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Stroke imaging
Johan Wikström MD PhD
Associate Professor of Radiology
Uppsala University
StrokeInfarct: -Arterial thrombosis/embolus-Hypoxic/ischemic-Venous thrombosis
Non-traumatic hemorrhage:-Intracerebral-Subarachnoid
2
Why image stroke patients?• Identification of patients w infarct who may benefit from
therapy (i.v. thrombolysis or endovascular)
• Identification of patients with bleeding or other diagnoses
Salvageable tissue?
ICH/SAH?
Ischemic lesion?
yes no
yesyes
no
Other diagnosis?
yes no
no
Treatment of infarct
Higher likelihood of good outcome after i v thrombolysis (tPA) if:-Symptom duration ≤4.5 h-No hemorrhage-Infarct ≤33% of media territory -No occlusion of carotid siphon branching-Tissue at risc of infarction (penumbra) ≥20% av perfusion deficit
4
Treatment of infarct
• I a thrombolysis or thrombectomy can be considered if: -Proximal occlusion (and available interventionist)
5
Methods for infarct diagnosis
• CT• CTA• CTP• MR• MRA• MRP
6
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
7
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
8
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
• Swelling
Acute
Chronic
9
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
• Swelling• Dense vessel
10
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
• Swelling• Dense vessel
1h
11
• Sensitivity 1:st 24h: 58%*
Diagnosis of acute infarct with CT
1h 24h
(*Yousem, Grossman: Neuroradiology. The requisites)12
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
• Swelling• Dense vessel• CTA: arterial
occlusion
CTA MIP
13 14
Why CTA?
• Find arterial occlusion: confirms diagnosis, identify lesions that can be endovascularly treated
• Dissection• Carotid stenosis• Sinus thrombosis• Aneurysm/AVM
15
CTA technique in suspected stroke
• I v injection rate 5-6 ml/s• Synchronization of injection and scanning w test bolus
or triggering techniques• Volume and scan time dependent on scanner• Thin collimation• Low pitch• Evaluation: source images and MIP (4/2mm) 3 planes
16
MIP 1 mm MPR 1 mm
17
MIP 5 mm MPR 5mm
18
MIP 50 mm MPR 50 mm19
Diagnosis of acute infarct with CT
• Gray-white matter differentiation (e.g. insular ribbon)
• Swelling• Dense vessel• CTA: arterial
occlusion• CTP: penumbra
20
CTP
• Mean transit time (MTT) (s)• Cerebral blood flow (CBF) (ml/s x 100g)• Cerebral blood volume (CBV) (ml/100g)
21
Hemodynamic changes in ischemia
MTT
CBV
CBF
Decreasing perfusion pressure
Autoregulation range
Penum
bra
Infarct
CTP in acute ischemia
Penumbra ( ): mismatch mellanMTT och CBV
23
CTP in acute ischemia
• CBV< 2 ml/100g : infarct• rMTT> 145% : threatening infarct
24
AJR 2011;196:53-60
25
CBF CBV1h
26
CBF 24h 27
• Right-sided symptoms, 2 h
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MTT CBV
29
CBV
24 h post i.v. thrombolysisAt admission
Problems with CTP
• No standardised computation algorithms• No standardiserad limits• Complicated relation between perfusion deficit, time
and evolution of infarct• Value of penumbra identification for selection of
thrombolysis candidates not shown in randomised studies
30
Diagnosis of acute infarct with MRI
• 2/3 with FLAIR whithin 6h• DWI in minutes• DWI: 90-95% sensitivity • DWI: <5% reversible restriction• Penumbra: mismatch DWI/MTT
31
• Glucose and oxygen depletion causes dysfunction of ATP-dependent cell membrane Na-K-pump
• Cell swelling
• Increase in ICF, decrease in ECF
• Intracellular changes?
