Neuroimaging is the use of various techniques to either directly or indirectly image the structure, function of the nervous system.  Neuroimaging plays a pivotal role in the diagnosis of central nervous system (CNS) disorders.  Main modalities of neuroimaging techniques are CT scan and MRI.

1. Workshop on Neuroimaging
Dr. Aminur Rahman
FCPS (Med), MD(Neuro) ,FINR (Switzerland),
Member ACP (USA), Member AAN(USA),
Fellow Interventional Neuroradiology (Thailand)
Assistant Professor
Department of Neurology
Sir Salimullah Medical College

2. Medicine is learned by bedside and
not in the classroom.
Sir William Osler (1849-1919)

3. Scheme of the Workshop
• Introduction
• Basic principles of CT scan
• Illustrations of CT scan in stroke
• Illustrations of MRI brain in stroke

4. Introduction
• Neuroimaging is the use of various techniques to
either directly or indirectly image the structure,
function of the nervous system.

5. Introduction
• Neuroimaging plays a pivotal role in the
diagnosis of central nervous system (CNS)
disorders.
• Main modalities of neuroimaging techniques
are CT scan and MRI.

6. Introduction..
• CT remains useful because of short imaging
times, widespread availability, ease of access,
sensitive detection of calcification and
hemorrhage, and resolution of bony detail.

7. Introduction..
• MRI offers superior soft-tissue contrast,
excellent visualization of vascular structures,
fewer artifacts, and imaging in any plane.

8. Brief History of Neuroimaging

9. History
• Sir Godfrey Hounsfield , engineer who invented
computed tomography in 1972 and won the
Nobel prize for medicine in 1979.
• Original scanners took approximately 6 minutes
to perform a rotation (one slice) and 20 minutes
to reconstruct.

10. History…..
• Rabi et al 1st observed NMR phenomenon in
1939.
• Bloch detected strong proton signal from H in
1946 and later on won Nobel prize in early 50s.
• Jasper Jakson produced 1st MR signal from a
live animal in 1967.
• Lauterbur in 1974 produced 1st image of live
animal by adding magnetic gradient. He won
the noble prize for physics in the year 2003.

11. Basic principles of CT imaging
• Uses X rays applied in
sequence of slices
across the organ
• Images reconstructed
from X ray absorption
data
• X ray beam moves
around the patient in
a circular path
Figure: Modern helical CT scanning technique
comprising a rotating x-ray tube and a fixed
array of detectors

12. Basic principles of CT imaging…
• CT scan provides a 3D display of the
intracranial anatomy built up from a vertical
series of transverse axial tomograms.
• Using computer processing, slice thickness
(typically ranging from 3-5 mm for routine
scanning) can be varied according to the level
of details that is required for image
interpretation.

13. Attenuation Coefficient
• The tissue contained within each image unit
(called a pixel) absorbs a certain proportion of
the x-rays that pass through it (e.g., bone
absorbs a lot, air almost none). The ability to
block x-rays as they pass through a substance
is known as Attenuation.

14. Attenuation Coefficient ..
• In CT, these attenuation coefficients are
mapped to an arbitrary scale of between
−1000 Hounsfield units (HU) (air) and
+1000 HU (bone).

15. Appearance and Density of Tissues on CT Head
Appearance:
Black → → → → → → → → → → White
−1000 HU → → → → → → → → +1000 HU
Air, fat, CSF, white matter, gray matter, acute hemorrhage, bone
Important Densities:
Air = −1000 HU
Water = 0 HU
Bone = +1000 HU
CSF, Cerebrospinal fluid; HU, Hounsfield units.

16. Figure : Hounsfield scale ranging from -1000 to + 1000

17. CT scan of Head is expressed in terms of density
 X-rays are absorbed to different degrees by
different tissues
 Brain parenchyma is the reference density
A. Isodense: For CT head, normal brain parenchyma is
isodense.
B. Hypodense: Darker than normal brain parenchyma.
C. Hyperdense: Whiter / Higher density than normal
brain parenchyma.

18. Densities in CT Scan

19. Slice thickness may vary, but
in general, it is between 3
and 5mm for a routine Head
CT
Technique…..

20. Slice thickness is between 3 and 5 mm for a routine head CT

21. Sections of CT Scan of Brain
•Axial sections are most important in a head CT

22. Abnormalities in CT Scan Head
Common abnormalities (95%) Uncommon abnormalities(5%)
1. Infarct :
a. Cortical
b. Sub-cortical
c. Cerebellar
d. Brainstem
2. Haemorrhage,
3. Space occupied lesion
(SOL)
1. Hydrocephalus:
a. Obstructive.
b. Non obstructive.
2. Diffuse brain oedema.
3. Abnormal calcification.

