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1. Arterial Anatomy
of brain and Imaging of
Strokes
MODERATOR: DR.MANASA M.D
PRESENTOR: N.LAKSHMI CHAITANYA

2. ARTERIAL ANATOMY
 The anterior circulation consists of the intradural internal
carotid artery (ICA) and its branches plus its two
terminations, the anterior cerebral artery (ACA) and middle
cerebral artery (MCA). Both the anterior communicating
arteries (ACoAs) and the posterior communicating arteries
(PCoAs) are also considered part of the anterior circulation.

3.  The is composed of the vertebrobasilar
trunk and its branches, including its terminal bifurcation
into the two posterior cerebral arteries (PCAs).

4. Intracranial Internal Carotid Artery
 C1 (cervical) segment
 C2 (Petrous) ICA Segment.
 C3 (Lacerum) ICA Segment
 C4 (Cavernous) ICA Segment
 C5 (Clinoid) ICA Segment
 C6 (Ophthalmic) ICA Segment.
 C7 (Communicating) ICA Segment.

6. Variants and Anomalies
Aberrant ICA
(AbICA),
Persistent
stapedial
artery, and
Embryonic
carotid-basilar
anastomosis.

7. Aberrant ICA
 Congenital vascular anomaly that enters the posterior
middle ear cavity from below and hugs the cochlear
promontory as it crosses the middle ear cavity.
 present with pulsatile tinnitus.
 otoscopic examination - a vascular appearing retrotympanic
mass lying in the anteroinferior mesotympanum.

8.  An AbICA mimics the clinical appearance of paraganglioma
(glomus tympanicum, glomus jugulare)
 Never –biopsy.
 The appearance of an AbICA on CT is pathognomonic. Axial
bone CT shows a tubular lesion that crosses the middle ear
cavity from posterior to anterior

11.  Coronal images show a round, well-delineated soft tissue
density lying on the cochlear promontory.
 Angiography (DSA, CTA, MRA) shows that the AbICA has a
more posterolateral course than normal. A distinct
angulation that resembles a 7 is often present, together
with a change in contour and caliber (pinched appearance)
before the segment resumes its normal course.

12. Persistent Stapedial Artery.
 Rare congenital vascular anomaly in which the embryonic
stapedial artery persists postnatally.
 A PSA arises from the C2 (petrous) ICA at the genu between
the vertical and horizontal segments.
 The PSA passes through the stapes footplate and doubles
the size of the anterior (tympanic) facial nerve segment.
Intracranially, the PSA becomes the middle meningeal
artery (MMA).

13.  Pathognomonic imaging findings are
 (1) the absence of the foramen spinosum (because the
MMA arises from the PSA, not the ECA) and
 (2) an enlarged tympanic segment of the facial nerve.

15. Embryonic Carotid-Basilar Anastomoses.
 Four types of PCBA.
 From superior to inferior, these are
 1)persistent trigeminal artery (CN V),
 2)persistent otic artery (CN VIII),
 3)persistent hypoglossal artery (CN XII), and
 4)proatlantal intersegmental artery (C1-3)

17. CIRCLE OF WILLIS

18. ACA

21. MCA

23. PCA

27. Acute Cerebral
Ischemia-Infarction

28.  The distinction between cerebral ischemia and
cerebral infarction is subtle but important.
 In cerebral ischemia, the affected tissue remains viable
although blood flow is inadequate to sustain normal
cellular function.
 In cerebral infarction, frank cell death occurs with loss of
neurons, glia, or both.
 Hyperacute stroke designates events within the first 6
hours following symptom onset.

29.  In hyperacute stroke, cell death has not yet
occurred, so the combined term acute cerebral
ischemia-infarction is often used.
 Acute strokes are those 6-48 hours from onset.

30. Pathophysiology of stroke

34.  Neurons in the CA1 area of the hippocampus, neocortex
layers III, V, and VI, and the neostriatum are more
vulnerable than other regions
 The MCA is the most common site of large artery
thromboembolic occlusion , followed by the PCA
and vertebrobasilar circulation.

