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Table of Contents    
LETTER TO EDITOR
Year : 2017  |  Volume : 65  |  Issue : 2  |  Page : 400-402

Persistent trigeminal artery trunk giant aneurysm and its management


1 Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Neurosuergry, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication10-Mar-2017

Correspondence Address:
Vivek Gupta
Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/neuroindia.NI_259_16

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How to cite this article:
Gupta V, Prabhakar A, Ahuja CK, Bajaj A, Gupta SK, Khandelwal N. Persistent trigeminal artery trunk giant aneurysm and its management. Neurol India 2017;65:400-2

How to cite this URL:
Gupta V, Prabhakar A, Ahuja CK, Bajaj A, Gupta SK, Khandelwal N. Persistent trigeminal artery trunk giant aneurysm and its management. Neurol India [serial online] 2017 [cited 2017 Nov 24];65:400-2. Available from: http://www.neurologyindia.com/text.asp?2017/65/2/400/201854


Sir,

Persistent trigeminal artery (PTA) is seen in 0.02–0.6% of patients undergoing cerebral angiography. Aneurysms arising in relation to a PTA are uncommon. These usually arise from the junction of the internal carotid artery (ICA) and PTA.[1] An aneurysm arising from the mid-third of the PTA is very rare. Here, we present a case of an unruptured, partially thrombosed, large PTA aneurysm arising from the trunk of the PTA as well as discuss its management.

A 62-year-old female patient presented with a history of headache and vomiting of 5 days duration followed by left sided ptosis. Clinically, left IIIth, IVth, and VIth cranial nerve palsy was noted. Plain computed tomography (CT) revealed a hyperdense left cavernous sinus lesion [Figure 1]a. On CT angiography, a partially thrombosed aneurysm [Figure 1]b measuring 15 × 15 × 25 mm was seen in the left cavernous sinus region with a large patent portion directed inferiorly [Figure 1]c. Subsequent diagnostic angiography confirmed the aneurysm [Figure 2]a and revealed an abnormal vessel arising from the cavernous portion of the left ICA [Figure 2]c up to the mid basilar artery [Figure 2]b and [Figure 2]c. The aneurysm was arising from its mid-portion and involved the entire circumference of the arterial wall with no discernible neck. The distal basilar artery and its branches were filling through this artery [Figure 2]b. The left posterior cerebral artery (PCA) had a fetal origin. The basilar artery proximal to its junction was mildly hypoplastic. On vertebral injection, the flow in the distal posterior circulation was normal with contrast reflux into this artery and minimal filling of the aneurysm [Figure 2]d. Thus, a diagnosis of PTA, Saltzmann Type I/II, with a truncal aneurysm was made.
Figure 1: NCCT (a) and CT angiography (b,c) images, showing a left cavernous sinus heterogeneous mass with central hyperdensity (black arrows in a, b) likely due to thrombosed portion of the aneurysm and a large patent aneurysmal sac (white arrows in b, c)

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Figure 2: DSA images of left ICA AP (a-c) and left vertebral artery injection (d). Patent portion of the aneurysm (black arrow in a,) and persistent trigeminal artery is seen (c) which is filling the basilar artery (c). Aneurysm is also filling on vertebral injection (d). Hypoplastic segment of basilar artery (d) is also seen

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As the posterior circulation was adequately filling from the vertebral arteries, decision was taken to coil the aneurysm without preserving the PTA. A 6F guiding catheter was placed in the left ICA via the right transfemoral route. An Echlon-14 (eV-3 Inc.) microcatheter was introduced into the aneurysm sac and 10 coils were used to pack the aneurysm. Post procedure digital subtraction angiography (DSA) revealed no filling of the aneurysm [Figure 3]a. The posterior circulation was being adequately supplied by the basilar artery [Figure 3]b. There were no post-procedural neurological sequelae. One-year follow-up revealed improvement in the cranial nerve palsies.
Figure 3: Post coiling left ICA (a) and right vertebral injection (b) images. There is complete occlusion of the aneurysm and mid part of PTA. Proximal PTA (black arrow in a) and distal PTA (black arrow in b), however, remains patent

