Telencephalic variant of the anterior choroidal artery: clinical significance and management considerations

Introduction

The anterior choroidal artery (AChA) is a vital vessel arising from the internal carotid artery (ICA), with its embryological development influencing its adult anatomy. During development, structural changes such as distal annexation can result in atypical variants, including hypertrophic or telencephalic arteries. These anomalies, though rare, hold significant clinical implications, particularly in neurovascular interventions, as they can mimic other cerebral arteries such as the fetal posterior cerebral artery (PCA). Understanding the embryological basis of these variants is essential for accurate diagnosis and safe surgical or endovascular procedures (1-3).

Image in medicine and surgery

AChA is a phylogenetically conserved vessel that derives from a branch of the cranial division of the primitive ICA. In the early embryonic period, during the choroidal stage, which takes place around five weeks, the vertebrobasilar system is not yet fully developed and the AChA has a large telencephalic territory, supplying branches to the temporal, parietal, and occipital territories. Such angioarchitecture is modified with the loss of cortical regions mediated by transfer to the caudal branch of the ICA, which subsequently forms the P2 to P4 segments, by an event named “distal annexation”. The AChA that supplies the cortical regions perfused by the PCA is designated as hypertrophic AChA or telencephalic AChA. Although this variant is rare and lacks a precise embryological origin, the persistence of telencephalic branches of this artery, possibly due to incomplete “distal annexation” is plausible (1-3).

Anomalous telencephalic AChA in many cases has been confused with the fetal PCA. Initially identified by Blackburn in 1907, this variation was designated as accessory PCA, replaced PCA, or true fetal PCA. Takahashi and collaborators later categorized it into 4 subtypes according to the blood supply to the PCA distribution areas. Subtypes 1, 2, and 3 correspond to the vascular supply of the anterior temporal branch, both the anterior and posterior temporal branches, and the calcarine and choroidal arteries, as well as the occipitoparietal arteries, respectively. Takahashi type 4 involves the original PCA being almost totally replaced by the anomalous AChA (1,4,5).

It is a rare condition, with prevalence reported as 0.55% on intracranial 3-dimensional time-of-flight magnetic resonance angiography (TOF MRA) and 1.1–2.3% on digital subtraction angiography. Anomalous hypertrophic AChA is often accompanied by an intracranial aneurysm. The incidence of aneurysm of anomalous hypertrophic AChA (4–17%) is much higher than that of general AChA aneurysm (0.4–0.5%) (1,4,5).

Although rare, the proper recognition of this variation of AChA is essential for neurosurgeons and neuroradiologists in practice, and they need to be aware of it to avoid critical and unintentional events during endovascular procedures and microsurgeries. The mature anatomy of the AChA comprises three branches: the telencephalic branch, which includes the uncus, piriform cortex, and amygdaloid nucleus; the diencephalic branch, which supplies the thalamus, lateral geniculate body, optic tract, and cranial nerve II; and the choroidal branches. This structural configuration facilitates targeted embolization beyond the choroidal point, where cortical branches are absent. Variants of the AChA originating from the telencephalon provide vascular supply to the cortical areas of the temporal, parietal, and occipital lobes. Consequently, clinical outcomes following AChA occlusion range from asymptomatic to manifestations of varying severity of AChA syndrome (6,7).

The reported image demonstrates a case of coiling procedure for a ruptured posterior communicating artery aneurysm accompanied by fetal PCA in a patient with Takahashi type 1 telencephalic AChA variant (Figure 1). This is a rare anatomical variation, and the case aims to reinforce the importance of embryological knowledge applied to the practice of neurointerventionists during diagnosis and endovascular management to minimize complications to the patient.

Figure 1 Digital subtraction angiography (A-C) and angiogram skull mask (D) following left internal carotid artery injection (white circumflex), showing a telencephalic anterior choroidal artery. (A) Posteroanterior view and (B) lateral view showing a ruptured posterior communicating artery aneurysm (red asterisk) accompanied by fetal posterior cerebral artery (white asterisk) and a Takahashi type 1 telencephalic anterior choroidal artery variant (white arrows). (C) Left oblique view showing initial procedure coiling procedure for a ruptured posterior communicating artery aneurysm (red asterisk), highlighting the telencephalic anterior choroidal artery variant (white arrows). (D) Lateral view after coiling procedure, showing no distal embolization and satisfactory aneurysm occlusion.

Conclusions

We discuss the importance of understanding embryological principles in managing these anomalies, illustrating with a case of coiling procedure for a ruptured posterior communicating artery aneurysm accompanied by fetal PCA in a patient with a telencephalic AChA variant. This case underscores the necessity of integrating embryological knowledge into clinical practice for optimal patient outcomes. It provides a concise overview of the topic, highlighting key points such as embryological development, clinical significance, management considerations, and a specific image illustration.

Acknowledgments

None.

Footnote

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-211/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Takahashi S, Suga T, Kawata Y, Sakamoto K. Anterior choroidal artery: angiographic analysis of variations and anomalies. AJNR Am J Neuroradiol 1990;11:719-29.
2. Komiyama M, Morikawa T, Ishiguro T, Matsusaka Y, Yasui T. Anterior choroidal artery variant and acute embolic stroke. Case report. Interv Neuroradiol 2002;8:313-6. [Crossref] [PubMed]
3. Lasjaunias P, Berenstein A, Brugge KG. Surgical Neuroangiography. 2nd ed., Springer; 2001.
4. Doi K, Mizuno T, Shigematsu Y, Kobayashi O, Takezaki T, Muta D, Nishi T. A new type of hyperplastic anterior choroidal artery. J Clin Neurosci 2018;51:72-4. [Crossref] [PubMed]
5. Hyun DK, Shim YS, Park HS, Oh SY. Thromboembolic complication following neurointervention in ruptured anomalous hyperplastic anterior choroidal artery aneurysm. Neuroradiol J 2014;27:103-7. [Crossref] [PubMed]
6. Youn S, Park SK, Kim MJ. Coil embolization and recurrence of ruptured aneurysm originating from hyperplastic anterior choroidal artery. J Cerebrovasc Endovasc Neurosurg 2024;26:181-6. [Crossref] [PubMed]
7. Triantafyllou G, Papadopoulos-Manolarakis P, Piagkou M. Accessory Posterior Cerebral Artery-The Hyperplastic Anterior Choroidal Artery Variant. J Craniofac Surg 2024; Epub ahead of print. [Crossref]