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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
What happens in tonsillar herniation?
Raised intracranial pressure causes the cerebellar tonsils to move through the foramen magnum, pushing the cerebellum onto the brain stem.
26
What happens when damage occurs to the brainstem, through ischaemia or compression?
Nausea, headache, loss of consciousness, cardiorespiratory failure, death
27
How do you treat raised intracranial pressure?
▪️Management to alleviate pressure (e.g. elevation of head) ▪️Surgical intervention (e.g. decompressing craniectomy, Burr holes)
28
What are secondary complications of TBI?
▪️Hydrocephalus (particularly with subarachnoid bleeding) ▪️Low CSF pressure states ▪️Intracranial infection ▪️CSF leak ▪️Epilepsy ▪️Long term neurodegeneration?
29
What is CTE?
Chronic traumatic encephalopathy - multiple small head impacts (concussions), often seen in sport, which may lead to later onset of progressive neurological deterioration
30
What is dementia pugilistica?
A form of chronic traumatic encephalopathy, well documented in boxers, presenting with characteristics of dementia. aka punch drunk syndrome
31
What are the main symptoms of CTE?
▪️Parkinsonism, e.g. dysarthria, movement difficulties, tremor ▪️Dementia, particularly memory problems ▪️Alcohol sensitivity ▪️Behavioural change
32
What are the main pathological findings of CTE?
▪️Cerebellar scarring ▪️Cerebral atrophy ▪️Tau deposition and NFTs ▪️Cavum septum pellucidum ▪️Acute axonal damage
33
What is the main pathognomonic feature of CTE?
Tau deposition in the grey matter depths of sulci BUT is this really the primary dementia-causing pathology or a comorbidity?
34
What is the proposed mechanism for tau-protein deposition in CTE?
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
35
What is metabolic injury?
The disruption of the maintenance of metabolism, such a anoxia, hypoglycaemia, or carbon monoxide poisoning
36
Which brain areas are most vulnerable to anoxic brain injury?
Areas with high metabolic demand such as: ▪️Grey matter ▪️Basal ganglia, particularly if on antipsychotics ▪️Hippocampal formation ▪️Cerebellum (loss of Purkinje cells) ▪️Association cortices
37
In what situations is the brain particularly vulnerable to anoxia?
Periods of increased metabolism/overactivity such as during an epileptic seizure, or alcohol withdrawal. Les vulnerable when cold!
38
What are watershed infarcts?
Ischaemia lesions along the border of 2 major arteries, usually caused by a sharp drop in blood pressure
39
What are the main neuroimaging signs of anoxic brain injury?
▪️Basal ganglia 'lit up', especially globus pallidus ▪️Hippocampal atrophy ▪️Global cerebral atrophy BUT might not show anything despite clear deficits
40
What are the two main causes of DAI?
Trauma and anoxia
41
What is Wernicke's encephalopathy?
A degenerative brain disorder caused by thiamine (B1) deficiency, most commonly seen in alcohol abuse
42
What is the role of thiamine?
It acts as a co-enzyme in aerobic respiration and the breakdown of glucose, playing an important role in metabolism
43
Which brain areas are particularly vulnerable to Wernicke's encephalopathy?
▪️Mammillary bodies ▪️Medial thalamus ▪️Periaqueductal grey matter
44
What cognitive neuropsychiatric sequelae are common to most brain injury pathologies?
▪️Slowed information processing ▪️Concentration and memory impairment ▪️Dysexecutive problems
45
What behavioural neuropsychiatric sequelae are common to most brain injury pathologies?
▪️Poor/chaotic organisation ▪️Self-centred, thoughtless, suspicious ▪️Inflexible, rigid ▪️Irritable, labile
46
What emotional neuropsychiatric sequelae are common to most brain injury pathologies?
▪️Labile ▪️Anxious ▪️Depressed
47
What neuropsychiatric symptoms is characteristic of a subarachnoid haemorrhage from the anterior communicating aneurysm?
Confabulation
48
What are the four main neuropsychiatric symptoms of Korsalov syndrome?
▪️Disorientation ▪️Anosognosia ▪️Amnesia ▪️Confabulation (Zangwill quadrad)
49
What specific neuropsychiatric sequelae may be indicative of anoxic brain injury?
▪️Parkonsonism/dyskinesia/myoclonus ▪️Severe cognitive impairment with poor prognosis ▪️Significant behavioural problems - may reflect self harm as cause
50
What are the three key considerations when linking neuropsychiatric symptoms to brain injury?
1. Misattribution (e.g. influence of media, litigation, what's normal?) 2. Reverse causality 3. Psychological effects
51
What risk factors for brain injury might interfere with the attribution of neuropsychiatric symptoms to the injury?
▪️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
What is the best predictor of injury prognosis?
Post-traumatic amnesia
53
Which type of TBI is more susceptible to psychological effects?
Mild
54
What factors are used to assess brain injury severity?
▪️Glasgow coma scale soon after injury ▪️Loss of consciousness ▪️Post-traumatic amnesia
55
What is posttraumatic amnesia?
