particularly vulnerable to Wernicke’s encephalopathy?

A

▪️Mammillary bodies
▪️Medial thalamus
▪️Periaqueductal grey matter

44
Q

What cognitive neuropsychiatric sequelae are common to most brain injury pathologies?

A

▪️Slowed information processing
▪️Concentration and memory impairment
▪️Dysexecutive problems

45
Q

What behavioural neuropsychiatric sequelae are common to most brain injury pathologies?

A

▪️Poor/chaotic organisation
▪️Self-centred, thoughtless, suspicious
▪️Inflexible, rigid
▪️Irritable, labile

46
Q

What emotional neuropsychiatric sequelae are common to most brain injury pathologies?

A

▪️Labile
▪️Anxious
▪️Depressed

47
Q

What neuropsychiatric symptoms is characteristic of a subarachnoid haemorrhage from the anterior communicating aneurysm?

A

Confabulation

48
Q

What are the four main neuropsychiatric symptoms of Korsalov syndrome?

A

▪️Disorientation
▪️Anosognosia
▪️Amnesia
▪️Confabulation

(Zangwill quadrad)

49
Q

What specific neuropsychiatric sequelae may be indicative of anoxic brain injury?

A

▪️Parkonsonism/dyskinesia/myoclonus
▪️Severe cognitive impairment with poor prognosis
▪️Significant behavioural problems - may reflect self harm as cause

50
Q

What are the three key considerations when linking neuropsychiatric symptoms to brain injury?

A
  1. Misattribution (e.g. influence of media, litigation, what’s normal?)
  2. Reverse causality
  3. Psychological effects
51
Q

What risk factors for brain injury might interfere with the attribution of neuropsychiatric symptoms to the injury?

A

▪️Young age and male
▪️History of alcohol or drug abuse
▪️Previous head injury
▪️Psychotropic prescription in previous year
▪️Lower IQ/SES/unemployed
▪️Adverse life events

52
Q

What is the best predictor of injury prognosis?

A

Post-traumatic amnesia

53
Q

Which type of TBI is more susceptible to psychological effects?

A

Mild

54
Q

What factors are used to assess brain injury severity?

A

▪️Glasgow coma scale soon after injury
▪️Loss of consciousness
▪️Post-traumatic amnesia

55
Q

What is posttraumatic amnesia?

A

The interval between injury and return to continuous day-to-day memories

56
Q

What GCS, LoC, and PTA scores are indicative of a mild TBI?

A

▪️GCS = 13-15
▪️LoC < 30 minutes
▪️PTA < 24 hours

57
Q

What GCS, LoC, and PTA scores are indicative of a severe TBI?

A

▪️GCS < 9
▪️LoC > 24 hours
▪️PTA > 1 week

58
Q

How long does neuropsychiatric sequelae typically persist in mild TBI?

A

~ 3 months

59
Q

What is the turning point for PTA that predicts return to work following severe TBI?

A

1 month - PTA that lasts longer than this is prognostic of long-term significant disability

60
Q

What other factors should be consider in the assessment of a TBI?

A

▪️Neuroimaging findings (~70% of mTBI DONT show abnormalities)
▪️Neuropsychological testing
▪️Time course of symptoms
▪️Migraine
▪️Benign paroxysmal positional vertigo (BPPV)
▪️Nerve damage
▪️Medication effects
▪️Pituitary function

61
Q

What factors might affect recovery of symptoms after mild TBI?

A

▪️Other causes of WM abnormalities such as SES, depression, or ADHD
▪️Sporting injury with multiple concussions
▪️Greater number of symptoms
▪️Is it somatisation disorder?

62
Q

What personality changes might be apparent with severe TBI?

A

▪️Apathy
▪️Anger and aggression
▪️Agitation
▪️Impulsive and disinhibjtef
▪️Irritable
▪️Labile
▪️Self-centred and thoughtless

63
Q

What is commonly seen alongside personality change in severe TBI?

A

Dysexecutive syndrome, loss of emotional control

(seen with rule breaking in verbal fluency tasks and deviation in multiple errand test)

64
Q

What are the main factors that distinguish confabulation from delusion?