35.  ischemic core -The center of the affected brain
parenchyma-typically has a CBF < 6-8 cm³/100 g/min.
 Neuronal death with irreversible loss of function occurs in
the core of an acute stroke.
 ischemic penumbra- area surrounding the central core.
CBF in the penumbra is significantly reduced, falling from a
normal of 60 cm³/100 g/min to 10-20 cm³/100
g/min.(salvageable tissue)

37. THE FOUR "MUST KNOW" ACUTE STROKE QUESTIONS
• Is there intracranial hemorrhage (or a stroke "mimic")?
• Is a large vessel occluded?
• Is part of the brain irreversibly injured?
• Is an ischemic "penumbra" present?

38. CT Findings
 A complete multimodal acute stroke CT protocol includes
nonenhanced head CT, an arch-to-vertex CTA, and dynamic
first-pass perfusion CT (pCT)
 Recent studies have demonstrated that CTA with or without
CTP improves diagnostic accuracy compared with NECT alone
and does not delay IV tPA or endovascular therapy.

39. NECT
 Initial NECT scans—even those obtained in the first
6 hours—are abnormal in 50-60% of acute ischemic strokes
if viewed with narrow window width.
 The most specific but least sensitive sign is a
hyperattenuating vessel filled with acute thrombus

40. CT Early signs of ischemia
ACUTE PHASE(2-6 HOURS)
 Obscuration of lentiform nucleus
 Dense MCA sign
 Insular ribbon sign
SUB-ACUTE PHASE(6-12 HOURS)
 Sulcal effacement and low attenuation in region of infarct that
extends to the periphery involving grey and white matter
cytotoxic edema

45. Alberta stroke programme early CT score
(ASPECTS)
 The Alberta stroke programme early CT score (ASPECTS) is a 10-
point quantitative topographic CT scan score used for patients
with middle cerebral artery stroke(MCA). It has also been
adjusted for the posterior circulation
 An ASPECTS score less than or equal to 7 predicts a worse
functional outcome at 3 months as well as symptomatic
hemorrhage.

47. Posterior circulation
 Variations of the ASPECT scoring system have been described for
use in the posterior circulation and referred to as pc-ASPECTS.
 thalami (1 point each)
 occipital lobes (1 point each)
 midbrain (2 points)
 pons (2 points)
 cerebellar hemispheres (1 point each)

49. CT ANGIO
 CTA (with or without CT perfusion) quickly answers
the second "must know" stroke question i.e., is a major
vessel occlusion with a "retrievable" intravascular thrombus
present?
 CTA localizes and defines the extent of the intravascular
thrombus, assesses collateral blood flow, and also
characterizes atherosclerotic disease.

51. PERFUSION CT
 pCT has three major parameters: cerebral blood volume
(CBV), cerebral blood flow (CBF), and mean transit time
(MTT).
 CBV is defined as the volume of flowing blood in a given
volume of brain.
 CBF is the volume of flowing blood moving through a given
volume of brain in a specified amount of time.
 MTT is the average time it takes blood to transit through a
given volume of brain.

52.  The standard color scale is graduated from shades of red
and yellow to blue and violet.
 With CBV and CBF, perfusion is portrayed in
red/yellow/green (highest) to blue/purple/black
 In normal brain, there is bilaterally symmetric perfusion in
the cerebral hemispheres with higher CBF and CBV in gray
matter (cortex, basal ganglia) compared with white matter.

53.  Well-perfused gray matter appears red/yellow, white
matter appears blue, and ischemic brain is blue/purple.
 Totally nonperfused areas (i.e., the ventricles and
densely ischemic central core of a major infarct) are black.

54.  Of the three standard parameters, MTT shows the
most prominent regional abnormalities.
 Here the color scales are reversed to emphasize
the abnormally prolonged transit time in the ischemic
brain.
 With MTT, the slower the transit time, the closer to the red
end of the scale. Brain with normal transit time appears
blue.