The interval between injury and return to continuous day-to-day memories
56
What GCS, LoC, and PTA scores are indicative of a mild TBI?
▪️GCS = 13-15 ▪️LoC < 30 minutes ▪️PTA < 24 hours
57
What GCS, LoC, and PTA scores are indicative of a severe TBI?
▪️GCS < 9 ▪️LoC > 24 hours ▪️PTA > 1 week
58
How long does neuropsychiatric sequelae typically persist in mild TBI?
~ 3 months
59
What is the turning point for PTA that predicts return to work following severe TBI?
1 month - PTA that lasts longer than this is prognostic of long-term significant disability
60
What other factors should be consider in the assessment of a TBI?
▪️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
What factors might affect recovery of symptoms after mild TBI?
▪️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
What personality changes might be apparent with severe TBI?
▪️Apathy ▪️Anger and aggression ▪️Agitation ▪️Impulsive and disinhibjtef ▪️Irritable ▪️Labile ▪️Self-centred and thoughtless
63
What is commonly seen alongside personality change in severe TBI?
Dysexecutive syndrome, loss of emotional control (seen with rule breaking in verbal fluency tasks and deviation in multiple errand test)
64
What are the main factors that distinguish confabulation from delusion?
▪️Not generally grandiose or persecutory ▪️Filling in memory gaps based on real memories ▪️Only sometimes bizarre ▪️Fleeting and variable ▪️Often DMS
65
When does confabulation usually occur in TBI?
Early on post-injury
66
What is the main issue with diagnosing depression following TBI?
Many symptoms overlap with the direct effects of TBI (e.g. poor concentration, Irritability, fatigue)
67
What symptoms may be indicative of depression that is NOT a direct consequence of the injury?
▪️Changes in self attitude ▪️Low self-esteem ▪️Feelings of hopelessnesd ▪️Self-deprication
68
How might persistent labile mood present long after injury and how do you treat it?
Mood swings, irritability, aggression, paranoia Often responds well to SSRIs
69
How might emotions change post-injury?
Not uncommon to see early upbeat mood and optimism alongside lack of insight followed by depression and pessimism on improved insight
70
Does TBI increase risk of suicide?
Yes BUT those with TBI are also lore likely to have self harmed before injury too.
71
How do you treat emotional disorders following TBI
1. Rehabilitation and support 2. CBT 3. Drug treatment if 1 and 2 not effective
72
Are antidepressants as effective in depression after TBI?
Not necessarily - reduced effectiveness of amitriptyline and sertraline
73
What medication shows the best effectiveness for emotional disorders following TBI?
Methylphenidate - particularly for apathy and fatigue
74
What has CBT shown to improve following mild to moderate TBI?
▪️Quality of life ▪️Depression ▪️Anxiety
75
What is the first step for managing post-TBI agitation and aggression?
Check for an underlying cause such as: ▪️Pain ▪️Fluid retention ▪️UTI ▪️Anxiety ▪️Medication ▪️Drug/alcohol withdrawal
76
What is the first line of treatment for post TBI agitation and aggression?
Psychosocial strategies (comfort, sleep, rest, family) Possibly consider transfer to neurobehavioural unit
77
What are the main principles for medication in TBI?
▪️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
What is the usual first line of treatment for post-TBI agitation and aggression in outpatient clinics?
Mood stabilisers and anticonvulsant, particularly carbamazepine (Also valproate or lamotrogine)
79
What should you consider when choosing a medication for long term management of TBI sequelae, particularly agitation and aggression?
▪️Comorbidities, such as depression, mood disturbance, epilepsy, paranoia, or psychotic symptoms ▪️PTA - danger of increasing confusion ▪️Other medical problems and medications ▪️Tolerability
80
What is the most reliably effective medication for post-TBI agitation and aggression and when should it be used?
Antipsychotics, but not usually used until other medications haven't worked
81
Which antipsychotics are better suited for inpatient post-TBI treatment of agitation and aggression?
Olanzapine and quetiapine (can be monitored)
82
Which antipsychotics are better suited for outpatient post-TBI treatment of agitation and aggression?
Risperidone (doesn't need monitoring as closely)
83
What is a midline shift?
The movement of the brain over to the side due to injury on the opposite side (usually a large subdural/subarachnoid haemorrhage)
84
What is a craniectomy?
The removal of part of the skull to alleviate swelling (cerebral oedema)
85
What are the signs of opisthotonic posturing?
▪️Arched back due to muscle spasms ▪️Arms closed in ▪️Hot, flushed, and sweaty
86
What is a ventriculoperitoneal shunt?
A tube surgically inserted to help drain CSF from the brain if the pressure is high
87
What is the Syndrome of the Trephined?
Neurological problems due to low pressure CSF, which causes movement of the brain and brainstem within the skull Seen with craniectomies
88
What symptoms are indicative of a medial orbitofrontal injury?
Social problems such as personality change and disinhibited behaviour, and anosmia
89
What is Anton syndrome and when might it be seen in TBI?
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
What neuropsychiatric sequelae might be seen with frontal meningioma?
Personality change, headache, mania, and disinhibition

Neuropsychiatric Disorders (30 decks)

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