Role of CT in CVA

1. CT-CVA
(CEREBRO VASCULAR ACCIDENT)
OSR
Dr. Yash Kumar Achantani

2. Introduction
• CVA or Stroke is an acute CNS injury that results in neurologic
deficits, brought on by a reduction or absence of perfusion to
a territory of the brain. The disruption in flow is from either
an occlusion (ischemic) or rupture (hemorrhagic) of the blood
vessel.
• Ischaemic stroke results from a sudden cessation of adequate
amounts of blood reaching parts of the brain.
• Ischaemic strokes can be divided according to territory
affected or mechanism.

3. Stroke
 Infarction 85%
• Cerebral
atherothrombosis 30-
40%
• Cardiogenic embolism
20-25%
• Penetrating artery
disease (lacune) 20%
• Other unusual causes 5%
 Hemorrhage 15%

4. Epidemiology
• Stroke is the third most common cause of morbidity
worldwide (after myocardial infarction and cancer) and is
the leading cause of acquired disability.
• Risk factors for ischemic stroke are:
• age, gender
• family history
• smoking, alcohol
• hypertension
• hypercholesterolaemia
• diabetes

5. Clinical presentation
• An ischemic stroke typically presents with rapid onset
neurological deficit, which is determined by the area of brain
that is involved.
• The symptoms often evolve over hours, and may worsen or
improve, depending on the fate of the ischemic penumbra.
• The vascular territory affected will determine exact symptoms
and clinical behaviour of the lesion

6. Patho-physiology

7. • Cerebral blood volume (CBV): the volume of blood
per unit of brain tissue(G/W:4/2 ml/100gm)
• Cerebral blood flow (CBF): the volume of blood flow
per unit of brain tissue per minute(G/W:60/25
ml/100gm/min)
• Mean transit time (MTT): defined as the time
difference between the arterial inflow and venous
outflow(G/W:4/4.8sec)

8. • Normal cerebral blood flow (CBF) is 50–60 mL/100 g brain
tissue/min.
• Cerebral autoregulation responds to a fall in cerebral
perfusion pressure (CPP) with vasodilatation and recruitment
of collateral vessels, thus increasing cerebral blood volume
(CBV) and reducing resistance, in order to maintain CBF
• The average time a blood cell remains with a particular
volume of tissue rises due to vasodilatation and collateral
flow, resulting in a prolonged mean transit time (MTT) and
thereby allowing improved oxygen delivery.

9. • After the vessels are fully dilated the autoregulatory system
cannot properly respond to any further reduction in CPP and
therefore CBF starts to decline.
• Oxygen extraction goes up to compensate, but once this is
maximal any further fall in CBF causes cellular dysfunction
• The loss of normal neuronal electrical function occurs when
CBF falls to 15–20 mL/100 g/min.
• This may be reversible, depending on the severity and
duration of the ischemia,
• Irreversible infarction is likely to occur within minutes if the
CBF <10, but moderate ischemia (10–20) may be reversible
for a few hours

10. • At levels of CBF <10, hypoxaemia leads to failure of the ATP-
driven cell integrity systems, resulting in cell depolarisation
and influx of Na+ and water.
• Cellular swelling and cell death occurs (cytotoxic oedema).
• In time, structural breakdown of the blood–brain barrier
occurs due to ischemic damage to capillary endothelium.
• Leakage of intravascular fluid and protein into the
extracellular space and later net influx of water to the
infarcted area cause vasogenic oedema.

11. The Penumbra Model
• Following a thromboembolic cerebral arterial occlusion, the
decline in regional CBF in the affected brain parenchyma is
not uniform.
• It has a centred infarct core with very low CBF and cell
depolarisation.
• A peripheral zone—the penumbra—has moderately
diminished CBF, resulting in loss of electrical function but
preserved cell integrity.
• The duration of ischemia in the penumbra is critical, and
strategies to recanalise the vessel and restore normal CBF are
likely to convey the greatest benefit.

12. • Failure or, more crucially, a delay in achieving this, however,
may lead to progression to infarction, especially as this tissue
is poorly autoregulated and more vulnerable.
• Surrounding the penumbra is a zone of benign oligaemia.
Here CBF is only mildly impaired and tissue is likely to survive.

