1. Imaging of INTRACRANIAL HEMORRHAGE
Sattam S. Lingawi MD, FRCPC, ABR
Assistant Professor of Radiology – King Abdulaziz University
President of Radiological Society of Saudi Arabia

2. Acute hemorrhage
A NECT should be done when there is a question of acute hemorrhage.

3. Acute hemorrhage
There is linear relation between CT attenuation & hematocrit ,hemoglobin concentration.
Retracted clot has a high globin content, hence its hyperdensity compared to normal brain

4. Subacute hemorrhage
The attenuation of uncomplicated ICH decrease with time at an average of 1.5 HU/day.
Between 1-6 weeks subacute ICH becomes
isodense with adjacent brain
may show peripheral enhancement.
MR is much more sensitive for evaluation of subacute & chronic hemorrhage.

5. Axial CT scan with intravenous contrast infusion, obtained at the same level as Picture 6, demonstrates the right isodense subdural hematoma (red arrow), enhancing veins (green arrow), and enhancement of the membrane (blue arrow).
Inward buckling indicate extraaxial mass effect

6. Chronic hemorrhage
Chronic hemorrhage
Unless re-bleeding has occurred ,chronic hematomas are hypodense copmared to adjacent brain
Rim enhancement of resolving hematoma (target sign) can be seen if re-bleeding takes place within an organizing hematoma.

7. Pitfalls
Thin linear clot near the skull base or calvarial bones are difficult to detect.
Window width between HU may be helpful in separating them from adjacent bony structures.

8. Pitfalls
Occasionally acute cerebral hematoma appears isodense with adjacent brain due to:
Sever anemia (Hb < 8g/dL)
Coagulation disorders
Thrombolytic therapy
Fluid-fluid level can occur in 50% of these clots.

9. Axial CT scan above the lateral ventricles shows extra-axial material (arrow) of approximately the same density as brain parenchyma, displacing the grey-white matter interface internally. Mild midline shift is seen.
Hyperdense Hypodense

10. Hematoma w fluid level
Fluid-Fluid level

11. Evolution of hemorrhage by MRI
The sequential oxidation products of hemoglobin affects the relaxation time of T1 & T2 due to changes in magnetic properties (magnetic susceptibility).

12. Evolution of hemorrhage by MRI
Time (Days)
RBC
Hb state T1 T2
Few hrs.
intact
Oxy Hb
Iso/dark
bright
Up to 2 days
Deoxy Hb
Dark
2-14
IC Met Hb
Bright
10-21
Lysed
EC Met Hb
>21
Hemosiderin
dark

13. Evolution of hemorrhage by MRI
Oxy Hg.
Deoxy Hg.
I.C Hg.
E.C Hg.
Hemosiderin
T 1
- / 0 1
T 2

14. Evolution of hemorrhage by MRI
I.C Hemoglobin

15. Evolution of hemorrhage by MRI
E.C Methemoglobin

16. CLASSIFICATION
Intra-axial hemorrhage
Extra-axial hemorrhage

17. Intra-axial hemorrhage

18. Intra-axial hemorrhage
Hypertensive hemorrhage is seen in:
putamen 35-50%
Subcortical white matter 30%
Cerebellum15%
Thalamus 10-15%
Pons 5-10%
Amyloid angiopathy.
Vascular malformation :
AVM
cavernous malformation,
Telangiectasias
venous malformations.

19. 59-year-old female with hypertension who presented with left-sided weakness demonstrated a right putaminal hemorrhage on noncontrast CT examination of the head. Tiny hyperdense foci in the basal ganglia and pineal gland represent calcifications.

20. 62-year-old female with hypertension presented with acute-onset ataxia and confusion. Noncontrast CT examination of the head showed a large right cerebellar hemorrhage, which was evacuated to relieve the mass effect on the brainstem and fourth ventricle.

21. Amyloid angiopathy: parenchymal hemorrhage is of lobar nature.
It is not associated with systemic vascular amyloidosis.
Affects elderly individuals.
Associated infarcts & hemorrhage.

