Traumatic brain injury

Question 1

Learning objectives

• To have a basic understanding of the neuropathology / neuroimaging of the common causes of single incident non-focal acquired brain injury (ABI) in adult life
• To appreciate the neuropsychiatric sequelae of the different causes of ABI; what is common and what is more specific
• To appreciate the importance of base rates of “brain injury” symptoms in the general population, that ABI is not random, the role of pre-injury constitution on post injury outcome, and reverse causality
• To be able to assess whether brain injury is likely playing a part in mental symptoms after injury
• To have some understanding of the assessment of the severity of brain injury, particularly as applied to traumatic brain injury (TBI)

Answer 1

• To have some understanding of diagnosis of common mental disorders in the presence of ABI
• To understand the role of secondary complications and other factors in symptom formation
• To appreciate the role of psychological factors and brain injury after mild TBI
• To be able to advise on the management of agitation and aggression after ABI

Question 2

Epidemiology

Answer 2

• According to the epidemiological catchment area study 8.5% of people report a head injury with loss of conciousness (LOC) or confusion
• Around 80% of head injuries are mTBI
• Ratio 3:1 male:female
• Most commonly seen in 15-25 years age group, alcohol and lower socioeconomic class

Question 3

What can primary brain injuries be classified as

Answer 3

1. Focal
2. Diffuse

Question 4

What causes focal lesions?

Answer 4

Often from direct impact or acceleration/ deceleration forces

Question 5

Coup

Answer 5

Contusion or lesion is directly beneath the area of impact

Question 6

Contrecoup

Answer 6

Contusion or lesion is contralateral (opposite) the area of impact

Question 7

Which areas are most affected?

Answer 7

Orbito-frontal/ temporal poles

Question 8

Diffuse (axonal) injury

Answer 8

Shearing or stretching of axons due to rotational forces of the brain inside the skull

Question 9

What are the most common brain injuries

Answer 9

Subdural haematoma and extradural haematoma

*Intracerebral and subarachnoid are also very common

Question 11

Neuroimaging

Which imaging modaility is first line

Answer 11

CT

Question 12

Secondary injures

What are some secondary complications of TBI

Answer 12

• hydrocephalus
• low csf pressure states (syndrome of the trephined)
• post surgical intracranial infection
• CSF leak
• epilepsy
• potentially neurodegenerative conditions in the long term

Syndrome of the trephines - slowed processing speed, dizziness, depression

Question 13

Craniotomy

Question 14

Craniectomy

Question 15

Cranioplasty

Question 16

What is the key marker of diffuse axonal injury

Answer 16

Shearing haemorrhages

Question 17

Where are DAI commonly seen on imaging

Answer 17

Parafalcine parallel to the falx (leathery division between the two hemispheres
White and grey matter interface

Question 19

What imaging can be used to visualise DAI

Answer 19

Gradient echo imaging
Wusceptibility weighted imaging

*CT may appear normal

Question 20

Diffusion tensor imaging fractional anisotrophy

Answer 20

DTI shows the movement of water across white matter tracts to map out white matter tracts and visualise their intergrity to see if any damage has occured

*not used much in clinical settings

changes are not unique to brain injury

Question 21

Subacute changes post TBI

Answer 21

• white matter atrophy
• ventriculomegaly
• thinning of the corpus callosum

These are passive benign processes

However these changes need to be distinguished from developing hydrocephalus due to raise ICP

Question 22

What finding on FA would suggest damage

Answer 22

Increased diffusion of water

Question 24

Imaging corpus callosum

Answer 24

Midslice of coronal aspect above the ventricles. The space is thinner if the ventricles are enlarged

Question 26

# *Direction of movement* Uncal herniation

Answer 26

Downward movement of unicate process of temporal lobe below the tentroium cerebelli

Question 27

# *Features* Uncal herniation

Answer 27

- third cranial nerve palsy - posterior cerebral artery infarct - contralateral temporal horn hydrocephalus - ipsilaterla paresis/ paralysis by compression of the contralateral tracts

Question 28

# *Direction of movement* Central herniation

Answer 28

Downward movement of teh thalamic regions below the tentorium cerebelli

Question 29

# *Features* Central herniation

Answer 29

- third cranial nerve palsy - progressive decrease in GCS - Cushing's triad

Question 31

Cushing's triad

Answer 31

1. Widening pulse pressure (***increasing systolic*** pressure and ***decreasing diastolic*** pressure) 2. bradycardia 3. irregular respirations

Question 32

# *direction of movement* Subfalcine herniation

Answer 32

sideways movement of the cingulate gyrus to contralateral hemisphere

Question 33

# *features* Subfalcine herniation

Answer 33

- hydrocephalus due to compression of the foramen of munroe - anterior cerebral artery compression - ipsilateral leg weakness

