The Trade-off Between the Bony Carotid Canal and Internal Carotid Artery | Neurology | JAMA Neurology | JAMA Network
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March 22, 2021

The Trade-off Between the Bony Carotid Canal and Internal Carotid Artery

Author Affiliations
  • 1Department of Neurology, West China Hospital, Sichuan University, Chengdu, China
  • 2Department of Neurosurgery, West China Hospital, Sichuan University, Chengdu, China
JAMA Neurol. 2021;78(5):611-612. doi:10.1001/jamaneurol.2021.0344

A 24-year-old woman presented with sudden-onset slurred speech and right-side weakness. Ten months previously, she had had an episode of transient consciousness loss. The patient denied smoking, had no history of miscarriage, was not taking oral contraceptives, and had a body mass index (calculated as weight in kilograms divided by height in meters squared) of 21.2. She denied any family history of stroke. On admission, her blood pressure was 103/65 mm Hg in the right arm and 76/40 mm Hg in the left arm. Her body temperature, heartbeat, and respiration rate were within normal limits. Simultaneous palpation of pulses in the 2 arms revealed that the left radial pulse was weak. A neurological examination revealed clinically significant right-side hemiparesis and dysarthria. Other findings of general physical and neurological examinations were normal. The patient’s blood work results were unremarkable, aside from an elevated erythrocyte sedimentation rate (90.0 mm/h) and C-reactive protein level (4.06 mg/dL [to convert to milligrams per liter, multiply by 10.0]). Hypercoagulable laboratory studies, chest radiography, transthoracic echocardiography, electrocardiography, and 24-hour Holter monitoring yielded normal findings. Head computed tomography (CT) images showed an acute infarct in the left basal ganglia. Head-and-neck CT angiography with digital subtraction angiography revealed left carotid artery occlusion and subclavian artery stenosis (Figure 1). These findings were believed to be consistent with Takayasu arteritis. The patient was given prednisolone (initial dosage, 60 mg/d, tapered very slowly). Regular clinical follow-up, including physical examinations, radiographic evaluations, and other medical tests, was performed every 6 to 12 months.

Figure 1.  Computed Tomography (CT) Angiography
Computed Tomography (CT) Angiography

Computed tomography angiography (A) with digital subtraction angiography (B) showed left common carotid artery occlusion and left subclavian artery stenosis.

Axial CT angiographic images obtained on initial evaluation and at the first follow-up visit showed symmetrical, normally sized carotid canals bilaterally (Figure 2A). Unexpectedly, a CT performed 2 years after diagnosis revealed left-right asymmetry of the bony carotid canals. Thereafter, the size of the left carotid canal decreased gradually year by year (Figure 2B). The unusual CT finding of thickening along the petrous carotid canal cortex attributable to new periosteal bone formation aided differentiation of this condition from congenital hypoplasia.

Figure 2.  Initial and Repeated Computed Tomographic (CT) Images
Initial and Repeated Computed Tomographic (CT) Images

An initial axial CT image (A) through the horizontal portion of the carotid canals showed bilateral symmetrical carotid canals of a normal size (arrowheads); 6 years later, a repeated CT image (B) showed that the left carotid canal had become significantly smaller than before (arrowheads).

Discussion

Understanding of associations between bony structures and the cranial vasculature has increased in recent decades.1 The cranial vasculature plays a crucial role in forming the cranial bony structures.2

Narrowing of the carotid canal is commonly used to differentiate hypoplasia from acquired internal carotid artery shrinkage, based on the presumption that the carotid canal size correlates with the ipsilateral internal carotid artery size during normal development and is immutable after childhood.1-4 In the present case, however, bony carotid canal narrowing occurred after the development of internal carotid artery occlusion in adulthood. Thus, small bony carotid canals in adults do not necessarily represent congenital internal carotid artery hypoplasia. Additionally, the use of bony carotid canal measurements to determine moyamoya disease onset is questionable.3 This case represents a so-called black swan, raising doubt about traditional assumptions regarding associations between bony structures and the cranial vasculature. A previous report4 raised the same concern, although the chronology of carotid canal changes was not presented as in this case. Thus, the distinction of congenital and acquired conditions is essential when a CT image of the skull base shows a small carotid canal.

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Article Information

Corresponding Author: Muke Zhou, MD, Department of Neurology, West China Hospital, Sichuan University, No. 37, Guoxuexiang, Chengdu 610041, China (muke.zhou@scu.edu.cn).

Published Online: March 22, 2021. doi:10.1001/jamaneurol.2021.0344

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

Additional Information: Drs Chen and Cao contributed equally to this work.

References
1.
Osborn  RE, Mojtahedi  S, Hay  TC, DeWitt  JD.  Internal carotid artery hypoplasia.   Comput Radiol. 1986;10(6):283-287. doi:10.1016/0730-4862(86)90032-6 PubMedGoogle ScholarCrossref
2.
Kim  C, Lee  SH, Park  SS,  et al.  A quantitative comparison of the vertebral artery and transverse foramen using CT angiography.   J Clin Neurol. 2012;8(4):259-264. doi:10.3988/jcn.2012.8.4.259 PubMedGoogle ScholarCrossref
3.
Watanabe  A, Omata  T, Koizumi  H, Nakano  S, Takeuchi  N, Kinouchi  H.  Bony carotid canal hypoplasia in patients with moyamoya disease.   J Neurosurg Pediatr. 2010;5(6):591-594. doi:10.3171/2010.3.PEDS09417PubMedGoogle ScholarCrossref
4.
Wyse  E, Sorte  DE, Jordan  L, Gailloud  P.  The observation of an ipsilateral carotid canal hypoplasia cannot be used to ascertain the congenital nature of a carotid artery occlusion.   J Neuroradiol. 2015;42(3):188-189. doi:10.1016/j.neurad.2015.02.003 PubMedGoogle ScholarCrossref
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