Diagnostic Imaging of Subarachnoid Hemorrhage

Diagnostic Imaging of Subarachnoid Hemorrhage

1. C.N.S.
Subarachnoid Hemorrhage

2. Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology
Department , Zagazig University Hospitals
Egypt
FINR (Fellowship of Interventional
Neuroradiology)-Switzerland
[email protected]

5. Knowing as much as
possible about your enemy
precedes successful battle
and learning about the
disease process precedes
successful management

6. Subarachnoid Hemorrhage
a) Causes
b) Distribution of SAH
c) Grading of SAH
d) Complications of SAH
e) Diagnosis & Investigation

7. a) Causes :
1-Trauma (Most common cause)
2-Ruptured Intracranial Aneurysm
3-Bleeding From Vascular Malformation
4-Extension From Parenchymal Hematoma
5-Perimesencephalic Hemorrhage
6-Miscellaneous
*N.B. :
-No cause of the SAH is identified in up to 22 % of cases

8. 1-Trauma : Most common cause
-Tends to have peripheral distribution in sulci
rather than concentrated in basal cisterns
2-Ruptured intracranial aneurysm : Most common
cause of non-traumatic SAH
-Potentially devastating condition with 50 %
immediate mortality and high long-term
morbidity

9. Traumatic SAH , high density blood (arrowheads) fills the sulci over the
right cerebral convexity in this subarachnoid hemorrhage

10. 3-Bleeding from vascular malformation :
-Cerebral or Spinal
-5 %
4-Extension From Parenchymal Hematoma :
-Often hypertensive bleed
-5 %

11. 5-Perimesencephalic Hemorrhage :
-Low pressure probable venous hemorrhage
-Few symptoms and signs
-Good prognosis
6-Miscellaneous :
-Anticoagulants & Vasculopathy

12. b) Distribution of SAH :
-The pattern of SAH may provide a clue to the location
of the ruptured aneurysm, however, multiple
aneurysms are seen in up to 20 % of patients with
SAH and subarachnoid blood may redistribute if the
patient was found down
1-Hemorrhage in the anterior interhemispheric fissure
suggests an ACOM aneurysm (33 % of intracranial
aneurysms)

13. Ruptured ACOM aneurysm , (a) NECT shows small amount of blood in the
anterior interhemispheric fissure and some sedimentation in the right
occipital horn , (b) CTA shows a small aneurysm of the ACOM

14. Ruptured ACOM aneurysm , (a) NECT shows nearly symmetric SAH & a small
interhemispheric or midline parenchymal hematoma (white arrow) , (b)
DSA confirms ACOM aneurysm (black arrow) suspected for rupture , small
MCA & ICA aneurysms were also detected (black arrow heads)

15. 2-Hemorrhage in the suprasellar cistern suggests a
PCOM aneurysm (also 33 % of intracranial
aneurysms)
3-Hemorrhage in the sylvian fissure suggests a MCA
aneurysm (20 % of intracranial aneurysms)
4-Perimesencephalic SAH :
*Suggests either a basilar tip aneurysm (5 % of
intracranial aneurysms) or the relatively benign non-
aneurysmal perimesencephalic SAH
*Perimesencephalic SAH is a type of nonaneurysmal
SAH that is a diagnosis of exclusion with a much
better prognosis than hemorrhage due to a ruptured
aneurysm

16. *The hemorrhage must be limited to the
cisterns directly anterior to the midbrain
*95% of cases have a normal cerebral
angiogram and the source of bleeding is not
identified, the cause is thought to be a venous
bleed, the other 5% of cases are due to
a vertebrobasilar aneurysm and the prognosis
is worse

17. Ruptured MCA aneurysm , (a) NECT shows SAH in the sylvian fissure (white
arrowhead & parenchymal hematoma (black arrowhead) , (b) CTA
confirms MCA aneurysm ((white arrow) , a 2
nd
unruptured MCA aneurysm
is present (open arrow)

18. Ruptured MCA aneurysm , (a,b) NECT at 2 locations , show asymmetric SAH &
focal hematoma , expanding the LT sylvian fissure

21. 1-Interhemispheric fissure
2-Suprasellar cistern
3-Sylvian fissure
4-Interpeduncular cistern
5-Ambient cistern
6-Quadrigeminal cistern

23. c) Grading of SAH :
-Hunt & Hiss Score is the clinical grading scale for aneurysmal
SAH and is based solely on symptoms , without imaging
Grade I : is the lowest grade with only mild headache
Grade IV : is the most severe with coma
-Fisher Grade classifies the CT appearance of SAH :
Grade 1 : negative on CT
Grade 2 : < 1 mm thick
Grade 3 : > 1 mm thick
Grade 4 : Diffuse SAH or intraventricular or parenchymal
extension

26. d) Complications of SAH :
1-Vasospasm :
-The most common cause of morbidity & mortality in
patients who survive the initial episode of SAH
-The peak incidence of vasospasm occurs
approximately 7 days after the initial ictus
-Vasospasm may lead to stroke or hemorrhage
-The medical treatment of vasospasm is triple-H
therapy of hypertension, hypervolemia &
hemodilution
-Endovascular treatment of vasospasm involves intra-
arterial infusion of vasodilators

