CT

1. CT BRAIN / MR – An introduction to
Normal Anatomy, Interpretation and
Some Common Pathologies
Anupama Chandrasekharan
Associate Professor & Consultant Radiologist
Dept of Radiology and Imaging Sciences
Sri Ramachandra Medical College & Research Institute
Chennai

2. Indications for CT / MR ……..
 Stroke
 Trauma
 Altered sensorium
 Neurological deficit
 Seizures
 Headache

3. How the CT study is usually planned…
15-20 degree
angulation to
canthomeatal line
to decrease
radiation to the
lens.

4. Plain CT Contrast CT

5. Indications for a contrast CT….
 Seizures
 Infections
 Venous thrombosis
 Tumors
 Atypical stroke findings on plain CT
 Atypical hemorrhage on plain CT
 Focal edema on plain CT

6. Brain Window Bone Window

18. Descriptive Terms …….
 Hypodense / Hypointense
 Isodense / Isointense
 Hyperdense / Hyperintense

19. Lesions appearing Hypodense
on Plain CT
 Infarct (non
hemorrhagic)
 Edema

20. Lesions appearing Hyperdense
on Plain CT
 Hemorrhage
 Calcifications

21. Normal Intracranial Calcifications

24. NINDS trial
Thrombolysis
CT criteria
No hemorrhage
CT criteria
No hemorrhage
Parenchymal hypodensity
in  1/3 MCA
ECASS

25. Purpose of imaging in stroke
 Definite diagnosis of stroke.
 To document the presence or absence of
hemorrhage
This information is critical since
anticoagulation is a standard therapy for
ischemic stroke
 Identify ischemic penumbra
 Assess location & extent of brain damage
(e.g. impending herniation)
 To exclude stroke mimics.

26. Ischemic Penumbra

27. Stroke Frequency Based on Aetiology :
Harvard Stroke Series
Ischaemic (82%) Atherosclerotic Thrombosis – 22%
Embolism – 30 %
Lacunar – 18 %
Indeterminate
Cerebral Venous
Dissection
 Haemorrhagic (18%)
Primary Intracerebral Hematoma –
12%
AVM + Aneurysm – 4%
Others: Cavernoma, AVF, bleeding
disorders -2 %

28. Stroke Based on Territory
 Anterior circulation stroke
Embolus : 70%
Thrombosis : 30%
 Posterior circulation stroke
Thrombosis : 70%
Embolus : 30%

30. Normal in 50% of ischemic strokes < 6
hrs

31. 2 hrs 24 hrs

32. CT in Hyperacute Stroke ( 0-6 hrs )
 Not v.sensitive for infarction
 Sensitive for a/c hemorrhage & gross
lesions precluding thrombolytic therapy
20 % within 2 hrs
82 % within 6 hrs
Neuroradiology.1996
Jan;38(1):31-33

33. Hyperacute Stroke On CT
EARLY ISCHEMIC CHANGES
 Hyperdense vessel sign
 Attenuation of lentiform
nucleus
 Loss of insular ribbon
 Effacement of sulci
 Loss of
corticomedullary
differentiation

34. Significance of Early Ischemic Signs
No contraindication to thrombolysis
Patel et al JAMA 2001;286:2830–2838
Indicate more extensive ischemia
AJNR 2004;25:933-938
Hyperdense vessel sign
Obscuration of basal ganglia
Loss of grey-white matter interface
Effacement of sulci
Strong association with later hemorrhagic
transformation AJNR 1991;12:1115-1121

36. Subacute infarct (1-7 days )
 Hemorrhagic transformation in 5-40 % of all
ischemic stroke Neurology 2001; 57:1603-1610
Stroke 1999;30:761-764

38. Lacunar Infarcts

39. Diffusion Weighted Imaging
Radiology 2000;217:331-345
Detects Infarct As
Early As 15-30
minutes

40. AJNR 2003 ;24:878-885
• 46 patients with acute stroke
• CT and DWI within 6 hours
• Mean delay 24.5 min. (R 10–41 min.)
• EIC on CT - 33/46 (Sn 73%)
• DWI 42/45 - (Sn 93%)
CT vs DWI