13. Causes
• Large Vessel Thromboembolic Stroke (40%)
• Cardioembolic Stroke (15–30%)
• Small Vessel or Lacunar Stroke (15–30%)

14. Large Vessel Thromboembolic Stroke
(40%)
• Most commonly due to thrombus at the site of atherosclerotic
plaque or embolisation more distally (artery-to-artery).
• Sites: carotid bifurcation > intracranial internal carotid artery
(ICA) > proximal MCA (> anterior cerebral artery (ACA));
vertebral artery origins > distal vertebral (VA) > basilar artery.
• Also vasculopathy (e.g. large vessel vasculitis, dysplasia such as
fibromuscular dysplasia (FMD)), dissection.

15. Cardioembolic Stroke (15–30%)
• Intracardiac thrombus: myocardial infarct, enlarged left atrial
appendage, aneurysm, arrhythmia (especially paroxysmal
atrial fibrillation (AF)); valvular disease—endocarditis,
prosthetic valves, inadequate anticoagulation; right-to-left
shunts.
• Cardiac tumours.

16. Small Vessel or Lacunar Stroke (15–
30%)
• Small infarcts (<1.5 cm) in deep perforator territories; typically
• Lenticulostriate perforators from M1 segment of MCA
with infarcts in the lentiform nuclei, internal capsules
and corona radiate.
• Thalamic branches from posterior choroidal perforators
from basilar tip, proximal PCAs and posterior
communicating arteries cause infarcts in the thalami
and posterior internal capsules.
• Perforators from the basilar artery and its major
branches resulting in brainstem infarcts.

17. Borderzone Infarction
• Also known as watershed ischemia. This occurs at the
boundaries of the major vessel territories—superficially
between the leptomeningeal collaterals of the MCA and ACA
which also extend into the corona radiata deep to the
superior frontal sulcus, and those of the MCA and PCA.
• In the deep white matter of the inferior corona radiata and
external capsules lies the deep borderzone between the
cortical branches and deep M1 perforators of the MCA
• Postulated mechanisms include local (e.g. carotid stenosis)
and global (e.g. cardiac insufficiency) hypoperfusion, but
embolic infarcts at these sites can also occur.

18. • Borderzone ischaemia in the posterior fossa is uncommon but
usually occurs between the superior cerebellar artery (SCA)
and posterior inferior cerebellar artery (PICA) territories, and
occasionally between the SCA, PICA and anterior inferior
cerebellar artery (AICA) territories.

20. In addition to bilateral chronic small vessel ischaemic change, on the left there is
patchy cortical infarction in a borderzone distribution.

21. Global Hypoxic–Ischaemic Injury
• Inadequate oxygen supply to the entire brain can be the
consequence of severe hypotension or impaired blood
oxygenation.
• Global hypoperfusion can result in watershed infarcts, but
profound hypoxia can also cause symmetric ischaemia in the
basal ganglia, thalami and hippocampal formations.
• Anoxia due to defective blood oxygenation such as in carbon
monoxide poisoning tends to cause infarcts in sensitive regions.

23. Diffuse low attenuation is seen throughout
the brain in keeping with severe cerebral
ischaemia.

24. Stroke Classification
• Deep white matter infarcts are typically small vessel in
nature but can result from emboli originating from
large vessel atheroma or from a cardiac source.
• Middle cerebral artery (MCA) territory infarcts can
arise from emboli from the heart or carotid artery, or
from in situ thrombosis in the middle cerebral artery.
• Small peripheral infarcts in a vascular territory are
usually embolic but the source is not always clear (i.e.
cardiac vs carotid vs MCA)
• Peripheral infarcts involving multiple vascular
territories must be from a proximal source and most
likely the heart.

