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Flashcards in CNS Trauma: Neuropathology Deck (27)
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Types of head trauma

- non missile (acceleration/deceleration, rotation, RTA, falls, assaults)
- missile (conflict-related)
- focal (fractures, intracerebral contusions, bleeding (SAH, extradural/subdural, intracerebral)
- diffuse (Diffuse axonal injury (DAH): damage to connections between regions)


How to determine the extend of damage from head trauma without imaging?

GCS]- learn fully

13+: mild brain injury
9-12: moderate brain injury
8 or less: severe injury


What is ischaemia?

Lack of oxygen AND nutrients (i.e. lack of blood supply providing these)


Define scalp laceration

Breach of the scalp


Define cerebral contusion

Bruise on the surface of the brain


Define cerebral laceration

Breaching of the pia and meninges- extends to parenchyma (disturbance of the actual brain substance)


Difference between diffuse axonal injury and (diffuse) traumatic axonal injury?

- Diffuse axonal injury- interpreting radiology in terms of likely outcome

- (Diffuse) Traumatic injury- a pathological phenomenon (can physically be seen in the tissue)


Where do fissure fractures often extend to?

Base of the skull
(may pass through middle ear/anterior cranial fossa and cause CSF leakage)

-> otorrhea/rhinorrhea (+infection risk)


Signs of skull base fractures?

- Battle's sign (just behind the ear)

- Racoon eyes (peri-orbital haemorrhage)


What causes a contusion?

Collision of brain with the skull (causing surface bruising)


Difference between "coup" and "contrecoup"

- Coup: damage on site of impact

- Contrecoup: damage on opposite side of impact


[When looking at pathology specimen]- You can't see any midline structures?

You are looking at an end piece of brain


Most common CNS trauma that causes coma?

Diffuse axonal injury


Diffuse axonal injury affects which particular structures?

Midline structures:

- corpus callosum
- rostral brainstem
- septum pellucidum


How to grade diffuse axonal injury (DAI)?

Grade 1: parasagittal frontal (white matter from longitudinal fissure), internal capsule, cerebellum

Grade 2: As Grade 1 plus corpus callosum

Grade 3: As Grade 2 plus dorsal brainstem


Molecular pathogenesis of DAI?

[calcium influx at the site of tear] -> activation of calcium dependent proteases (e.g. calpain) -> membrane sealing + cytoskel disruption -> swelling

Primary axotomy: immediate disconnect

Secondary axotomy: stabilising -> secondary insult -> late disconnection


How to detect traumatic axonal injury?

Immunostaining for amyloid precursor protein (APP)

[NB: this is not always detectable using silver staining methods]


What does a midline shift indicate?

Space-occupying lesion (could be blood though)


Describe the causes of brain swelling

- vasodilatation and increased cerebral blood volume -> congestion

- blood vessel damage (vasogenic oedema)

- increased water content of cells -> cytotoxic cerebral oedema


3 main sites of herniation within cranial cavity?

- Subfalcine herniation (cingulate cortex pushed under falx)]- rarest, due to SOL above tentorium

- Transtentorial herniation (medial temporal lobe pushed into posterior cranial fossa)(Supratentorial raised ICP)

- Tonsillar herniation (inferior cerebellum pushed through foramen magnum)]- Base of skull (global raised ICP/supratentorial raised ICP) ----also seen in coning when an LP is done at a raised ICP


Difference between necrosis and apoptosis

- Necrosis = passive cell death

- Apoptosis = programmed cell death that requires an energy supply


Role of inflammation in CNS trauma?

(initially seen as protective response)- but goes on for too long in brain

Involved in chronic, long term, degenerative conditions

BBB breakage -> immune cell infiltration -> activation of microglial cells

- Proinflammatory
- Neuroprotective -> regeneration

Microglial cells- balance of inflammatory M1 and neuroprotective M2


Relationship between acute head injury and Alzheimer's

Acute head injury has been shown to have Aβ and tau pathology, just like Alzheimer’s


Relationship between chronic traumatic encephalopathy (CTE) and Alzheimer's

Both involve astrocytic tau


Key cytological features of CTE pathology

Perivascular distribution of tau pathology in astrocytes- found at the base of the sulci


Major clinical presentations of CTE?

- behaviour/mood variants (generally younger onset)

- cognitive impairment (generally older onset)


Available methods to treat CNS trauma?

- Treat/prevent secondary damage: (neuroprotection, anti-inflammatories, protease inhibitors)

- Hypothermia- minimise metabolic + breakdown activity

- Hyperbaric treatment