Cerebellopontine Angle Meningioma Presenting as Trigeminal Neuralgia in a Patient with Meningiomatosis: A Case Report

Abstract

Introduction: Trigeminal neuralgia (TN) is a paroxysmal neuropathic facial pain that is classified as classical, idiopathic or secondary. Space-occupying lesions account for approximately 4–6% of TN presentations, and meningioma is one of the most frequent culprits. The coexistence of TN with meningiomatosis—two or more spatially separate meningiomas—is uncommon, and in such patients the clinician must determine which lesion is responsible for the pain before rational treatment can be planned.

Case Illustration: A 51-year-old woman attended the neurology outpatient clinic of a regional general hospital in Gianyar, Bali, Indonesia, with a 2-year history of left-sided facial pain that had progressively worsened over the preceding year despite consultations at several hospitals. The pain was electric shock-like, predominantly periocular, lasted from seconds to 1 minute, and was triggered by light touch, wearing a face mask, chewing, tooth-brushing and face-washing. She also reported rotatory dizziness aggravated by positional change with nausea and vomiting, which had improved at presentation. Examination revealed hyperaesthesia in the territories of the left ophthalmic (V1) and mandibular (V3) divisions with trigger points in the left periorbital and mandibular regions; cerebellar testing was normal. Contrast-enhanced magnetic resonance imaging with angiography (MRI-MRA) demonstrated two strongly enhancing extra-axial masses with dural tails: a left temporal/cerebellopontine angle (CPA) lesion measuring 4.14 × 2.63 × 4.40 cm that encased the cavernous segment of the left internal carotid artery, extended to the posterior sphenoid sinus and compressed the left pons, and a right temporo-occipital lesion measuring 2.68 × 3.86 × 3.84 cm, consistent with meningiomatosis. Laboratory investigations were not performed. The patient was diagnosed with secondary TN attributed to the left CPA meningioma and was treated with carbamazepine 200 mg three times daily, mecobalamin 500 µg twice daily and betahistine 12 mg twice daily.

Discussion: Strict clinicoradiological correlation identified the left CPA–petroclival component, not the contralateral temporo-occipital lesion, as the pain generator. Involvement of the porus trigeminus/Meckel’s cave and pontine root entry zone explains the paroxysmal V3 pain, whereas extension along the lateral wall of the cavernous sinus explains the unusual V1 predominance. Hyperaesthesia, V1 involvement and concomitant vestibular symptoms are red flags that should prompt MRI in every patient with TN. Sodium-channel blockers are appropriate first-line symptomatic therapy, but secondary TN is more often refractory; definitive control of tumour-related pain is achieved more reliably with microsurgical decompression than with tumour-targeted radiosurgery, while the second, asymptomatic lesion may be kept under surveillance. HLA-B*15:02 carriage, which is prevalent in Indonesia, must be considered when carbamazepine is prescribed.

Conclusion: TN may be the index manifestation of meningiomatosis. Early contrast-enhanced MRI, lesion-by-lesion clinicoradiological correlation, pharmacogenomically safe symptomatic therapy and timely referral for multidisciplinary neurosurgical decision-making are essential to optimise outcomes, particularly in secondary-care settings.