Traumatic Head and Spinal Cord Injury & Raised Intracranial Pressure

Question 1

What are secondary effects of traumatic brain injury?

Answer 1

Ischaemia - can be acute
Hypoxia - can be acute
Cerebral swelling (raised ICP)
Infection
Epilepsy

Question 2

Epi/extradural haematoma is caused by

Answer 2

rupture of MMA

Question 3

Epi/extradural haematoma is less likely in

Answer 3

old age; dura increasingly adheres to skull with age

Question 4

Subdural haematoma is caused by

Answer 4

subdural veins; can be acute or chronic

Question 5

Subdural haematoma is more common in

Answer 5

old age; as the brain shrinks there is stretch put on the subdural veins where they enter the sagittal sinus and they can rupture w/less force than that causing an extradural haematoma

Question 6

Contusion is what type of necrosis?

Answer 6

Haemorrhagic

Question 7

Where can contusions occur?

Answer 7

Coup (impact site), contrecoup (opposite), and inferior lobes (frontal, lateral temporal)

Question 8

How do cerebral contusions heal?

Answer 8

macrophages remove dead tissue and blood, leaving collapsed gyri that are orange in colour (haemosiderin)

Question 9

Where is the cerebral tissue vulnerable to tearing?

Answer 9

ponto-medullary junction (pons and medulla in brainstem), results in instant death

Question 10

What is traumatic/diffuse axonal injury (TAI/DAI)?

Answer 10

damage to individually axons in cerebral tissue, not necessarily with contusions, haemorrhaging, or tearing; the corpus callosum is particularly susceptible

Question 11

What is diffuse vascular injury?

Answer 11

Tearing of small vessels, give spotty haemorrhages; usually occurs with TAI/DAI

Question 12

What is an axonal spheroid?

Answer 12

indicator of axonal injury/transsection; axoplasm continues to send proteins down axon, get a buildup of neurofilaments and axonal material

Question 13

What are the long-term effects of DAI?

Answer 13

brain atrophy, enlargement and dilation of the ventricles, thinning of the corpus callosum and white matter relative to cortical tissue

Question 14

What are the long-term sequelae of brain trauma?

Answer 14

infection - especially in open skull fracture; hydrocephalus (dilated ventricles compress brain tissue, occurs to blockage of CSF drainage or overproduction); epilepsy; chronic traumatic encephalopathy (brain atrophy due to neuronal loss, deposition of proteins and plaques - ie in boxers, footballers)

Question 15

What is the initial response to expanding brain lesions?

Answer 15

expulsion of CSF to decrease ventricular size, gyral-sulcal flattening, and expulsion of venous blood - then ICP starts to rise

Question 16

As ICP approaches arterial pressure

Answer 16

brain perfusion ceases

Question 17

How can CSF caused raised ICP?

Answer 17

overproduction, obstruction to absorption or flow

Question 18

What are the two types of cerebral oedema?

Answer 18

vasogenic and cytotoxic

Question 19

Vasogenic cerebral oedema

Answer 19

due to BBB disruption with increased vascular permeability; predominantly involves white matter; responsive to steroids and other tx

Question 20

Cytotoxic cerebral oedema

Answer 20

increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury - occurs in strokes and infarcts; does not respond to tx; affects grey and white matter

Question 21

What is subfalcine herniation?

Answer 21

cingulate gyrus is pushed underneath the falx

Question 22

What is transtentorial/medial herniation?

Answer 22

medial temporal lobe is pushed through tentorium cerebelli

Question 23

What is tonsilar herniation?

Answer 23

cerebellar tonsils pushed into spinal canal due to pressure on brainstem from herniating cerebral tissue

Question 24

What are Duret haemorrhages?

Answer 24

Secondary to raised ICP pushing the brainstem downwards, tearing of blood vessels in the brainstem occurs because they are fixed relative to the cerebral tissue; causes further brainstem damage

Question 25

What are causes of raised ICP?

Answer 25

Trauma
Tumour
Infarction
Haemorrhage
Infection
Cerebral oedema
Overproduction or obstruction of flow or absorption of CSF