Intracranial Pressure and Brain Injury Flashcards
What are the major components of ICP?
brain
CSF
blood
> increased volume of any one will raise ICP, unless compensatory reduction in one/both of other components
> if ICP continues to increase, compensatory mechanisms will fail
Describe compensatory mechanism in intracranial pressure?
- reduction in the CSF space > within and around the brain
- pressure atrophy of the brain > which occurs most commonly with slow-growing extrinsic lesions, e.g. meningiomas
- reduction in blood volume e.g. within the intracranial venous sinuses
What are the consequences of intracranial space-occupying lesions?
- raised intracranial pressure
- intracranial shift and herniation
- epilepsy
- hydrocephalus
- systemic effects
What are the characteristic clinical signs and symptoms of raised intracranial pressure?
- papilloedema: due to accumulation of axoplasm in optic papilla
- nausea and vomiting: due to pressure on vomiting centres in the pons and medulla
- headache: due to compression and distortion of pain and stretch receptors
- impairment of consciousness, ranging from drowsiness to deep coma, related to the level of increased intracranial pressure
What are the common causes of raised ICP?
- intracranial expanding lesions (“space-occupying lesions”) – e.g. tumour, haematoma, abscess
- hydrocephalus (excess CSF)
- cerebral oedema – increase in brain water content, due to blood-brain barrier problem
> localised (e.g. around tumours)
> generalised (e.g. following severe head injury or hypoxic brain damage)
Name the sites of brain herniation?
- subfalcine
- (trans)tentorial
- tonsillar
- also through skull defect in trauma or before sutures fuse
Describe decompensation?
causes shifts and herniation
What is Cushing reflex?
a physiological nervous system response to acute elevation of intracranial pressure resulting in Cushing triad of
1. widened pulse pressure (increasing systolic, decreasing diastolic)
2. bradycardia
3. irregular respirations
> haemodynamic changes
(raised BP, slowed pulse)
What causes a subfalcine herniation?
(=supracallosal or cingulate hernia)
- usually due to primary abnormality in one cerebral hemisphere
- ipsilateral cingulate gyrus herniates under the free edge of falx
What arteries are affected by a subfalcine herniation?
- pericallosal arteries are compressed > possible cerebral infarction
- anterior cerebral artery may also be affected > larger infarct
Describe a tentorial herniation?
- medial aspect of temporal lobe through tentorium
> affects hippocampus - midbrain compressed and distorted
> compressed aqueduct impairs CSF flow (obstructive hydrocephalus)
> haemorrhage in pons and midbrain
Tentorial herniation poses a risk to what structures?
- ipsilateral 3rd nerve
- posterior cerebral artery
- opposite cerebral peduncle
Describe tonsillar herniation?
- cerebellar tonsils move down – with medulla form “cone” shape
- exit from 4th ventricle blocked impairing CSF flow (obstructive hydrocephalus)
Clinical consequences of tonsillar herniation?
compression of breathing and cardiac centres in medulla
> causing Cushing reflex and even death
What is the effect of transtentorial herniation?
Ipsilateral 3rd cranial nerve compression
Ipsilateral 6th cranial nerve compression
Posterior cerebral artery compression
Cerebral peduncle compression
Brainstem compression and haemorrhage