Neuro-ophthalmic complications following eighth cranial nerve microvascularx decompression

Abstract

Purpose

To discuss a novel diagnosis of post-surgical iatrogenic AICA vasospasm following eighth cranial nerve microvascular decompression as the most likely etiology for a lateral pontine infarct.

Observations

A 49-year-old male presented with tinnitus, vertigo, binocular and monocular diplopia following left occipital decompressive craniectomy and microvascular decompression of cranial nerve VIII. Magnetic resonance imaging demonstrated patent vasculature with evolution of a subacute infarct of the left lateral pons and middle cerebellar peduncle in the territory of the left AICA.

Conclusions

We report a unique case of lateral pontine infarction without vascular occlusion acutely following surgical microvascular decompression of CN VIII, most consistent with post-surgical AICA vasospasm. This case provides a clear example of vestibular and neuro-ophthalmic complications of CN VIII microvascular decompression.

A 49-year-old Hispanic male presented to the Houston Methodist Hospital Neuro-ophthalmology clinic in November 2022 with tinnitus, vertigo, binocular and monocular diplopia following left occipital decompressive craniectomy and microvascular decompression of cranial nerve (CN) VIII.

He was in his usual state of health until March 2022 when he developed new onset tinnitus. After failing maximum medical therapy for tinnitus, he elected to undergo microvascular decompression of an aberrant dolichoectatic vertebrobasilar artery seen in magnetic resonance imaging (MRI) and MR angiography. The dolichoectatic artery was compressing the left CN VIII and at the time of surgery, a Teflon pad was placed between the artery and CN VIII. A titanium plate was used to close the cranial defect. Post-operatively the patient developed severe headache. A repeat cranial MRI showed only postoperative changes with fluid collection at the site. Cerebrospinal fluid (CSF) analysis revealed a CSF pleocytosis (>400 white blood cells/mm³) and a markedly elevated CSF protein level (102 mg/dL).

On post-operative day 16, he returned to the operating room for drainage of the infectious/inflammatory fluid collection and removal of the titanium plate. The Teflon pad remained in place. Fluid cultures grew Enterococcus faecalis, which was treated with vancomycin, linezolid, and cefixime. Two days following the second intracranial surgery and drainage, the patient developed nystagmus, dizziness, vertigo, and binocular diplopia.

Past medical history was significant for hypertriglyceridemia and hypercholesterolemia. Family history was non-contributory. He has never smoked or used smokeless tobacco. He stopped drinking alcohol in February 2022 and has no history of drug use. His medications at the time of presentation were Thealoz (trehalose), Nootropil (piracetam for myoclonus, not FDA approved), and Oroxadin (ciprofibrate, not FDA approved).

Neuro-ophthalmic examination in November 2022 found a visual acuity of 20/20 bilaterally (OU). Intraocular pressure was 14 mmHg in the right eye (OD) and 15 mmHg in the left eye (OS). Pupils were 4 mm in darkness and 2 mm when exposed to light OU. There was no anisocoria or relative afferent pupillary defect. Ocular motility examination showed a unidirectional, left-beating, small amplitude nystagmus observed in left gaze only. There was no primary position or bidirectional nystagmus and no evidence of skew deviation. Cup-to-disc ratio was 0.3 without papilledema OU. Optical coherence tomography showed retinal nerve fiber layer thickness of 101 (OD) and 110 (OS) μm. On dynamic visual acuity testing, he lost 3 lines of vision compared to May 2022, compatible with vestibulo-ocular reflex (VOR) mismatch. He underwent electronystagmography testing with otolaryngology who recommended empiric treatment with corticosteroids and vestibular rehabilitation.

An MRI at the time of the second surgery showed inflammatory change in the postsurgical bed of the left cerebellopontine angle along with a round, lobulated, low intensity, 9.7 mm structure (Fig. 1A), surgically identified as a granuloma, and a subacute infarct (Fig. 1B). MR venogram showed no venous occlusion. MR arteriography (MRA) demonstrated patent cerebral arterial vasculature. Serial computed tomography (CT) scans demonstrated evolution of the subacute infarct of the left lateral pons and the middle cerebellar peduncle in the territory of the left AICA.

Fig. 1.

MRI of the brain showing the granuloma that resulted from Teflon pad placement and subsequent AICA infarct. (A) At the described location of the Teflon pad placement (white arrow), within the left pontocerebellar angle and adjacent to CN VII and CN VIII, there is a round structure with lobulated borders, low intensity, and a major axis of 9.7 mm. Following this MRI, this structure was surgically confirmed to be a granuloma surrounding the Teflon pad. (B) Subacute infarct at the intersection of the left lateral aspect of the pons and middle cerebellar peduncle within the territory of the AICA.

