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Mikael Häggström: /* MRI - timing and therapeutic windows */ CT

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MRI - timing and therapeutic windows: CT

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|author1=[[User:Mikael Häggström|Mikael Häggström]]
|author2=Authors if integrated Creative Commons article<ref name=Mirza2016>{{cite web|url=http://www.smgebooks.com/neuroimaging/chapters/NI-16-06.pdf|title=Neuroimaging in Acute Stroke|author=Shazia Mirza and Sankalp Gokhale|date=2016-07-25}}<br>[https://creativecommons.org/licenses/by/4.0/ Attribution 4.0 International (CC BY 4.0)]</ref>
|author3=
}}
==Planning==
{{Stroke - choice of investigation}}

==Conventional MRI==
MR sequences usually used in acute strokes are: T1-weighted spin echo, T2-weighted fast
spin-echo, fluid-attenuated inversion recovery-FLAIR, DWI for acute ischemia, MRA and PWI
for penumbra. T2-weighted gradient-echo- GRE- for hemorrhage and gadolinium-enhanced T1-
weighted spin-echo sequences. Typical findings in acute ischemia include: hyper-intense signal in
white matter on T2-weighted images and fluid-attenuated inversion recovery images, and similar
to CT findings; grey-white matter distinction loss, sulcal effacement and intravascular signal
intensity changes due to occlusion. Hemorrhage is seen as abnormal blooming and while MRI is
effective at detecting bleeds, thrombolytic guidelines utilize CT based evidence alone. With the
onset of Diffusion weighted imaging, the conventional MR sequences play a minor role in acute
stroke evaluation (Figure 7A,B,C).<ref name=Mirza2016/>

<gallery mode=packed heights=200>
File:FSE T2 MRI of cerebral infarction.png|Figure 7A: Fast spin echo T2-weighted fat suppressed image demonstrates increased signal intensity and effacement of the right temporal lobe, consistent with sub-acute infarct of the right middle cerebral artery.<ref name=Mirza2016/>
File:T1 MRI of cortical border zone infarcts.png|Figure 7B: These are T1 weighted MRI images of a patient with bilateral cortical border zone infarcts (secondary to hypotension). T1 bright staining is seen along cortical grey matter suggestive of Cortical Laminar Necrosis.<ref name=Mirza2016/>
File:FLAIR MRI of cerebral infarction.png|Figure 7C: MRI axial FLAIR images of brain show an infarct involving left frontal lobe anterior to the Sylvian fissure,an area which corresponds to the superior division of the left middle cerebral artery.<ref name=Mirza2016/>
</gallery>

==MR angiography==
High resolution imaging of the cranial vasculature can be obtained using a non-contrast 3D
time-of-flight (TOF) MR angiography (MRA). The basis of this technique is that protons in tissue
are saturated by repeated radiofrequency excitation and have low signal intensity but protons
coming in through the vessels are unsaturated and have a high signal intensity producing flow
dependent imaging. TOF can be 2D or 3D and does not expose the patient to radiation, or contrast.
It is limited by both patient motion and flow artifact often resulting in over-estimation of the
stenosis or occlusion. Since it obtains imaging over a short time period, it provides no data on
the speed or direction of blood flow (important to study collateral supply). To overcome this, 4-D
MRA (and CTA) have been developed. This involves reimaging the field of interest at several time
points after the radiofrequency pulse (or contrast injection in CTA) with results similar to those
of catheter angiography . Several studies show that TOF is not as accurate as other modalities
such as DSA or CTA with a sensitivity of 84.2% and specificity of 84.6% . Contrast enhanced
MRA (with gadolinium) is the technique used for extra-cranial vasculature imaging allowing
improved anatomical details with an advantage of better diagnosis of arterial dissections to be
balanced with side-effects of contrast in renally compromised patients and nephrogenic systemic
fibrosis (Figure 8 A,B & C).<ref name=Mirza2016/>