23. Hypodense (black) lesions Hyperdense (white) Lesions
1. Air, e.g., In nasal cavity,
paranasal sinuses
1. Bones
2. Fluid, except blood, e.g.,
CSF, water.
2. Acute haemorrhage:
Blood pigments ( bilirubin,
biliverdin) are radio-opaque.
3. Infarct. 3. Calcification
4. ISOL. 4. Contrast material.
5. Old haemorrhage (>2-3
weeks).
Lesions seen in CT Scan Head

24. Hyperdense (white) Lesions in Brain
A. Bones
B. Calcification
C. Acute haemorrhage: Blood pigments
( bilirubin, biliverdin) are radio-opaque
D. Contrast material

25. Physiological calcifications
1. Falx cerebri
2. Choroid plexus ( suspended in the post.
horns of lateral ventricle)
3. Pineal gland (in third ventricle)
4. Basal ganglia ( speckle calcifications)

26. Physiological calcifications

27. Bilateral basal ganglia
calcification in Fahr’s
disease
Pathological calcifications

28. Sub-ependymal
calcifications in
Tuberous Sclerosis

29. Non contrast axial CT scan of the head showing Gyriform
cortical calcifications with ipsilateral atrophy and enlarged
choroid plexus - Sturge-Weber syndrome

30. Illustrations of CT scan in stroke

31. Acute haemorrhage stroke/ Haematoma
(Hypertensive )

32. • The most common etiology of primary hemorrhagic
stroke (intracerebral hemorrhage) is hypertension,
with at least two thirds of patients with primary
intraparenchymal hemorrhage due to preexisting or
newly diagnosed hypertension.
• Non-contrast CT (NCCT) remains the gold standard
means of detecting intracranial haemorrhage in acute
stroke.
Acute haemorrhage stroke/ Haematoma
(Hypertensive )

33. Left parieto-temporal
(putamen) region
sided ICH with
minimal midline shift

34. Right fronto-parieto-temporal
region (Ganglio-thalamic
region), sided ICH with
ventricular extension

35. Brain stem (pons)
haemorrhage with
hydrocephalus

36. Left sided Cerebellar
Hemorrhage

37. Fig: Common sites of hypertensive intracerebral hemorrhages

38. Resolving haematoma
2 days 2 weeks 2 months

39. Resolving haematoma
Haematoma in left Ganglio-
thalamic region with ventricular
extension
Resolved haematoma with
formation of Encephalomalatia /
Porencephalic cavity.

40. Various stages of haemorrhagic stroke

41. Amount of blood in ml = ½ (Total number of Haemorrhagic slide
– 1) X ( Height X breath in cm of largest haemorrhage)
How to measure the amount of haemorrhage in CT scan

42. Others causes of Haematoma

43. Primary intraventricular
haemorrhage with
secondary SAH.

44. Cortical ICH in left
parietal lobe due to
Intracerebral AVM

45. Intracerebral Arterio-venous malformation
IV contrast CT scan of the
head showing prominent
abnormal vessels in left
parietal lobe- Intracerebral
Arterio-venous
malformation

46. Cortical Haemorrhage in
vasculitis with perilesional
oedema
D/D:
1. AVM
2.Venous stroke
3.Drugs- thrombolytic, Warin

47. Left sided Cortical
haemorrhage in parietal
lobe with generalized
cerebral oedema.
D/D:
1. AVM,
2. Vasculitis

48. 4th ventricular haemorrhage
with hydrocephalus

49. 3rd ventricular haemorrhage

50. Fig: non contrast Axial CT scan of head
Left Ganglio-thalamic
region ICH with a fluid
level., most probably
resolving due to: H/O taking
Clopidogrel for IHD.

51. Multiple irregular
hyperdense shadow on the
brain stem and cerebellum.
Due to Aspirin induce
haemorrhage in brain stem
and cerebellum

52. Multiple intra-cerebral
haemorrhage.
This is a ct scan of a 50
yrs old lady of breast
cancer with multiple
brain metastasis.

53. Rt. ICH with ventricular
extension with Infarct in
Rt. MCA territory.
( This infarct form due to
reflex vascular spasm after
ventricular).

