INTRODUCTION
Hemifacial spasm (HFS) is caused by compression of the facial nerve root exit zone (REZ) by either branch vessels of the vertebrobasilar artery system or the vertebral artery (VA) itself [1], and microvascular decompression (MVD) is the gold standard for radical treatment. Several case reports have documented successful outcomes of endovascular treatment for HFS caused by VA aneurysms [2-11]. However, the efficacy of endovascular treatment for HFS caused by a deviated branch vessel associated with an aneurysm remains unclear.
Here, we describe the endovascular treatment of an HFS with a lesion in a branch vessel associated with a VA aneurysm.
CASE REPORT
A 45-year-old female with a history of hypertension presented with a right HFS that had been present for approximately 3 years and had increased in frequency over the last 6 months. Magnetic resonance angiography revealed a fusiform aneurysm of the VA immediately proximal to the posterior inferior cerebellar artery (PICA) origin (Fig. 1A). 3D rotation angiography revealed a fusiform aneurysm with a maximum diameter of 9 mm in the V4 portion of the VA (Fig. 1B) without evidence of arterial dissection. Magnetic resonance imaging (MRI) images suggested that the right PICA was the vessel responsible for the HFS (Fig. 1C), which revealed that the PICA contacted the facial nerve at its proximal side to the detachment point from the brainstem (Fig. 1D). The occlusion test indicated that the patient was tolerant of ischemia.
The patient agreed to endovascular treatment for the right VA aneurysm but declined surgical MVD, given the mild nature of the HFS symptoms. Based on the clinical course and imaging findings, we suspected that the enlargement of the VA aneurysm had altered the VA course, causing PICA displacement, which likely led to HFS development. As a treatment for HFS, choosing a device that straightens the parent vessel and keeps the PICA away from the REZ was prioritized. We chose a neck-bridge stent and selected the LVIS Jr. (Terumo) for its balance between aneurysm embolization efficiency and its ability to straighten the parent vessel.
Aspirin (100 mg/day) and clopidogrel (75 mg/day) were started 1 week before treatment, which was performed under general anesthesia. Systemic heparinization was initiated after inserting a 6-Fr sheath through the right femoral artery and adjusting the activated coagulation time to 200–250 seconds during the procedure. A 6-Fr Slimguide (Medikit) was inserted into the right VA. The Headway 17 (Terumo) was advanced to the basilar artery for stenting, and the Phenom 17 (Medtronic) was inserted using a Synchro Select Standard (Stryker) for aneurysm embolization. A Hydrocoil 3D 5 mm×14 cm (Terumo) was inserted into the aneurysm as the first coil, and an LVIS Jr. stent was deployed. A stent was implanted to lengthen the proximal side of the right VA, including the PICA, to straighten its outward curvature. Embolization of the jailed catheter was performed to achieve Raymond–Roy class I. There were no perioperative complications, and no ischemic changes were observed on diffusion-weighted imaging the day after surgery. The HFS showed no improvement for 3 months after the procedure. Thereafter, it gradually improved, with near-complete resolution at 9 months and complete remission at 1 year and 9 months postoperatively, with no subsequent recurrence. The VA aneurysm was confirmed to be completely occluded by angiography 1 week postoperatively and remained occluded 1 year later.
Comparison of digital subtraction angiography images at 1-year post-procedure with preoperative images revealed straightening of the stented VA with outward curvature (Fig. 1E, F). Comparison of the PICA origin position against craniocaudal reference lines suggested lateral deviation associated with VA outward curvature and demonstrated a reduction in PICA diameter. Regarding the spatial relationship of the PICA from its origin to its loop associated with the VA outward curvature, we compared coronal MRI time-of-flight images obtained before treatment and at a 2-year follow-up (Fig. 1G, H). Comparative analysis showed that the PICA was displaced laterally and caudally on coronal images, suggesting that the PICA had moved away from the pontine surface where the facial nerve courses. PICA deviation was quantitatively evaluated using cone-beam computed tomography by measuring the vertical distance from the petrous bone plane at the internal auditory canal level to the nearest point of the PICA loop. Comparison with 1-year post-treatment measurements showed a reduction from 7.21 mm to 5.28 mm, confirming lateral displacement of the PICA from the root REZ toward the petrous bone.
DISCUSSION
HFS is caused by mechanical compression of the facial nerve in the REZ [1]. While vascular compression is the most common cause, lesions such as tumors, arteriovenous malformations, and aneurysms can occasionally be responsible [12]. Among these, HFS due to VA aneurysms is rare, occurring in only 0.5% of cases [1]. Although there have been only a few reports of direct surgery [13], recent years have seen increasing reports of endovascular treatment (Table 1) [2-11]. Various treatment modalities, including coil embolization [8], stent-assisted coil embolization [7,9], flow diverter (FD) placement [6], and parent artery occlusion, have been used to dissect VA aneurysms and saccular/fusiform aneurysms [2-5,10,11].