<gallery mode=packed heights=190>
File:TOF MRI angiography of right middle cerebral artery stenosis.png|Figure 8A: 3-D Time Of Flight (TOF) Non contrast MR Angiography of brain shows severe right MCA proximal main stem (yellow arrow) with sparse cortical branches of right MCA compared to left (green arrow).<ref name=Mirza2016/>
File:T2-star FLAIR MRI of sluggish arterial flow.png|Figure 8B: The same case as above shows faint serpiginous high signal on T2* axial FLAIR (due to sluggish flow in the sparse cortical branches of the MCA) known as the “ivy sign” in the right perisylvian area (yellow arrows).<ref name=Mirza2016/>
File:MR angiography of bilateral internal carotid dissection.png|Figure 8C: An MR angiogram of a patient with bilateral internal carotid artery dissection showing
narrowing of lumen. The lumen is black (blood imaging) and a white hematoma can be visualized in the vessel wall.<ref name=Mirza2016/>
</gallery>

==Diffusion-weighted imaging (DWI)==
MR with diffusion is quickly becoming the gold standard in acute stroke imaging, as it can
be obtained within 10 minutes at certain centers . DW MRI uses fast (echo-planar) imaging
technology, and is resistant to patient motion artefacts with an imaging time of a few seconds to
2 minutes . The sensitivities and specificities are 100% and 86%, respectively, for diffusionweighted
MRI versus 18% and 100% for conventional MRI . Hence, DW MRI plays an essential
role in the diagnosis of acute infarctions and to rule out stroke mimics.
[[File:DWE MRI of cerebral infarction.png|thumb|300px|Figure 9:(A and B) Restricted water diffusion in the region of infarct (right middle cerebral
artery) results in an increased signal intensity on diffusion-weighted imaging (A) and decreased
signal on apparent diffusion coefficient imaging (B).<ref name=Mirza2016/>]]

Principle: is based on the random (Brownian) motion of water molecules in tissues. A change
in the water content of cells affects the rate of molecular diffusion in these tissues. Using T2
weighted spin-echo MR imaging sequence with 2 extra gradient pulses (equal magnitude, opposite
directions) results in signal changes: greater loss of signal is seen in tissues with higher rates of
diffusion and vice versa. Hence, in acute stroke (cytotoxic edema with decreased rate of molecular
diffusion in the affected tissue), ischemic tissue appears brighter than normal brain tissue. DW
MRI cannot be used to calculate the diffusion coefficient, which is obtained from orthogonal
diffusion weighted MR images in all 3 planes and is called Apparent Diffusion Coefficient ADC.
ADC maps are used because occasionally areas on diffusion imaging have a high signal due to
vasogenic edema, but will appear dark on ADC map proving it is not an acute infarct.
In humans restricted diffusion is seen as early as 30 minutes decreasing to reach a low at
3–5 days (hyper intense signal with reduced ADC values due to restricted diffusion), and reaches
baseline at 1–4 weeks, explained by the development of vasogenic edema alongside the cytotoxic
edema, replaced by gliosis which carries an increase in extracellular water (high intensity signal
due to increased T2 signal: T2 shine through and variable ADC values for months). Hence DWI
cannot be reliably used to estimate infarct age without the help of ADC maps.
DW imaging has high sensitivity and specificity with studies showing 94% accuracy for afinal
diagnosis of stroke, compared with a yield of 71%-80% when using conventional MRI (T2W/
PDW or FLAIR sequences) . DWI demonstrated infarct volumes also correlate (with statistical
significance) with NIH Stroke Score and other scales . However false negatives with DWI can
occur in small lacunar infarcts of the brainstem or deep nuclei . False positives may be seen in
abscesses, tumors but can be easily ruled out. Diffusion imaging may show no abnormality in the
setting of ischemia, hence normal DWI with altered perfusion images indicate tissue at risk, and
prompt initiation of therapy (Figure 9).<ref name=Mirza2016/>

==Perfusion-weighted imagin (PWI)==
The main advantage of Perfusion weighted imaging is its ability to image entire brain and
detect the ischemic penumbra. This technique requires a method of achieving contrast for
perfusion either exogenous (IV contrast agent-gadolinium) or endogenous (labeling hydrogen-1
protons in water or arterial spin labeling).<ref name=Mirza2016/>

