Case Report
A 70-year-old hypertensive and diabetic lady presented with a right hemiparesis of 1-month duration. Her echocardiogram and lipid profile were unremarkable. Cranial magnetic resonance imaging (MRI) showed an infarct in the left basal ganglia. Computed tomography (CT) angiogram revealed severe kinking of the cervical internal carotid arteries (ICAs) bilaterally, resembling a python [Figure 1a and b]. Despite being on aspirin, she had three episodes of transient unilateral weakness over the next 6 months that abated with double antiplatelets.
Figure 1.

(A) Computed tomography (CT) angiogram (volume rendered images) showing severe coiling cervical internal carotid arteries bilaterally, resembling a python (B)
Discussion
Anatomical variations of ICA have been clearly recognized for ages. Looping and kinking of the ICA is commonly observed in infants. ICA is formed from the third aortic arch and the dorsal aorta, hence, it is normally kinked in the embryo.[1] The persistence of the original fetal morphology produces different types of undulations and variations in the anatomy of ICA. Whether or not these are independent stroke risk factors or markers is controversial.[2]
Marked coiling of ICA may be a risk factor for stroke.[3] Though considered to be normal variation at some point, it is now believed that the presence of these undulations may be attributed to increased blood pressure. Long-standing aortic insufficiency with resultant high pulse pressure may also be contributory in causation of these undulations.[4]
Most available literature suggest that these carotid anomalies are rarely symptomatic unless other additional vascular risk factors are present in an individual.[2] Although an indisputable evidence for a connection between carotid anomalies and occurrence of vascular events does not exist, it is believed that “….development of symptoms may at times depend on the fortuitous positioning of the head in a such a way that the vessels are kinked rather than merely elongated.”[3,5]
Alleviation in the symptoms of patients after straightening of kinked carotid vessels has also been reported in literature,[5,6,7] providing an indirect evidence of the causal relationship between the two.
Our patient had extremely coiled carotid vessels and no other source of atheroembolism, with recurrent cerebrovascular events despite being on antiplatelet agents. The anomalies, when detected, deserve due consideration and should not be passed on as normal or benign variants. Their presence may warrant the need for an aggressive medical or surgical treatment to prevent adverse outcomes.
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Conflicts of interest
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References
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