54. Haemorrhagic transformation
of Lt. MCA territory infarct

55. Haemorrhagic transformation
of Infarct in Rt. MCA territory
due to Reperfusion injury

56. The most common cause of atraumatic
hemorrhage into the subarachnoid space is
rupture of an intracranial aneurysm.
Sensitivity of ct scans for detecting subarachnoid
blood ranges from 90% to 100% when performed
within the first 24 hours after symptom onset.
Subarachnoid haemorrhage (SAH)

57. Subarachnoid haemorrhage
(SAH) with hydrocephalus
probably rupture left MCA
aneurysm.

58. Sub arachnoids
haemorrhage with
hydrocephalus. Most
probably rupture
ACOM artery
aneurysm.

59. SAH
ACOM aneurism rupture MCA aneurism rupture (left)

60. Hypodense lesion in brain
Causes:
1. Infarct
2. SOL
3. Oedema

61. Acute Ischaemic stroke in CT scan

62.  The overall sensitivity of CT to diagnose
stroke is 64% and the specificity is 85%.
Role of CT in acute ischemic stroke

63. Role of CT in acute ischemic stroke
A. To Rule out bleed: Non contrast CT is sufficient
to rule out most important infarct mimic that is
bleed which is an absolute contraindication for
thrombolytic therapy.
B. Can detect early stage acute ischemia : by
depicting features such as the
1) Hyper dense vessel sign,
2) Insular ribbon sign and
3) Reduced parenchymal attenuation with
effacement of cortical sulci.

64. Time course of ischemic stroke on NECT
Shows the early CT sign (<6h)
of ischemic stroke with
hyperdensity of MCA
representing an acute
embolus lodged into left MCA
known as “hyperdense MCA
sign”.
Immediate(< 6 hours):

65. Shows the early CT sign (<6h) of
ischemic stroke with “loss of gray-
white matter differentiation” in
basal ganglia.
Immediate(< 6 hours):

66. Early hyperacute: ˃3–12 hours
Diffuse cerebral swelling
with loss of cortical sulci
and compression of
ventricular system (right).

67. The hypodensity of
insular cortex known as
“insular ribbon sign”.
Early hyperacute : ˃3–12 hours

68. 1. No bleed.
2. Faint low attenuation involving right insular cortex and adjacent basal
ganglia - 'insular ribbon' sign.
3. Effacement of right hemispheric cortical sulci.
1 2 3

69. Acute: 12 hours -7 days
Large areas of
hypodensity within the
left and (Left) middle
cerebral artery vascular
territories, due to
cytotoxic oedema.

70. Subacute:2 -4 weeks
Shows the “fogging
effect” occurs during
subacute phase. Left CT
image is obtained at
36hrs with bilateral
occipital hypodensities.
Right image is taken at
18 days showing the
isodense appearance of
previous infarct.

71. Chronic: ≥6 weeks– months
Shows the
encephalomalacic
changes in right
fronto-parietal
region

72. Alberta stroke program early CT score
(ASPECTS)

73. Alberta stroke program early CT score (ASPECTS):
• Segmental assessment of the MCA vascular territory is made
and 1 point is deducted from the initial score of 10 for every
region involved:
Caudate
Putamen
Internal capsule
Insular cortex
M1: "anterior MCA cortex," corresponding to frontal operculum
M2: "MCA cortex lateral to insular ribbon" corresponding to
anterior temporal lobe
M3: "posterior MCA cortex" corresponding to posterior
temporal lobe
M4: "anterior MCA territory immediately superior to M1"
M5: "lateral MCA territory immediately superior to M2"
M6: "posterior MCA territory immediately superior to M3

74. Clinical use
• An ASPECTS score less than or equal to 7 predicts a
worse functional outcome at 3 months as well as
symptomatic haemorrhage.
• According to the study performed by R. I. Aviv et al.,
patients with ASPECTS score less than 8 treated with
thrombolysis did not have a good clinical outcome.

75. Cerebral infraction according to vascular territory

76. Shows multiple small
hypodense shadows in
bilateral thalamoganglionic
regions - bilateral lacunar
infarcts.

77. Porencephalic cyst/cavity
after stroke.

78. Bilateral infarct in
hypoxic ischaemic
encephalopathy

79. Recent / New infarct
1. Hypodense.
2. Larger.
3. Ventricles- pressure
effect.
4. Sulcus obliterated in same
side.
Old infarct
1. More hypodense
2. Smaller – due to gliosis in
surrounding area.
3. Ventricles- no pressure
effect but may be enlarged.
4. Sulcus prominent.
Age determination of infarction in CT

80. Illustrations of MRI brain in stroke

81. Imaging of stroke in MRI
• More sensitive in early detection of acute
ischaemic stroke .
• Can detect acute infarct within 30 mints

82. • Once bleed is ruled on CT.
• MRI is to confirm an infarct with better
evaluation.