41. Hyperacute hemorrhage
2.5 hr 18 hr
GRE T2* WI
MRI as sensitive as CT for acute hemorrhage
More sensitive than CT for chronic hemorrhage
(JAMA 2004;292:1823-30)

42. CT sensitivity for SAH
 Day of SAH – 98 %
 After Day 1 – 90 %
 After Day 5 – 80 %
 After 1 wk – 50 %
Neuroradiology 1982:23:153-156

43. Acute SAH - 100 %
Chronic SAH – 63 %
Chronic SAH ( CT ) – 46 %
Radiology .1995;196(3):773-777
Radiology.1997;203(1):257-262

44. Acute hemorrhage
 MRI – 96% sens. 99% accuracy
 CT - 89% sens. 98% accuracy
Chronic hemorrhage
•MRI – 96% sens. 99% accuracy
•CT - 40% sens. 78 accuracy
HEME study

45. CT Angiography
 Site of occlusion
 Length of occluded
segment
 Arteries beyond occluded
segment – collateral flow
 Detection & exclusion of
large vessel intracranial
occlusion – sens – 98.4%
and spec.-98.1%
JCAT 2001; 25(4):520-8

46. CT Perfusion
 If no penumbra…..increased risk of bleed with
thrombolysis
RCNA 44(2006)41-62

47. MTT rCBV
rCBF
DWI ADC

50. Can MR replace CT as first imaging
modality in hyperacute stroke?
Yes
 MR immediately available
 Protocol is optimized
 Skilled personnel

51. Unlikely to replace CT .......
• Cost
• Limited availability
• Time
• Lack of evidence that MR has a positive influence
on
prognosis

52. Delta Sign

55.  Extradural
haematoma
 Subdural
haematoma
 Subarachnoid
haemorrhage
 Intraventricular
haemorrhage
 Cerebral contusions
 Intracerebral
haemorrhage
 Diffuse cerebral
edema
EXTRA-AXIAL LESIONS INTRA-AXIAL LESIONS
Imaging in Craniocerebral Trauma

56. Extradural
Hematoma
Acute Subdural
Hematoma

62. Diffuse Axonal Injury

64. 23 yr old male c/o fever and intense headache

65.  Ring enhancing lesions – granuloma /
abscess
 Calcifications
 Cerebritis
 Meningeal abnormalities
 Complications

67. Differential Diagnosis of Ring
Enhancing Lesions
 Granulomas
 Brain abscess
 Tumors – metastasis,
glioma
 Resolving hematoma

75. Encephalitis
 MRI – within 48 hrs
 CT - at least 3-5 days

76.  Widely available
 Cost
 Quick
 Hemorrhage
 Trauma
 Hyperacute infarcts
 Posterior fossa
 Diffuse axonal injuries
 White matter diseases
 Subtle abnormalities
of neuroparenchyma

77. Contraindications for MRI
 Metallic implants
 Pacemakers
 Prosthetic valves
 Aneurysm clips
 Claustrophobia

78. Thank U

81. Epidural Abscess Subdural
Empyema
 Notice the rim enhancing
epdural fluid collection
(arrowheads)
).

82. Encephalitis
 Diffuse nonfocal brain parenchymal
inflammatory process
 Most common agents - viruses
 Immunocompetent individuals - Herpes viruses
 Immunocompromised individuals
 Human immunodeficency virus (HIV)
 Cytomegalovirus (CMV)
 Papovavirus

83. Tuberculous meningitis

86. Cerebellar Atrophy
Cerebral Atrophy

87. ARTERIOVENOUS MALFORMATION

88. ARTERIOVENOUS MALFORMATION

90. SUBACUTE SDH

91. ACUTE ON CHRONIC SDH

92. CONTUSION SAH

93. Complications
EARLY
 ABSCESS
 SUBDURAL/EPIDUR
AL EMPYEMA
 VENTRICULITIS
 INFARCTION
 VENOUS
THROMBOSIS
LATE
 SUBDURAL/
EPIDURAL EFFUSION
 ENCEPHALOMALACIA
 HYDROCEPHALUS
 ATROPHY

