overall investigations of ischemic stroke in short

1. Investigations of ischemic stroke
Dr. Muhammad Rezeul Huq
Resident phase B
Department of neurology
BSMMU

2. Immediate Diagnostic Studies:
Evaluation of a
Patient With Suspected Acute
Ischemic StrokeAll patients
• Noncontrast brain CT or brain MRI
• Blood glucose
• Oxygen saturation
• Serum electrolytes/renal function tests*
• Complete blood count, including platelet count*
• Markers of cardiac ischemia*
• Prothrombin time/INR*
• Activated partial thromboplastin time*
• ECG*

3. CT vs MRI
Emergency imaging of the brain is recommended before
initiating any specific therapy to treat acute ischemic
stroke (Class I; Level of Evidence A). In most instances,
NECT will provide the necessary information to make
decisions about emergency management.
Either NECT or MRI is recommended before intravenous
rtPA administration to exclude ICH (absolute
contraindication) and to determine whether CT
hypodensity or MRI hyperintensity of ischemia is present .

4. CT vs MRI
•Patients with transient ischemic neurological
symptoms should undergo neuroimaging
evaluation within 24 hours of symptom
onset or as soon as possible in patients with
delayed presentations. MRI, including DWI,
is the preferred brain diagnostic imaging
modality. If MRI is not available, head CT
should be performed.

5. CT vs MRI
CT
• widespread immediate
availability
• relative ease of
interpretation and
• acquisition speed (most
common modality used in
acute ischemic stroke
imaging).
MRI
• ability to distinguish acute, small
cortical, small deep, and posterior
fossa infarcts
• the ability to distinguish acute
from chronic ischemia
• the avoidance of exposure to
ionizing radiation
• DWI has a high sensitivity (88%
to 100%) and specificity (95% to
100%) for detecting infarcted
regions, even at very early time
within minutes of symptom onset.

6. CT vs MRI
CT
• the ability of observers to
detect these on NECT is
quite variable and occurs in
≤67% of cases imaged within
3 hours
• NECT is relatively
insensitive in detecting acute
and small cortical or
subcortical infarctions,
especially in the posterior
fossa
• radiation.
MRI
• cost
• relatively limited availability
• relatively long duration of the
test
• increased vulnerability to
motion artifact
• patient contraindications
(claustrophobia, cardiac
pacemakers, patient
confusion, or metal
implants).

7. MRI
Immediate
Hyperintense Artery sign
DWI -restricted diffusion
ADC-hypointense lesion
Perfusion alterations
Absence of normal flow void
Intravascular contrast enhancement
<12 hrs
T1WI (sulcal effacement, gyral edema, loss
of gray-white interfaces)
12 to 24 hrs
Hyperintensity in T2WI
Meningeal enhancement
CT(<24 hours)
Hyperdense Artery
- Dense artery
- Dot sign
Insular ribbon sign
Poor gray white
differentiation
Effacement of sulci &
fullness of gyri
Obscuration of lentiform
nucleus

9. MRI OF BRAIN
DWI & ADC mapping – most sensitive method for imaging
acute ischemia.

10. Ischemic penumbra in acute stroke –Magnetic
resonance perfusion weighted image

11. CT
1 to 3 days
increasing mass effect
wedge shaped hypodense area
haemorrhagic transformation
4 to 7 days
Mass effect persists
Gyral enhancement
> 1 wk
Mass effect resolves
> 2 wk
Fogging
Months to years
Encephalomalacic change
MRI
1 to 3 days
increasing mass effect
signal abnormalities striking on
T1WI, T2WI
haemorrhagic transformation
4 to 7 days
Mass effect
Gyral enhancement
> 1 wk
Mass effect resolves
> 2 wk
Fogging
Months to years
Encephalomalacic change

12. Figure: (A) 12 hours after symptom onset- obscuration of right basal ganglia and insular ribbon
sign
(B) & (C) 4 days later- wedge shaped MCA territory infarct

16. Bilateral ACA territory infarct

17. Acute ischemic stroke in the territory of anterior
cerebral artery

18. Acute ischemic stroke in the territory of posterior
cerebral artery

19. Chronic ischemic stroke

20. Pathophysiology of cerebral infarction
with corresponding imaging findings
PATHOPHYSIOLOGY IMAGING FINDINGS
Cytotoxic edema • Decreased density with loss of gray-white
interface on CT
• Increased T1 and T2 relaxation times on MRI
• Restricted diffusion on DWI
• Regional mass effect
Intravascular enhancement • Reduced blood flow
Parenchymal enhancement/ Gyral enhancement • Disruption of blood brain barrier
• Leaky neocapillary
Hemorrhagic transformation or neocapillary growth
Decreased edema
Fogging
Glial scar and cystic necrosis • Low density on CT
• Prolonged T1 and T2 relaxation times on MRI
• Evidence of volume loss