[[File:CT and MR perfusion of cerebral infarction.png|thumb|300px|Figure 10A: Patient presents with a stroke involving left middle cerebral artery. MR perfusion shows areas of increased time to peak (TTP) which correspond to decreased flow and volume. Visual key:<br>- For TTP, higher scale (red) means longer TTP (compromised), and lower scale (blue) means shorter TTP (intact).<br>- For CBF (cerebral blood flow), higher scale (red) means faster flow (preserved), and lower scale (blue) means less flow (compromised).<br>- For CBV (cerebral blood volume), higher scale (red) means more volume (generally preserved), and lower scale (blue) less volume (generally compromised).<ref name=Mirza2016/>]]
Principles: Passage of contrast in the vessels causes transient loss of signal (T2 effect).
Tracking these signal change results in a time-signal curve which can create perfusion maps of
cerebral blood volume and mean transit time. Using the arterial spin technique encompasses
using radiofrequency to invert the spin polarity of the protons entering the image plane which
measurably affects the image intensity as they perfuse the tissue. Subtracting the flow sensitive
image from the flow insensitive image gives a measure of the protons perfusing that image plane,
in essence a perfusion map.<ref name=Mirza2016/>

PWI detects areas of reduced flow contrasted to DWI which depicts areas of injury. The
difference between the DWI defect and the PWI defect is the ischemic penumbra which helps to
guide further stroke therapy. This is the subject of multiple clinical trials for patients with a DWIPWI
mismatch who will benefit from thrombolysis . In certain cases, DWI defect is larger
than PWI defect which is seen in early reperfusion (Figure 10 A, B).<ref name=Mirza2016/>

<gallery mode=packed heights=200>
File:MR perfusion in cerebral infarction.png|Figure 10B: TTD -time to drain, (similar to TTP), shows decreased flow in entire middle cerebral artery territory in a case of infarction. CBF is down in the lenticulo-striate area, but relatively good over the temporal lobe. CBV is increased implying that temporal lobe vascular bed has dilated effectively, thereby increasing its volume and almost normalizing temporal lobe CBF.<ref name=Mirza2016/>
</gallery>

This is the preferred MRI sequence to rule out acute or chronic hemorrhage including a
hemorrhagic transformation. It is a T2 weighted sequence sensitive to the change in local
magnetic fields due to the iron in blood and degradation products. As the hemoglobin in the
parenchyma becomes deoxygenated, unpaired electrons make it para-magnetic (non-uniform
field) resulting in a signal loss- known as susceptibility effect seen as hypointense (dark) lesions.
This sequence is used to image acute stroke patients in whom ICH is suspected or has to be ruled
out for thrombolytic therapy and is found to be as accurate as CT in the detection of acute ICH and
more accurate in cases of chronic ICH (Figure 11 A, B).<ref name=Mirza2016/>

<gallery mode=packed heights=180>
File:T2-star MRI of cerebral infarction.png|Figure 11 A: Arterial infarct with hemorrhagic transformation show a low signal intensity (yellow arrow) on T2* GRE (areas of bleed) in the region of infarct.<ref name=Mirza2016/>
File:FLAIR, T2-star and DW MRI of cerebral infarction.png|Figure 11 B: MRI axial FLAIR study shows focal hyperintensity in the region of corpus callosum (yellow arrow) which corresponds to the low signal intensity on T2* GRE (green arrow). DWI shows the corresponding focus of ischemia (red arrow).<ref name=Mirza2016/>
</gallery>

==MRI - timing and therapeutic windows==
Treatment with thrombolytics is time dependent (within 3-4.5 hours) hence strokes that
occur in sleep or unwitnessed pose a unique therapeutic challenge for which neuroimaging can
provide decision making criteria. MRI sequences have been proposed to identify strokes in the
therapeutic time window.<ref name=Mirza2016/>

