How to Differentiate Carotid Obstructions

Atherosclerosis
Atherosclerotic plaques are mostly located at the level of the bulbus. Atherosclerosis  is usually bilateral and frequently calcifications can be seen. 

Subtotal stenosis
In a high-grade atherosclerotic stenosis the flow through the internal carotid is  severely decreased and results in a collapse and consequently a small caliber of the vessel distal to the occlusion.    

Occlusion
In a total occlusion the contrast has a { or curly bracket-like configuration.

Dissection
In the case of a ICA dissection the bulbus is not involved and the contrast in the proximal ICA has a flame-shaped  configuration. The total diameter of the ACI is widened due to the formation of a mural hematoma. The narrowed eccentric true lumen is surrounded by a crescent-shaped mural on transversal imaging. The compressed true lumen can be occluded in case of severe compression.    

Pseudo-occlusion
This simulates an occlusion of the lower cervical part of the internal carotid, but is actually the result of a stop at the carotid T-top. Contrast that tries to enter the internal carotid will give a waterpaint appearance due to this outflow obstruction.    

Carotid web
This is  a thin shelf-like luminal protrusion of the intimal fibrous tissue that extends from the posterior aspect of the proximal internal carotid artery bulb into the lumen. The carotid web is increasingly being associated with ischemic stroke in young individuals, especially females.   

There is a problem diagnosing carotid dissection versus pseudo-obstruction.

In a study in which the CTA-findings were compared to tDSA (golden standard for carotid lesions), the results showed that there was a high accuracy in diagnosing atherosclerotic occlusions and high grade stenoses of the internal carotid artery.
Only one atherosclerotic stenosis was misdiagnosed as a pseudo-occlusion.

On the other hand pseudo-occlusions were misdiagnosed as carotid dissection and dissections were misdiagnosed as pseudo-occlusions quite frequently (red circles).

In the chapters below we will discuss how to differentiate dissection from pseudo-occlusion.

Tandem occlusions are intracranial occlusions combined with a severe (>70% ) stenosis or occlusion of the ICA.
They are found in up to 30% of all patients presenting with a large vessel occlusion.
The accompanying ICA pathology is not a contra-indication for endovascular therapy for the intracranial occlusion, regardless of the underlying  ethiology of the ICA stenosis/occlusion. 

However identifying carotid pathology is important for planning and execution of the endovascular procedure.

Typical findings in an atherosclerotic stenosis or occlusion are:

• Atherosclerotic stenosis of the ACI is mostly located at the level of the bulbus.
• Frequently there are calcified plaques.
• Atherosclerosis is usually a bilateral disease.

These patients are usually older and have cardiovascular risk factors.

ICA stenosis measurement

The illustration shows the formula for measuring the degree of stenosis according to the NASCET (North American Symptomatic Carotid Endarterectomy Trial).

The diameter of the stenosis (a) should be measured perpendicular to the longitudinal axis of the vessel (green line) and not in a pure axial plane (red line), because then you may underestimate the degree of stenosis.
It is compared to the diameter of the normal vessel at about 6 cm distal to the stenosis (b).
In the formula the degree of stenosis is calculated.

Calcifications are common in atherosclerotic stenosis and CTA has a high sensitivity in detecting these calcified structures.

Sometimes a bias in the exact evaluation of stenosis degree may be caused by the high attenuation values of the calcified plaques.
This might lead to an overestimation of the degree of stenosis.
Furthermore, heavily calcified plaques can be a challenge for the interventional neuroradiologist as the stenosis needs to passed with a large bored guiding catheter or long sheath (at least 6 Fr).

Near occlusion

In a severe stenosis or near occlusion the diameter of the ACI above the level of the stenosis is diminished and less than the caliber of the contralateral ICA and the ipsilateral ECA.

In a total occlusion the contrast has a { or curly bracket-like configuration, which is unlike an occlusion in a dissection or in a pseudo-occlusion.

Near occlusion (2)

In this case the common carotid artery has a normal diameter (image 1).
There is a severe stenosis with a partly calcified plaque at the level of the bulbus (2).
The ICA above the stenosis shows a small caliber (3). See also the arrow in the sagittal reconstruction.