In MVD, most cases show immediate resolution of HFS postoperatively when contact between the responsible lesion and facial nerve is eliminated. Early remission of HFS has been reported in endovascular treatment cases where aneurysms were the responsible lesions. However, as this treatment does not alter the position of the aneurysm itself, it is hypothesized that the resolution of HFS is related to the cessation of aneurysmal pulsation against the facial nerve. In a case of FD placement for VA aneurysm with HFS [6], although HFS improved significantly after treatment, complete remission took 6 months. Furthermore, while subsequent angiography confirmed complete aneurysm occlusion, MRI showed no changes in aneurysm size or its relative position to the facial nerve. This supports the hypothesis that HFS resolves when aneurysmal pulsation ceases due to thrombosis and complete occlusion. Additionally, there are multiple reports of rapid HFS improvement in cases of coil embolization for saccular aneurysms [7,8], suggesting that rapid intra-aneurysmal occlusion by coil embolization plays a role. The time interval between symptom onset and treatment has also been considered as another contributing factor [8]. Conversely, there is a report of endovascular treatment resistance where subsequent endoscopic observation during craniotomy revealed PICA contact with the REZ, and remission was achieved only after additional MVD [10].
Based on these findings, endovascular treatment appears safe and effective, specifically in cases where an aneurysm itself is the cause of HFS. Treatment selection can be considered based on the severity of HFS symptoms.
The facial nerve originates from the upper edge of the supraolivary fossette at the pontobulbar groove and courses along the ventral surface of the pons for 8–10 mm, firmly adhered by the pia mater and connective tissue. Tomii et al. [14] defined the origin point as the root exit point (REP) and the point where the facial nerve detaches from the pons as the detach point (DP). The segment between the DP and the transitional zone (TZ), where the facial nerve transitions from central to peripheral myelination, is known as the proximal cisternal segment (PCS) [15]. While the facial nerve distal to the TZ is resistant to mechanical compression due to peripheral myelination, the central portion from REP to PCS is highly susceptible, potentially leading to HFS. The reported frequencies of compression vary by location: REP-DP (10–96%), PCS (up to 64%), TZ (22%), and other cisternal segments (3%) [16]. In the present case, contact with the PICA was confirmed during REP-DP. Based on pre- and postoperative imaging findings, we concluded that the HFS pathogenesis most likely involved medial PICA displacement due to VA course alterations associated with vertebral aneurysm enlargement. The gradual VA straightening and outward curvature post-procedure led to lateral PICA displacement, which resolved the contact with the facial nerve, resulting in HFS remission. The reduction in PICA diameter may have also contributed to the resolution of HFS, suggesting that multiple factors were involved in the therapeutic outcome.
Regarding the treatment strategy, we selected the LVIS Jr. stent for treatment and achieved favorable outcomes. While various studies have reported parent vessel straightening following stent deployment, a comparative analysis of four intracranial stents (LVIS, LEO [Balt], Enterprise VRD [Cerenovus/ Johnson & Johnson], and Neuroform [Stryker]) demonstrated that the LVIS stent exhibited the lowest radial force but the highest axial force among the compared devices [17]. Furthermore, in vitro studies have reported that while braided stents have low radial force, they exhibit high axial force [18]. Regarding FD, which are braided stents, there are reports about straightening of the parent artery itself. In terms of FD composition as a factor in straightening, it has been reported that cobalt-chromium stent tends to cause more straightening compared to nitinol stent [19]. Regarding the time required for vessel straightening, previous studies have documented that laser-cut stents can induce changes from immediate post-deployment through 1-year follow-up, with a higher incidence observed in bifurcation-type aneurysms [20]. Conversely, since there are no reports regarding the displacement of branch vessels in the stented area associated with straightening, the timing of occurrence and the degree of variation remain unclear. In our patient, although HFS remission took more than 1 year, considering that the stent was deployed in the parent vessel rather than at a vessel bifurcation, we speculate the vessel straightening presumably occurred more gradually, and this timeline is consistent with our clinical course given that the PICA displacement was a secondary change. Based on post-treatment imaging findings showing lateral displacement of the PICA origin and subsequent symptom improvement, the proposed mechanism of HFS is that aneurysm enlargement caused medial displacement of the PICA, resulting in contact with the facial nerve running along the anterior surface of the pons. However, it remains unclear whether VA straightening by stent placement can cause PICA displacement, leading to HFS improvement, and it should be noted that this was merely a secondary effect of aneurysm treatment.
Endovascular treatment becomes challenging when VA aneurysms affect branch vessels, causing HFSs. While VA straightening may cause secondary PICA displacement, leading to HFS improvement, this process likely requires time; therefore, it is not a viable treatment option for HFS. However, when there is time to evaluate the clinical course of HFS alongside aneurysm treatment, longitudinal imaging assessment can be useful for determining effectiveness.
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