21. Lacunar infarct

22. Water shed infarct
Involves the border zones between the vascular territories
of the major cerebral arteries.
Types
 Superficial, between the territories of the major branches
of the circle of Willis
• Anterior watershed infarcts between the proximal
territories of the anterior and middle cerebral arteries
• Posterior watershed infarcts between those of the middle
and posterior cerebral arteries.
Deep border zone infarcts between the superficial and
deep branches of a cerebral artery.

23. Water shed infarct
• Bilateral, roughly symmetrical watershed infarcts result
from global cerebral hypoperfusion caused by heart
failure, hypoxia .
• In unilateral cases, one of these factors is usually
coupled with arterial stenosis or occlusion, which can be
evaluated with MRA or CTA of the carotid and vertebral
arteries.

24. Acute ischemic stroke in the left anterior
watershed area

25. Water shed infarct

26. Vascular imaging
• Duplex study of neck vessels
• Trans cranial Doppler (TCD)
• CT/ MR angiogram
• Digital subtraction angiogram

27. Modality TCD DUPLEX CTA MRA
Site intracranial extracranial both both
Sensitivity 55 -90 83% to 86% (for>70%) 92% - 100%(intra)
>90% (extra)
60% -85% stenoses
80% -90%occlusions
62% to 91%(extra)
Specificity 90-95 87% to 99% 82% - 100% (intra)
>95% (extra)
86% to 97% (extra)
Advantages -Microembolic signals
(extracranial or cardiac
sources).
-Predict, as well as
enhance, intravenous
rtPA outcomes.
-Safe and inexpensive
for imaging the carotid
bifurcation and
measuring blood
velocities.
-(100%) negative
predictive value for
excluding >70%
stenosis.
-Can be performed in
an additional
2 to 4 minutes
-useful in identifying
acute proximal large-
vessel occlusions
-can be performed in an
additional
2 to 4 minutes
Disadvantages -Limited in case of poor
bony windows. –
Operator dependent.
-For posterior
circulation stroke, not
helpful.
-Increased risk of
hemorrhage.
-Influenced by equipment,
the specific lab and the
technologist.
-Limited in extracranial
vasculature proximal or
distal to the bifurcation.
-Can’t differentiate severe
stenosis & occlusion
-Provides a static image
- Inferior to DSA for the
demonstration of flow
rates and direction
-High osmolality
contrast agent
-Cannot reliably identify
distal or branch
occlusions
-Provides a static image
-Can’t differentiate
severe stenosis &
occlusion

28. DSA Advantages DSA Disadvantages
1. Gold standard
2. High-resolution
3. Most informative technique when
making decisions about invasive
therapies
4. Valuable information about collateral
flow, perfusion status, and other occult
vascular lesions that may affect patient
management
5. Particularly useful in cases of carotid
dissection
6. Nonionic contrast media
1. Stroke or
death in <1% of DSA procedures
2. Procedure related complications
3. Renal impairment

29. Duplex study of neck vessels
Ultrasound assessment of carotid arterial atherosclerotic disease
• Become the first choice for carotid artery stenosis screening
• Permitting the evaluation of both the macroscopic appearance of plaques
as well as flow characteristics in the carotid artery
• To estimate the severity of stenosis.

30. Duplex study of neck vessels contd..
Society of Radiologists in Ultrasound (SRU) consensus
Normal:
• ICA PSV is <125 cm/sec and no plaque or intimal thickening is
visible sonographically
• Additional criteria include ICA/CCA PSV ratio <2.0 and ICA
EDV <40 cm/sec

31. Duplex study of neck vessels
•<50% ICA stenosis:
• ICA PSV is <125 cm/sec and plaque or intimal thickening is
visible
• ICA/CCA PSV ratio <2.0 and ICA EDV <40 cm/sec
•50-69% ICA stenosis:
• ICA PSV is 125-230 cm/sec and plaque is visible
• ICA/CCA PSV ratio of 2.0-4.0 and ICA EDV of 40-100 cm/sec
•≥70% ICA stenosis but less than near occlusion:
• ICA PSV is >230 cm/sec and visible plaque and luminal
narrowing are seen at gray-scale and colour Doppler ultrasound
• ICA/CCA PSV ratio >4 and ICA EDV >100 cm/sec