94. SUBDURAL EMPYEMA

95. EXTRA-AXIAL INTRA-AXIAL

99. Hypertensive Hemorrhage
 Hypertensive hemorrhage accounts for
approximately 70-90% of non-traumatic primary
intracerebral hemorrhages. It is commonly due to
vasculopathy involving deep penetrating arteries
of the brain. Hypertensive hemorrhage has a
predilection for deep structures including the
thalamus, pons, cerebellum, and basal ganglia,
particularly the putamen and external capsule.
Thus, it often appears as a high-density
hemorrhage in the region of the basal ganglia.
Blood may extend into the ventricular system.
Intraventricular extension of the hematoma is
associated with a poor prognosis.

100. Haemorrhagic Stroke
Etiology
 Hypertension
 Vascular malformation
 Aneurysm
 Trauma
 Amyloid angiopathy
 Tumor
 Coagulopathy
 Hemorrhages can occur in the intraparenchymal,
subarachnoid, intraventricular, subdural and
extradural spaces.
 Location of hypertensive hemorrhage:
Putamen, external capsule, thalamus, pons,
cerebellum, subcortical white matter

101. Subarachnoid hemorrhage
 In the absence of trauma, the most common cause
of subarachnoid hemorrhage is a ruptured cerebral
aneurysm. Cerebral aneurysms tend to occur at
branch points of intracranial vessels and thus are
frequently located around the Circle of Willis.
Common aneurysm locations include the anterior
and posterior communicating arteries, the middle
cerebral artery bifurcation and the tip of the basilar
artery. Subarachnoid hemorrhage typically presents
as the "worst headache of life" for the patient.
Detection of a subarachnoid hemorrhage is crucial
because the rehemorrhage rate of ruptured
aneurysms is high and rehemorrhage is often fatal.

102. Subarachnoid hemorrhage
 CT is currently the imaging modality of choice because
of its high sensitivity for the detection of subarachnoid
hemorrhage. CT is most sensitive for acute
subarachnoid hemorrhage. After a period of days to
weeks CT becomes much less sensitive as blood is
resorbed from the CSF. If there is a strong clinical
indication, LP may be warranted despite a negative CT
since small bleeds can be unapparent on imaging.
On CT, a subarachnoid hemorrhage appears as high
density within sulci and cisterns. The insular regions
and basilar cisterns should be carefully scrutinized for
subtle signs of subarachnoid hemorrhage.
Subarachnoid hemorrhage may have associated
intraventricular hemorrhage and hydrocephalus.


103. MR Spectroscopy
Normal Infarct

104. Venous Sinus Thrombosis with Venous
Infarct
 Clinical symptoms – head ache, seizures
 Pathology is due to decrease in perfusion pressure as
the venous pressures elevate due to occlusion.
 Predisposing conditions are dehydration, infection,
polycythemia, sickle cell disease, hypercoagulable
states, peripartum, OCP poisoning.
Imaging findings
 Unilateral / bilateral parenchymal hypodensities
 Not limited to an arterial territory
 May be associated with hemorrhage
 Signs: Delta sign, Enhancement of walls of sinus than
their contents.

105. MR Spectroscopy
 Dynamic study depicting intracellular
metabolism of cerebral ischemia.
 Within the region of infarct, lactate
appears elevated whereas NAA and
total creatinine are reduced.

106. Radionucleotide studies in acute
stroke
 PET is an accurate method of quantifying
changes in cerebral hemodynamics.
 As cerebral blood flow (CBF) falls, cerebral
blood volume (CBV) and oxygen extraction
factor (OEF) increase.
 PET measures changes in CBF, CBV and OEF
using O15
 Plays a limited role due to limited availability .
 SPECT with Tc 99m HMPAO or ECD will show
a perfusion defect.

107. Radionucleotide Studies in Acute Stroke
 SPECT – Tc99m HMPAO
 PET – O15
 Adv – Early detection
 Limitation - Not widely
available

108.  MRI has been increasingly utilized in
early stroke since it is more sensitive
than CT in the first twelve hours
 Bright on Diffusion weighted images
(detected as early as 15 to 30 min after
vessel occlusion).

