= blood between pia + arachnoid membrane

Cause:

1. Spontaneous
   1. Ruptured aneurysm (72%)
   2. AV malformation (10%)
   3. Hypertensive hemorrhage
   4. Hemorrhage from tumor
   5. Embolic hemorrhagic infarction
   6. Blood dyscrasia, anticoagulation therapy
   7. Eclampsia
   8. Intracranial infection
   9. Spinal vascular malformation
   10. Cryptogenic in 6% (negative 4-vessel angiography; seldom recurrent)
2. Trauma (common)
   concomitant to cerebral contusion
   1. Injury to leptomeningeal vessels at vertex
   2. Rupture of major intracerebral vessels (less common)
      Location:
      1. focal, overlying site of contusion / subdural hematoma
      2. interhemispheric fissure, paralleling falx cerebri
      3. spread diffusely throughout subarachnoid space (rare in trauma): convexity sulci >basal cisterns

Pathophysiology: irritation of meninges by blood and extra fluid volume increases intracranial pressure → vasospasm in 2–41%

• acute severe headache (“worst in life”), vomiting
• altered state of consciousness: drowsiness, sleepiness, stupor, restlessness, agitation, coma
• spectrophotometric analysis of CSF obtained by lumbar puncture

NECT (60–90% accuracy of detection depending on time of scan; sensitivity depends on amount of blood; accuracy high within 4–5 days of onset, 90% sensitive within 1^st day):

• increased density in basal cisterns, superior cerebellar cistern, sylvian fissure, cortical sulci, intraventricular
• along interhemispheric fissure = on lateral aspect irregular dentate pattern due to extension into paramedian sulci with rapid clearing after several days
• “cortical vein” sign = visualization of cortical veins passing through extraaxial fluid collection

MR (relatively insensitive within first 48 hours):

• hyperintense sulci and cisterns on FLAIR and T2* (more sensitive than CT for small amounts of blood)
• “dirty” CSF isointense to brain on T1WI + T2WI
• low signal intensity on brain surfaces in recurrent subarachnoid hemorrhages (hemosiderin deposition)

Prognosis: clinical course depends on amount of subarachnoid blood

Cx:

1. Acute obstructive hydrocephalus (in <1 week) ← intraventricular hemorrhage / ependymitis obstructing aqueduct of Sylvius or outlet of 4^th ventricle
2. Delayed communicating hydrocephalus (after 1 week) ← fibroblastic proliferation in subarachnoid space and arachnoid villi interferes with CSF resorption
3. Cerebral vasospasm + infarction (develops after 72 hours, at maximum between 5–17 days, amount of blood is a prognostic parameter)
4. Transtentorial herniation (cerebral hematoma, hydrocephalus, infarction, brain edema)