Francesco Comacchio

Background: Persistent Postural Perceptual Dizziness (PPPD) unifies several preceding diagnoses that share persistent non-vertiginous dizziness and visually or posturally triggered unsteadiness. Whether clinically meaningful subtypes exist within PPPD remains debated. We aim to characterise demographic, clinical, and psychological profiles of untreated PPPD patients and test for differences across subtypes corresponding to historical entities: Chronic Subjective Dizziness (CSD), Phobic Postural Vertigo (PPV), Space Motion Discomfort (SMD), and Visual Vertigo (VV). Methods: Retrospective observational study of consecutive PPPD patients evaluated in a single neurotology practice (2023–2025). All underwent standard vestibular work-up, symptom profiling, and psychological assessment (Beck Anxiety Inventory, Beck Depression Inventory-II, and clinician-rated attitudes). Results: Eighty-eight patients (mean age 40 years; female predominance) met PPPD criteria. PPV was most frequent (>two-thirds), followed by CSD. Instability predominated (54%), whereas dizziness was less common (19%), indicating mainly postural disturbance. Subtyping showed attitude differences (p=0.0006): SMD/VV patients more often displayed obsessive attitudes and less frequent anxious attitudes, while PPV patients were less often obsessive and more often anxious. Anxiety and depression scores did not differ significantly across subtypes. SMD/VV was strongly linked to acute vestibular triggers (all unilateral vestibular neuritis), whereas CSD frequently occurred without prior vestibular disease. Psychosocial triggers and prior psychiatric diagnoses clustered in specific subgroups. Conclusions: PPPD could be considered a heterogeneous spectrum with subtype-specific clinical–psychological profiles. Integrating subgroup profiling and systematic psychological assessment may guide personalised treatment, prioritising cognitive–behavioural strategies for obsessive/visual profiles and vestibular rehabilitation for postural-dominant presentations; longitudinal studies should validate tailored pathways and refine prognostic stratification.

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.

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.

Posterior semicircular canal dehiscence (PSCD) has been demonstrated to result in a third mobile window mechanism (TMWM) in the inner ear similar to superior semicircular canal dehiscence (SSCD). Typical clinical and instrumental features of TMWM, including low-frequency conductive hearing loss (CHL), autophony, pulsatile tinnitus, sound/pressure-induced vertigo and enhanced vestibular-evoked myogenic potentials, have been widely described in cases with PSCD. Nevertheless, video-head impulse test (vHIT) results have been poorly investigated. Here, we present six patients with PSCD presenting with a clinical scenario consistent with a TMWM and an impaired vestibulo-ocular reflex (VOR) for the affected canal on vHIT. In two cases, an additional dehiscence between the facial nerve and the horizontal semicircular canal (HSC) was detected, leading to a concurrent VOR impairment for the HSC. While in SSCD, a VOR gain reduction could be ascribed to a spontaneous “auto-plugging” process due to a dural prolapse into the canal, the same pathomechanism is difficult to conceive in PSCD due to a different anatomical position, making a dural herniation less likely. Alternative putative pathomechanisms are discussed, including an endolymphatic flow dissipation during head impulses as already hypothesized in SSCD. The association of symptoms/signs consistent with TMWM and a reduced VOR gain for the posterior canal might address the diagnosis toward PSCD.

The role of intercalatus nucleus of Staderini (INS), the most caudal of the perihypoglossal nuclei, is much debated. Last research seems to suggest that this nucleus plays a role as a vertical eyes movements integrator. The few clinical reports present in the literature that describe isolated lesions of the INS have described patients presenting in acute with up-beating vertical spontaneous nystagmus. Isolated acute lesion of INS is, in fact, much rare, and, without other neurological signs, is exceptional. We present a case of acute isolated vertigo with no other neurological signs or symptoms, due to INS ischemia provoked by vertebral artery stenosis. The patient presented with spontaneous vertical up-beating nystagmus that showed at videonystagmographic recording, a clear exponential decay of angular slow-phase velocity, that is considered a typical sign of neural integrator impairment. This case seems to represent a further confirm that INS is part, as a vertical-to-position neural integrator, of the neural circuit controlling the vertical eyes movements.(c) 2023 PLA General Hospital Department of Otolaryngology Head and Neck Surgery. Production and hosting by Elsevier (Singapore) Pte Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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.

Vestibular neuritis (VN) mostly involves the superior vestibular nerve. Isolated inferior vestibular neuritis (IVN) has been more rarely described. The diagnosis of IVN is based on an abnormal head impulse test (HIT) for the posterior semicircular canal (PSC), pathological cervical vestibular-evoked myogenic potentials (C-VEMPs), and spontaneous downbeat nystagmus consistent with acute functional loss of inner ear sensors lying within the inferior part of the labyrinth. HIT for both lateral and superior semicircular canals is normal, as are ocular VEMPs and bithermal caloric irrigations. The etiology of IVN is debated since peripheral acute vestibular loss with a similar lesion pattern can often be associated with ipsilesional sudden hearing loss (HL). Viral inflammation of vestibular nerves is considered the most likely cause, although reports suggest that VN usually spares the inferior division. On the other hand, an ischemic lesion involving the terminal branches of the common cochlear artery has been hypothesized in cases with concurrent HL. Debated is also the lesion site in the case of IVN without HL since different instrumental patterns have been documented. Either isolated posterior ampullary nerve involvement presenting with selective PSC functional loss on video-HIT, or only saccular lesion with isolated ipsilesional C-VEMPs impairment, or inferior vestibular nerve damage (including both saccular and posterior ampullary afferents) exhibiting an impairment of both C-VEMPs and PSC-HIT. We report an interesting case of a patient with an acute vestibular loss consistent with IVN without HL who developed a PSC ossification on follow-up, questioning the viral origin of the lesion and rather orienting toward an occlusion of the posterior vestibular artery. To the best of our knowledge, this is the first report of PSC ossification after a clinical picture consistent with IVN.

Background and Objectives: Bilateral sequential vestibular neuritis (BSVN) is a rare condition in which an inflammation or an ischemic damage of the vestibular nerve occurs bilaterally in a sequential pattern. We described four cases of BSVN.Subjects and Methods: Every patient underwent video-head impulse test during the first and the second episode of vestibular neuritis (VN), furthermore they have been studied with radiological imaging.Results: Contralateral VN occurred after a variable period from prior event. Vestibular function recovered from the first episode in one case. The other three patients developed contralateral VN. One case was due to a bilateral VN in association with a Ramsay-Hunt syndrome, in another patient clinical records strongly suggested an ischemic etiology, whereas in two cases aetiology remained uncertain. Two patients subsequently developed a benign paroxysmal positional vertigo involving the posterior canal on the side of the latest VN (Lindsay-Hemenway syndrome).Conclusions: Instrumental vestibular assessment represents a pivotal tool to confirm the diagnosis of VN and BSVN.