The criteria for near occlusion are:

• Caliber of distal ICA smaller compared to the contralateral ICA (image 3).
• Caliber of the distal ICA less than the ipsilateral external carotid (ECA on image 3).

The peak velocity with US-doppler normally increases in relation to the severity of a stenosis, but when there is a near-occlusion the systolic peak velocity will drop to very low levels like in this case (20 cm/sec).

Continue with the sagittal images...

You can scroll through the sagittal images.

Notice the calcified plaque at the level of the bulbus and the small caliber of the distal ICA, which is less than the caliber of the ECA.

Treatment
Treatment strategy for near occlusion (NO) is still controversial. In the analyses conducted in randomized controlled trials such as the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST), it was reported that the risk of stroke was low with medical treatment, and surgical therapy was not beneficial for internal carotid NO.However, an 11%–33% risk of ipsilateral stroke within the first year has also been reported in medically treated patients.

Furthermore, other authors have reported a significantly lower risk of future stroke after Carotid endarterectomy or Carotid artery stenting in these patients.

Seeking safe interventional procedures could, therefore, be worthwhile especially with the current improvements in carotid stenting technique .

Occlusion

In a total atherosclerotic occlusion the contrast has a { or curly bracket-like configuration.
The stop will be at the level of the bulbus.

A carotid dissection is the result of a tear in the intima of the vessel wall.
As blood enters between the layers of the vessel wall an intramural hematoma is created.

This intramural hematoma results in the following:

• Dilatation of the total ICA-diameter 
• Compression of the true lumen
• The hematoma can be a source of emboli and lead to a cerebrovascular accident

Dissections cause about 2% of all ischemic strokes, but account for 10%−25% of ischemic strokes in young people.
Patients sometimes present with pain in the neck and may have a history of a previous trauma.

On CTA a dissection presents with the following findings:

• On axial images there is an eccentric and narrowed lumen of the ICA.
• There is expansion of the ICA (↑ of the total diameter).
• The bulbus is spared unlike in atherosclerotic disease.
• A dissection generally stops prior to entering the skull.
• The emboli that originate from the intramural hematoma are erythrocyte rich thrombi and result in very dense thrombi in the intracerebral vessels on a non-enhanced CT (dens vessel sign).

Flame-shaped ICA

These images show the typical flame-shaped presentation of a carotid dissection on sagittal CTA reconstructions and DSA.

Notice that on the CTA reconstruction you can follow the contours of the dilated ICA above the level where the contrast stops.
Also notice how similar the images are, when you compare the CTA with the DSA.

String sign

In most cases a dissection will present with a flame-shaped appearance like in A, but when the lumen is less compressed and still partially patent you may get the "string sign" as in B.

Look below the skull base

When you consider the possibility of a dissection, t is important to study the axial images just below the skull base as in this case.

On the left side there is a normal ICA and ECA (the high density structure in between them is the styloid process).
On the right side we see a normal ECA and medial to the jugular vein is the dilated ICA (circle).
The lumen does not fill with contrast.
The combination of an occlusion in an enlarged and dilated ICA means that we are dealing with a dissection.

A dissection stops at the skull base

This patient has a carotid dissection.
In A we see the compressed lumen in an eccentric position (green arrow).
The diameter of the ICA is enlarged by the intramural hematoma (red arrowheads).

When we follow the ICA cranially, the dissection continues up to image E (arrowheads).
At the level of the skull base, where the ICA enters the carotid canal (vertical petrous segment) , the dissection stops and the ICA has a normal appearance (yellow arrow).

Hyperdense thrombi

A typical finding in dissection are hyperdense thrombi as in these two patients.
Whenever you see these kind of extremely hyperdense thrombi, think of dissection and scroll down to just below the skull base.
These thrombi are almost completely composed of erythrocytes.

Dissection on DSA

All the findings that we discussed on CTA are similar and even more obvious on DSA.

