Calcified cerebral embolus
Calcified cerebral embolus is an uncommon and often overlooked cause of embolic ischemic stroke.
Epidemiology
Although emboli are a common cause of ischemic stroke, calcified cerebral emboli are considered rare. With only a paucity of literature regarding calcified cerebral emboli – only 48 reported cases as of 2014 – it is difficult to truly gauge the incidence of stroke via this etiology . However, one relatively large 2014 study found that calcified cerebral emboli were detected in 2.7% of all patients undergoing non-contrast CT with the clinical indication of stroke, many of these cases only detected retrospectively during the study .
Clinical presentation
The presentation is that of acute ischemic stroke, which is discussed in more detail elsewhere (see ischemic stroke) . However, these emboli may also be found incidentally without prior evidence of stroke .
Pathology
Calcified cerebral emboli are generally small in size, with a diameter of 2-3 mm .
Etiology
Causes include :
- spontaneous (~90%)
- calcific aortic stenosis (most common)
- mitral annular calcification
- calcified carotid, vertebral, brachiocephalic, and aortic arch plaques
- iatrogenic
- complication of procedures such as cardiac valve or coronary surgery
- complications of carotid intervention (endarterectomy or endovascular stenting)
- idiopathic
Radiographic features
CT
These emboli, having a calcified component, are unsurprisingly hyperdense on non-contrast CT . If multiple are present, the salted pretzel sign may be seen .
Moreover, it may be of therapeutic and prognostic significance to differentiate this hyperdensity from that of a ‘regular’ intramural thrombus (see hyperdense MCA sign and MCA dot sign) by observing the shape and by measuring the radiographic density of the embolus :
- calcified cerebral emboli tend to have a round or ovoid shape, in comparison to ‘regular’ thrombi which tend to fill up the vessel in a tubular configuration
- with region-of-interest density measurements, calcified cerebral emboli are more attenuated (~160 HU) in comparison to ‘regular’ thrombi which attenuate at typically 50-70 HU
However, once calcium is suspected (especially if found incidentally), it is important to differentiate it from mimics such as hemorrhage, vessel wall calcification, infection (e.g. neurocysticercosis), cavernomas, or other causes of vascular intracranial calcification .
CT angiography
As these emboli are hyperdense on CT, they may appear isodense to the iodinated contrast used in CT angiography, which may give the impression that the vessel is patent when it really is not, especially in early-phase images . This has been described in one case report as 'pseudo-patency' .
MRI
Although MRI is more sensitive than CT for detecting acute ischemic stroke , CT is generally considered superior to MRI for detecting calcified cerebral emboli themselves both in terms of its accessibility and sensitivity . However, studies examining the role of sequences such as SWI filtered phase imaging have not yet been performed (as of August 2017).
Treatment and prognosis
Current stroke guidelines do not make a distinction between calcified and 'regular' non-calcified cerebral emboli with regard to thrombolysis , and there is mixed case series-level evidence regarding its effectiveness . There is also currently (as of August 2017) very limited and mixed evidence, even at a case report-level, regarding experience with endovascular embolectomy of calcified cerebral emboli, however, the current consensus seems to be that it may be a riskier procedure .
In terms of prognosis, calcified cerebral emboli may be a risk factor for recurrent stroke, with one study finding that nearly half of all patients had repeat embolic ischemic stroke . Thus, it is paramount to also investigate for and treat any causative lesions (e.g. calcific aortic stenosis) in order to prevent recurrence .
History and etymology
Calcified cerebral emboli were first noted radiographically by Douglas H. Yock, an American radiologist, in his 1981 seminal paper .
Differential diagnosis
- vascular hyperdensity
- hyperdense artery of thromboembolism
- myelography contrast (e.g. Lipiodol) spread to cranial subarachnoid space
- bone cement embolism
- parenchymal hyperdensity
- oligodendroglioma (especially in the setting of subacute infarction)
- infections (e.g. neurocysticercosis, cerebral sparganosis etc...)