25. Scoring and classification systems
• Alberta stroke program early CT score (ASPECTS)
• TOAST classification
• NIH Stroke Scale
• Orgogozo Stroke Scale
• Canadian Neurological Scale
• Mathew Stroke Scale
• Scandinavian Stroke Scale

26. TOAST classification in acute ischemic
stroke
• The TOAST (trial of ORG 10172 in acute stroke
treatment) classification denotes five sub types
of ischaemic stroke.
– large-artery atherosclerosis (embolus / thrombosis)
– cardioembolism (high-risk / medium-risk)
– small-vessel occlusion (lacune)
– stroke of other determined aetiology
– stroke of undetermined aetiology

27. Alberta stroke program early CT score
• The Alberta stroke programe early CT score (ASPECTS) is a
10-point quantitative topographic CT scan score used in
patients with middle cerebral artery (MCA) stroke.
• caudate
• lentiform
• 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"

28. A = anterior circulation; P = posterior circulation;
C = caudate; L = lentiform;
IC = internal capsule; I = insular ribbon;
M1 = anterior middle cerebral artery (MCA) cortex;
M2 = MCA cortex lateral to insular ribbon;
M3 = posterior MCA cortex;
M4, M5 and M6 are anterior, lateral and posterior MCA territories immediately superior to M1,
M2 and M3, rostral to basal ganglia.

29. • Two NECT axial slices are examined
• level of basal ganglia and internal capsule;
• bodies of the lateral ventricles
• Ten regions are identified (four deep and six cortical)
• Starting with a score of 10, 1 point is deducted for
each of these areas that is involved.
• If the score is <7, the infarct is considered >1/3 of
an MCA territory

30. Radiographic features
• In many institutions with active stroke services which provide
reperfusion therapies a so-called code stroke aimed at
expediting diagnosis and treatment of patients will include:-
• Non-Contrast CT brain,
• CT perfusion
• CT angiography.

31. Objectives of NECT in Acute Stroke
• To exclude haemorrhage and allow administration of
aspirin therapy
• To exclude an alternative cause of the fixed
neurological deficit. Around 30% of patients presenting
with a stroke-like episode have a non-vascular cause
• To exclude infarcts > 1/3 MCA territory
• In cases of suspected posterior circulation stroke, to
attempt to identify an obviously thrombosed basilar
artery

32. Infarct Imaging Signs

33. Immediate
• The earliest CT sign visible is a hyperdense segment of a
vessel, representing direct visualisation of the intravascular
thrombus / embolus and as such is visible immediately.
• Although this can be seen in any vessel, it is most often
observed in the middle cerebral artery (hyperdense middle
cerebral artery sign).

34. Dense Artery sign

37. Early (1-3 hours)
• Within the first few hours a number of signs are visible
depending on the site of occlusion and the presence of
collateral flow.
• Early features include:
– loss of grey-white matter differentiation, and hypo
attenuation of deep nuclei:
• lentiform nucleus, changes seen as early as 1 hour
after occlusion, visible in 75% of patients at 3 hours
– cortical hypodensity with associated parenchymal swelling
with resultant gyral effacement
• cortex which has poor collateral supply (e.g. insular
ribbon) is more vulnerable.

39. Lentiform nucleus sign

42. Insular ribbon sign

43. First week (3-7days)
• With time the hypo-attenuation and swelling become more
marked resulting in significant mass effect.
• Maximum Edema
• This is a major cause of secondary damage in large infarcts.

44. Second and third week (7-21 days)
• Petechial Hemorrhage-Hemorrhagic transformation
• Correlates with BBB breakdown and Gyral enhancement
• Fogging Effect
– CT in 2nd week post infarction
– Decrease in edema and accumulation of protein from cell lysis
balance each other out, hence can have a normal appearance
on CT.
• Imaging a stroke at this time can be misleading as the affected
cortex will appear near normal.
– Rule of 3’s
• Peaks 3days to 3weeks and resolves by 3months

45. Left MCA territory infarct with hemorrhagic transformation

47. Hemorrhagic Transformation-
The Spot sign

48. • 30-90days
– BBB repair, loss of enhancement
• Months Post infarct
– CSF takes up the previously occupied brain
– Ex vacuo dilatation of adjacent ventricle
– Widening of adjacent Sulci
– Gliotic scar and encephalomalacia

49. Extensive area with attenuation of CSF replacing part of the brain parenchyma in the
vascular territory of the right middle cerebral artery. Ex vacuo dilatation of the
ipsilateral lateral ventricules.

