Station 4: head injury

Question 1

What is the usual cause of death in severe head injuries with a variable period of survival?

Answer 1

Raised intracranial pressure - as a result of either brain swelling or of a haemorrhage accumulating inside the skull.

Question 2

What is the most usual neuropathological cause of long-term disability after a head injury?

Answer 2

Damage to axons and hypoxic-ischaemic damage, sustained at time of injury.

Question 3

What are the two important mechanisms involved in head injury?

Answer 3

Impact to the head and movement of the brain.

Question 4

What are the two most useful ways to classify head injury?

Answer 4

Focal or diffuse

Question 5

What does the term focal indicate in head injury?

Answer 5

Pathology that can be seen on CT or MRI - which may be neurosurgically treatable.

Question 6

What does the term diffuse indicate in head injury?

Answer 6

Microscopic damage which cannot be demonstrated by any of the current imaging techniques, clinicians diagnose this when they have an unconscious patient whose scan shows very little obvious damage.

Question 7

What types of skull fracture are there?

Answer 7

Depressed, comminuted, linear

Question 8

What type of skull fracture is most likely to occur from a RTA involving a motorcyclist wearing a helmet?

Answer 8

Linear fracture

Helmet dissipates force

Question 9

How does papilloedema develop in head injury?

Answer 9

Optic disc swelling

A raised intracranial pressure following head trauma can cause bilateral optic disc swelling.
The optic nerve sheath is continuous with the subarachnoid space, the increased ICP is transmitted to the subarachnoid space surrounding the optic nerve. The pressure prevents axonal flow back along the nerve, causing swelling and protrusion of the optic nerve at its head into the globe. Ultimately compressing the optic nerve and impeding its venous return.

Question 10

What is visible papilloedema?

Answer 10

Retinal veins that produce capillary leak around optic disk

Question 11

What is the Cushing’s reflex and how does it develop in head injury?

Answer 11

Trauma -> raised ICP -> compression of blood vessels supplying the brain -> reduced blood flow to the brain resulting in ischaemia -> sympathethic peripheral vasoconstriction and increased cardiac output -> increase arterial BP -> increase perfusion of the brain (to perfuse the brain, arterial blood pressure = MAP must be greater than that of intracranial pressure so CPP = MAP - ICP) -> baroreceptors in carotid bodies -> bradycardia

Triad: hypertension, bradycardia and irregular respirations in a patient with increased ICP

Question 12

What is the battle sign that you can develop in head injury?

Answer 12

Mastoid ecchymosis
Middle cranial fossa basilar skull fracture (base of skull fracture) - fractures of petrous temporal bone
Periosteal bleeding, draining towards exterior from basilar fracture, develops for several hours following trauma

Question 13

How does a facial nerve palsy develop following head trauma?

Answer 13

The facial nerve runs through the temporal bone.
Skull fracture across temporal bone (basilar fracture) or shearing contents in middle ear -> facial nerve contusion/transection leading to paralysis hours or days post trauma.

Question 14

What is an indication in head trauma to test the facial nerve?

Answer 14

Haemotympanum (blood seen in the tymanic cavity of the middle ear) indicating a base of skull fracture

Question 15

What are common features of an anterior cranial fossa fracture?

Answer 15

CSF rhinorrhoea

Racoon eyes

Question 16

What are the common features of middle cranial fossa fracture?

Answer 16

CSF otorrhoea
Haemotympanum
Battle sign
Facial nerve palsy (CNVII)

Question 17

What are the common features of a posterior cranial fossa fracture?

Answer 17

Bruising over suboccipital area

Cranial nerve injuries

Question 18

What are the possible causes of ‘mass effect’ in the brain?

Answer 18

Space occupying lesion: trauma, haematoma, tumour, cerebral oedema

Question 19

What is the Monro-Kellie hypothesis?

Answer 19

Pressure-volume relationship, aiming to keep a dynamic equilibrium among essential non-compressible components inside the rigid compartments of the skull.

Question 20

What is the average intracranial volume of an adult and what is it composed of?

Answer 20

Average volume around 1700ml.
Composed of:
Brain tissue (1400ml)
CSF (150ml)
Blood (150ml)

The volume of each remains nearly constant in a state of dynamic equilibrium so a decrease in one should be compensated by an increase in another.

Question 21

What is the main protection to the brain when the intracranial volume increases?

Answer 21

Blood and CSF

Question 22

What happens when there is intracranial pathology?

Answer 22

The volume of one component within the cranium increases e.g. heamatoma, brain swelling. When the initial compensatory mechanisms are exhausted (which tries to prevent major changes in the ICP), there is a marked increase in ICP -> reduction CPP -> cerebral ischaemia

Question 23

Explain the phases of the ICP-volume compliance curve

Answer 23

Beginning of curve (A+B):
Compensation phase -> ICP nearly constant with an increase in intracranial volume initially

Steep curve (C+D):
Decompensation phase -> ICP increase rapidly with increase ICV as buffers exhausted.

Question 24

What system is the blood in the cranial cavity mostly contained in?

Answer 24

Low pressure venous system - venous compression serves as a means of displacing blood volume

Question 25

What happens as a result of a rapidly increase ICP?

Answer 25

Herniation

Question 26

What are the later signs of raised ICP?