Question 34

# *direction of movement* transcalvarial herniation

Answer 34

extracranial herniation of cerebral tissue

Question 35

# *features* transcalvarial herniation

Answer 35

cerebral ischaemia secondary to venous infarction

Question 36

# *direction of movement* ascending herniation

Answer 36

upwards movement of cerebellar tonsils through the tentorium cerebelli

Question 37

# *features* ascending herniation

Answer 37

- nausea and vomiting - progressive decrease in GCS - posterior circulation artery/ superior cerebellar artery compression

Question 38

# *direction of movement* tonsillar herniation

Answer 38

downward movement of cerebellar tonsils through the foramen magnum (coning)

Question 39

# *features* tonsillar herniation

Answer 39

- Cushing's triad - brainstem aterial supply compression (breathing) - obstructive hydrocephalus

Question 40

What is CTE

Answer 40

Chronic traumatic encephalopathy - caused by multiple small head impacts - seen often in contact sports - may lead to late onset progressive neurological deterioration

Question 41

What is the clinical presentation of CTE

Answer 41

- behavioural change (irritability, agitation, paranoia) - concentration and memory difficulties - intolerance of alcohol - movement disorder (dysarthria, slowing, balance problems, tremor = *parkinsonism*) - dementia

Question 42

What is the pathology of CTE | *Postmortem findings*

Answer 42

- cerebellar scarring - cerebral atrophy - neurofibrillary tangles - *tau deposition in the sulci* | - cavum septum pellucidum

Question 43

*'dementia pugilistica'*

Answer 43

punch drunk syndrome

Question 44

Tau deposition

Answer 44

- Protein - important for the normal structure of microtubules in neurons - Tau becomes phosphorylated and clumps together/ phosphorylated tau thought to be pathogenic

Question 45

Hypoxic brain injury

Answer 45

Affects: grey matter basal ganglia Made worse by epilepsy and excess alcohol

Question 46

# imaging Hypoxic brian injury

Answer 46

Basal ganglia and globus pallidus involvement atrophy of hippocampi global cerebral atrophy completely normal

Question 48

What is a common cause of hypoxic ichaemic injury

Answer 48

cardiac arrest

Question 49

What are the hallmarks of hypoxic injury on MRI

Answer 49

- watershed infarcts - basal ganglia changes particularly in the globus pallidus - hippocampal atrophy

Question 50

What is wernicke's encephalopathy

Answer 50

- caused by thiamine deficiency (vitamin B1) - commonly in alcohol depedent individuals

Question 51

what is the significance of thiamine

Answer 51

thiamine acts as a coenzyme in aerobic respiration | Aerobic respiration is the breakdown of sugars

Question 52

what are the hallmarks of wernicke's encephalopathy on MRI

Answer 52

High signal (areas appears bright white) - periacqueductal grey - mamillary bodies - medial thalamus | high signal/ hyper intensity for bright white areas on MRI ## Footnote vs high attenuation on CT

Question 53

Cognitive impairment in TBI

Answer 53

- anterograde amnesia - inaccurate recall - poor monitoring - poor insight - confabulation - procedural (implicit) memory remains relatively intact | Concept of cognitive reserve

Question 54

Dysexecutive syndrome

Answer 54

Deficits are seen in organisation, planning, scheduling, prioritising, monitoring and multitasking | *Multiple errands task*

Question 56

Personality change

Answer 56

Most often an enhanced version of premorbid characteristics.

Question 57

What percentage of people who experience personality change post TBI would meet scale criteria for certain personality traits?

Answer 57

Approximately 30%

Question 58

Which *three* trait personalities are common after TBI?

Answer 58

1. avoidant personality 2. impulsive personality 3. borderline paranoid

Question 59

What percentage of peopel develop maladaptive personality traits?

Answer 59

Around 20%

Question 60

# *Where is the lesion?* Disinhibition/ poor judgement

Answer 60

Orbitofrontal region

Question 61

# *Where is the lesion?* Poor motivation

Answer 61

Mesial frontal region

Question 62

# *What is the symptom(s)?* Lesion in the orbitofrontal region

Answer 62

Disinhibition/ poor judgement

Question 63

# *What is the symptom?* Lesion in the mesial frontal region

Answer 63

Poor motivation

Question 64

# *Abbrv* PPCS

Answer 64

Persistant post concussional syndrome

Question 65

What are some early 'neurological' symptoms of PPCS or **mTBI**

Answer 65

- headache - dizziness - double vision - impaired information processing - concentration - fatigue - noise sensitivity

Question 66

Pseudobulbar affect

Answer 66

e.g. crying but feeling fine. The external affect presentation does not match the internal state

Question 67

Emotional lability

Answer 67

rapid cycling through different mood states which are actually being felt but can distract them from their mood