109. CT / MR Perfusion imaging
 Concentrates on the assessment of mean
transit time (MTT), relative cerebral blood
volume (RCBV) and derived relative cerebral
blood flow. RCBF = MTT / RCBV
 Prolonged MTT is the earliest & most consistent
sign of impaired perfusion.
 In addition to this, there is a simultaneous drop
in RCBV indicating tissue at risk for infarction.

110. Stroke in Children
 Constitutes 3% of cerebral infarcts
 Most common cause is congenital heart
disease. Other causes are vasospasm &
vasculitis,
 Echo, CT, MRI & catheter angiogram
should be performed as and when
required.

111.  There are several advantages to performing a CT scan
instead of other imaging modalities. A CT scan:
- Is readily available
- Is rapid
- Allows easy exclusion of hemorrhage
- Allows the assessment of parenchymal damage
The disadvantages of CT include the following:
- Old versus new infarcts is not always clear
- No functional information (yet)
- Relatively limited evaluation of vertebrobasilar system
A CT is 58% sensitive for infarction within the first 24 hours
(Bryan et al, 1991). MRI is 82% sensitive. If the patient is
imaged greater than 24 hours after the event, both CT and
MR are greater than 90% sensitive.

112. Epidural Hematoma
 An epidural hematoma is usually associated with a skull
fracture. It often occurs when an impact fractures the
calvarium. The fractured bone lacerates a dural artery or a
venous sinus. The blood from the ruptured vessel collects
between the skull and dura. On CT, the hematoma forms a
hyperdense biconvex mass. It is usually uniformly high
density but may contain hypodense foci due to active
bleeding. Since an epidural hematoma is extradural it can
cross the dural reflections unlike a subdural hematoma.
However an epidural hematoma usually does not cross
suture lines where the dura tightly adheres to the adjacent
skull

113. Cerebral Contusion
 Cerebral contusions are the most common
primary intra-axial injury. They often occur
when the brain impacts an osseous ridge or a
dural fold. The foci of punctate hemorrhage
or edema are located along gyral crests. The
following are common locations:
- Temporal lobe - anterior tip, inferior surface,
sylvian region
- Frontal lobe - anterior pole, inferior surface
- Dorsolateral midbrain
- Inferior cerebellum

114. Cerebral Contusion
 On CT, cerebral contusion
appears as an ill-defined
hypodense area mixed with
foci of hemorrhage.
Adjacent subarachnoid
hemorrhage is common.
After 24-48 hours,
hemorrhagic transformation
or coalescence of petechial
hemorrhages into a
rounded hematoma is
common.

115. Diffuse Axonal Injury
 Diffuse axonal injury is often referred to as "shear injury". It is the most
common cause of significant morbidity in CNS trauma. Fifty percent of all
primary intra-axial injuries are diffuse axonal injuries. Acceleration,
deceleration and rotational forces cause portions of the brain with
different densities to move relative to each other resulting in the
deformation and tearing of axons. Immediate loss of consciousness is
typical of these injuries. The CT of a patient with diffuse axonal injury may
be normal despite the patient's presentation with a profound neurological
deficit. With CT, diffuse axonal injury may appear as ill-defined areas of
high density or hemorrhage in characteristic locations. The injury occurs in
a sequential pattern of locations based on the severity of the trauma. The
following list of diffuse axonal injury locations is ordered with the most
likely location listed first followed by successively less likely locations:
- Subcortical white matter
- Posterior limb internal capsule
- Corpus callosum
- Dorsolateral midbrain

116. Encephalitis
 CT scan is often normal , especially early in
the disease.
 Ill defined hypodense lesions may be seen
e.g. temporal lobe changes are predominant
in Herpes Encephalitis.
 MRI is far more sensitive in the evaluation of
patients with encephalitis

117. Skull Fractures
 Skull fractures are categorized as linear or depressed,
depending on whether the fracture fragments are
depressed below the surface of the skull. Linear
fractures are more common. The bone windows must
be examined carefully. A skull fracture is most clinically
significant if the paranasal sinus or skull base is
involved. Fractures must be distinguished from sutures
that occur in anatomical locations (sagittal, coronal,
lambdoidal) and venous channels. Sutures have
undulating margins both sutures and venous channels
have sclerotic margins. Venous channels have
undulating sides. Depressed fractures are characterized
by inward displacement of fracture fragments.

