Basic concepts of computed tomography scan of the brain 2.ppt

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1. Basic concepts of
computed tomography scan of the brain
Part 2
By
Amir AbdelGhaffar
Lecturer of neurology
Al-Azhar faculty of medicine

2. Imaging for stroke
•"Stroke" is a clinical diagnosis; however imaging plays an
increasingly important role in its diagnosis & management.
•Decisions concerning therapy are dependent on the diagnosis
and may include the following:
- in ischemic stroke:
- Is the patient a thrombolysis candidate?
- in hemorrhagic stroke:
- Neurosurgery or neurology patient?
About 5% of clinically definite "strokes" are found to be a result of some
other pathology such as SOL, subdural hematoma or CNS infection.
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3. CT scan in stroke
Advantages of CT scan over other imaging modalities:
- Widely available.
- 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).
- Limited evaluation of vertebrobasilar system & post fossa structures.
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.
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4. CT pathophysiology in stroke
•After a stroke, edema progresses, and brain density
decreases proportionately.
•Ischemia results in:
–3% focal increase in the intraparenchymal water within 1
hour (This corresponds to 7-8 Hounsfield Unit decrease in brain density).
–6% increase in water at 6 hours.
•The degree of edema is related to:
–The severity of hypoperfusion.
–The adequacy of collateral vessels.
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5. Use of non-contrast CT scan to exclude acute
hemorrhage followed by
CTA to confirm vascular stenosis or occlusion and
CTP in suspected cerebral ischemia prior to IV
thrombolysis with rTPA.
Proper
CT work-up for stroke
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6. CT Findings of Stroke
Analyzing the CT of a potential stroke victim requires:
–The presence or absence of hemorrhage.
–Dense middle cerebral artery or a dense basilar artery,
which corresponds to thrombus in the affected vessel.
–Other subtle changes of acute ischemia due to edema
include the following:
- Obscuration of the lentiform nuclei.
- Loss of insular ribbon.
- Loss of gray/white distinction.
- Sulcal effacement.
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7. HyperDense Vessel Sign
•A hyperdense vessel is a denser vessel than its
counterpart and denser than any non-calcified vessel
of similar size.

•This is seen in 25-50% of stroke patients.

•This sign indicates poor outcome and poor response
to IV-rtPA therapy.
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8. Dense MCA
High density in the right MCA (arrowheads)
compare with the normal left MCA (arrow)
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9. Dense Basilar Artery
Dense basilar artery (arrow)
Dense basilar artery (arrow). Compare this to
the normal ICA (arrowhead)
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10. Treatment of brain edema
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11. Lentiform Nucleus Obscuration
•Lentiform nucleus (glopus pallidus & putamen)
obscuration is due to cytotoxic edema in the basal
ganglia.

•This sign indicates proximal MCA occlusion, which
results in limited flow to lenticulostriate arteries.
•Lentiform nucleus obscuration can be seen as early
as one hour post onset of stroke.
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12. Lentiform Nucleus Obscuration
Hypodensity in the left hemisphere
(arrows) involving the caudate
nucleus and lentiform nuclei (glopus
pallidus & putamen)
Nonenhanced CT scan obtained 5 hours after the onset of
stroke in a Pt with MCA occlusion demonstrates
obscuration of the lentiform nucleus (long white arrow)
and of the head of the caudate nucleus (arrowhead) as well
as hypoattenuation of the insular ribbon (short white
arrow) and effacement of the sulci of the temporo-parietal
MCA territory (black arrows).
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13. Insular Ribbon Sign
•The insular ribbon sign is the loss of the gray-white
interface in the lateral margins of the insula.

•This area is supplied by the insular segment of MCA
and is particularly susceptible to ischemia because it
is the most distal region from either anterior or
posterior collaterals.

•The insular ribbon sign may involve only the
anterior or the posterior insula.
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14. Insular ribbon
The cortex of the left insular ribbon
is not visualized (arrow).
Axial unenhanced CT image, obtained in a Pt 2.5
hours after the onset of left hemiparesis, shows
hypoattenuation & obscuration of the posterior part of
the right lentiform nucleus (white arrow) and a loss of
gray matter-white matter definition in the lateral
margins of the right insula (black arrows).
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15. Diffuse Hypodensity and Sulcal
Effacement
•Diffuse hypodensity and sulcal effacement is the
most consistent sign of infarction.
•Extensive parenchymal hypodensity is associated
with poor outcome.
•If hypodensity is greater than half (1/2) of the MCA
territory there will be, on average, an 85% mortality rate.
•Hypodensity in greater than one-third (1/3) of the MCA
territory is generally considered to be a contra-indication to
thrombolytic therapy.
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16. Sulcal Effacement
Diffuse hypodensity and sulcal effacement
(arrowheads) in the rt MCA distribution
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17. CT of Subacute Infarction
The CT of a subactue infarction has the following findings
according to the post-stroke period:
•In 1-3 days:
- Increasing mass effect.
- Wedge shaped hypodensity.
- Hemorrhagic transformation!!.
•After 4 - 7 days:
- Gyral enhancement.
- Persistent mass effect.
•In 1-8 weeks:
- Mass effect resolves.
- Enhancement may persist. 17

