Procedure Details:
We reviewed the cases of patients with previously confirmed ischemic stroke of the past 2 years of the Department of Radiology and Medical Imaging of the University Emergency Hospital of Bucharest,
selecting eloquent aspects for each pathology.
The scanners used were a 16-row CT for emergencies,
a 64-row CT for follow-up and a 1.5Tesla MRI.
Findings:
We divide findings according to the mechanism of stroke as seen in Fig. 1,
inspired by TOAST classification [10].
Penetrating artery disease
Lacunar ischaemic stroke is defined as a stroke that is attributable to a recent small infarct <1.5 (or some say 2) cm diameter in the white matter,
basal ganglia,
pons or brainstem,
and is consistent with a lacunar clinical syndrome.
The mechanisms proposed are either embolic - occluding lenticulostriate arteries,
atheromatous – atheromas in the parent artery extending to cover the penetrating branches,
intrinsic small vessel disease with thickening vessel wall and secondary luminal occlusion[11].
Such vascular changes are too discrete to be visualised directly,
magnetic resonance imaging managing to detect parenchymal changes [12].
Cardiac
Embolism of cardiac origin accounts for about one fifth of ischaemic strokes.
Strokes due to cardioembolism are in general severe and prone to early recurrence [2].
The suspicion for a cardioembolic source for stroke is raised with a large vessel occlusion or when strokes occur in multiple vascular territories ( Fig. 2 ).
Haemorrhagic transformation happens in up to 71% of cardioembolic strokes and as many as 95% of hemorrhagic strokes are cardioembolic.
Emboli from the heart are distributed evenly throughout the body,
with more than 80% of symptomatic emboli affect the brain.[13].
Imaging of the heart was performed either as an extension on the CTA or subsequently,
to determine the source of the stroke.
Atrial Fibrillation (AF)
AF is a powerful risk factor for stroke,
independently increasing risk 5-fold throughout all ages,
with particular impact at 80 to 89 years of age,
where it accounts for 23.5% of strokes [14].
Both atrial and ventricular thrombi have to be distinguished from either contrast filling defects and papillary muscles,
both of which have higher HU in contrast studies.
Visualization of the cerebral arteries can point out filling defects consistent with emboli.
Fig. 3
Endocarditis
Infective endocarditis ( Fig. 4 )is complicated by stroke in about 10% of cases.
Emboli can be multiple,
especially in the case of infection of prosthetic valves and in infections due to aggressive agents,
such as Staphylococcus aureus [2].
Serious complications and deaths related to left-sided infective endocarditis are due to either cerebral emboli causing severe neurologic deficits or to intracardiac suppurative complications,
which can cause severe valvular regurgitation and perivalvular abcesses[15].
Cardiac imaging can confirm valvular vegetation and the presence of complications ( Fig. 5) .
Atrial Septal Defect
Atrial wall anomalies play a dual role in stroke.
On the one hand,
the combination of patent foramen ovale and atrial septal aneurysm may provide both an locus for in situ thrombosis and site for right to left embolization[16].
On the other,
patients with atrial septal defects have a higher chance of developing AF,
especially as they age[17] Fig. 6 .
Left Ventricular Thrombus Fig. 7
Myocardial infarction is associated with ventricular wall immobility and may lead to left ventricular thrombus formation and cardioembolic stroke.
The stroke rate from acute myocardial infarction (AMI) is 1%–3% from any AMI and 2%–6% anterior wall MI.
The presence of LV Thrombus increases it to 15% at 3 months[18].
Atrial Myxoma
Myxomas are the most common primary heart neoplasm and are generally located in the atria.
They have significant association with embolic events.
The main differential diagnosis is with thrombi.
Myxomas are larger in size (1-15cm),
may change position during cardiac cycle and may have contrast enhancement [19].
Atherosclerotic Disease
Carotid atherosclerosis is one of the most common causes of death and disability in the western countries.
The main criteria evaluated for risk stratification has been the degree of luminal stenosis,
being a well-known risk factor for the development of neurologic.
Recent research has concluded that a number of other plaque features contribute to the occurrence of neurologic symptoms,
introducing the “vulnerable plaque”,
responsible for almost half of stroke cases.
The main mechanism seems to be that of artery-to-artery embolization [4].
Carotid plaques are typically classified into smooth,
irregular or ulcerated ( Fig. 9),
with the last having high clinical significance for neurological symptoms,
as much as a four-fold increase.
The term smooth cad be used for a plaque with regular luminal morphology,
irregular can be used for plaques whose surface fluctuates <1 mm,
whereas the term ulceration is reserved for cavities measuring at least 1-2 mm[20].
Each ulcer is characterized by a neck and a base,
both of varying sizes and resulting in various shapes,
but none of them of particular increased risk.
What is correlated with increased complications is plaque hemorrhage,
which can be indirectly determined if the plaque presents enhancement [21] Fig. 10 .
Basically,
ulceration can be diagnosed when contrast medium is identified extending beyond the vascular lumen (and within the plaque limits) for at least 1 mm in at least two planes [22] and hemorrhage by observing plaque post-contrast enhancement.
Lastly,
measurement of degree of stenosis can be done by following NASCET criteria: % ICA stenosis = (1 - [narrowest ICA diameter/diameter normal distal cervical ICA]) x 100.
One has to keep in mind that measurements need to be done perpendicularly to the vessel axis and mentioning which modality was used in the report.
Fig. 11
Aortic Atheroma
Aortic atheromas a discrete protrusion of the intimal surface of the vessel >2 mm in thickness,
different in appearance from the adjacent intact intimal surface.
The presence of protruding atheromas in the aortic arch has been recognized as a potential cause of cerebral or peripheral embolization in the elderly,
with studies showing that protruding aortic atheroma (>4–5 mm) is 3–9 times more common in stroke patients than in healthy [2].
Findings indicate that the risk of ischemic stroke in elderly patients with arch atheromas is more strongly related to the complexity of the lesion than to its size.
Complex atheromas present either a mobile component or ulcerations as previously defined[23] ( Fig. 12).
Other causes
Iatrogenic
Many vascular procedures present a risk of stroke,
but few are as serious as the ones that generate fat emboli.
Even though it is a rare complication,
trauma is responsible for 90% of cases,
but also liposuction,
burns and cardiopulmonary bypass [24] Fig. 13 .
Dissection Fig. 15
Craniocervical artery dissection is rare,
but in young and middle-aged patients,
spontaneous craniocervical artery dissection is the cause of up to one-fourth of strokes,
with a peak prevalence in the fifth decade of life.
As a suggested mechanism,
intramural hemorrhage forms through ruptures of the vasa vasorum without intimal tear,
especially if the wall is arteriopathic [25].
Arteritis
Lastly,
recent CTA studies demonstrated that CTA can easily measure carotid artery wall thickness (CAWT) and found that,
by using a 1 mm threshold,
there was a 8 fold increase in stroke in patients with thicker (≥1 mm) CAWT [7] Fig. 16 .