50. CT PERFUSION

51. CT Perfusion
• CT perfusion has emerged as a critical tool in selecting
patients for reperfusion therapy as well as increasing the
accurate diagnosis of ischaemic stroke among non-expert
readers four fold compared to routine non-contrast CT.
• It allows both the core of the infarct (that part destined to
never recover regardless of reperfusion) to be identified as
well as the surrounding penumbra (the region which although
ischemic has yet to go on to infarct and can be potentially
salvaged).

52. • The key to interpretation is understanding a number of
perfusion parameters:
• cerebral blood volume (CBV)
• cerebral blood flow (CBF)
• mean transit time (MTT)
• time to peak (TPP)
• Areas which demonstrate matched defects in CBV and MTT
represent the unsalvageable infarct core, whereas areas
which have prolonged MTT but preserved CBV are
considered to be the ischemic penumbra.

53. Objectives of Penumbral Imaging
• To more accurately delineate the size of the core infarct
• To establish whether a penumbra of salvageable tissue is
present
• To evaluate the size and severity of ischemia of the penumbra

54. • Large core infarcts have a poorer outcome, regardless of
penumbra size or severity. Specifically, core volumes greater
than 70 mL are associated with adverse outcomes regardless of
recanalisation therapy.
• Core infarcts with small penumbra are described as ‘matched’
defects and carry reduced reperfusion benefit. However, some
units proceed with thrombolysis in this situation because of the
possibility of partial reversibility.
• Large areas of salvageable tissue, known as ‘mismatch,’ are
likely to benefit most from recanalisation therapy.
• Areas of mildly ischemic penumbra may reperfuse
spontaneously—known as ‘benign oligaemia’.
• Appropriate patient selection using penumbral imaging may
extend the therapeutic time window beyond 4.5 hours.

55. Case of a 67 year old male patient who presented with hemiplegia
No acute haemorrhage. Loss of grey-white differentiation at the caudate head
and insula ribbon. Hyperdense left M1 segment.

56. There is a large region of reduced CBV, CBF and time to peak perfusion affecting the
whole left cerebral hemisphere. This is in keeping with a large left MCA infarct. A very
small region of mismatch reduced time to peak perfusion is suggestive of only a tiny
penumbra.

57. Expected evolution of known left MCA territory infarct with left cerebral hemisphere loss
of grey-weight differentiation with oedema and positive mass effect. Hyperdense left
MCA again demonstrated. No haemorrhagic transformation.

58. CT Angiography
• May identify thrombus within an intracranial vessel, and may
guide intra-arterial thrombolysis or clot retrieval.
• Evaluation of the carotid and vertebral arteries in the neck
– establishing stroke aetiology
(eg. atherosclerosis, dissection)
– access limitation for endovascular treatment (e.g.
tortuosity, stenosis)

60. Case of right hemiparesis in a 84 year old female
CT shows increased attenuation of the proximal portion of left the MCA, as well the
onset of a ​​ill-defined hypoattenuation area involving the left capsular region
(ischemia).

61. CTA study confirms the occlusion of proximal left MCA and no involvement of the left
ACA.

62. Goals of Acute Stroke Imaging
• Parenchyma: Assess early signs of acute stroke and rule out
hemorrhage
• Pipes: Assess extracranial and intracranial circulation for
evidence of intravascular thrombus
• Perfusion : Assess cerebral blood volume, cerebral blood flow, and
mean transit time
• Penumbra : Assess tissue at risk of dying if ischemia continues
without recanalization of intravascular thrombus
Rowley HA. AJNR 2001;22:599–601.

63. Venous infarct
Causes of cerebral venous thrombosis include trauma, infection (particularly
subdural empyema) and hypercoagulability disorders including those due to oral
contraceptives.
Venous infarcts do not conform to arterial territories and are often haemorrhagic
and multifocal.
The superior sagittal sinus is most commonly involved, which can lead to bilateral
parasagittal infarcts. Isolated occlusion of the transverse sinus or the deep cerebral
veins can occur.
On unenhanced CT acute thrombosis will cause a venous sinus to appear expanded
and hyperdense.
IV contrast medium causes more intense enhancement of the walls of the sinuses
than of their contents, the so-called ‘delta sign’ .

