|
1
|
|
|
2
|
- Acute change in neurological status.
- Symptoms persist longer than 24 hours.
- Resolution in less than 24 hours = TIA
- Ischemia 80%
- Hemorrhage 20%
|
|
3
|
- Rapid clinical and imaging evaluation.
- “Stroke team” needed
- Thrombolytic therapy for appropriate patients
- <3 hours from onset of Sx
- No contraindications to tPA (long list)
- Involvement of large area of brain a contraindication
- Risk of hemorrhage from tPA
- Assessed by imaging and clinical evaluation
- CT usually negative in the first few hours
|
|
4
|
- CT without IV contrast
- Rapid
- Reliable to exclude hemorrhage
- High sensitivity for acute blood
- Acute blood appears bright on CT relative to brain tissue.
- IV contrast only if suspicion of another etiology, e.g. tumor or AVM
|
|
5
|
|
|
6
|
|
|
7
|
- 1st 6 hours:
- 60% normal
- Vague hypodensity in ischemic area.
- Insular ribbon sign
- Sulcal effacement from slight swelling
- Loss of grey/white interface
- 12-24 hours
- More apparent hypodensity
- Minimal mass effect
|
|
8
|
- After 24 hours
- Well circumscribed hypodensity
- 3-5 days
- Peak mass effect
- Mass effect gone by 2-4 weeks
- Long term
- Ex vacuo dilatation of ventricles
- Encephalomalacia in infarcted area
|
|
9
|
|
|
10
|
|
|
11
|
|
|
12
|
|
|
13
|
- Thrombus in vessel is hyperdense relative to flowing blood
|
|
14
|
- Equivalent to dense MCA sign
|
|
15
|
|
|
16
|
- Minimal mass effect
- Well circumscribed infarct
- Cytotoxic edema pattern
|
|
17
|
- Cytotoxic
- Grey and white matter
- Wedge shape
- Infarct
- Vasogenic
- Almost exclusively in white matter tracts
- Finger-like projections
- Infection, XRT, tumor
|
|
18
|
|
|
19
|
|
|
20
|
- Contrast enhancement
- Not usually indicated unless there’s suspicion of a different process
- Enhancement in infarcted area begins after about three days
- Enhancement more than 6-8 weeks after ictus suggests another etiology
- New role:
- “Perfusion” scans of brain with rapid IV contrast infusion.
|
|
21
|
- Low sensitivity for acute ischemic infarct
- Decision to use thrombolytic based on absence of CT findings
- Potential use of thrombolytic in patients without thrombotic or embolic
infarct
- Arterial dissection
- Postictal state
- Infection or tumor
- Up to 40% of acute strokes are not from causes amenable to thrombolysis
- 20% without defect seen on angiogram
- 10-20% from small vessel disease or arterial dissection
|
|
22
|
- MRI
- Diffusion weighted images take only ~2 minutes
- highly sensitive for acute ischemia
- Contraindications
- Pacer, AICD, aneurysm clip, etc
- Full imaging takes ~30 minutes
- Special MR compatible life support and monitoring equipment needed
|
|
23
|
- Glossary - types of pulse sequences
- T1WI- images where signal depends on T1 of tissues
- T2WI- images where signal depends on T2 of tissues
- FLAIR = FLuid Attenuated Inversion Recovery
- Images with pathology bright and CSF dark
- DWI = Diffusion Weighted Imaging
- Fast acquisition where signal depends on ability of water to diffuse
in all directions
|
|
24
|
- Acute stroke appears as
- Normal to low signal on T1WI
- High signal on T2WI
- High signal on FLAIR
- High signal on DWI
- FLAIR and DWI most sensitive
|
|
25
|
- Abnormal area becomes bright on DWI within 30 minutes of onset of
ischemia
- High signal visible on T2WI in about 8 hours
- T1WI image becomes abnormal after ~16 hours
|
|
26
|
- Infarcted area remains bright on T2WI forever.
- As encephalomalacia occurs, infarct becomes progressively darker on T1WI
until it matches signal of CSF
|
|
27
|
- Requires high field magnet with rapid gradients
- In ischemic tissue, diffusion of water molecules in 3 dimensions is
restricted
- Magically, these areas appear as bright areas on DWI
- Ask a physicist how it works…
|
|
28
|
- Area of ischemia visible within 30 minutes
- 10-14 days later, diffusion is “normal”
- Brain becomes isodense
- Late, with encephalomalacia, area shows low signal
- T2WI becomes progressively brighter with respect to DWI as infarct ages
- crossover at about 3-7 days
|
|
29
|
|
|
30
|
- Super-sensitive
- Not super-specific
- False positives:
- Hemorrhage
- MS
- Abscess
- Lymphoma and other tumors
- In uncertain situations, repeat in 2 weeks
- Infarct should normalize on DWI
|
|
31
|
|
|
32
|
- Dark on T1WI, bright on T2WI and FLAIR, very bright on DWI
|
|
33
|
|
|
34
|
- Good for seeing larger intracerebral vessels only.
- Not generally useful unless intervention is planned very early.
- In most strokes, treatment is not usually affected by identification of
an occluded vessel.