32. Duplex study of neck vessels
Near occlusion of the ICA:
• Velocity parameters may not apply, since velocities may be
high, low, or undetectable
• Diagnosis is established primarily by demonstrating a markedly
narrowed lumen at colour or power Doppler ultrasound
Total occlusion of the ICA:
• No detectable patent lumen at gray-scale US and no flow with
spectral, power, and colour Doppler ultrasound
• There may be compensatory increased velocity in the
contralateral carotid

33. Doppler ultrasound with tight stenosis. Spectral
display
of duplex Doppler flow velocities suggesting 75% to
90% internal
carotid artery stenosis, with high systolic (654 cm/sec)
and diastolic
velocities (205 cm/sec)

34. Atherosclerotic plaque. Longitudinal B-mode image of
an atherosclerotic plaque in the region of the carotid
bifurcation and
proximal internal carotid artery, with possible crater
formation (arrow).

35. Duplex study of neck vessels
• Plaque severity can be classified by thickness, with
minimal (1.1–2.0 mm), moderate(2.1–4.0 mm), and severe
(>4.0 mm)
• Plaque morphology, surface features (smooth, irregular,
crater), echodensity and texture (homogeneous,
heterogeneous)
• The presence of hypoechoic plaques and plaques that are
quite heterogeneous with prominent hypoechoic regions
(complex plaque) identify an increased risk of stroke
• Measurement of the intima-media thickness.

36. Different Angiography
A, MRA reveals moderate luminal narrowing in mid to distal portion of basilar artery.
B, Three-dimensional reconstruction of CTA images reveals irregular narrowing with
65% stenosis. C, DSA most accurately depicts the stenotic region with high temporal
and spatial resolution.

38. Angiography contd..
A, Three-dimensional reconstructed CTA image of left ICA reveals severe stenosis
B, DSA confirms severe stenosis seen on CTA due to an atherosclerotic plaque.

39. Immediate Diagnostic Studies:
Evaluation of a
Patient With Suspected Acute
Ischemic StrokeSelected patients
• Toxicology screen
• Pregnancy test
• Arterial blood gas tests (if hypoxia is suspected)
• Chest radiography (if lung disease is suspected)
• Lumbar puncture (if subarachnoid hemorrhage is
suspected and CT scan is negative for blood)
• Electroencephalogram (if seizures are suspected)

40. Other investigation to assess the
risk factors
•Fasting blood sugar, 2 hours after
breakfast, HbA1c
•Fasting lipid profile
•Echocardiogram

41. Special investigation for young stroke
• ANA, anti DS DNA, antiphospholipid antibody- SLE,
antiphospholipid antibody syndrome
• Serum homocystine- homocystinuria
• P-ANCA, C-ANCA- vasculitis
• VDRL , TPHA- neurosyphilis
• Hb electrophoresis –sickle cell anaemia
• Blood and CSF lactate –MELAS

42. Special investigation for young stroke contd..
• Thrombotic screening: Protein C, protein S, anti-thrombin
lll
• Blood culture and echocardiogram – infective endocarditis
• Color Doppler and trans esophageal echocardiogram -
congenital heart disease and valvular heart disease.
• Digital subtraction angiogram – moyamoya disease,
vascular malformation.

45. Investigation for complications of stroke
• Complete blood count
• Urine routine microscopic test and culture
• Serum electrolytes
• Chest X ray P/A view
• X Ray shoulder joints

46. VENOUS STROKE

48. Venous stroke

49. Hemorrhagic transformation of infarct
ECASS II classification (European Cooperative Acute Stroke Study)
• Haemorrhagic infarction type 1 (HI1)
• petechial haemorrhages at the infarct margins
• Haemorrhagic infarction type 2 (HI2)
• petechial haemorrhages throughout the infarct
• no mass-effect attributable to the haemorrhages
• Parenchymal hematoma type 1 (PH1)
• ≤30% of the infarcted area
• minor mass-effect attributable to the haematoma
• Parenchymal hematoma type 2 (PH2)
• >30% of infarct zone
• substantial mass-effect attributable to the haematoma

51. Referrences
• Adams and Victor’s Principles of Neurology, 10th edition
• Bradley’s Neurology in Clinical Practice,7th edition
• CT and MRI of the Whole Body by JOHN R. HAGGA, 5th
edition
• Diagnostic Neuroradiology by Anne G. Osborn, 1st edition
• Guidelines for the Early Management of Patients With
Acute Ischemic Stroke, Stroke 2013;44:870-947
• Moyamoya Disease and Moyamoya Syndrome, N Engl J
Med 2009; 360:1226-1237
• http://www.radiologyassistant.nl
• https://radiopaedia.org/

52. THANK YOU