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PTA has been classified by Saltzmann into Types I, II, and III. In Type I, the PTA inserts into the basilar artery distal to anterior ICA and proximal to the superior cerebellar arteries (SCA). The basilar system proximal to the PTA may be hypoplastic. In such patients, the PTA is the major vascular supply to the distal SCA and posterior cerebral arteries (PCA). In Type II, the PTA joins the basilar artery at the level of SCAs, which are supplied by it. PCAs are fetal in origin with hypoplasia of the P-1 segments of PCA. A combination of both types 1 and 2 may exist, in which the PTA supplies bilateral SCAs and the contralateral PCA. The ipsilateral PCA has a fetal origin. In type III, PTA continues as one of the one of the cerebellar arteries without communication with the basilar artery. Anatomically, the PTA may be classified on the basis of its course as the medial and lateral types.[2]

The incidence of aneurysms occurring in the brain in association with PTA varies from 14% to 32%.[1] However, after a detailed review of the published reports, we could find only 14 cases of PTA trunk aneurysms, reported by Kai et al.,[1] Ladners et al.,[3] and Bai et al.[4] Endovascular management was performed in only 5 of these patients.[1],[3]

Surgical management is challenging due to the deep location of the aneurysms and the presence of cranial nerves in the vicinity.[1] Endovascular management techniques include coil embolization of the aneurysms alone or with stent/balloon assistance, stent grafts, or occlusion of the PTA.[1],[5] In general, if the aneurysm is saccular in configuration, coiling with balloon/stent-assisted techniques is successful. However, if the aneurysm is fusiform in shape or is significantly incorporating the parent arterial wall, the treatment becomes difficult. If the PTA forms the major supply to the distal basilar circulation or is terminating as one of the cerebellar arteries, its preservation is essential. However, if the posterior circulation can be sustained by the basilar artery and the posterior communicating arteries, coiling of the aneurysm along with parent artery occlusion can be contemplated. Prior to parent vessel occlusion for large aneurysms in the region of the circle of Willis, a pre-procedural balloon occlusion test may be performed to detect hypoperfusion.[6],[7] In our case, the left PCA was fetal in origin. As there was adequate redundancy in the blood supply of the posterior circulation via the right posterior communicating and the basilar artery, balloon occlusion test was not performed. Flow diverter placement across the diseased arterial wall is also possible. This results in a gradual thrombosis of the aneurysm with preservation of the flow through the PTA.

The risks associated with endovascular management of PTA aneurysms are similar to any other intracerebral aneurysm. However, because the PTA may be the dominant supply to the posterior circulation, its occlusion may compromise the flow to the basilar artery leading to brainstem ischemia.[2] In addition, various arteries such as the meningohypophyseal trunk, anterior inferior cerebellar artery, pontine perforators, and branches to the trigeminal ganglion may arise from the PTA, thus increasing the risk of infarcts if the parent artery is occluded.[2]

In conclusion, PTA in the brain is usually an uncommon and asymptomatic variant. Aneurysms may form along its course. Coiling is a safe method of treatment; however, it is essential to evaluate the anatomical relationship and flow pattern of the artery to prevent any ischemic complications.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Kai Y, Ohmori Y, Watanabe M, Morioka M, Hirano T, Kawano T, et al. Coil embolization of an aneurysm located at the trunk of the persistent primitive trigeminal artery. Neurol Med Chir 2011;51:361-4.  Back to cited text no. 1
    
2.
Azab W, Delashaw J, Mohammed M. Persistent primitive trigeminal artery: A review. Turk Neurosurg 2012;22:399-406.  Back to cited text no. 2
    
3.
Ladner TR, Ehtesham M, Davis BJ, Khan IS, Ghiassi M, Ghiassi M, et al. Resolution of trigeminal neuralgia by coil embolization of a persistent primitive trigeminal artery aneurysm. BMJ Case Rep 2013;2013.  Back to cited text no. 3
    
4.
Bai M, Guo Q, Sun Y. Rare saccular aneurysm in a medial type persistent trigeminal artery trunk and literature review. Surg Radiol Anat SRA 2014;36:299-302.  Back to cited text no. 4
    
5.
Zhao QP, Li TL, Duan CZ, Chen GZ. Combined neuroform intracranial stent and bioactive matrix detachable coil for embolization of a broad-necked persistent primitive trigeminal artery aneurysm. Interv Neuroradiol 2005;11:63-8.  Back to cited text no. 5
    
6.
Misra BK. Treatment of giamt intracranial aneurysms: What is the best option? Neurol India 2015;63:138-141.  Back to cited text no. 6
[PUBMED]  [Full text]  
7.
Zhang Z, Lv X, Yang X, Shiqing M, Wu Z, Shen C, et al. Endovascular management of giant aneurysms: An introspection. Neurol India 2015;63:184.  Back to cited text no. 7
[PUBMED]  [Full text]  


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