18. Aging of stroke
This image was taken 4 hours after the infarction.
This image, from the same patient, was
taken 2 days after the infarction.
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19. Acute cerebral infarction often cannot be seen by CT in the first
6-12 hrs after the event, then edema & cell death lead to
hypodensity.
Over weeks-months the brain tissue surrounding the infarct may
shrink leading to enlarged ventricle.
Persistent hypodense areas
in brain may be present as a
result of gliosis or brain
necrosis and replacement
with CSF
(encephalomalacia).
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20. Sharply circumscribed hypodense
edema (arrowheads) in the Rt MCA
territory
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21. Enhancement in Infarctions
•Approximately 35% of infarcts enhance on CT with contrast
by 3 days. 90% enhance at 1 week after the infarct.
•Faint enhancement begins near the pial surface or near the
infarct margins.
•The enhancement is initially smaller than the area of
infarction. It subsequently becomes gyriform.
•Enhancement occurs as a result of:
–Breakdown of the BBB,
–Neovascularity, and
–Reperfusion of damaged brain tissue.
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22. Post contrast CT demonstrating gyriform enhancement of subacute rt frontal lobe infarct (arrow)
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23. )A) Postcontrast brain CT shows right MCA territory infarction and a hypodense
lesion in right internal carotid artery (ICA) (arrowhead(
)B) A hypodense lesion (arrowhead) in right distal internal carotid artery has a
Hounsfield unit of –83, indicating a fat macroembolus instead of an air density.
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24. Hemorrhagic Stroke
•Hemorrhagic strokes account for 20% of all strokes.
•There are two major categories of hemorrhagic
stroke.
–Intracerebral hemorrhage (ICH) is the most common,
accounting for 12% of all strokes.
–Subarachnoid hemorrhage (SAH), due to rupture of a
cerebral aneurysm, accounts for 8% of all strokes.
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25. Intracerebral Hemorrhage
•Causes of non-traumatic intracerebral hematoma:
–Hypertensive hemorrhage (the most common).
–Amyloid angiopathy.
–Ruptured vascular malformation.
–Coagulopathy.
–Hemorrhage into a tumor.
–Venous infarction.
–Drug abuse.
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26. Hypertensive Hemorrhage (HH)
•HH accounts for approximately 70-90% of non-
traumatic primary intracerebral hemorrhages.
•HH is commonly due to vasculopathy involving
deep penetrating arteries of the brain.
•HH has a predilection for deep structures including
the thalamus, pons, cerebellum, basal ganglia
(particularly the putamen) and external capsule.
Blood may extend into the ventricular system. Intraventricular
extension of the hematoma may be associated with a poor
prognosis.
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27. HTN bleed
Hemorrhage in the cerebellum (arrow).
Thalamic hemorrhage (arrow) extending
into the lateral ventricle (arrowheads)
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28. HTN bleed
Basal ganglia hemorrhageTemporal intracerebral hematoma
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29. Coagulopathy Related Intracerebral
Hemorrhage (CRIH)
•CRIH can be due to anticoagulants or a systemic
abnormality such as thrombocytopenia.
•On imaging, this hemorrhage often has a
heterogeneous appearance due to incompletely
clotted blood.
•A fluid level within a hematoma suggest
coagulopathy as an underlying mechanism.
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30. Coagulopathy Bleed
Notice the fluid level within the
hematoma (arrow).
Sequential axial non-contrasted CT of the head
demonstrating a large left frontal hge with
multiple fluid blood levels & intraventricular
extension.
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31. Hemorrhage Due to Arteriovenous
Malformation (AVM)
•An underlying AVM may or may not be visible on a
CT scan.
•However, the following may suggest AVM as an
underlying pathology:
–Prominent vessels adjacent to the hematoma.
–Some AVMs contain dysplastic areas of calcification
seen as serpentine enhancing structures after contrast
administration.
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32. Hemorrhage Due to AVM
Hemorrhage (arrow) due to underlying AVM
(arrowheads).
Axial contrast-enhanced CT scan shows a tangle
of intensely enhancing tubular structures
embedded in the left parietal lobe, a finding that
is compatible with a nidus.
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33. Subarachnoid hemorrhage (SAH)
Traumatic
•SAH occurs with injury of small arteries or veins on the surface of the
brain. The ruptured vessel bleeds into the space (above the pia & below
the arachnoid matter).
•The most common cause of SAH is trauma. In the absence of
significant trauma, the most common cause of SAH is the rupture of a
cerebral aneurysm.
•When traumatic, SAH occurs most commonly over the cerebral
convexities or adjacent to otherwise injured brain (i.e. adjacent to a
cerebral contusion). If there is a large amount of SAH, particularly in
the basilar cisterns, the physician should consider whether a ruptured
aneurysm led to the subsequent trauma.
•On CT, SAH appears as focal (or linear) hyperdensity in sulci &
fissures.
•Again, the most common location of posttraumatic SAH is over the
cerebral convexity. This may be the only indicator of cerebral injury.
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34. Subarachnoid hemorrhage (SAH)
Aneurysmal
•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 & posterior communicating arteries,
–The middle cerebral artery bifurcation and
–The tip of the basilar artery.
•SAH typically presents as the "worst headache of life" for the patient.
•Detection of a SAH is crucial because the rehemorrhage rate of ruptured
aneurysms is high and rehemorrhage is often fatal.
•CT is most sensitive for acute SAH. 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, SAH appears as hyperdensity within sulci & cisterns. The insular
regions and basilar cisterns should be carefully inspected for subtle signs of
SAH.
•SAH may have associated intraventricular hemorrhage and hydrocephalus.
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35. SAH
High density fills the cisterns (arrowheads)
in this pt with hemorrhage from the Lt
MCA. Note the MCA aneurysm (arrows)
SAH Lt MCA
High density (arrowheads) fills the sulci over
the right cerebral convexity in this SAH
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36. SAH
Non-contrast head CT demonstrates SA blood over the right cerebral convexity (white arrow).
The surrounding brain parenchyma is edematous.
The superior sagittal sinus appears expanded and is of abnormally high attenuation, worrisome
for sinus thrombosis (black arrow). This is known as the dense cord sign.
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37. 37Ct in CNS disorders by Amir
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