118. Ventriculitis / Ependymitis
 Inflammation and enlargement of the
ventricles characterizes ventriculitis.
Ependymitis shows hydrocephalus with
damage to the ependymal lining and
proliferation of subependymal glia. A CT of
patients with these conditions reveals the
presence of periventricular edema and
subependymal enhancement. Ventriculitis and
Ependymitis affect approximately 30% of the
adult patients and 90% of the pediatric
patients with meningitis.

119. Cerebrovascular Complications of
Meningitis
 The development of cerebrovascular problems is
the most common complication of meningitis.
Arterial infarction can occur which often affects
the basal ganglia due to the occlusion of small
perforating vessels. Hemispheric infarction can
also occur due to major vessel spasm. Venous
infarctions are also common and can include
cortical venous occlusion or the involvement of
the superior sagittal sinus.

120. Subdural Empyema
 Subdural empyema is usually due to
meningitis, sinusitis, trauma or prior surgery.
It is a neurosurgical emergency. Subdural
empyema leads to rapid clinical deterioration,
especially if it is due to sinusitis. On CT it
appears as an isodense or hypodense extra-
axial mass. It has a lentiform or crescentic
shape.
The margin of collection often enhances with
contrast material administration due to the
presence of granulation tissue or subjacent
cortical inflammation.

121. Extra-axial CNS Infection
 Extra-axial CNS infections can cause epidural
abscess or subdural empyema. Extra-axial CNS
infections account for 20-30% of CNS infections.
Fifty percent of extra-axial infections are
associated with sinusitis, usually frontal sinusitis.
The infection occurs by direct extension or septic
thrombophlebitis. Thirty percent of extra-axial
infections occur post-craniotomy. Finally, 10-15%
of extra-axial CNS infections are related to
meningitis. CT findings include a focal fluid
collection usually with an enhancing margin in a
subdural or epidural location.

122. Pathophysiology
Flow abnormalities - Perfusion
Cellular dysfunction – DWI / CT/ MR
Structural breakdown – CT / MRI

123. Ischemic Stroke
 Occurs due to obstruction of cerebral arteries or cerebral veins.
 The clinical spectrum of ischemia includes
TIA (Transient ischemic attacks)
RIND (Reversible ischemic neurological deficit)
PRIND (partially reversible ischemic neurological
deficit)
Evolved stroke
 Pathophysiology:
Normal cerebral blood flow to the brain cortex is approximately
50 to 66 ml/100gm/min. When cerebral perfusion pressure falls
below critical levels (<15ml/gm/min) ischemia results. Ischemia
produces energy depletion in the affected cells. This results in
accumulation of Ca++, Na+ and Cl-, along with osmotically
obligated water. This secondary accumulation of water results
in the imaging features of stroke such as edema and mass
effect.

124. Hyperdense vessel sign
 Seen in 25% of stroke patients.
 In patients presenting with clinical deficit
referable to the middle cerebral artery territory,
the hyperdense vessel sign is present 35-50% of
the time.
 This sign

125. Lentiform Nucleus Obscuration
 Due to cytotoxic edema in the basal
ganglia
 Indicates proximal middle cerebral
artery occlusion, which results in limited
flow to lenticulostriate arteries
 Can be seen as early as one hour post
onset of stroke.

126. Insular Ribbon Sign
 Loss of the gray-white interface at the lateral
margins of the insula.
 Supplied by the insular segment of the middle
cerebral artery
 Particularly susceptible to ischemia because it
is the most distal region from either anterior
or posterior collaterals
 May involve only the anterior or the posterior
insula

127. Diffuse Hypodensity and Sulcal
Effacement
 Most consistent sign of infarction.
 Extensive parenchymal hypodensity is associated
with poor outcome.
 If > 50% of MCA territory involvement ,there is,
on average, an 85% mortality rate. Hypodensity
in greater than one-third of the middle cerebral
artery territory is generally considered to be a
contra-indication to thrombolytic therapy.

