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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}}
===Configuration===
Initially without IV contrast.
==Non-contrast CT==
Non-contrast CT in early infarction has a variable detection rate of about 65% in cases imaged within 6 hours. A description of these signs is below.<ref name=Mirza2016/>
;Hyperdense artery/MCA sign
This is a result of a thrombus or embolus (usually in the MCA) resulting in an increased density
of the blocked vessel. The prevalence ranges from about 27% in all types of strokes to 41% with
MCA infarct with a specificity of 100%, but sensitivity of only 30% . This sign disappears with
resolution of the thrombus in a few days. False positives are due to calcification of the walls or a
high hematocrit (Figure 1).<ref name=Mirza2016/>
;Hypo-attenuating brain tissue
Ischemia causes cytotoxic edema; an increase in brain water by 1% results in a CT attenuation
decrease of 2.5 HU (Hounsfield Units) . The specificity of ischemic edema on NCCT for brain
infarcts is 85% and sensitivity was 64%, with lack of early CT findings resulting in better 90 day
clinical outcomes and vice versa . Also seen is cortical sulcal effacement (Figure 2).<ref name=Mirza2016/>
<gallery mode=packed heights=270>
File:CT of dense media sign.png|Figure 1. Hyperdense Artery Sign. The “Dense MCA or hyperdense vessel/artery sign” is one of the early signs of acute middle cerebral artery (MCA) territory infarction. This corresponds to a hyper-dense cord like MCA seen in the regionof the Sylvian fissure on non-contrast CT which represents thrombotic material in main stem of the MCA.<ref name=Mirza2016/>
File:CT of cerebral infarction.png|Figure 2. Left middle cerebral artery (MCA) infarction. Axial nonenhanced computer tomography shows foci of hypoattenuation in the left parenchyma (arrows) and sulcal effacement in the left MCA territory, consistent with infarction.<ref name=Mirza2016/>
</gallery>
;Obscuration of the lentiform nucleus
Also called blurred basal ganglia; it is one of the most common and earliest seen sign of
infarction (MCA) due to terminal blood supply pattern. The loss of the grey-white matter interface
and CT hypodensity results in the ‘obscuration’ of the lentiform nucleus.<ref name=Mirza2016/>
;Insular ribbon sign
Another early and indicative sign of infarction (MCA) refers to hypodensity and swelling of
the insular cortex results in loss of the insular ribbon (Figure 3).<ref name=Mirza2016/>
[[File:CT of insular ribbon sign.png|thumb|Figure 3: Insular ribbon signrefers to loss of the normal grey-white matter differentiation in the
insular cortex. It is one of the earliest imaging signs of middle cerebral artery territory infarction.
The yellow arrow shows a normal insular cortex (ribbon visble). However upon infarction leading
to cytotoxic edema, this ribbon is lost (red arrow).<ref name=Mirza2016/>]]
;Hemorrhagic infarct
There is usually a sharp contrast between blood (high attenuating- seen as brighter white areas) and CSF (low attenuating-dark areas) (Figure 4 A & B).<ref name=Mirza2016/>
<gallery mode=packed heights=250px>
File:CT of subarachnoid hemorrhage.png|Figure 4A: Axial nonenhanced CTshows “bright” or hyper attenuating dense subarachnoid hemorrhage throughout the perimesencephalic cistern (arrow), along the tentorium (double arrows), and from there to the 4th (double arrowheads) and 3rd (arrowhead) ventricles.<ref name=Mirza2016/>
File:CT of basal ganglionic hemorrhage.png|Figure 4B: Nonenhanced axial CT demonstrates a large right basal ganglionic hypertensive bleed (*) complicated by mass effect, midline shift (subfalcine herniation)to the left (arrows). The blood is seen as hyper-attenuating or bright.<ref name=Mirza2016/>
</gallery>
By altering standard viewing parameters, the sensitivity and specificity of stroke detection can be increased.<ref name=Mirza2016/>
==Quantification of ischemic involvement - ASPECTS==
[[File:Cerebral regions by ASPECTS.png|thumb|270px|Alberta Stroke Program Early Ct Score (ASPECTS). Schematic diagram showing various areas
used for scoring on the ASPECTS. Level of internal capsule & insula: M1 - cortical area anterior
to Sylvian fissure; M2 - cortical area just posterior to Sylvian fissure; M3 - more posterior cortical
area in MCA distribution at same level.