27. Vasospasm , two coronal MIP from CTA , (a) shows severe narrowing of the
basilar artery , left AICA (RT not visible) and distal vertebral arteries , (b)
the follow up study was performed after endovascular treatment which
shows a normal caliber of the basilar & LT vertebral arteries

28. 2-Hydrocephalus :
-20-30 % of patients with SAH will develop acute
hydrocephalus due to obstruction of arachnoid
granulations, treatment is ventriculostomy
3-Superficial Siderosis :
-Is a condition caused by iron overload of pial
membrane due to chronic or repeated subarachnoid
bleeding
-On imaging, the iron causes hypointensity on T2
outlining the affected sulci

29. Superficial Siderosis , T2 show a thin hypointense interface at the junction of
the sulcal surfaces & the subarachnoid space (arrows) of the basal cisterns
(a) & the MCA territory temporal lobes (b)

30. e) Diagnosis & Investigation :
1-CT
2-Lumbar Puncture
3-MRI
4-Catheter Angiography

31. 1-CT :
-Most sensitive in first few days (98 % on day 1,
only 50 % positive by 7 days), CTA may be
performed
-Noncontrast CT is the initial imaging modality in
suspected SAH, on CT, subarachnoid blood
appears as high attenuation within the
subarachnoid space
-High attenuation material in the subarachnoid
space may be due to SAH (by fat the most
common cause), meningitis, leptomeningeal
carcinomatosis or prior intrathecal contrast
administration

34. 2-Lumbar Puncture :
-Negative CT scan doesn’t exclude SAH,
especially if scan performed days after ictus,
therefore lumbar puncture mandatory if CT
negative to look for Xanthochromia

35. 3-MRI :
-Late MRI more sensitive than CT
-Proton Density, Gradient Echo T2 and FLAIR sequences most
sensitive
-Acute SAH appears hyperintense on FLAIR & demonstrates
susceptibility artifact on gradient sequences
-D.D. for increased FLAIR signal in the subarachnoid space is
similar to the differential for high attenuation subarachnoid
material seen on CT including SAH, meningitis,
leptomeningeal carcinomatosis and residual contrast
material, note that meningitis & carcinomatosis will typically
show leptomeningeal enhancement in addition to the
abnormal FLAIR signal

36. 4-Catheter Angiography :
-Now used less often in initial work-up as CTA
often used at time of diagnosis of aneurysmal
SAH and for planning therapy
(neurointerventional versus surgical)

37. **N.B. Reversible Cerebral Vasoconstriction
Syndrome :
-The pathophysiology of RCVS is not well-understood
-Pregnancy, migraines, exposure to certain vasoactive
drugs (pseudoephedrine, selective serotonin
reuptake inhibitors, triptans, ergot derivatives and
cocaine) and trauma have been associated with this
condition
-Not to be confused with posterior reversible
encephalopathy syndrome (PRES)

38. -A thunderclap headache is the usual main
symptom, often occipital but also potentially diffuse,
there may be a history of recurrent thunderclap
headaches over days or weeks, headache may be
associated with photophobia, nausea and vomiting,
focal neurological deficits can occur secondary to
ischemia
-Radiographic Findings :
1-Angiography (CTA/MRA/DSA) demonstrated
multifocal narrowings in the circle of Willis branches
or arteries forming circle of Willis, post stenotic
segments show dilatation giving classical beaded
appearance/sausage shaped arteries

39. 2-No CT evidence of SAH (although recent
studies shown the association of SAH and
intraparenchymal hemorrhage with RCVS
more commonly SAH which is seen in about
11-25% of the cases, cortical SAH was the
most common pattern seen)
3-Confirmation of the diagnosis rests on
eventual resolution of angiographic findings
within 12 weeks

40. Marked narrowing of the basilar artery (measuring 1.1 mm in diameter) and
proximal PCAs with beaded irregular areas of narrowing and dilation in
the distal PCAs

41. (a) MRA showing segmental narrowings (arrows) of the middle and anterior
cerebral arteries , (b) DSA showing segmental narrowings of the branches
of the anterior cerebral artery (arrows)

42. FLAIR shows focal SAH blood in the precentral sulci and superior frontal sulci
(arrow) , the cisterns and sylvian fissures were free

43. (a) MRA at presentation shows segmental narrowing of the anterior , middle
(arrow) and posterior cerebral arteries bilaterally , (b) 3 months follow-up
angiogram shows resolution of arterial narrowing