57.  An important ancillary finding
in patients with large
MCA infarcts is reduced
perfusion in the opposite
cerebellar hemisphere
 large MCA infarcts cause
hypoperfusion with reduced
CBF in the contralateral
cerebellum, a phenomenon
called crossed
cerebellar diaschisis

58. MRI
 T1W1: T1WI is usually normal within the first 3-6 hours
 Subtle gyral swelling and hypointensity begin to develop
within 12- 24 hours and are seen as blurring of the GM-
WM interfaces.
 T2/FLAIR: hyperintensity on FLAIR scans within the first 4
hours.
 Nearly all strokes are FLAIR positive by 7 hours following
symptom onset. T2 scans become positive slightly
later, generally within 12-24 hours.

59.  Intraarterial hyperintensity on FLAIR is an early sign of
stroke and indicates slow flow (not thrombosis).
 FLAIR-DWI "mismatch" (negative FLAIR, positive DWI) has
been suggested as a quick indicator of viable ischemic
penumbra and eligibility for thrombolysis.
 T2* GRE:Intraarterial thrombus can sometimes be
as "blooming" hypointensity on T2* (GRE, SWI) studies

60.  T1 C+:Parenchymal enhancement is uncommon in
acute/hyperacute ischemia
 DWI and DTI: Cellular swelling begins to develop within
minutes following an ischemic insult. ADC values decrease,
producing high signal intensity on DWI images.
 Around 95% of hyperacute infarcts show diffusion
restriction on DWI, with hyperintensity on DWI and
corresponding hypointensity on ADC.
 DTI is even more sensitive than DWI, especially for pontine
and medullary lesions.

61.  PMR: Restriction on DWI generally reflects the densely
ischemic core of the infarct, whereas pMR depicts the
surrounding "at-risk" penumbra.
 A DWI-PWI mismatch is one of the criteria used in
determining suitability for intraarterial thrombolysis.

64. Subacute Cerebral Infarcts
 Early subacute strokes have significant mass effect and often
exhibit HT, whereas edema and mass effect have mostly
subsided by the late subacute period.
 CT Findings. On NECT, the wedge-shaped area of decreased
attenuation seen on initial scans becomes more sharply
defined. Mass effect initially increases, then begins to decrease
by 7-10 days following stroke onset. HT develops in 15-20% of
cases and is seen as gyriform cortical or basal
ganglia hyperdensity.

65.  CECT follows a "2-2-2" rule. Patchy or gyriform
enhancement appears as early as 2 days after stroke onset,
peaks at 2 weeks, and generally disappears by 2 months.
 T1WI: Non hemorrhagic subacute infarcts are hypointense
on T1WI and demonstrate moderate mass effect with sulcal
effacement. Strokes with HT are initially isointense with
cortex and then become hyperintense

66.  T2WI: Subacute infarcts are initially hyperintense compared
with nonischemic brain. Signal intensity decreases with time,
reaching isointensity at 1-2 weeks (the T2 "fogging effect").
 FLAIR: Subacute infarcts are hyperintense on FLAIR. By 1 week
after ictus, "final" infarct volume corresponds to the FLAIR-
defined abnormality.
 • T2*:○ "Blooming" HT ; ○ Prominent medullary veins
 DWI ○ Pseudonormalization ○ T2 "shine-through"

67. Chronic Cerebral Infarcts
 NECT scans show a sharply delineated wedge-shaped hypodense area
that involves both gray matter (GM) and white matter (WM).
 The adjacent sulci and ipsilateral ventricle enlarge secondary to volume
loss in the affected hemisphere.
 Chronic infarcts older than 2-3 months typically do not enhance on CECT.
 MR scans show cystic encephalomalacia with CSF-equivalent signal
intensity on all sequences.
 Marginal gliosis or spongiosis around the old cavitated stroke is
hyperintense on FLAIR.

68. Watershed ("Border
Zone") Infarcts
 Two distinct types of vascular border
zones are recognized: an external
(cortical) WS zone and an internal
(deep) WS zone.

69. Artery of Percheron Infarction

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