At cut near top of the lateral ventricles: M4 - anterior third of cortex; M5 - middle third of
cortex; M6 - posterior third of cortex.<ref name=Mirza2016/>]]
A major reason for quantifying the volume in ischemic involvement is because extensive cerebral ischemia further increases the risk of secondary hemorrhage if thrombolysis is given.
Alberta Stroke Program Early CT score (ASPECTS) is a 10-point quantitative topographic CT
scan score offering a reproducible grading system to score early ischemia in
anterior circulation strokes to better direct treatment and reduce the variability of observations. Using two standard axial CT slices; one at the level of the thalamus and basal ganglia, and
one just rostral to the basal ganglia, the MCA territory is divided into 10 regions, each accounting
for one point in the total score, for each involved area, a point is subtracted. This score correlated
inversely with the NIHSS (National Institutes of Health Stroke Score) with clinicians agreeing it
superior and more systematic compared to the conventional 1/3 MCA rule to exclude thrombolytic
treatment. The ASPECTS method is not without its limitations; such as difficulty in scoring
due to age related periventricular white matter changes or streak artifacts in the base of the skull
or tilt and motion artifacts..<ref name=Mirza2016/>
{|class="wikitable"
|+ CT findings that generally contraindicate thrombolysis<ref name="FrankGrotta2013">{{cite journal|last1=Frank|first1=Benedikt|last2=Grotta|first2=James C.|last3=Alexandrov|first3=Andrei V.|last4=Bluhmki|first4=Erich|last5=Lyden|first5=Patrick|last6=Meretoja|first6=Atte|last7=Mishra|first7=Nishant K.|last8=Shuaib|first8=Ashfaq|last9=Wahlgren|first9=Nils G.|last10=Weimar|first10=Christian|last11=Lees|first11=Kennedy R.|title=Thrombolysis in Stroke Despite Contraindications or Warnings?|journal=Stroke|volume=44|issue=3|year=2013|pages=727–733|issn=0039-2499|doi=10.1161/STROKEAHA.112.674622}}</ref>
|-
| Edema, dense middle cerebral artery sign, loss of insular ribbon, lenticular hypodensity, acute infarction, sulcal effacement, or ASPECT-score of 8 or 9
|-
| Mass effect, infarction of >1/3 of the middle cerebral artery territory, midline shift, or ASPECT-score of ≤7
|-
| ASPECT-score of ≤7
|}
==Computed tomography angiography (CTA)==
CTA is a minimally invasive study with an optimally timed rapid injection of iodinated
contrast through a peripheral IV (intravenous) line to cause vascular opacification, obtaining
thin section CT images and using software to stitch the images allowing for a 3-dimensional
image of cerebral and neck vasculature (from the aortic arch to the circle of Willis). This allows
for identification of stenosis and occlusions; assisting therapeutic decisions such as IV or intraarterial
TPA, mechanical clot retrieval or in cases of carotid dissection, against such a therapy.
CTA also identifies vascular abnormalities such as arterio-venous malformations and aneurysms.
CTA demonstrated occlusion does correlate with the NIH Stroke Score and outcome of TPA
(Figure 4C, 5A, B, C, D).<ref name=Mirza2016/>
<gallery mode=packed heights=220>
File:CT angiography of a vascular malformation with intraventricular hemorrhage.png|Figure 5A: Sagital reformatted images from CT angiogram identify an enhancing vascular malformation (arrow), which was the etiology of the intraventricular hemorrhage.<ref name=Mirza2016/>
File:CT angiography of basilar tip aneurysm.png|Figure 5B: Computed tomography angiogram in the axial projection demonstrates a focal basilar tip artery aneurysm (arrow).<ref name=Mirza2016/>
File:Volume rendered CT angiography of anterior communicating artery aneurysm.png|Figure 5C: Volume rendering of cerebal computed tomography angiogram (CTA) with
skull surface overlay demonstrates an anterior communicating artery aneurysm (1). Dedicated images from CTA of the Circle of Willis isolate the aneurysm (arrow) (2).<ref name=Mirza2016/>
File:Volume rendered CT angiography of posterior communicating artery aneurysm.png|Figure 5D: This patient had subarachnoid hemorrhage on non-contrast CT scan. Left image is a maximum intensity projection and right is a volume rendering CTA (to identify source of hemorrhage) which show aneurysm like pouching (red arrows) in the PCOM (2). On conventional angiography, these aneurysms were proved to be the infundibulum of vessels. The diagnosis of aneurysms <3 mm on CTA is often tenuous and requires angiographic confirmation.<ref name=Mirza2016/>
File:Volume rendered CT angiography of subtle anterior communicating artery aneurysm.png|Two more volume renderings of the same case, also showing an aneurysm-like pouching in the ACOM.<ref name=Mirza2016/>
</gallery>
