Pearls & Oy-sters: Labyrinthine Infarction Mimicking Vestibular Neuritis

Concomitant Labyrinthine and Cerebellar Infarction

Given the common vascular supply to the cerebellar flocculus and inner ear, mostly from the anterior inferior cerebellar artery (AICA; Figure, F),^1,2 findings of acute unilateral peripheral vestibulopathy may be ascribed to concomitant labyrinthine infarction that is hardly visualized with current imaging technique in our patient. The diagnosis of labyrinthine infarction is usually made when patients show combined loss of hearing and peripheral vestibular function in association with brainstem or cerebellar infarction in the territory of AICA.³ Occasionally, diffusion-weighted images (DWI) can also visualize an infarction directly involving the vestibulocochlear nerve or the labyrinth.⁴ Given the common vascular supply of the vestibulocochlear nerve and the labyrinth,¹ infarctions are hardly expected to involve the vestibular nerve only and spare the cochlear nerve.² Indeed, only 4% of patients with infarction in the territory of AICA present with acute vestibulopathy in isolation.³ However, as in our patient, the auditory symptoms may not be striking in embolic labyrinthine infarction when the anterior vestibular artery is preferentially involved.^1,5 Indeed, laboratory evaluation showed predominant involvement of the HC. Given the normal angiogram, steno-occlusion of the proximal portion of the AICA and subsequent recanalization or embolism may be presumed as the mechanism.

Differentiation of Labyrinthine Infarction From Vestibular Neuritis

The diagnostic hallmarks of vestibular neuritis are spontaneous contralesional horizontal-torsional nystagmus, positive HITs for the ipsilesional canals, and ipsilesional canal paresis. Unlike Ramsay-Hunt syndrome or labyrinthitis that can show swelling or gadolinium enhancement in the vestibular nerve or labyrinth,⁶ conventional MRIs of the inner ear are almost always normal in vestibular neuritis.⁷ As such, the diagnostic utility of MRIs is limited unless using high-dose gadolinium or a 4-hour delayed 3D fluid-attenuated inversion recovery images.⁸ Thus, the diagnosis of labyrinthine infarction should be based on findings of history taking and clinical evaluation. Absence of antecedent infection and the hyperacute onset of vertigo are also atypical for vestibular neuritis.

Catching the Subtle Auditory and Central Ocular Motor Signs

Although the 3-item bedside eye movement screening head impulse, nystagmus, test of skew (HINTS) shows excellent sensitivity, it can be misleading in AICA infarction.⁹ Moreover, DWI often fails to detect the labyrinthine infarction, which can be a harbinger of AICA infarction.¹⁰ Thus, scrutinized neurotologic evaluation is important for diagnosing infarction involving the labyrinth and cerebellum. In our patient, the diagnosis of labyrinthine infarction was challenging because the auditory symptoms were subtle and transient. Patients may not notice hearing impairments during an attack of vertigo when the hearing loss is subtle.¹¹ In this case, the finger rub test may help detect asymmetric hearing at bedside.¹² Because HINTS may fail to detect labyrinthine infarction,¹³ detection of hearing loss using the finger rub test (HINTS-plus) is important for diagnosing vascular inner ear damage.¹²

Even though floccular infarction was found on MRI, our patient did not show ipsilesional spontaneous nystagmus, GEN, impaired smooth pursuit, or increased gain of the VOR during rotatory chair test, which are ocular motor signs indicating floccular dysfunction. However, the small corrective saccades for the contralesional right HC may be ascribed to a partial involvement of the left flocculus or adaptation to the labyrinthine infarction.¹⁴

A thorough history taking and neurotologic evaluation are important for differentiating labyrinthine infarction from inflammatory disorders involving the labyrinth.