83. Role of Diffusion-Weighted Imaging(DWI)
• Acute stroke causes excess intracellular water
accumulation or “cytotoxic oedema”, with an
overall decreased rate of water molecular diffusion
within the affected tissue.
• Areas of cytotoxic oedema (restricted motion of
water molecules) appear bright on DWI
As early as 30 minutes after onset of ischemia
High signal up to 5 days
Mildly increased signal 1-4 wks

84. Role of DWI….
• Mild hyperintense DWI with pseudonormal ADC
from 1 -4wks .
• After several wks DWI signal varies (T2 effect)
with increased ADC .
• DWI alone cannot be used and should always be
compared with ADC to assess the age of infarct.

85. Accuracy of diagnosis ischaemic stroke in DWI
CT/ conventional MRI:
• Sensitivity and specificity < 50%
DWI:
• Sensitivity 88-100%
• Specificity 86-100%
False -ve DWI:
• Lacunar infarcts of brain stem
• Small deep grey matter infarcts
False +ve DWI:
• Abscess
• Cellular tumours like lymphoma

86. Role of Apparent Diffusion Coefficient maps
(ADC Map)
• Decreased from 30 minutes after onset to 5
days.
• Then increases and reaches normal in 1-4
weeks.
• Likely due to development of vasogenic
oedema with cytotoxic oedema.

87. Role of FLAIR
• Sensitivity to pick an infarct is arbitrarily
comparable to CT.
• If an infarct seen on diffusion and not seen FLAIR
called FLAIR / Diffusion Mismatch indicate hyper
acute infarct - reversible ischemic changes and
salvageable tissue or tissue at risk.
• If changes are marked on FLAIR indicate already
infracted and non salvageable tissue.

88. Early hyper acute (2 to 4 hours)
• Within minutes of arterial occlusion
demonstrates
• Increased DWI signal (hyper intense) and
• Reduced ADC values (hypo intense).
• At this stage, the affected parenchyma
appears normal on other sequences.
A.Prof Frank Gaillard et al.

89. Early hyper acute (2 to 4 hours)
DWI= Hyperintense
ADC= Isointense
FLAIR= Isointense

91. Late hyper acute (≥ 6 hours-16 hrs)
• Generally, after 6 hours, hyper intense T2
signal will be detected, initially more easily
seen on FLAIR than conventional Fast Spin
Echo T2.
• This change continues to increase over the
next day or second day.
• T1 hypo intensity is only seen after 16
hours and persists.
A.Prof Frank Gaillard et al.

92. DWI= Hyperintense
ADC=Hypointense
FLAIR= Hyperintense
T2= Isointense Late hyper acute (≥ 6 hours-16 hrs)

94. Acute (≤ first week)
• During the first week, the infarcted parenchyma continues to
demonstrate
– high DWI signal and low ADC signal, although by the end of
the first week ADC values have started to increase.
• As early as 3 days demonstrate
– T1 signal remains low, although some cortical intrinsic high
T1 signal may be seen after infarction.
• During the first 4 days
– The infarct remains hyper intense on T2 and FLAIR, with T2
signal progressively increasing during the first 4 days.
• After day 5 the cortex usually demonstrates contrast
enhancement on T1 C+ 1.
A.Prof Frank Gaillard et al.

95. Acute Ischaemic stroke (≤ first week)
DWI= Hyperintense
FLAIR= Hyperintense
T2= Hyperintense
T1= Hypointense

96. Acute lacunar infarct in the left thalamus
DWI= Hyperintense
FLAIR= Hyperintense
T2= Hyperintense
T1= Hypointense
Francois Moreau.
DOI: (10.1161/STROKEAHA.111.647859)

97. Sub acute(between ≥1-2 weeks)
• ADC demonstrates pseudonormalisation typically
occurring between 8-14 days. As ADC values
continue to rise, infarcted tissue progressively
gets brighter than normal parenchyma.
• In contrast, DWI remains elevated due to
persistent high T2/FLAIR signal (T2 shine
through) .
• T2 fogging is also encountered typically between
1 and 5 weeks, most commonly around week 2.
A.Prof Frank Gaillard et al.