1. The catheter is at the level of the bulbus, which is normal.
   A couple of centimeters above the bulbus the lumen of the ICA is eccentric and compressed by a mural hematoma (better seen on detailed view 2).
   At the level of the skull base (yellow stippled line) the vessel returns to normal.
2. Detailed view showing contrast material that has entered the hematoma.
   Notice that the total diameter of the ICA is enlarged. Arrow indicates the true lumen.
3. After endovascular treatment the patency of the ICA has been restored.
   The mural hematoma is for a large part lysed through the iv-treatment of recombinant tissue plasminogen activator (rt-PA, alteplase) prior to endovascular treatment. The intima flap is still visible. Again you can seen the intimal flap stopping at the level of the skull base.
   

Pseudo-occlusion of the cervical internal carotid artery refers to an isolated occlusion of the distal intracranial ICA that mimicks an extracranial ICA occlusion on CTA or DSA.

In pseudo-occlusion it looks as if there is a total occlusion in the ICA just above the level of the bulbus.
The contrast that enters the ICA has difficulty to move up further cranially, because of the stagnant blood within the ICA, since the ICA has no major side branches. 
The contrast will only slowly penetrate this stagnant blood column and this results in a waterpaint appearance.

On CTA you will see a gradually diminishing contrast density in the ACI with a water paint appearance.

The problem is the outflow obstruction at the level of the carotid T-top.  

A pseudo-occlusion is never seen in combination with a more distal occlusion.
For example, in case of a M2 occlusion there will be sufficient outflow of the distal ICA through the other patent  M2 division and the ACA. 

Two cases of a carotid pseudo-occlusion.

In the first case (left) the contrast stop is rather abrupt, although a small zone of diminishing contrast density can be seen.
In this case the differentiation between a pseudo-occlusion and a dissection or atherosclerotic occlusion can be difficult.
However, we do not see the typical flame shape configuration of the bulbus as seen in a dissection and we see no signs of atherosclerosis (no plaque or calcifications). 

In the second case the gradually dimishing contrast density is cleary seen over a longer course (arrowheads).
This is clearly a carotid pseudo-occlusion.

Continue with the DSA images...

Pseudo-occlusion with DSA

The DSA gives us comparable images.

In this patient during catheter angiography, first there was a typical waterpaint appearance of the contrast in the ICA, which simulated a proximal occlusion in the ICA.

However the catheter could easily be  advanced  into the distal  ICA.
After a more forceful contrast injection there is a typical carotid-top occlusion on the lateral view (just above the level of the ophthalmic artery.
There is no contrast filling of the intracerebral vessels.

On the saggital view there is a longitudinal filling defect in the proximal internal carotid artery (arrowheads).
This filling defect is a floating thrombus attached to a atherosclerotic plaque located at the carotid bulb (white arrow). 

In the axial plane this floatig thrombus causes a central filling defect in the ICA also now as a “donut sign” (arrowhead). 

In case of an accompanying intracranial occlusion of a large vessel endovascular therapy is initiated to open this intracranial occlusion.
An isolated floating thrombus (no large vessel occlusion) is treated with heparine or anti-platelet therapy .

A carotid web is a shelf-like lesion along the posterior wall of the internal carotid artery bulb and an under-recognized cause of stroke in young individuals.
Several studies suggest that patients with a carotid web have a high risk of recurrent stroke.

In the MR CLEAN study 30 patients with a carotid web ipsilateral to the stroke were identified.
In this study 1 out of every 6 patients with a symptomatic carotid web had a recurrent stroke within 2 years, suggesting that medical management alone may not provide sufficient protection for patients with a carotid web.

On the saggital view of the CTA the shelf-like protusion on the dorsal wall of the ICA bulbus is seen. 

This is the typical configuration location for a carotid web. 

However, for the definite diagnosis of a carotid web a ridge connecting the lateral and medial wall of the internal carotid artery must be seen in the axial view (arrow right image). 

Carotid webs can differ in size.
In this case the carotid web is much smaller than in te previous example.
However, the imaging criteria for the diagnosis of a carotid web still apply.
On the sagittal images a self-like protrusion is seen on the dorsal aspect of the internal carotid artery (arrow left image).
On the axial images the ridge of the carotid web is seen connecting the lateral and medial wall of the internal carotid artery (arrow).