AICA infarction, also known as lateral pontine syndrome, classically results in sudden onset severe vertigo, vomiting, nystagmus, falling to the side of the lesion, ipsilateral loss of sensation of the face, ipsilateral facial paralysis, and ipsilateral hearing loss and tinnitus.¹ These symptoms correspond with damage to structures within the lateral pons that are vascularly supplied by the AICA or damage to the inner ear, which is vascularly supplied by the labyrinthine artery, which originates from the AICA in the majority of patients. In cases of incomplete infarction of the area, a patient may present with only select findings from this collection of symptoms, like those seen in our patient's presentation (Fig. 1B). The nystagmus with which our patient presented likely arose from an asymmetric otolithic input following ischemic depolarization of left inner ear otolithic neurons, thereby simulating a left head turn with subsequent eyes drifting to the right and beating to the left. Patients undergoing microvascular decompression within the cerebellopontine angle are at risk of adverse events, including neuronal and vascular damage. The subsequent complications, including hearing loss, tinnitus, vertigo, and hemifacial paresis typically result from direct damage to the cranial nerves, the pons, or the vasculature.²

Meningitis increases the risk of vasospasm, thus, though we believe that the pontocerebellar angle granuloma is the primary driver of the vasospasm and subsequent AICA infarction, it is likely that meningitis also contributed to this event.

Our patient's symptoms arose following microvascular decompression (MVD), which is a well described surgical procedure to relieve mass effect and compression of specific cranial nerves (e.g., trigeminal neuralgia (CN V), glossopharyngeal neuralgia (CN IX), or hemifacial spasm (CN VII)). Recently, MVD has been performed for CN VIII dysfunction.³ In carefully selected patients, MVD is a useful surgical technique to treat neurovascular conflicts, which are a rare cause of unilateral tinnitus and vertigo, potentially minimizing the risk of long-term recurrence and complications. However, the decision-making process should be determined on a case-by-case basis. In appropriately selected cases, such patients should undergo thorough history, clinical examination and consistent follow-up, as their postoperative symptoms may uncover a serious ischemic event.

In our patient, the acute onset of symptoms in conjunction with the surgical microvascular decompression of CN VIII suggests post-surgical AICA vasospasm as the most likely etiology of the lateral pontine infarct and subsequent symptoms. Clinicians should be aware of the vestibular and neuro-ophthalmic complications of CN VIII microvascular decompression.

CRediT authorship contribution statement

Stanley M. Saju: Writing – review & editing, Writing – original draft, Formal analysis, Data curation, Conceptualization. Patrick J. Hunt: Writing – review & editing, Writing – original draft, Formal analysis, Data curation, Conceptualization. Pamela Davila-Siliezar: Writing – review & editing, Writing – original draft, Formal analysis, Data curation, Conceptualization. Noor Laylani: Writing – review & editing, Writing – original draft, Formal analysis, Data curation, Conceptualization. Andrew G. Lee: Writing – review & editing, Formal analysis, Data curation, Conceptualization.

Patient consent

Consent to publish this case report has been obtained from the patient in writing.

Claims of priority

After conducting a literature review on November 15th, 2022 utilizing PubMed, Google Scholar using the key words (Microvascular Decompression, Postoperative Iatrogenic AICA Infarct, CN VIII), we did not find any prior reports of a postoperative iatrogenic AICA infarct secondary to vasospasm after microvascular decompression.

Publication originality statement

We confirm this publication is original.

Authorship

All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, take responsibility for the integrity of the work, and have given their approval for this version to be published.

Statement of authorship

Category 1:

• a. Conception and design: Stanley M. Saju, Patrick J. Hunt, Pamela Davila-Siliezar, Noor Laylani, Andrew G Lee.

• b. Acquisition of data: Stanley M. Saju, Patrick J. Hunt, Pamela Davila-Siliezar, Noor Laylani.

• c. Analysis and interpretation of data: Stanley M. Saju, Patrick J. Hunt, Pamela Davila-Siliezar, Noor Laylani, Andrew G Lee.

Category 2:

• a. Drafting the manuscript: Stanley M. Saju, Patrick J. Hunt, Pamela Davila-Siliezar, Noor Laylani.

• b. Revising it for intellectual content: Pamela Davila-Siliezar, Noor Laylani, Andrew G Lee.

Category 3:

• a. Final approval of the completed manuscript: Stanley M. Saju, Patrick J. Hunt, Pamela Davila-Siliezar, Noor Laylani, Andrew G Lee.

Authorship

All authors attest that they meet the current ICJME critieria for Authorship.

Funding

No funding or grant support

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.