Introduction: Masseter vestibular evoked myogenic potentials (M-VEMPs) are a recent tool for assessing a vestibulo-trigeminal pathway departing from the saccule, similarly to cervical VEMPs (C-VEMPs), that evaluate saccular function via the sternocleidomastoid muscle. M-VEMPs may offer a complementary diagnostic value in vestibular neuritis (VN). Methods: This retrospective study analysed M-VEMPs and C-VEMPs in 28 monolateral patients and 1 bilateral (30 ears) diagnosed with VN between 2023 and 2024. Diagnostic evaluation included video head impulse tests (VHIT), caloric tests, ocular VEMPs, and, in a few cases, electromyography (EMG) of the sternocleidomastoid muscle. M-VEMPs were elicited using 500 Hz tone bursts at 97 dB nHL. Results were compared based on the topography of vestibular involvement and muscle response concordance. Results: M-VEMPs were always present in patients with superior VN and intact saccular function, showing consistent results with normal C-VEMPs. In some cases, with saccular dysfunction, M-VEMPs were preserved despite the absence of C-VEMPs, suggesting greater robustness. One patient with herpes zoster (HZ) involving both the VIII and trigeminal nerves showed absent M-VEMPs, indicating trigeminal pathway involvement. Edentulous patients showed reduced or absent M-VEMPs due to compromised masseter muscle electromyography activity. Conclusions: M-VEMPs are reliable and often concordant with C-VEMPs in VN but may reveal additional diagnostic information in discordant or complex cases. They are particularly useful in identifying trigeminal involvement but are limited in patients with poor masseter muscle function. Further studies are needed to clarify their full diagnostic potential.
(1) Background: Patients affected by Ménière’s disease can experience Tumarkin’s syndrome, which is characterized by postural instability, gait abnormalities, and, occasionally, an abrupt loss of balance known as vestibular drop attack or Tumarkin’s crisis. In this study, semicircular canal plugging is proposed as the definitive treatment for this condition. The outcomes of this type of surgery are discussed. (2) Methods: A total of 9 patients with a confirmed diagnosis of Ménière disease suffering from Tumarkin crisis underwent posterior semicircular canal plugging. These patients were assessed with Video Head Impulse Tests, vestibular evoked myogenic potentials, and Pure Tone Audiometry preoperatively and postoperatively. (3) Results: VHIT showed a postoperative decrease in PSC gain median (Preop. 0.86 and postop. 0.52; p < 0.009). No statistically significant differences were described for the anterior semicircular canal and the lateral semicircular canal. No patient experienced new Tumarkin crisis after the surgical treatment. (4) Conclusions: Our ten years of experience with posterior semicircular canal plugging in Ménière disease patients with Tumarkin’s syndrome has shown that this type of surgical procedure is successful in controlling Tumarkin’s crisis, with high patient satisfaction and little worsening in hearing level.
The association between acoustic neuroma and positional vertigo with paroxysmal positional nystagmus is relatively rare, but, when present, it certainly represents a challenge for the otoneurologist. There are few reports in the literature on this particular issue, and some questions are still unanswered, particularly regarding the characteristics of positional nystagmus that may distinguish between a true benign paroxysmal vertigo and a positional nystagmus associated with the tumor. We present the videonystagmographic patterns of seven patients with acoustic tumor who had paroxysmal positional nystagmus and analyzed its features. A concomitant true benign paroxysmal positional vertigo may be present during the follow-up of a non-treated patient, as the paroxysmal positional vertigo may be the first symptom of the tumor, and it may show characteristics that are very similar to a posterior semicircular canal canalolithiasis or a horizontal canal “heavy or light cupula”. The possible mechanisms are discussed.
Background: The posterior labyrinth is particularly vulnerable to ischemic injury. Vertigo can occasionally be the only presenting symptom of acute myocardial infarction (AMI). Acute Bilateral Vestibular Neuropathy (ABVN) is an extremely rare condition, with only three cases previously reported in the literature. Its exact pathophysiological mechanisms remain unclear. Case Presentation: We present the case of a 76-year-old male who presented to the emergency department (ED) with vertigo and severe postural unsteadiness. Subsequently, a silent AMI was diagnosed, prompting cardiac stenting. Vestibular function assessments over the following eight months confirmed the diagnosis of ABVN. A cycle of vestibular rehabilitation yielded limited objective benefit, although the patient reported subjective improvement as measured by the Dizziness Handicap Inventory (DHI). Discussion and Conclusions: This case suggests a potential association between peripheral vestibular dysfunction and acute hemodynamic impairment due to myocardial infarction. Notably, it represents the first reported case of ABVN following a silent AMI, presenting solely with vestibular symptoms.