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A previously healthy 70-year-old woman presented with sudden left-sided weakness and facial paralysis. She had no prior comorbidities, addictions, or neck trauma. Her initial assessment revealed a Glasgow Coma Scale of E4V5M6, blood pressure of 100/52 mm Hg, a regular pulse of 86 beats per minute, and normal pupils. She had complete left-sided weakness (0/5) with facial weakness and mute left plantar reflex. National Institutes of Health Stroke Scale score was 10. The other system examinations were unremarkable. Imaging revealed right-sided internal and external watershed infarcts between the anterior and middle cerebral arteries on non-contrast computed tomography (CT) of the brain Figure 1a. CT angiography of the brain and neck vessel highlighted a dissection in the right common carotid artery (CCA), showing unusual bilateral retropharyngeal carotids Figure 1b-f. Subsequent magnetic resonance imaging with angiography and vessel wall imaging confirmed the abnormal course of CCA and dissection Figure 2. Laboratory tests showed normal hemogram, coagulation, renal, liver, thyroid, and lipid profiles, with slightly elevated inflammatory markers. Cardiac evaluation showed a right bundle branch block without ischemic changes; 2D transthoracic echocardiography was normal. She received dual antiplatelet, statin, and other standard stroke care measures.Figure 1: (a) NCCT head showing right external watershed territory chronic infarcts (yellow arrows); (b) CT angiography of the neck vessels showing gradual reduction in contrast opacification, and non-visualization of right mid-distal CCA (double headed blue arrow), with reformation at the CCA bifurcation via External carotid Artery (ECA), likely due to mid-distal CCA dissection; (c) CT angiography of neck vessels showing carotid plaque at the bifurcation of the CCA (Orange arrow); (d-f) Long-segment dissection noted in the CCA, with extrinsic thrombosed false lumen (green arrow) and contrast opacification within true lumen (red arrow)Figure 2: MRI brain (a) FLAIR (Fluid-Attenuated Inversion Recovery) sequence showing gyral (cortical and subcortical) hyperintensity in the right posterior frontal, right parietal and right posterior temporal region (external watershed) with slight mass effect as effaced sulci (yellow arrows); (b) with concomitant diffusion restriction. VWI (Vessel Wall Imaging); (c,d and e) non-contrast T1 sagittal (c), and post-contrast axial (d) and sagittal (e), showing enhancing dissection flap arising from proximal CCA (blue, red and green arrows)DISCUSSION Variations in the extracranial internal carotid arteries (ICAs) are observed in about 5%–10% of the general population, with certain endovascular case studies indicating abnormal ICA pathways in up to 39% of cases.1 Typically, the carotid arteries maintain a straight trajectory through the neck; yet they can exhibit variations, such as elongation, kinking, or coiling. These deviations usually occur during embryogenesis, with the bilateral CCAs and proximal segments of ICAs developing from the third aortic arch. As the heart descends into the thoracic cavity, these arteries usually straighten, but incomplete alignment may result in kinks. This phenomenon is more commonly observed in ICA than in CCA. The Weibel–Fields classification categorizes ICA tortuosity into three distinct types: Type 1 encompasses arteries elongating into "C," "U," or "S" shapes; Type 2 includes arteries forming loops or coils around an axis; and Type 3 describes arteries that are kinked into a "V" shape.2 A notable variation of ICA tortuosity is the bilateral occurrence, termed as the "kissing carotid artery." This specific variant, where ICAs are closely juxtaposed, is even more rare. Various factors like age, gender, hypercholesterolemia, obesity, atherosclerosis, hypertension, enlarged heart dimensions, Marfan syndrome, fibromuscular dysplasia, and connective tissue disorders are associated with these arterial variations. Although often asymptomatic, tortuous CCA or ICA can have clinical implications, such as pulsating neck masses and dysphagia. They may cause luminal constriction, turbulent blood flow, intimal ulceration, and embolic events. Patients might exhibit symptoms akin to those arising from atherosclerotic disease at the carotid artery bifurcation, including strokes, hemispheric transient ischemic attacks, or amaurosis fugax. Riser et al. were the pioneers in documenting cerebrovascular symptoms linked to "kissing carotids."3 Nonetheless, the unequivocal causal nexus between these vascular aberrations and cerebrovascular incidents is yet to be definitively established. Progressive age, female sex, hypertension, and atherosclerotic changes are recognized as potential aggravators. In a longitudinal study, Del Corso et al.4 meticulously examined the interplay between ICA abnormalities and the incidence of stroke or atherosclerotic vascular diseases. Over a year, the study analyzed 469 subjects to understand how atherosclerosis, hypertension, and aging contribute to carotid irregularities. The results revealed that aging was a more significant factor than atherosclerosis. In addition, Vannix et al.5 reported a four-fold greater occurrence of carotid kinking in women compared to men. The debate extends to the implications of arterial tortuosity on cerebrovascular blood flow, with theoretical assertions suggesting that such vascular deviations could attenuate cerebral perfusion, potentially culminating in cognitive decline.6 Although there is a recognized link with stroke, cases of retropharyngeal carotid dissection that occur spontaneously remain uncommon. The primary concern with this atypical pathway of the carotid artery lies in the challenges it poses during mechanical thrombectomy for treating ischemic stroke and in the surgical planning for head, neck, and vascular surgeries. In summary, an aberrant course of the carotid artery might be a potential risk factor for stroke, particularly in older adults. However, this hypothesis warrants confirmation through detailed clinical scrutiny of additional cases and more comprehensive research. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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Archita Makharia
All India Institute of Medical Sciences Bhopal
Savyasachi Jain
Shailesh Gaikwad
All India Institute of Medical Sciences
Annals of Indian Academy of Neurology
All India Institute of Medical Sciences
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Makharia et al. (Tue,) studied this question.
synapsesocial.com/papers/68e5b9bbb6db6435875528c5 — DOI: https://doi.org/10.4103/aian.aian_327_24