44. -Differential Diagnosis :
1-The presence of SAH necessitates differentiating vasospasms secondary
to aneurysmal rupture from those secondary to RCVS
*In RCVS, at the time of presentation, the patient has the multifocal
vasospasms which are characteristic of the same, however, in cases of
aneurysmal rupture with SAH, there was delayed vasospasm in a time
setting of about 1-2 weeks after hemorrhage
*Ruptured aneurysmal SAH has various patterns depending on the region of
involvement :
a) ACOM aneurysm is suggested by blood in the cisterna lamina terminalis,
anterior pericallosal cistern and interhemispheric fissure
b) PCOM aneurysm : blood is usually seen diffusely within the cisterns
c) MCA aneurysm is characterized by blood in the sylvian fissure and a
hematoma in the temporal lobe which may rupture into the adjacent
temporal horn
d) Posterior fossa aneurysms mostly have no characteristic localizing findings
on CT
*In RCVS, the blood is found in the cortical sulci
*Vasospasms can also occur in correlation to a ruptured aneurysm, these
spasms are most commonly seen in the vessels closest to the site of
leakage

45. 2-Primary angitis of the CNS :
-Has no characteristic radiological findings, it can have
diffuse white matter lesions, multiple infarctions
involving multiple vascular territories and multiple
intraparenchymal hemorrhages
-The differentiation from RCVS is predominantly based
on the clinical presentation, Primary angitis of the
CNS tends to have a dull aching pain of insidious
onset and is progressive in nature, in RCVS there is a
sudden and severe onset of headache

46. Cerebral Cisterns & Subarachnoid Spaces
1-Premedullary cistern
2-Prepontine cistern
3-Cerebellopontine cistern
4-Cisterna magna
5-Superior cerebellar cistern
6-Interpeduncular cistern
7-Ambient cistern
8-Quadrigeminal cistern
9-Suprasellar cistern

47. sagittal T1
1-Premedullary
cistern
2-Pons
3-Medulla
4-Cerebellum

48. axial T1
1Premedullary
cistern
2-Medulla
3-Cerebellum

49. coronal T1
1-Basilar artery
in premedullary
cistern
2-Spinal cord
3-Hippocampus

50. sagittal T1
1-Prepontine
cistern
2-Pons
3-Medulla
4-Cerebellum
5-Splenium,
corpus callosum

51. axial T1
1-Basilar artery in
prepontine cistern
2-Pons
3-Cerebellum
4-Cranial nerve V

52. coronal T1
1-Basilar artery
in prepontine
cistern
2-Hippocampus
3-Lentiform
nucleus

53. axial cut
(magnification) T2-
1-Cerebellopontine
cistern
2-Pons
3-Internal acoustic
meatus
4-Fourth ventricle
5-Cerebellar
hemisphere

54. coronal cut
(magnification) T2
1-Cerebellopontine
cistern
2-Temporal lobe
(right side)
3-Pons
4-Hippocampus
5-Internal acoustic
meatus

55. sagittal T1
1-Cisterna
magna
2-Medulla
3-Pons
4-Midbrain
5-Cerebellum

56. axial T1
1-Cisterna
magna
2-Cerebellum
3-Medulla

57. coronal T1
1-Cisterna
magna
2-Cerebellum
3-Corpus
callosum

58. sagittal T1
1-Superior
cerebellar cistern
2-Tentorium
cerebelli
3-Cerebellum
4-Pons
5-Midbrain

59. axial T1
1-Superior
cerebellar
cistern
2-Cerebral
aqueduct

60. coronal T1
1-Superior
cerebellar cistern
2-Lateral ventricle
3-Cerebellar
hemisphere
4-Tentorium
cerebelli

61. sagittal T1
1-Interpeduncular
cistern
2-Midbrain
3-Pons
4-Medulla
5-Fourth ventricle
6-Cerebellum
7-Third ventricle
8-Corpus callosum

62. Axial T1
1-Interpeduncular
cistern
2-Cerebral
aqueduct
3-Hippocampus

63. coronal T1
1-Interpeduncular
cistern
2-Hippocampus
3-Third ventricle
4-Lateral ventricle

64. sagittal T1
1-Ambient
cistern
2-Splenium,
corpus callosum
3-Cerebellum
4-Pons

65. coronal T1
1-Ambient
cistern
2-Cerebral
aqueduct
3-Lateral
ventricle

66. axial T1
1-Ambient
cistern
2-Lateral
ventricle
3-Fourth
ventricle
4-Cerebellar
hemisphere

67. sagittal T1
1-Quadrigeminal
cistern
2-Midbrain
3-Pons
4-Medulla
5-Cerebellum

68. axial T1
1Quadrigeminal
cistern
2-Cerebral
aqueduct
3-Optic chiasm

69. coronal T1
1-Quadrigeminal
cistern
2-Lateral ventricle
3-Fourth ventricle
4-Cerebellar
hemisphere

70. sagittal T1
1-Suprasellar
cistern
2-Pituitary gland
3-Pons
4-Third ventricle
5-Corpus
callosum

71. axial T1
1-Suprasellar
cistern
2-Pituitary stalk
3-Cerebral
aqueduct
4-Hippocampus

72. coronal T1
1-Suprasellar
cistern
2-Anterior
cerebral artery
3-Lateral
ventricle
4-Caudate
nucleus