CTA Source Images: CTA SI using the images in a CTA, cerebral perfusion can be assessed as
low density/dark areas in contrast to hyper-attenuated contrast areas allowing for an estimation
of tissue perfusion and a better assessment of tissue at risk compared to NCCT potentially
removing the need for a separate CT perfusion study.<ref name=Mirza2016/>
==Computed tomography perfusion imaging (CTP)==
CTP (like CTA) tracks an IV bolus of iodinated contrast over time with sections of the brain
imaged repeatedly. This allows the measurements of parameters such as cerebral blood volume,
cerebral blood flow, mean transit time (time difference between arterial inflow and venous
outflow), time to peak enhancement (time from the beginning of the contrast injection to the
maximum concentration in a region of interest). These parameters can be extrapolated to
delineate areas of hypo-perfusion and irreversible infarction by creating perfusion maps. CTP
has shown incremental increased sensitivity and specificity in diagnosing acute ischemic stroke
compared to NCCT or CTA . CTP is easily available and can be performed on a standard helical
CT after NCCT. Clinically, in acute stroke CTP provides information on the penumbra (increased
mean transit time, moderately decreased cerebral blood flow and normal to high cerebral blood
volume due to auto regulation or if blood flow is markedly decreased then decreased cerebral
blood volume) and on the infarcted tissue (severe decrease in cerebral blood flow, and blood
volume with increased mean transit time) with defined cut-offs for each criteria. A drawback of
CTP is the need to analyze several brain slices for accurate flow data, requiring a multi detector
CT with higher slice row, (currently at 2 slices, evolving to 64 slices) and high radiation exposure.
Different techniques are employed such as Dynamic Contrast-enhanced CT and Perfusedblood-
volume Mapping . Dynamic contrast enhanced CT consists of monitoring the passage
of iodinated contrast bolus which causes a transient increase in attenuation which is in linear
relation to the amount of contrast in the region used to generate curves for arterial and venous
Regions of Interest which are converted using mathematical models into the perfusion parameters
and color coded perfusion maps.<ref name=Mirza2016/>
[[File:CT perfusion in M1 artery occlusion.png|thumb|300px|Figure 6B: This perfusion map gives a quick visual estimate of the anterior cerebral artery (ACA) and middle cerbral artery (MCA) collaterals on the convexity in a case of M1 artery occlusion. This patient underwent CT perfusion study in setting of acute aphasia and hemiparesis. A prominent mismatch is present on CT perfusion with delay in time to peak (TTP) but relatively preserved rCBV, (cerebral blood volume) indicating adequate collateral supply with the exception of basal ganglia (M1 thrombus will nearly always take out the lenticulostriate vessels which are effectively end-arteries without significant collaterals).<ref name=Mirza2016/>]]
Perfusion maps can give a quick visual read for color changes indicative for perfusion deficits
or through measurements (usually not required). Perfused-blood-volume Mapping consists
of subtracting the unenhanced CT data from the CTA source image data giving cerebral blood
volume data with the advantage of allowing evaluation of the whole brain. However, since it does
not allow determination of the mean transit time, blood flow and hence the ischemic penumbra,
it clinically has a lesser use (Figure 6A,B).<ref name=Mirza2016/>
<gallery mode=packed heights=200>
File:CT perfusion with flow and volume maps in cerebral infarction.png|Figure 6A: (1) Regional cerebral blood flow map from computed tomography perfusion in a case of left middle cerebral artery infarct shows a large perfusion defect in the left frontal and temporal lobes, evidenced by a lack of color display. (2) Regional cerebral blood volume map demonstrates a penumbra of decreased perfusion (indicated with arrows around blue areas) surrounding the defect (purple), indicating potentially reversible ischemia around the perfusion defect.<ref name=Mirza2016/>
</gallery>
==Subsequent MRI==
MRI is seldom performed after CT of stroke in Swedish practice,<ref>{{NU Hospital Group}}</ref> but can offer additional diagnostics:
[[File:Stroke imaging algorithm.png|thumb|350px|center|Algorithm.]]
{{Main|MRI of the head in stroke}}
==Reporting==
Report even the absence of:
*Intracranial hemorrhage
*Delineable infarction
In case of angiography, report:
*Normal/Unremarkable contrast filling of larger vessels of the cerebrum and cerebellum (or pathology thereof).
{{Reporting}}
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