23. T2-weighted MRI through the thalami of a hypertensive patient demonstrates two small areas of decreased signal in the right thalamus, representing hemorrhagic lacunes.
T2-weighted gradient-echo MRI through the thalami demonstrates multiple, bilateral foci of signal loss, correlating with expected locations of hypertensive petechial hemorrhages that were not seen on regular T2-weighted images (
T2 FSE T2 GRE

24. Intra-axial hemorrhage
Named after its anatomic location.
Etiology:
HTN
Anticoagulation
Amyloid Angiopathy
Vasculitis
Medical not Surgical.

25. Intra-axial hemorrhage
Putamenal Pontine Parenchymal

26. Intra-axial hemorrhage
I.V Extension Mass effect

27. Hemorrhagic Transformation

28. Infarction

29. Arteriovenous malformation:
80-90 are seen supratentorial.
AVM have 2-3 annual risk of bleeding.
Angiography is the definitive method of evaluation for an AVM anatomy.
NECT will show a mixed attenuation lesion.
MR will show an AVM as a tangle of enlarged vessels without mass effect.
Contrast will increase conspicuity of the AVM

30. Cerebral angiogram, lateral projection, of a right internal carotid artery injection demonstrates a right frontoparietal arteriovenous malformation (AVM), with prominent early draining veins (arrow) extending cephalad to the superior sagittal sinus from the AVM nidus. (The patient is facing to the left.)

31. Cavernous malformations:
Thin walled sinusoidal vessels, not seen on Angiogram.
MR will show a reticulated enhancing lesion.

32. Multiple cavernous hemngioma
Multiple cavernous hemngioma.chronic hematoma surrounded by rim of hemosidren containing macrophages.

33. Venous malformation (venous angiomas) seen in 1-2 % of patient studiedby contrast MR ,seen as an enhancing stellate lesion extending to the ventricle or cortex.

34. Extra-axial hemorrhage

35. Extra-axial hemorrhage
Relationship to Meningeal reflection.
Epi-dural (Extra-dural)
Sub-dural
Sub-arachnoid
Etiology:
Trauma
Aneurysm
Surgical not medical.

36. Epidural (Extra-axial hemorrhage)

37. Epidural (Extra-axial hemorrhage)
Hyperacute – Swirl Sign

38. Epidural (Extra-axial hemorrhage)
Venous Hemorrhage

39. Subdural (Extra-axial hemorrhage)
Acute

40. Subdural (Extra-axial hemorrhage)
Subacute
Iso-dense C+

41. Subdural (Extra-axial hemorrhage)
Acute on Chronic

44. Subdural (Extra-axial hemorrhage)

45. Subdural (Extra-axial hemorrhage)

48. Subarachnoid hemorrhage
SAH is most commonly the result of:
aneurysm rupture %
AVM malformation %
Trauma, dissection
Drug abuse
Coagulopathies.
Congenital berry aneurysm (1-2%)
Risk increases with smoking and positive FH.

49. Approximately 15-20 % of patient with SAH will have multiple aneurysm
CT sensitivity:
> 95% for detection of acute SAH
Drops to 66% after 3 days.
50% by the end of 1st wk.
Approximately % of patient with SAH will have multiple aneurysm
Detailed selective 4 vessels angiogram is needed on initial evaluation.
The combination of MRI & MRA will detect the vast majority of aneurysm greater > 3 mm.

50. Detailed selective 4 vessels angiogram is needed on initial evaluation.
Negative angio 15% of SAH
Repeat is positive in 5%