A

▪️Not generally grandiose or persecutory
▪️Filling in memory gaps based on real memories
▪️Only sometimes bizarre
▪️Fleeting and variable
▪️Often DMS

65
Q

When does confabulation usually occur in TBI?

A

Early on post-injury

66
Q

What is the main issue with diagnosing depression following TBI?

A

Many symptoms overlap with the direct effects of TBI (e.g. poor concentration, Irritability, fatigue)

67
Q

What symptoms may be indicative of depression that is NOT a direct consequence of the injury?

A

▪️Changes in self attitude
▪️Low self-esteem
▪️Feelings of hopelessnesd
▪️Self-deprication

68
Q

How might persistent labile mood present long after injury and how do you treat it?

A

Mood swings, irritability, aggression, paranoia

Often responds well to SSRIs

69
Q

How might emotions change post-injury?

A

Not uncommon to see early upbeat mood and optimism alongside lack of insight followed by depression and pessimism on improved insight

70
Q

Does TBI increase risk of suicide?

A

Yes BUT those with TBI are also lore likely to have self harmed before injury too.

71
Q

How do you treat emotional disorders following TBI

A
  1. Rehabilitation and support
  2. CBT
  3. Drug treatment if 1 and 2 not effective
72
Q

Are antidepressants as effective in depression after TBI?

A

Not necessarily - reduced effectiveness of amitriptyline and sertraline

73
Q

What medication shows the best effectiveness for emotional disorders following TBI?

A

Methylphenidate - particularly for apathy and fatigue

74
Q

What has CBT shown to improve following mild to moderate TBI?

A

▪️Quality of life
▪️Depression
▪️Anxiety

75
Q

What is the first step for managing post-TBI agitation and aggression?

A

Check for an underlying cause such as:

▪️Pain
▪️Fluid retention
▪️UTI
▪️Anxiety
▪️Medication
▪️Drug/alcohol withdrawal

76
Q

What is the first line of treatment for post TBI agitation and aggression?

A

Psychosocial strategies (comfort, sleep, rest, family)

Possibly consider transfer to neurobehavioural unit

77
Q

What are the main principles for medication in TBI?

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

78
Q

What is the usual first line of treatment for post-TBI agitation and aggression in outpatient clinics?

A

Mood stabilisers and anticonvulsant, particularly carbamazepine

(Also valproate or lamotrogine)

79
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

80
Q

What is the most reliably effective medication for post-TBI agitation and aggression and when should it be used?

A

Antipsychotics, but not usually used until other medications haven’t worked

81
Q

Which antipsychotics are better suited for inpatient post-TBI treatment of agitation and aggression?

A

Olanzapine and quetiapine (can be monitored)

82
Q

Which antipsychotics are better suited for outpatient post-TBI treatment of agitation and aggression?

A

Risperidone (doesn’t need monitoring as closely)

83
Q

What is a midline shift?

A

The movement of the brain over to the side due to injury on the opposite side (usually a large subdural/subarachnoid haemorrhage)

84
Q

What is a craniectomy?

A

The removal of part of the skull to alleviate swelling (cerebral oedema)

85
Q

What are the signs of opisthotonic posturing?

A

▪️Arched back due to muscle spasms
▪️Arms closed in
▪️Hot, flushed, and sweaty

86
Q

What is a ventriculoperitoneal shunt?

A

A tube surgically inserted to help drain CSF from the brain if the pressure is high

87
Q

What is the Syndrome of the Trephined?

A

Neurological problems due to low pressure CSF, which causes movement of the brain and brainstem within the skull

Seen with craniectomies

88
Q

What symptoms are indicative of a medial orbitofrontal injury?

A

Social problems such as personality change and disinhibited behaviour, and anosmia

89
Q

What is Anton syndrome and when might it be seen in TBI?

A

Lack of insight into and denial of blindness

Seen with uncal herniation, when the posterior cerebral artery is squeezed and causes damage to the visual cortex

90
Q

What neuropsychiatric sequelae might be seen with frontal meningioma?

A

Personality change, headache, mania, and disinhibition

Neuropsychiatric Disorders (30 decks)

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