One imaging combination includes: DWI to detect lesions within minutes of ischemia and
FLAIR which is sensitive for subacute ischemia. Hence a positive DWI with FLAIR negative
mismatch (94% specific) is likely to provide a time window for safe thrombolysis .
An imaging combination of DW-PWI mismatch helps identify the tissue at risk, and potential
benefit from interventions even if outside the 3-4.5 hour window.<ref name=Mirza2016/>

Several studies have been conducted to determine the “best” imaging modality in acute stroke,
but the reality is that both CT and MRI will co-exist and complement each other for a long time.
The main drawbacks to CT are that an ischemic brain stroke may not appear in a CT scan for
up to 48 hours period, and that CT does not image the vertebra-basilar (up to 15% of strokes).
While the MRI does provide superior quality of images and anatomical details, in an acute setting
its advantages address the above-mentioned two drawbacks of CT. Important contraindications
to MRI are patients with magnetic material in their body such as pacemakers, pins, a vital point
to note as neurologically altered or aphasic patients may be unable to provide this information to
their providers.<ref name=Mirza2016/>

The sensitivities and specificities were 100% and 86%, respectively, for diffusion-weighted
MR imaging versus 18% and 100% for conventional MR imaging and 45% and 100% for CT .
New guidelines from the American Academy of Neurology state that doctors should use a diffusion
MRI scan to diagnose stroke instead of a CT scan which was published in the July 13, 2010, issue
of Neurology®, the medical journal of the American Academy of Neurology.
The imaging modality of choice will depend upon the specific situation: cost, availability,
clinical setting, contraindications etc. and it remains the purview of a well-educated provider to
determine the imaging to effectively guide the therapeutic goals.<ref name=Mirza2016/>

{|class="wikitable"
|+ Table 1: CT vs MRI<ref name=Mirza2016/>
! Characteristic !! CT !! MRI
|-
| Availability || Easily available in the emergency department || Not available in all emergency departments
|-
| Time || 5 mins || 15 mins
|-
| Perfusion study: volume assessed || 2–4 cm || Entire brain visualized
|-
| Side effects: Contrast
| Iodinated contrast has toxic effects on kidney, cannot be used in renally compromised patients, risk of anaphylaxis.
| Gadolinium: minimal toxicity on kidneys, risk of nephrogenic and systemic fibrosis
|-
| Side effects: Ionizing radiation || YES: increases risk of cancer || No ionizing radiation
|-
| Side effects: Claustrophobia || - || +++
|-
| Drawback: motion artefact || + || +++
|-
| Contraindication: Pacemaker, shrapnel, metal plates || - || +++
|-
!colspan=3| Purpose
|-
| Chronic hemorrhage || +/- || +++
|-
| Acute ischemic stroke || - || ++
|-
| Angiography || ++ || +++
|-
| Vertebro-basilar visualization || - || ++
|-
|colspan=3| Abbreviations: ICH: Intracerebral hemorrhage, SAH: Sub arachnoid hemorrhage, EDH: Extradural hemorrhage, SDH: Subdural hemorrhage. AVM: Arterio-venous malformation, TCD: transcranial Doppler, CDUS: Carotid duplex ultrasound, DSA: Digital subtraction Angiography.
|}

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@@ Line 136: / Line 136: @@
 An imaging combination of DW-PWI mismatch helps identify the tissue at risk, and potential
 benefit from interventions even if outside the 3-4.5 hour window.<ref name=Mirza2016/>
 ==See also==

@@ Line 190: / Line 190: @@
 |colspan=3| Abbreviations: ICH: Intracerebral hemorrhage, SAH: Sub arachnoid hemorrhage, EDH: Extradural hemorrhage, SDH: Subdural hemorrhage. AVM: Arterio-venous malformation, TCD: transcranial Doppler, CDUS: Carotid duplex ultrasound, DSA: Digital subtraction Angiography.
 |}
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MRI of the head in stroke - Revision history

Mikael Häggström: /* MRI - timing and therapeutic windows */ Moved to separate page

Mikael Häggström: /* MRI - timing and therapeutic windows */ CT

Mikael Häggström: From CC-BY article