98. Sub acute(between ≥1-2 weeks)….
• T1 weighted sequences continue to show hypointensity
with cortical intrinsic high T1 signal due to cortical
laminar necrosis or pseudolaminar necrosis.
• Cortical enhancement is usually present throughout
the subacute period.
• In cases of true restricted diffusion, the region of
increased DWI signal will demonstrate low signal on
ADC.
• In contrast, in cases of T2 shine-through, the ADC will
be normal or high signal.
A.Prof Frank Gaillard et al.

99. Sub acute(between ≥1-2 weeks)….

100. Sub acute(between ≥1-2 weeks)….

101. Chronic ≥ 4 wk
• T1 signal remains low with intrinsic high T1 in the
cortex if cortical necrosis is present.
• T2 signal is high. Cortical contrast enhancement
usually persists for 2 to 4 months.
• Importantly if parenchymal enhancement persists
for more than 12 week the presence of an
underlying lesion should be considered.
• ADC values are high, resulting in high signal.
• DWI signal is variable, but as time goes on signal
progressively decreases.
A.Prof Frank Gaillard et al.

102. Chronic ≥ 4 wk
DWI= Hypointense
FLAIR= Hyperintense
T2= Hyperintense
T1= Hypointense
Laura M. Allen et. al

103. Chronic: DWI- Hypointensity ,
ADC- hyperintensity
DWI ADC

104. Distinguish between new vs old
ischaemic stroke
• New / acute infraction : Bright on DWI
• Old / chronic infraction ( encephalomalacia):
low signal intensity in DWI

106. Comparison of the findings on T2WI with DWI
and ADC in time to evaluate of Ischaemic stroke

107. Temporal changes on time in ischemia on
FLAIR) and DWI and ADC map

108. Acute ischaemic stroke and DWI –
sequential changes with time

109. MRI Evaluation of Intracranial Hemorrhage

110. Goals of MRI in the Evaluation of ICH
• To recognize the presence of blood
• To localize and differentiate hemorrhages (intra-axial
versus extra-axial):
– if intra-axial, to locate the specific neuroanatomical
localization (stroke).
– if extra-axial, to differentiate subarachnoid hemorrhage
(SAH), subdural hematoma (SDH), and epidural
hematoma (EDH);
• To determine the age of the hemorrhage.
• To identify the etiology.
• To aid in managing the bleed and in ascertaining the
patient's prognosis.

111. Gradient-echo (GRE)
• GRE is T2* - based sequence, which is
extremely sensitive to local magnetic field
inhomogeneity and is especially useful for
detection of microhemorrhages, which may
be undetectable by other sequences.
• Microbleeds are usually defined as cerebral
bleeds less than 5-10 mm in size

112. Table: MRI Evaluation of Intracranial Hemorrhage
Stages Time T1 T2 FLAIR T2 GRE DWI
Hyper
acute
<24hours Isointense Hyperintense Hyperintense Variable Hyperintense
Acute ˃24 hr- <1week Isointense/
Hypointense
Hypointense Hypointense Hypointense Hypointense
Early
Subacute
˃1 wk- 2week Hyperintense Hypointense /
Isointense
Hypointense
/ Isointense
Hypointense /
Isointense
Hypointense
Late
Subacute
>2wk-4 week Hyperintense Hyperintense Hyperintense Hyperintense Hyperintense
Chronic ˃4week Isointense/
Hypointense
Hyperintense/
Isointense
Variable Isointense/
hyperintense
Variable
Jitendra L Ashtekar et al.

113. Mnemonic to help recall the signal changes at stages hemorrhage.

114. Hyperacute hematoma <24 hour
Stages Time T1 T2 FLAIR T2 GRE DWI
Hyper acute <24hours Isointense Hyperintense Hyperintense Variable Hyperintense
TIW T2W GRE
Jitendra L Ashtekar et al.

