CT

Non-contrast CT of the brain remains the mainstay of imaging in the setting of an acute stroke. It is fast,
inexpensive and readily available. Its main limitation, however, is the limited sensitivity in the acute setting.
Detection depends on the territory, the experience of the interpreting radiologist and of course the time of
the scan from the onset of symptoms. Whether tissue is supplied by end arteries (e.g. lenticulostriate
arteries) or has collateral supply (much of the cerebral cortex) will influence how quickly cytotoxic
edema develops 6. For example detection of MCA territory infarct has been shown to be approximately 60-
70% in the first 6 hours 3, although changes in the deep grey matter nuclei (especially lentiform nucleus)
can be visible within 1 hour of occlusion in up to 60% of patients 6.

The goals of CT in the acute setting are:

1. exclude intracranial hemorrhage, which would preclude thrombolysis

2. look for any "early" features of ischemia
3. exclude other intracranial pathologies that may mimic a stroke, such as tumor

Immediate
The earliest CT sign visible is a hyperdense segment of a vessel, representing direct visualization of the
intravascular thrombus / embolus and as such is visible immediately 7. Although this can be seen in any
vessel, it is most often observed in the middle cerebral artery (see hyperdense middle cerebral artery
sign and middle cerebral artery dot sign). It may be of therapeutic and prognostic value to differentiate this
hyperdense 'regular' thromboembolus from a calcified cerebral embolus.

Early hyperacute
Within the first few hours, a number of signs are visible depending on the site of occlusion and the presence
of collateral flow. Early features include:

 loss of grey-white matter differentiation, and hypoattenuation of deep nuclei:

o lentiform nucleus changes seen as early as 1 hour after occlusion, visible in 75% of patients at 3
hours 6
 cortical hypodensity with associated parenchymal swelling with resultant gyral effacement
o cortex which has poor collateral supply (e.g. insular ribbon) is more vulnerable 6

Acute
With time the hypoattenuation and swelling become more marked resulting in a significant mass effect. This
is a major cause of secondary damage in large infarcts.

Subacute
As time goes on the swelling starts to subside and small amounts of cortical petechial hemorrhages (not to
be confused with hemorrhagic transformation) result in elevation of the attenuation of the cortex. This is
known as the CT fogging phenomenon 5. Imaging a stroke at this time can be misleading as the affected
cortex will appear near normal.

Chronic
Later still the residual swelling passes, and gliosis sets in eventually appearing as a region of low density
with negative mass effect. Cortical mineralisation can also sometimes be seen appearing hyperdense.

CT perfusion
CT perfusion has emerged as a critical tool in selecting patients for reperfusion therapy as well as
increasing the accurate diagnosis of ischemic stroke among non-expert readers four-fold compared to
routine non-contrast CT 9.

It allows both the core of the infarct (that part destined to never recover regardless of reperfusion) to be
identified as well as the surrounding penumbra (the region which although ischemic has yet to go on to
infarct and can be potentially salvaged). CT perfusion may also demonstrate early evidence of
associated crossed cerebellar diaschisis.

The key to interpretation is understanding a number of perfusion parameters:

 cerebral blood volume (CBV)

 cerebral blood flow (CBF)
 mean transit time (MTT)
 time to peak (TTP)
Areas which demonstrate matched defects in CBV and MTT represent the unsalvageable infarct core,
whereas areas which have prolonged MTT but preserved CBV are considered to be the ischemic
penumbra 9.

These factors will be discussed further separately. See CT perfusion.

CT angiography
 may identify thrombus within an intracranial vessel, and may guide intra-arterial thrombolysis or clot
retrieval.
 evaluation of the carotid and vertebral arteries in the neck
o establishing stroke etiology (eg. atherosclerosis, dissection, web)
o access limitation for endovascular treatment (e.g. tortuosity, stenosis)
 may be necessary prior to thrombolysis in pediatric stroke
o some guidelines only advise that children with an arterial thrombus benefit from thrombolysis

Multiphase or delayed CT angiography

Multiphase or delayed CT angiography is showing benefit either replacing CT perfusion or as an additional
4th step in the stroke CT protocol as it guides patient selection for endovascular therapy by assessing
collateral blood flow in the ischemic and infarct tissue.

MRI
MRI is more time consuming and less available than CT but has significantly higher sensitivity and
specificity in the diagnosis of acute ischemic infarction in the first few hours after onset.

Early hyperacute
Within minutes of arterial occlusion, diffusion weighted imaging demonstrates increased DWI signal and
reduced ADC values 4,10. This correlates well with infarct core (for a detailed discussion of DWI and ADC in
stroke see diffusion-weighted MRI in acute stroke). At this stage, the affected parenchyma appears normal
on other sequences, although changes in flow will be detected (occlusion on MRA) and the
thromboembolism may be detected (e.g. on SWI). Slow or stagnant flow in vessels may also be detected as
a loss of normal flow void and high signal on T2/FLAIR and T1 C+ (intravascular enhancement).

If infarction is incomplete then cortical contrast enhancement may be seen as early as 2 to 4 hours 10.

Late hyperacute
Generally, after 6 hours, high T2 signal will be detected, initially more easily seen on FLAIR than
conventional fast spin echo T2 10. This change continues to increase over the next day or two.

T1 hypointensity is only seen after 16 hours 10, and persists.

Acute
During the first week, the infarcted parenchyma continues to demonstrate high DWI signal and low ADC
signal, although by the end of the first week ADC values have started to increase. The infarct remains
hyperintense on T2 and FLAIR, with T2 signal progressively increasing during the first 4 days. T1 signal
remains low, although some cortical intrinsic high T1 signal may be seen as early as 3 days after
infarction 10. After day 5 the cortex usually demonstrates contrast enhancement on T1 C+ 10. Less common
patterns of enhancement include arterial enhancement, encountered in approximately half of strokes and
becomes evident after 3 days, and meningeal enhancement which is uncommon and is usually seen
between 2 and 6 days 10.

Hemorrhage, most easily seen on susceptibility weighted imaging (SWI), is not a good indicator of age.
Although most commonly seen after 12 hours and within the first few days, it may occur earlier or as late as
5 days 10.

Subacute
ADC demonstrates pseudonormalization typically occurring between 10-15 days 10. As ADC values continue
to rise, infarcted tissue progressively gets brighter than normal parenchyma. In contrast, DWI remains
elevated due to persistent high T2/FLAIR signal (T2 shine through), unless hemorrhage (T2 blackout) or
cystic encephalomalacia 10. T2 fogging is also encountered typically between 1 and 5 weeks, most
commonly around week 2 10,11.

T1 weighted sequences continue to show hypointensity with cortical intrinsic high T1 signal due to cortical
laminar necrosis or pseudolaminar necrosis 10. Cortical enhancement is usually present throughout the
subacute period.

Chronic
T1 signal remains low with intrinsic high T1 in the cortex if cortical necrosis is present 10. T2 signal is high.
Cortical contrast enhancement usually persists for 2 to 4 months 10. Importantly if parenchymal
enhancement persists for more than 12 week the presence of an underlying lesion should be considered 10.

ADC values are high, resulting in high signal. DWI signal is variable, but as time goes on signal
progressively decreases.