128. Newer Imaging Techniques In Acute
Stroke
 MR Diffusion imaging:
 CT / MR Perfusion imaging
 Combined MR perfusion & Diffusion
imaging
 MR Spectroscopy
 Radionucleotide studies

129. Ventriculitis /
Ependymitis

130. Cerebral Blood flow for Survival
Average blood flow : 55ml/ 100gm/ mt
Ischemic threshold : 20 ml/ 100gm/ mt
Tissue death : <10 ml/ 100gm/ mt
Functional failure without cell death:
10-20ml/ 100gm/ mt.

131. Concept of Ischemic Penumbra
Ischemic Insult

Focal core area of infarct (irreversible)

Surrounded by viable neuronal cell on
the brink of cell death

“Ischemic Penumbra”
 
Geographic area of tissue
surrounding a profoundly
ischemic core. Identified
on DWI / per MRI
Saving this potential
salvageable area
leads to significant
chance of
improvement

132. Ischemic stroke
 Thrombotic stroke
 Embolic stroke
 Lacunar infarct
 Global cerebral hypoperfusion

133. • Ischemic Stroke (83-85%)
• Hemorrhagic Stroke (15-17%)

134. MRI in Hyperacute Stroke
 DWI – Infarct core
 FLAIR - SAH , Parenchymal changes
 T2* GRE – Intracranial hemorrhage
 PWI – Perfusion deficit
 MRA – Vessel occlusion

135. Diffusion Weighted Imaging
 Sensitivity : 88 – 100 %
 Specificity : 95 – 100 %
 Initial diffusion lesion volume
correlates well with final infarct
volume & neurologic and functional
outcome
 Multiple a/c lesions in diff.vasc
territories in pts. with 1 symptomatic
insult …. embolic
Neurology.1999 Jun 10;52(9):1784-
1792
Ann Neurol.1997 Aug;42(2):164-170

136. False Negative DWI
Brainstem infarct
Deep GM nucleus infarct
Neuroradiology2000;42:444–447
Stroke2000;31:1965–1972
AJNR 1999;20:1871–1875
Neurology 1999;52:1784-52

137. 4 h 24 h
Dept. Neurosciences Univ. of Rome La Sapienza

138. Reversibility of Ischemic lesions on
DWI
Occlusion of MCA 1 hour - DWI lesion  or resolution
Occlusion of MCA 2 hour - Lesion size same or 
Radiology 2000;217:331-345
Successful thrombolysis may revert DWI changes

139. Diffusion changes in TIAs
• 29% to 67% will show restricted diffusion
• May reverse or persist
• Perfusion deficits 
Stroke vs TIA
DWI lesions of TIA are less intense
Stroke 2004;35:1095
AJNR 2004;25:1645-52

141. Hyperacute Hemorrhage
Wiesmann M, et al. Eur Radiol.
2001;11:849-53.

142. Stroke 2004;35:502-506

147. Nederkoorn PJ et al. Stroke 2003;34:1324-32

148. MR Spectroscopy in acute stroke
Stroke 2003;34:e82-87
6 pts within 7 hrs of stroke onset
Lactate alone – metabolic injury - Reversible
Lactate +  NAA- more severe – Irreversible
Lac/Cho ratio from acute lesions improves
the prediction of stroke outcome
Neurology 2000;55:498

151. CT Venography

154. 25 yr old lady c/o fever and altered sensorium x 1
wk. Had 1 episode of GTC seizures. Admitted
elsewhere , LP done showed proteins-55 mg % and
sugar –105 mg % ..
ABG- pH – 7.55
HCO3 – 28.3 , PCO2-32.9, PO2 –322.9,SPO2-99.8
CT – Normal
Discharged at request.
H/o fever,headache and vomitting on and off x 5
mths -