If you only look at the axial images, you may miss a web.
The red arrow points at the ICA and ECA, but no web is seen..
Only with by angulating the axial plane perpendicular to the longitudinal axis of the ICA (green line and green arrow) you will notice the web  (ridge connecting the lateral and medial wall of the ICA.
Of course the sagittal reconstructions are superior for detecting a web.

Correlation carotid web and cerebral ischemia

These DSA images cleary demonstrate the mechanism by which carotid webs cause cerebral infarctions.
On the first angiographic images  you might first a stenosis (white arrow left image).
On the next image the web is clearly  delineated (yellow arrow).
On in the late arterial phase  view t stasis of contrast  is seen directly cranial of the web. 
It is clear, that in this region, due to turbulence and stasis thrombi can develop and can cause cerebral emboli.

An isolated carotid means that the ICA supplies blood to the ipsilateral anterior and middle cerebral artery, but that there is no connection to the contralateral side or posterior circulation, because the anterior (Acom) and posterior (Pcom) communicating artery are missing as an anatomic variant.
This is one of the many variants of the circle of Willis.

Patent circle of Willis

Let us first describe the most common situation.
In 90% of patients the circle of Willis is patent.
When these patients present with an acute stroke as a result of a dissection, they usually have an embolus in the middle cerebral artery.
In those cases it is sufficient to treat the intracranial occlusion and the dissected carotid artery can be left untreated.
The collateral circulation over the patent circle of Willis will take over the blood flow to the middle cerebral artery.

Non-patent circle of Willis

In 10% of cases the circle of Willis is insufficient.
In this case both the anterior and posterior communicans artery are absent.
If there is an occlusion of the ACI, then the patient is at risk for a massive stroke in both the anterior and middle cerebral artery territory, since there is no collateral flow from the contralateral ICA.
We will demonstrate this scenario in the following case...

Case

A 35-year-old woman presented at the ER with speech difficulties and a paresis of the right arm.

The NECT did not show signs of a bleeding or infarction.
On the CECT there was normal enhancement of the intracerebral vessels, which means no intracerebral occlusion.

Within 20 minutes she was treated with IV trombolyse, which resulted in partial recovery.

One hour later however there was a deterioration with hemiparalysis on the right and aphasia.
The NIHSS was 27.

Subsequently she was transported to the intervention center.
Continue with the CTA of the neck...

The CTA of the neck shows the typical flame shape of the proximal ICA indicating a dissection.

Continue with the axial slices...

The axial image shows a dilated left ICA with an eccentric compressed lumen.

In conclusion there is a 35-year old women with a massive stroke (NIHSS = 27), a carotid occlusion as a result of a dissection, but no intracranial occlusion.

At that moment the questions were:

• Could there be a variant of the circle of Willis?
• And if so, why was there normal contrast enhancement of the left middle cerebral artery on the CTA?

The DSA of the left ICA confirmed the dissection (arrowheads) by demonstrating the flame shaped configuration of the proximal ICA .

Subsequently a DSA of the right ICA and the left vertebral artery was performed.
The angiography of the right ICA showed an absent Acom as not contrast crossed from right to left. In addition, contrast injection in the left vertebral artery showed an absence of a Pcom.

This was proof of the diagnosis "Isolated carotid artery".

Now what is the explanation for the contrast filling  of the left middle cerebral artery as the left ACI is occluded and there is no collateral flow through the circle of Willis?

The explanation is, that there are small collaterals between the external carotid artery (ECA) and the ICA.
This is enough to to fill the ACM with contrast , but this is not sufficient for adequate perfusion of the left hemisfere.
This is clearly demonstrated on the perfusion images.

During the interventional procedure the flow was restored due to repositioning of the intimal flap caused by the catheter manipulation. 

Carotid stent placement was considered but not performed.
The patient was treated with Fraxiparine

After 24 hours there was a NIHSS: 2 with only a mild aphasia, after 3 months the NIHSS was down to 0.

Follow-up MRI after one month showed a small left frontal infarction (white arrow).
The left ICA was patent and showed a remaining of the intramural hematoma with high signal on the T1W-image (arrowhead).