Changes in intra- and extracellular space in acute infarct causes diffusion restriction
Appearance of DWI changes
• Within minutes in animal models• Reported after 11 minutes in humans
DWI signal evolution
DWI
t
Early Late
• DWI signal affected by not only diffusion, but also T2
Speed of diffusion abnormality evolution?
Day after ictus
% positive DWI lesions (n=93)<1 100
1-4 965-9 9410-14 6015-19 0>20 0
Burdette, AJR:171, September1998
Accuracy of DW-MRI for acute infarct?
n Sens. (%)
Spec. (%)
Study
194 88 (133/151) 95 (41/43) Lövblad, AJNR 1998
356 83 (157/190) 96 (246/255) Chalela, Lancet 2007
Predictors of false negative DWI exam
• Brainstem• Time from ictus<3h• NIHSS score<4
Chalela, Lancet 2007;369:293-298
Reversibility of DWI changes
• In animal models• Anecdotal reports of spontaneous reversible DWI
lesions• Reversibility of DWI changes after iv
thrombolysis• ADC cut-off for reversibility?• -No, large heterogenity in cellular metabolic injury
in regions w ADC decreaseNicoli Stroke 2003, Guadagno Neurology 2006
Kidwell Ann Neurol 2000
Kidwell Stroke 1999, Marks Radiology 1996
Mintorovitch Magn Reson Med 1991
Differential diagnoses (intraaxial) with diffusion restriction
• Other causes of cytotoxic edema (seizures, migraine, tumor, trauma, toxic)
• Some blood products• Abscess
Images from scanner:
B0 B1000 ADC
Evaluation of DWI
1. Look at mean DWI 2. Confirm finding at ADC
DWI ADC
T2 shine through
B0 B1000 ADC
T2 shine through
DWI ADC
T2-shine through
• Signal intensity in DWI depends on initial (at b=0) SI and diffusivity (ADC)
• High initial SI can give high DWI SI without diffusion restriction!
0
Log SI
b1000
Equal DWI signal
High diffusion
Low diffusion
Brain stem infarct
CT T2w
Brain stem infarct
DWI ADC
Multiple lesions; what´s new?
DWI ADC
Non-traumatic hemorrhages
• Subarachnoid (SAH) • Intracerebral (ICH)
49
SAH
• Aneurysm• AVM• Dissection• Venous• (Traumatic)
50
Diagnosis of SAH
• CT: sensitivity 95% 1st 24h, <50% after 1w • MR: FLAIR high sens. but low spec.• LP
51FLAIR
• Flow artefacts
52FLAIR
SAH
• 80-90% of non-traumatic caused by ruptured aneurysms
• Age: peak at 40-60 y• M:F 1:2• risk rebleeding• disturbance of CSF flow• vasospasm, ischemia
53
Intracranial aneurysms
• Predilection sites: 90% at circulus Willisi+ a cer media-bifurcation
• Look at source images+thin MIPs (e.g. 4/2 mm)
54
ICH due to aneurysm
• Most often also SAH• ICH close to large
arterial branch (fissura Sylvii!)
• ICH in younger
55
ICH due to aneurysm
56
Evaluation of CTA
• Source images• MIP e.g. 4/2 mm, 3 planes• VRT for demonstration• 20% multiple! Which has bled?• Assess blood distribution, irregularity, spasm in
vicinity
57
Look in all three planes!
• Transverse: MCA, AComA• Coronal: BA, SCA, PICA• Sagittal: A Pericallosa, PComA
http://en.wikipedia.org/wiki/Circle_of_Willis
58
MIP 4/2
59
Diagnosis of ICH
• CT: high attenuation due to coagulation (60-80HU)• Low attenuation and possible levels in acute phase
and in coagulation disturbance
60
”Spot sign”
• Predicts hematoma expansion
61
Stroke. 2007; 38:1257-1262
Etiology ICH
• Hypertonia• Amyloid angiopathy• Anticoagulative treatment• Vasculitis• AVM• Aneurysm• Cavernoma• Tumour• Hemorragic infarct
62
Older:• Hypertonia• Arterial hemorrhagic infarct• Amyloid angiopathy• Tumour
Etiology ICHYounger:
• AVM
• Cavernoma
• Venous hemorrhagic infarct
• Vasculopathy
• Tumour
63
Investigation of ICH?