Answer 26

``` Loss of consciousness (reduced GCS) Cushing's triad Pupil asymmetry/dilatation Projective vomiting Hemiplegia/decorticate/decerebrate ```

Question 27

What is subfalcine herniation?

Answer 27

Displacement of brain (typically cingulate gyrus) beneath free edge of falx cerebri due to raised intracranial pressure --> diffuse hemispheric oedema, compressed/flattened gyri on affected side and midline shift

Question 28

What is tentorial/uncal herniation?

Answer 28

Transtentorial herniation has two subtypes: 1. Uncal = descending 2. Ascending transtentorial The uncus and adjacent part of temporal lobe glide downwards across tentorial notch compressing brainstem and posterior cerebral arteries in the ambient cistern.

Question 29

What is tonsillar herniation?

Answer 29

Inferior descent of the cerebellar tonsils below the foramen magnum. Tonsil compresses on the dorsal part of medulla which can be fatal as it can affect the cardiac and respiratory centres if left untreated.

Question 30

What effects does herniation have on the brain?

Answer 30

- Distorting and causing pressure on the brain - Compresses blood vessels leading to secondary ischaemic damage - Cranial nerves can be compressed

Question 31

Which type of herniation is the most common?

Answer 31

Subfalcine herniation

Question 32

Which artery can be occluded in cases of subfalcine herniation? What are the likely symptoms?

Answer 32

Anterior cerebral artery infarct - clinical symptom of contralateral leg weakness

Question 33

What is the triad of features which constitute the Cushing reflex (vasopressor response) as seen in raised ICP? What is it a late sign of?

Answer 33

1. Hypertension 2. Bradycardia 3. Irregular respiration (impaired brainstem function) Terminal stages of acute head injury - may indicate imminent herniation.

Question 34

What are the components of uncal herniation?

Answer 34

Oculomotor (CNIII) PS input to affected eye -> pupil dilates, fails to constrict in response to light Somatic motor -> down and out only CNIV and CNVI working Compress ipsilateral posterior cerebral artery - ipsilateral primary visual cortex - contralateral homonymous hemianopia Compress contralateral cerebral crus (corticospinal and corticobulbar tract) - ipsilateral hemiparesis (herniation) - contralateral hemiparesis (cerebral crus)

Question 35

Why may a herniating uncus result in a dilated pupil before it progresses to become in the down and out position with ptosis?

Answer 35

PS fibres surround motor fibres of CNIII therefore will be compressed first

Question 36

Tonsillar herniation (coning) is considered to be the most severe herniation. It compresses the medulla and therefore which regulatory centres?

Answer 36

Respiratory | Cardiac

Question 37

Projective vomiting can be a later stage of raised ICP, what causes this?

Answer 37

Good question sir - me don't know. Something to do with the vomiting centres??

Question 38

What is decorticate posturing? What is it a sign of?

Answer 38

Damage of one/both corticospinal tracts - Arms are adducted, flexed with wrist/finger flexed on the chest - Legs are stiffly extended and internally rotated - plantar flexion

Question 39

What is decerebrate posturing? What is it a sign of?

Answer 39

Damage to upper brain stem - Arms: adducted, extended - Wrists: pronated, fingers flexed - Legs: stiffly extended, plantar flexion

Question 40

What is a subarachnoid haemorrhage?

Answer 40

Bleed within subarachnoid space (between arachnoid and pia mater) Presentation: severe, sudden onset headache and vomiting.

Question 41

What is an extradural haemorrhage?

Answer 41

Bleeding into extradural space (between skull and endosteal layer of dura mater) Often hit head on pterion (middle meningeal artery), lucid period then collapse (younger people - dura gets thicker as get older so extradural more common in younger people) Biconvex shape, limited by cranial sutures but not by venous sinuses.

Question 42

What is a subdural haemorrhage?

Answer 42

Bleeding into subdural space (between meningeal layer of dura mater and arachnoid mater). Shearing of bridging veins that drain into adjacent dural sinus - elderly people, falls

Question 43

What is a brain contusion?

Answer 43

Foci of superficial bruising of the brain

Question 44

Where do brain contusions often occur?

Answer 44

On crests of gyri: brain moves over roughened floor of skull - inferior surface of frontal lobe - lateral/inferior surface of temporal lobe - region adjacent to lateral fissures - orbital poles

Question 45

Define 'coup' and 'contra-coup' injuries

Answer 45

Coup: point of impact Contra-coup: traumatic axonal and neuronal damage distant to primary impact -> result of stresses on decelerating brain when it collides with inside of skull

Question 46

What is the difference between diffuse and focal brain injury?

Answer 46

Diffuse: microscopic damage, can't be seen on imaging e.g. - diffuse axonal injury (DAI) - diffuse brain swelling - hypoxic-ischaemic damage - diffuse vascular injury Focal: pathology seen on CT/MRI -> neurosurgically treatable - contusion/laceration to scalp - fracture to skull - haemorrhage/infection to meninges - infection/laceration/haemorrhage/contusion to brain

Question 47

What is 'diffuse axonal injury' and what are its causes?

Answer 47

Result of shearing forces, typically from rotational acceleration (often deceleration). Shearing due to change in velocity has a predilection for axons at the grey-white matter junction. The forces often result in damage to the cells and result in oedema. Complete tearing of the axons is only seen in severe cases. Damage is more widespread than focal brain injury. Extensive lesions in white matter tracts -> LOC and vegetative state Outcome is frequently coma: more than 90% with DAI never regain consciousness :( DAI - most common and devastating head injury

Question 48

How is DAI classified?

Answer 48

Grade I: involves grey-white matter interfaces Grade II: Involves corpus callosum and stage I Grade III: involves brainstem + grade I and II locations MRI is best imaging