64. Delta sign in superior sagittal sinus thrombosis. (A) Young man with a seizure after several
days of headaches. An unenhanced CT shows a small right parietal acute haematoma. The
superior sagittal sinus is occluded by acute thrombus. It appears expanded and the same
density as the intraparenchymal clot (arrow). (B) Contrast-enhanced CT shows the dura
around the sinus (long arrow) is higher density than the lumen (short arrow).

65. NONTRAUMATIC INTRACRANIAL HAEMORRHAGE

66. Spontaneous SAH is due to a ruptured arterial aneurysm in 70–80 per
cent of patients and an arteriovenous malformation in about 10 per
cent. In the remaining approximately 15 per cent, no underlying cause
is found on angiography.
CT is positive for SAH in 98 per cent within 12 h of onset but this falls
to less than 75 per cent by the third day. Recent SAH causes increased
density of the cerebrospinal fluid (CSF) spaces on CT.
Most aneurysms are located on or close to the circle of Willis and
blood is therefore seen in the basal cisterns, although the entire
intracranial subarachnoid space may be opacified and intraventricular
blood is common.
SAH

67. Cerebral aneurysms may be saccular, fusiform, or dissecting. However
majority are saccular aneurysms, which are usually round or lobulated
and arise from arterial bifurcations. Giant aneurysms by definition
measure over 25 mm in diameter and account for approximately 5 per
cent of all cerebral aneurysms.
Around 90 per cent of intracranial aneurysms arise from the carotid
circulation, the remaining 10 per cent from vertebral or basilar
arteries.

68. Anterior communicating artery aneurysm rupture. (A) CT shows diffuse subarachnoid
haemorrhage (short arrows) and a small haematoma in the septum pellucidum indicating the
likely source is an aneurysm of the anterior communicating artery (long arrow). The temporal
horns of the lateral ventricles and anterior recesses of the third ventricle are enlarged
(arrowheads) due to secondary communicating hydrocephalus, an extremely common finding in
acute SAH. (B) A 3D angiogram shows a lobulated aneurysm in the predicted location (long
arrow). The left proximal anterior cerebral artery (short arrow), middle cerebral artery
(arrowhead) and internal carotid artery (open arrow) are clearly shown.

69. INTRACEREBRAL HAEMORRHAGE
Nontraumatic intracerebral haemorrhage in older people is frequently
from rupture of a small perforating vessel due to hypertension.
The preferential sites of hypertensive haemorrhage are the basal ganglia,
thalamus and pons. Larger hypertensive bleeds in the basal ganglia often
extend into the ventricles or Sylvian fissure.
Haemorrhage may also be due to vascular malformations and
‘recreational’ drugs such as cocaine.
Other causes include coagulopathies, anticoagulation, vasculitis, venous
infarcts and haemorrhagic transformation of arterial infarcts.
Intracerebral haemorrhage is reliably detected on CT appearing as
increased density.

70. Non-contrast CT of the brain demonstrates a large right temporo-parietal haemorrhage. It is
associated with moderate midline shift.

71. AVM’SIntracranial vascular malformations can be classified according to the
presence or otherwise of arteriovenous shunting. The former comprises
cerebral (or subpial) arteriovenous malformations (AVMs) and dural
fistulae; the latter includes developmental venous anomalies (DVAs),
cavernous angiomas (‘cavernomas’) and capillary telangiectasias.
Cerebral (subpial) AVMs are probably congenital anomalies consisting of
direct arteriovenous shunts without a normal intervening capillary bed.
Cerebral haemorrhage is the commonest clinical presentation, others being
epilepsy, headache or focal neurological deficit.
They are usually detectable on CT as serpiginous areas of high density
(with marked contrast enhancement). CT may show calcification. There
may be haemorrhage at different stages of evolution. AVMs may be
surrounded by areas of ischaemic damage that are low attenuation on CT.
Dilated feeding arteries and early opacification of draining veins are the
angiographic hallmarks of these lesions.

72. Noncontrast axial images demonstrating a serpiginous hyperdensity is in the left parietal region.
Arteriovenous malformation is located superficially in the parieto-occipital region on the left It
receives most of its supply from the left middle cerebral artery branches Venous drainage
appears predominantly superficial, with vein coursing posteriorly to drain into the superior
sagittal sinus. There is no evidence of haemorrhage or thrombosis or aneurysm formation.