• All?• Normotensive?• Depending on age?• CTA?• DSA?• MR?
64
Diagnosis of ICH: MRT
• As high sensitivitity as CT• Dependent on sequence type
65
Diagnosis of ICH: MRT
• As high sensitivitet as CT• Dependent on sequence type
66T1 TSE T2 TSE T2 GRE
MRI in ICH
• T1, T2, diffusion restriction, susceptibility effects
Oxy-Hb (hyperacute): Deoxy-Hb (acute): Met-Hbintracellular (early subacute):
Met-Hbextracellular (late subacute): Ferritin/Hemosiderin (chronic):
T1 T2 DWI ADC
?
or NAC
NAC
NAC: no accurate calculation
from ”Diffusion-weighted MR imaging of the brain”, Springer, 2nd ed 2009
NAC
Hypertonic hemorrhage
• Thalamus• Basala ganglia• Pons• Cerebellum• ....but can have any location!• ....and vascular anomalies in
25% of patients w HT and ICH
68
Acta Radiol 1997; 38:797–802
Amyloid angiopathy
• Amyloid replaces normal tissue in vessel wall• 27-33% of normal elderly• Causes 15-20% of sICH>60 y• Frontal and parietal lobes• Bleedings of different ages• MRI (GRE T2, SWI): microbleeds
69
Amyloid angiopathy
• Lobar hemorrhage• Remnants of old hemorrhages
70
Amyloid angiopathy
• MRI with blood sensitive sequence (T2 GRE, SWI) • Lobar microbleeds
71
AVM
72
Radiological findings in AVM
• Dilated arteries and veins• Intervening nidus• Shunting• Flow related aneurysms (a
and v)• Steal phenomena• MR: flow voids
73
Radiological findings in AVM
• Dilated arteries and veins• Intervening nidus• Shunting• Flow related aneurysms (a
and v)• Steal phenomena• MR: flow voids• CT: often Ca2+
74
• 7 år girl• Acute headache
75
CTA
76
DSA
77
Investigation of suspected AVM
• DSA golden standard• MR with dynamic MRA?
78
MR in AVM
• Preferrably 3T
• 3D TOF MRA
• Dynamic Gd-MRA
79
Investigation of suspected AVM
• DSA golden standard• MR with dynamic MRA?• CT with dynamic CTA/CTP?
80
Tumoral hemorrhage
• Astrocytoma grade III-IV• Metastases: lung,
breast, melanoma, kidney...
• Repeated bleedings; gives inhomogeneous appearance
• More edema, mass effect
81
Dual energy CT
• Separate enhancement from blood
82
AJNR Am J Neuroradiol 2012 33: 865-872
Virtual iodine
Virtual non-contrast enhanced Fusion
Plain Dual energy CTA
Take home points infarct
• Findings at plain CT: loss of gray-white matter differentiation, dense vessel, swelling
• CTA can confirm ischemic diagnosis and establish differential diagnoses (dissection, sinus thrombosis, AVM, aneurysm)
• CTP/MRP can establish diagnosis and possibly identify candidates for i v thrombolysis/i a thrombectomy
• DWI is highly sensitive for acute ischemia from early timepoint until around two weeks after ictus
83
Take home points non-traumatic hemorrhage
SAH: – CTA of good quality (>300 HU)– MIP e.g. 4/2 MM.– structured evaluation of predilection sites for aneurysms
ICH:– CTA on wide indications, especially younger– spot sign bad prognostic sign– dual energy technique can separate iodine and hematoma– amyloid angiopathy common source in elderly, often
characteristic microbleeds at MRT– consider sinus thrombosis– blood has varying appearance at MRI– blood can cause diffusion restriction (diff infarct, abscess!)
84