- Ask your neurologist if the information is useful.
|
|
35
|
- Vasculopathies:
- Diabetic
- Hypertensive
- Giant cell (temporal) arteritis
- Takayasu’s arteritis
- PAN
- Sarcoid
- Collagen vascular diseases esp. SLE
- Wegener’s granulomatosis
- drugs
- Larger vessel disease
- Moyamoya
- Fibromuscular dysplasia
- Infectious disease
- Nonvascular
- Global hypoxia
- CO poisoning
|
|
36
|
- CT best for finding acute bleeding
- Normal white matter = 30-34 HU
- Normal grey matter = 37-41 HU
- Attenuation of blood depends on hemoglobin conc.
- Blood with Hct of 45% = 56 HU
- Acutely extravasated blood will be denser than brain and easily
visible
- Clotted blood, e.g. subdural hematoma, will be even denser.
|
|
37
|
- Hounsfield Units
- Measure of CT density
- H20 = 0 HU
|
|
38
|
- Intraparenchymal
- Intraventricular
- Subarachnoid
- Subdural / epidural
|
|
39
|
- Acute bleed in anemic patient will be harder to detect.
- With Hct <30%, nonclotted blood may be isodense with brain.
- Highest clot density at about 72 hrs after bleed
- High density disappears after several weeks
|
|
40
|
- Hypertensive bleed - most common (80%)
- Basal ganglia
- Thalamus
- Pons
- Cerebellum
|
|
41
|
|
|
42
|
- Atypical locations like cerebral hemispheres
- AVM
- Aneurysm
- Trauma
- Amyloid angiopathy
- Tumor
- Vascular mets, primary tumors
- Vasculitis, cocaine, amphetamine, bleeding diathesis, anticoagulation,
etc
|
|
43
|
- Accompanied by vasogenic edema, some mass effect
- Consider enhanced scan for mass effect out of proportion to size of
hematoma
- Possibility of underlying tumor
- Later, some peripheral enhancement may be seen
- Confusion with other etiologies
- Much later, thin slit of hypodensity is seen at site of bleed.
|
|
44
|
|
|
45
|
- 80-90% of subarachnoid bleeds
- Prevalence 1-5%?
- Familial vs. sporadic
- Adult polycystic kidney disease (10% of pts)
- Marfan’s, Ehlers-Danlos
- Fibromuscular dysplasia
- Multiple in 15-20%
|
|
46
|
- Mortality 10-15%
- Often re-bleed in first day
- 50% will re-bleed within 6 months
- Angiogram and treatment early
- Before onset of arterial spasm leading to infarction
- MRA or CTA?
- Rapid (2-3 minutes)
- No need for specialized call personnel
- Endovascular therapy vs. surgery
|
|
47
|
- Usually traumatic in origin
- Subdural
- Venous bleed
- Low pressure
- Slow growth
- Epidural
- Arterial bleed
- High pressure
- Rapid growth
- Both may be life-threatening from mass effect and herniation
|
|
48
|
|
|
49
|
- Trauma
- Hypertension
- Aneurysm
|
|
50
|
- Signal from blood depends on pulse sequence, age of clot
- Hemoglobin contains iron
- Strong paramagnetic effects on signal from nearby protons
|
|
51
|
- Natural history of hemoglobin in clot
|
|
52
|
- Standard T1 and T2 weighted images are insensitive for small acute
hemorrhage
- Diffusion weighted images are highly sensitive for acute ischemia
- Area of acute infarction visible within 30 minutes of onset of ischemia
|
|
53
|
|
|
54
|
- Bleed or not?
- CT for initial evaluation of acute ΔMS
- MR more rapidly positive for acute ischemia
- DWI positive within 20 minutes.
- But: early identification of presence and size of infarct not usually
necessary.
- Only if thrombolysis is being considered
|
|
55
|
- Old or new stroke?
- CT: look for water density and dilatation of underlying ventricle = old
stroke.
- MRI: water signal on T1 and T2 and low signal on DWI = old stroke
- Cause of bleed?
- Know typical locations of hypertensive hemorrhages:
- Basal ganglia, cerebellum, pons
|
|
56
|
|
|
57
|
- Patients are candidates for tPA thrombolysis up to 24 hours after onset
of symptoms.
- MRI is the modality of choice for initial evaluation of acute stroke
symptoms.
- Diffusion weighted imaging shows acute infarction earlier than any other
modality.
- 50% are due to acute hemorrhage.
|
|
58
|
- Basal ganglia
- Temporal lobe
- Cerebellum
- Brainstem
|
|
59
|
- Contrast enhanced CT is not generally useful in early stroke diagnosis
- Persistence of contrast enhancement after 6-8 weeks suggests underlying
tumor.
- Contrast enhanced MRI is more useful than enhanced CT in early stroke.
- Perfusion CT may help diagnose major stroke as rapidly as MRI
|
|
60
|
- Beauchamp N et al. Imaging of acute cerebral ischemia.
Radiology:1999;212:307-324
- Von Kummer R et al. Acute stroke: usefulness of early CT findings before
thrombolytic therapy Radiology 1997; 205: 327-333.
- Hoeffner EG et al. Cerebral Perfusion CT: Technique and Clinical
Applications Radiology 2004 231: 632-644
- Provenzale JP et al. Assessment
of the Patient with Hyperacute Stroke: Imaging and Therapy Radiology
2003;229:347-359.
|
|
61
|
|