115. Hyperacute hematoma <24 hour
Stages Time T1 T2 FLAIR T2 GRE DWI
Hyper acute <24hours Isointense Hyperintense Hyperintense Variable Hyperintense

116. Acute hematoma ˃24 hr- < 1week
Stages Time T1 T2 FLAIR T2 GRE DWI
Acute ˃24 hr- <1week Isointense
/hypointense
Hypointense Hypointense Hypointense Hypointense

117. Acute hematoma ˃24 hr- < 1week
Stages Time T1 T2 FLAIR T2 GRE DWI
Acute ˃24 hr- <1week Isointense Hypointense Hypointense Hypointense Hypointense

118. Early subacute hematoma ˃1 wk- 2week
Stages Time T1 T2 FLAIR T2 GRE DWI
Early
Subacute
˃1 wk- 2week Hyperintense Hypointense /
Isointense
Hypointense
/ Isointense
Hypointense /
Isointense
Hypointense
TIW T2W GRE
Jitendra L Ashtekar et al.

119. Early subacute hematoma ˃1 wk- 2week
Stages Time T1 T2 FLAIR T2 GRE DWI
Early
Subacute
˃1 wk- 2week Hyperintense Hypointense /
Isointense
Hypointense
/ Isointense
Hypointense /
Isointense
Hypointense

120. Late subacute hemorrhage >2week-4 week
Stages Time T1 T2 FLAIR T2 GRE DWI
Late
Subacute
>2wk-4 week Hyperintense Hyperintense Hyperintense Hyperintense Hyperintense
TIW T2W GRE
Jitendra L Ashtekar et al.

121. Late subacute hemorrhage >2week-4 week
Stages Time T1 T2 FLAIR T2 GRE DWI
Late
Subacute
>2wk-4 week Hyperintense Hyperintense Hyperintense Hyperintense Hyperintense

122. Late subacute to chronic hematoma ˃4week
Stages Time T1 T2 FLAIR T2 GRE DWI
Chronic ˃4week Isointense/
Hypointense
Hyperintense/
Isointense
Variable Isointense/
hyperintense
Variable
TIW T2W GRE
Jitendra L Ashtekar et al.

123. Chronic hematoma ˃4week
Stages Time T1 T2 FLAIR T2 GRE DWI
Chronic ˃4week Isointense/
Hypointense
Hyperintense/
Isointense
Variable Isointense/
hyperintense
Variable

124. MRI findings of different stages of haemorrhage

125. Subarachnoid hemorrhage (hyperacute or acute hemorrhage)

126. Subarachnoid hemorrhage(old/chronic hemorrhage )

127. An extensive subarachnoid hemorrhage due to rupture
of the aneurysm Rt MCA

128. T2-weighted MRI shows rounded lesions that are centrally hypointense and
peripherally hyperintense. An isointense lesion with peripheral edema is seen
in the right basal ganglia. These lesions have central hyperintensity and
peripheral hypointensity on T1-weighted MRI. All of these lesions show
susceptibility on gradient-echo images, with minimal ring enhancement on
gadolinium-enhanced images.

129. Venous hemorrhagic infarcts
These appear as an isointense-to-hypointense signal on T1-weighted (T1W)
MRIs and hypointense on T2-weighted (T2W) MRIs. Also seen is blooming on
the gradient-echo (GRE) image with a rim of hyperintense vasogenic edema.

130. Venous angioma
Venous angioma shows characteristic flow void on T2-weighted (T2W)
MRI and mixed signal intensity on T1-weighted (T1W) MRI. Catheter
angiography (DSA) shows the typical caput medusa appearance of the
small parenchymal veins suggestive of a venous angioma.

131. Hemorrhages of various ages

132. Acute-to–early subacute hematoma

133. Hemorrhagic transformation of an infarct

134. Subacute subdural hematoma(late subacute hemorrhage)

135. Epidural hematomas (EDHs)
• Epidural hematomas (EDHs) evolve in manner
similar to that of SDHs.
• EDHs are differentiated from SDH on the basis
of their classic biconvexity versus medially
concavity and on the basis of the intensity of
the fibrous dura matter.

136. Epidural hematomas (EDHs- Hyperacute)

137. Conclusion
• As hemorrhage evolves, it passes through 5
well-defined and easily identified stages, as
seen on MRI.
• Knowledge of these stages may be useful for
dating a single hemorrhagic event or for
ascertaining if multiple hemorrhagic events
occurred at different times.

138. Conclusion
• Although CT may be more useful than MRI for
detecting hyperacute parenchymal hemorrhage
or early subarachnoid hemorrhage (SAH) or
intraventricular hemorrhage (IVH), MRI is
certainly more sensitive after 12-24 hours.
• MRI is also more specific than CT in determining
the age of a hemorrhage.
• Both T1- and T2-weighted MRIs should be
obtained to adequately characterize and stage a
hemorrhage.

139. Thank you