25. Differentials
• The major differential diagnosis of aSAH is traumatic SAH
(tSAH). aSAH is generally much more widespread, often filling
the basal cisterns. tSAH typically occurs adjacent to cortical
contusions or lacerations and is therefore most common in
the superficial sulci
26. • Perimesencephalic nonaneurysmal SAH (pnSAH) is much
more limited than aSAH and is localized to the interpeduncular,
ambient, and prepontine cisterns.
• Convexal SAH (cSAH) is, as the name implies, localized to superficial
sulci over the cerebral convexities. Often only a single sulcus is
affected. Causes of cSAH are numerous and include cortical vein
occlusion, amyloid angiopathy, vasculitis, and reversible cerebral
vasoconstriction syndrome (RCVS).
27. • Pseudo-SAH is caused by severe cerebral edema. The hypodensity of the
brain makes blood in the cerebral arteries and veins appear dense,
mimicking the appearance of SAH.
• Sulcal-cisternal FLAIR hyperintensity on MR is a nonspecific imaging
finding. It occurs with hemorrhage, meningitis, carcinomatosis,
hyperoxygenation, stroke, and gadolinium contrast (blood-brain barrier
leakage or chronic renal failure).
• FLAIR "bright" CSF can also result from flow disturbances and technical
artifacts (e.g., incomplete CSF nulling)
31. Fisher scale (modified)
• the risk of developing vasospasm progressively increases with
each grade
• grade 0
• no subarachnoid haemorrhage (SAH)
• no intraventricular haemorrhage (IVH)
• incidence of symptomatic vasospasm: 0% 3
• grade 1
• focal or diffuse, thin SAH
• no IVH
• the incidence of symptomatic vasospasm: 24%
•
32. • grade 2
• thin focal or diffuse SAH
• IVH present
• the incidence of symptomatic vasospasm: 33%
• grade 3
• thick SAH
• no IVH
• the incidence of symptomatic vasospasm: 33%
• grade 4
• thick SAH
• IVH present
• the incidence of symptomatic vasospasm: 40%