155.  O/E – GCS – E1V1M5
BP – 140/100 , PR – 116
Pupils – 4mm dilated , sluggish light reaction
Neck Rigidity +
Kernig’s & Brudeski’s - ve
 Hb-13.5
 TC- 12,200
 Platelets-4.2
 MP/MF – negative
 BUN, creatinine – normal
 Urine R/E – proteins +++, pus cells 5-8
 Coagulation Profile - WNL
 134/3.4/26/102

157. Q qq

160. HIV Encephalopathy

162. Thank You

163. Hyperdense artery
•SPECIFICTY 100%
•SENSITIVITY 10% TO 50%
Seen as early as 90 minutes
AJNR 1996; 17:79-85

164. Hyperdense MCA / Vessel Sign
 Persistent large vessel occlusion
 Large clot burden
 Not a contraindication for i.v. thrombolysis
Neurology 2001:57:1603-1610

165. Infarct VS Tumor

167. CT Findings in Stroke
Hyperacute infarct (<12 hrs)
 Normal (50 to 60%)
 Hyperdense MCA
 Obscuration of lentiform nucleus
Acute infarct (12 – 24hrs)
 Loss of grey - white matter interface (insular
ribbon sign)
 Low density basal ganglia
 Sulcal effacement.

168. Hyperdense vessel sign
• Indicates poor outcome and poor response to iv - TPA therapy.

169. CT Findings in Stroke (Contd)…
Subacute infarct (1- 7days)
 Mass effect
 Wedge shaped hypodensity involving grey &
white matter
 Hemorrhagic transformation.
 Gyral enhancement.
Chronic infarct ( 1 to 8 weeks)
 Encephalomalacic changes
 Reduced mass effect

170. Global Cerebral Hypoperfusion
 Consequence of global hypoperfusion.
 Common causes are hypotension, cardiac
arrest with successful resuscitation, neonatal
asphyxia and CO inhalation.
Imaging patterns
 1) Water shed infarct in the parieto-
occipital region & basal ganglia infarcts.
 2) Cortical laminar necrosis with
hemorrhagic foci in basal ganglia & cerebral
cortical gyri.
 3) In severe cases “reversal sign” is noted.

171. Reversal sign

172. Infarct With Hemorrhagic Transformation

174. CT VS MRI in the setting of acute
stroke
 MRI is more sensitive
 Diffusion weighted MR images has the
highest sensitivity & specificity for acute
cerebral infarction.
 CT is more sensitive to detect
hemorrhage.
 CT is more widely available in many
institutions.
 CT is less expensive
 CT is more rapid

175. CT Angiography
 Useful in MCA embolic stroke & predictive of
infarction volume in MCA territory
 Less useful –deep grey matter & brainstem
stroke
(Taipei)1999:62:255-260

176. Subacute SAH
 FLAIR + (GRE) T2*-weighted superior to
either alone
J Neurol Neurosurg
Psychiatry.200170(2):205-211

181. Hypertensive Hemorrhage

182. Subarachnoid hemorrhage

184. Combined MR Perfusion & Diffusion
Imaging
 In hyperacute stage, larger abnormality is
noted on the perfusion images than on
diffusion weighted images. This diffusion
perfusion mismatch is the ischemic
penumbra. This is the tissue at risk which
would benefit from thrombolysis.

185. Stroke Protocol
Normal Infarct Haemorrhage
Diffusion /
Perfusion
CT Perfusion Intraparenchymal SAH
HT Atypical site Angiogr
Angiogram
Mismatch Matches
Angiogr
Thrombolysis

186. To Summarize the Role of CT in
Stroke
 Haemorrhagic or non-haemorrhagic
 Arterial or venous
 Territory involved
 Acute,subacute or chronic
 Assess the mass effect
 Exclude Stroke mimics like subdural
hematoma, tumors

189. How the CT study is usually planned…
 Thinner sections
are studied
through the
posterior fossa

190. Hounsfield Units
AIR - - 1000
FAT - - 30 to -100
CSF - 0
GREY MATTER - 32 - 41
WHITE MATTER - 23 - 34
ACUTE BLOOD - 56 - 76
CALCIFICATION - 60 - 400
BONE - 1000