51. MR in SAH T1: T2: FLAIR: GRE:
The combination of MRI & MRA will detect the vast majority of aneurysm greater > 3 mm.

58. Ant comm A aneurysm w Hge

59. Ant comm A aneurysm w Hge
Interventricular Hge & hydrocephalus

61. Aneurysm
Basilar tip aneurysm

62. Aneurysm

63. Aneurysm

64. A. COM

68. Subarachnoid (Extra-axial hemorrhage)

71. A. Com

73. P.Com Aneurysm

74. PICA Aneurysm

79. Non-Aneurysmal Hg Perimesencephalic non-aneurysmal SAH.
Benign clinical entity with SAH.
Hydrocephalus and vasospasm are very rare.
Recurrence < 1%.
Blood location:
perimesencephalic and prepontine cisterns.
Blood does not extend to Sylvian fissure.
Angiogram:
Negative(90-95%).
Vertebrobasilar aneurysm (5-10%)

80. Non-Aneurysmal Hg

81. Non-Aneurysmal Hg

82. Non-Aneurysmal SAH

83. Hunt & Hess Classification
Grade
Description
% Vasospasm
Un-ruptured Aneurysm O% 1
Asymptomatic or mild H/A & slight nuchal rigidity
22% 2
Cr. N Palsy (e.g. III, VI) moderate to severe H/A, nuchal rigidity.
33% 3
Mild focal deficit, lethargy, or confusion.
52% 4
Stupor, moderate to severe hemiparesis, early decerebrate rigidity
53% 5
Deep coma, decerebrate rigidity, moribund appearance
74%

84. Fisher Grading Group Blood in CT % Vasospasm 1 2 3 4 NO blood detected2
Diffuse layer < 1mm 3
Focal or Diffuse layer > 1mm 23 4
Intraventricular / intracerebral

88. 50% Mortality
15% re-bleed within the first 24 hours
Vasospasm: 3-10 days (70-90% patients)

97. AVM

99. AVM

100. Speitz-Martin Grading system1 2 3
Size
<3
3-6
>6
Location NE E
Drainage
Superficial
Deep

102. Cavernous Angioma (Cavernoma)
Pathology:
Discrete multiloculated lesions formed of dilated endothelial spaces.
Multiple stages of hemorrhage.

103. Cavernous Angioma (Cavernoma)
Location:
80% are supratentorial (esp. frontal and temporal).
Spinal cord involvement is rare.
Extra-axial & intraventricular locations are rare.

104. Cavernous Angioma (Cavernoma)
Incidence:
The most common vascular anomaly (0.4%).
50% - 80% are multiple.
Age:
20-40 yrs.
Symptoms:
Seizure, Neuro. Deficit, H/A.
Hemorrhage:
1% per yr.
Previous large hg. & post. Fossa location

105. Cavernous Angioma (Cavernoma)
Angiographically occult.
CT:
Iso or hyperdense with Ca++.
No enhancement.
MRI: (GRE > T2 > T1)
Well defined mass of multiple intensities.
High signal core and low signal rim “popcorn”.
Presence of surrounding edema = recent hg.

107. Carotid Dissection

108. ICA DISSECTION

109. Dural Sinus Thrombosis
Incidence: Unknown
Uncommon cause of stroke, requires a high index of clinical suspicion to diagnose.
Sex: Female > Males
venous : Arterial 1 : 62.5

110. Dural Sinus Thrombosis Etiology
Unknown
Infection
Coagulopathies
Behcet;’s disease
SLE
Tumors

111. Dural Sinus Thrombosis Clinical presentation
Headache 75 %
Papillodema 49 %
Focal deficit 34 %
Cranial palsy 12%
LOC , Coma 30 %
Seizures 37 %
Meningeal sings 0 %
Amnestic syndrome 12 %

112. N
MILD
MODERATE
SEVER

113. Dural Sinus Thrombosis Diagnosis
Clinical Presentation.
Radiological Findings.

114. Dural Sinus Thrombosis
NECT:
Dense Sinus
Cord sign
Venous infarction
& Hemorrhage

115. Dural Sinus Thrombosis
CECT:
Empty Delta sign.
Dural Sinus Filling Defect

116. Dural Sinus Thrombosis
MRI:
Dense Sinus
Cord sign
Venous infarction
Filling Defect

117. Dural Sinus Thrombosis

118. Dural Sinus Thrombosis

119. Dural Sinus –NORMAL MRV

120. Dural Sinus Thrombosis