Nontraumatic convexal subarachnoid hemorrhage (cSAH)

David Goldemund M.D.
Updated on 18/02/2024, published on 06/04/2021


  • non-traumatic spontaneous subarachnoid hemorrhage at the convexity (non-traumatic convexal SAH – cSAH) is defined as a collection of blood in one or more adjacent sulci, in the absence of SAH in another localization
  • it is relatively rare, but the etiological DDx is quite broad

Clinical presentation

  • severe headache typical for classic SAH is usually not present [Beitzke, 2011]
    • headaches are generally present in cerebral venous thrombosis, RCVS, and PRES
  • transient focal symptoms (paresthesias, paresis) are frequent, which leads to suspicion of stroke/TIA (cSAH belongs to stroke mimics)
    • the etiopathogenesis of transient symptoms is unclear; cortical spreading depression triggered by blood in the SA space is considered [Beitzke, 2011]

Diagnostic evaluation

Computed tomography

  • the primary diagnostic method
  • a finding of sulcal hyperdensity leads to the indication of CTA (both arterial and venous phases)
    • CT sensitivity is approx. 90% in the acute phase but decreases quickly with time (the lesion becomes isodense)
  • given the wide DDx, it is advisable to add an MRI

Magnetic resonance imaging

  • perform the following sequences:
    • FLAIR
    • GRE or SWI
    • DWI+ADC
    • 3D TOF MRA + MR venography
    • T1 and T1 C+
  • FLAIR is highly sensitive to lesions in the subarachnoid space; cSAH appears as a hyperintense band
  • in DDx of cSAH exclude:
    • meningitis
    • leptomeningeal metastases (LMM) and leptomeningeal melanosis
    • post status epilepticus lesions
    • previous contrast examination with gadolinium
    • artifact
  • FLAIR further reveals other typical structural changes in the parenchyma (e.g., PRES, etc.)
  • GRE/SWI – confirms the hemorrhagic nature of sulcal hyperintensities and may also help in the detection of older hemorrhages or venous thrombosis
Non-traumatic convexal SAH


  • typical parenchymal abnormalities in ~ 50% of cases (edema, cortical infarction with/without a hemorrhagic component)
  • cSAH has been described in thromboses of both dural sinuses and superficial veins
  • it most likely results from cortical vein rupture due to venous hypertension
  • MRI GRE helps detect hemorrhagic lesions and thrombosis itself, including smaller superficial veins (GRE directly displays the thrombus)

see here

Non-traumatic convexal SAH in cerebral venous thrombosis

→ more about PRES here

  • hemorrhages occur in approx. 5-17% of PRES cases:
    • parenchymal hematoma
    • minor hemorrhages
    • cSAH
  • AVMs can be a source of ICH with SAH; isolated cSAH is rare
    • AVM is reliably detected on CTA
  • superficially localized cavernous malformations can rarely be the source of cSAH
    • extra-axial cavernous malformations are more vascularized and frequently show signs of bleeding on GRE/SWI
  • CAA tends to occur in patients > 60 years of age [Beitzke, 2011]
  • it is a degenerative angiopathy characterized by amyloid deposits in the walls of small and medium-sized vessels
  • in addition to lobar hematomas and microbleeds, superficial hemosiderosis due to cSAH has also been described
  • cSAH is most likely caused by the rupture of amyloid-attenuated leptomeningeal arteries
  • clinically, there is no headache but rather focal symptoms, including epileptic seizures
  • MRI GRE/SWI is optimal for hemorrhage detection
  • RCVS typically presents with headache, variable neurological deficit, and reversible vascular changes
  • headache is the most frequent and prominent symptom (often described as a “thunderclap” headache)
  • detection of vascular abnormalities on CTA/MRA/TCCD is essential for diagnosis
  • MRI shows parenchymal lesions, including cSAH
  • the diagnosis is confirmed by the regression of vascular changes within three months

→ Vasculitis

  • inflammation can lead to cortical artery rupture, resulting in cSAH
  • in DDx, it is necessary to exclude RCVS and PACNS
gender F > M M > F
onset sudden onset
course monophasic
chronic with fluctuations or fulminant
CSF commonly normal
pathologic finding
vascular imaging
always a pathological finding with severe vasospasms
resolution within a few weeks (< 3 months)
negative in up to 50% of cases
parenchymal imaging
usually normal
ICH, SAH, or edema (similar to PRES)
multiple ischemic lesions
possible leptomeningeal enhancement
vessel wall imaging
(T1C+ dark or black blood high-res images)
[Obusez, 2014]  [Mandell, 2012]
  • cSAH can be caused by the rupture of an infectious aneurysm (meningitis, endocarditis) or due to focal arteritis
  • rarely, cSAH has been described as a consequence of abscess (again due to focal arteritis)
  • clinical presentation: headache, general signs of infection (anorexia, fatigue, fever, etc.), or focal signs (caused by the mass effect of an abscess or ischemia and microhemorrhage)
  • typical for Moyamoya disease or moyamoya syndrome is intraparenchymal or intraventricular bleeding
  • cSAH is rare, most likely due to a rupture of dilated cortical arterioles
  • a typical angiographic findings confirm the diagnosis
  • in cases of hemodynamically significant extra- or intracranial stenosis, collateral circulation becomes involved
  • the rupture of a dilated, congested pial artery may lead to cSAH (Hacein-Bey, 2014)
  • FLAIR imaging shows serpiginous hyperintense structures, similar to the “ivy sign” described in moyamoya patients
  • cSAH due to malignancy can be provoked by coagulopathy, venous thrombosis, PRES, or RCVS (potential side effect of chemotherapy)
  • leptomeningeal metastases are a major consideration in DDx of cSAH
  • both conditions share similar findings on CT and FLAIR imaging
    • a sudden headache favors the diagnosis of SAH; however, it is often missing in cSAH
    • leptomeningeal dissemination is characterized by a gradual development of cranial nerves paresis and postcontrast enhancement of the meninges (on T1 or FLAIR)
    • in the subacute stage, cSAH appears hypointense on GRE

Differential diagnosis

  • traumatic SAH
    • history of trauma
    • usually, a more significant extent of SAH in imaging methods
    • concurrent contusions, sometimes only seen on a follow-up CT scan
    • skull bone trauma is visible in the bone window
  • cortical laminar necrosis
    • associated with hyperintense lesions on MR DWI
  • leptomeningeal metastases

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Nontraumatic convexal subarachnoid hemorrhage