see also:

• radiology
• arachnoid cysts
• hydrocephalus

• is there any cerebral oedema, if so, what type and where?
• is there evidence of a bleed, if so, what type of bleed, how old and where?
  • acute bleeds and clots are hyperdense
  • subacute bleed 2wks old is isodense with grey matter
  • chronic bleeds > 3-4wks old become “cystic” and appear hypodense like CSF
• is there mass effect?:
  • midline shift
  • assess fourth ventricle and foramen magnum including effacement of CSF around the midbrain
  • herniation
• is there any hydrocephalus - check the size of the anterior horns
• in sudden unconsciousness with an apparently normal CT brain, look for a dense basilar artery tip to indicate a basilar artery thrombus which may warrant urgent life saving clot retrieval or catheter-directed thrombolysis
  • see https://radiopaedia.org/articles/acute-basilar-artery-occlusion
• use a systematic approach
  • start at the vertex - assess grey-white matter differentiation, dura sinus, midline shift, look for subdurals, etc

• non-contrast CT brain
  • looking for a bleed
• CT carotid and Circle of Willis Angiogram
  • looking for occlusion, collaterals, ease of access for possible clot retrieval within 6hrs of symptom onset
  • eg. ICA embolus categorised as either:
    • ICA-T = fork shaped embolus extending up two branches of bifurcation
    • ICA-L = linear shaped embolus extending up one of the two branches of bifurcation
    • M1 = more distal embolus past the bifurcation
• CT Perfusion scan
  • assess degree of potentially salvageable ischaemic penumbra (some patients may still have this up to 14hrs post onset whereas others may have none by 8 hours)

• cytotoxic
  • BBB is intact and the pathophysiology is cellular swelling
  • CT features are loss of grey-white matter differentiation as BOTH become hypodense
  • due to either:
    • cerebral infarct
    • HSV encephalitis
    • hypoxic brain injury
• vasogenic
  • BBB is lost, oedema is extracellular
  • CT features are heightened grey-white matter differentiation as only the white matter becomes hypodense
  • due to either:
    • tumour
    • metastasis
    • abscess
  • these cases usually warrant a contrast CT scan as likely to have an enhancing lesion

• see https://radiopaedia.org/articles/cerebral-vascular-territories for details
• anterior cerebral artery (ACA) - fronto-medial
  • rare (2% of ischaemic strokes);
• middle cerebral artery (MCA) - lateral involving Sylvian fissures
• medial lenticulostriate arteries - fronto-medial aspects of basal ganglia
  • arise from the A1 segment of anterior cerebral artery (ACA), and supply the globus pallidus and medial portion of the putamen
• anterior choroidal arteries - central and lateral aspects of basal ganglia
  • rare and usually incomplete; characterised by the triad of hemiplegia, hemianaesthesia and contralateral hemianopia
• lateral lenticulostriate arteries - posterior aspects of basal ganglia
  • arise from the proximal middle cerebral artery (MCA) and supply the lateral portion of the putamen and external capsule as well as the upper internal capsule.
• posterior cerebral artery (PCA) - occipital lobe
• superior cerebellar artery (SCA) - cerebellum
• posterior inferior cerebellar artery (PICA)
  • usually causes vertigo, nausea and truncal ataxia
  • 30% have signs of a lateral medullary syndrome
  • see https://radiopaedia.org/articles/posterior-inferior-cerebellar-artery-pica-infarct
• anterior inferior cerebellar artery (AICA)
  • rare; presents with vertigo, ataxia, peripheral facial palsy and/or hypoacusis

• extra-axial
  • extradural
  • subdural
  • subarachnoid
  • intraventricular
• intra-axial
  • “primary”
    • hypertension
    • amyloid angiopathy
  • “secondary”
    • vascular malformation
    • tumour
    • haemorrhagic transformation of infarct
    • venous thrombosis
    • traumatic intraparenchymal
  • tip: if there is more oedema than haemorrhage, then think of an underlying tumour or infarct as a cause of the bleed