What is the Munro-Kellie Doctrine?
States that the cranial compartment is incompressible and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another.
Vcsf+Vblood+Vbrain+Vother = Vintracranial space = constant
How would you calculate cerebral perfusion pressure?
CPP = MAP - ICP
How do you calculate mean arterial pressure?
Diastolic BP + 1/3 pulse pressure
What is normal cerebral perfusion pressure?
What is normal MAP?
What is normal ICP?
What proportion of cardiac output does the brain receive?
How do neurones produce energy?
Entirely oxidative metabolism of gluocse or ketone bodies. There is little capacity for anaerobic metabolism
What happens if the brain is starved of oxygen?
Energy dependent processes cease, leading to irreversible damage within 3-8 minutes
What processes contribute to the control of blood flow into the brain?
- Myogenic mechnism - effect of transmural blood pressure changes, which are directly detected by the vascular smooth muscle in arterioles. Then, the calibers are adjusted accordingly to keep blood flow constant.
- Metabolic mechanism - driven by metabolic demand and oxygen delivery through cerebral blood flow and acts by means of a vasoactive substance.
- Autonomic mechanism - vascular smooth muscle actuators in the resistance arterioles are controlled via sympathetic innervation, receiving the input from the appropriate brainstem autonomous control center.
What is the most important autoregulation mechanism implicated in cerebral perfusion?
What happens to cerebral perfusion below a blood pressure of 50 mmHg systolic?
Arteries collapse and brain tissue becomes ischaemic
What happens to cerebral perfusion at blood pressures above 150 mmHg systolic?
Blood flow increases, causing force mediated dilatation of vessels, and vasogenic oedema to form
What happens to cerebral vessel diameter as blood pressure approaches 150 mmhg systolic?
Vessels reach maximal point of constriction in an attempt to maintain CBF and ICP
What are mass effect causes of raised ICP?
- Tumours (1o or mets)
- Infarction with oedema
- Chronic subdural/epidural haematoma
What are specific features of the headache seen in individuals with raised ICP?
- Lying down
- Bending forward
What are symptoms seen in someone with raised ICP?
- Nausea and vomiting
- Subtle personality change
What are signs of increased ICP?
- Evolving focal neurology
- False localising VI nerve palsy
- Decreased GCS
What focal neurological signs would point to a lesion in the temporal lobe?
- Dysphasia/Wernicke's Aphasia
- Confusional states
- Contralateral homonymous haemianopia/superior quadrantinopia
- Odd/inexplicable phenomena
What focal neurological signs would point to a lesion in the frontal lobe?
- Personality change
- Release phenomena (e.g. grasp reflex)
- Broca's dysphasia
- Unilateral anosmia
- Executive dysfunction
- Decreased verbal fluency
What personality changes can occur in someone with a frontal lobe lesion?
- Tendancy to pun
What are release phenomena?
Increased tone and hyperirritability of muscle-stretch reflexes that occur following damage of the upper portions of the extrapyramidal system
When is the presence of release phenomena considered signficant?
Only if unilateral
What is perseveration?
Unable to switch from one line of thinking to another
What is executive function?
Ability to plan tasks
What focal neurological features might you see in someone with a parietal lobe lesion?
- Hemisensory loss
- Decreased 2-point discrimination
- Sensory inattention
What is astereognosis?
Inability to recognise an object by touch alone
What focal neurological features would indicate a lesion in the occipital lobe?
- Contralateral visual field defects
- Visuospatial deficits
What is palinopsia?
Persisting images once the stimulus has left the field of vision
What is polyopia?
Seeing multiple images
What focal neurological features would point towards a lesion in the cerebellum?
- Ataxia (limb/truncal)
- Intention tremor
- Slurred speech
- Past pointing
What focal neurological features would point to a lesion in cerebellopontine angle?
- Ipsilateral deafness
- Decreased corneal reflex
- Facial weakness
- Ipsilateral cerebellar signs
- CNVI palsy
What focal neurological signs would point to a lesion in the midbrain?
- Failure of up/down gaze
- Light-near dissociation
- Nystagmus on convergent gaze
What are classes of causes of increased ICP?
- Mass effect
- Generalised brain swelling
- Increased venous pressure
- Onstruction of CSF flow +/- absorption
What are causes of generalised brain swelling which can lead to raised ICP?
- Ischaemic-anoxic states
- Acute liver failure
- Hypertensive encephalopthy
What are causes of increased venous pressure which can cause increased ICP?
- Venous sinus thrombosis
- Heart failure
- Obstruction o superior mediastinal/jugular veins
What are causes of obstruction of CSF flow/absorption which can lead to increases in ICP?
- Extensive meningeal disease - due to infection, carcinoma, granuloma
- Obstruction of cerebral convexities/superior sagittal sinuses
What level does the ICP have to rise to before small changes in brain volume cause marked elevations in ICP?
25 mmHg - due to failure of intracranial compliance
What is the main danger of raised ICP?
Reduces cerebral perfusion - leads to ischaemic brain tissue
What is the body's response to a fall in CPP?
Raise systolic BP and dilate cerebral blood vessels
Why does the body's response to a fall in CPP caused by raised ICP cause problems?
It increases cerebral blood volume, thus increasing ICP further, which lowers CPP even further - VICIOUS CYCLE
What can result from severely raised ICP caused by a unilateral SOL cause (e.g. acute haematoma)?
Midline shift - compresses ventricles and causes hydrocephalus
What is someones prognosis if they have midline shift present on imaging from a SOL relative to someone who has an SOL without midline shift?
Midline shift = much worse prognosis
What are secondary effects of increased ICP?
- Hernation syndromes
- Decreased cerebral perfusion - infarction
Why do individuals with increased ICP get nausea and vomiting?
Compression of vomiting centres in brainstem
How would you manage raised ICP?
- Surgery to relieve pressure - Heamatoma, ventricular shunt
- Osmotic agents - mannitol
- Nurse with head at 30-45o (Venous return)
- Reduce pain
- Hyperventilation - Maintain good PO2, reduce PCO2
- Reduce metabolism - reduce temperature, barbiturates
Why is hyperventilation used as part of treatment for raised ICP?
Causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP. This effect is mediated by pH changes in the extracellular fluid which cause cerebral vasoconstriction or vasodilation depending on the pH.
Why is mannitol used to manage increased ICP?
It is an osmotic diuretic and can have significant beneficial effects on ICP, cerebral blood flow and brain metabolism. Mannitol has two main mechanisms of action:
- Expands circulating volume by reducing cerebral parenchymal cell water
- Decreases blood viscosity
Through these actions it reduces ICP, which increases cerebral blood flow and cerebral oxygen delivery.
Why is mannitol only used for short term (approximately 72 hours) control of raised ICP only?
Rebound effect - It eventually enters the CSF, and subsequently raises ICP through osmotic shift
What investigations would you consider doing in someone with signs of raised ICP/SOL?
- CT +/- MRI
- Consider Biopsy
- Consider LP - after imaging to assess for coning
How would you manage someone with cerebral oedema?
- Mannitol - if ICP raised acutely