Project description:The aim of this study was to investigate the clinical characteristics and underlying pathogenesis of episodic vestibular syndrome (EVS) with hyperventilation-induced downbeat nystagmus (HV-DBN).
Project description:We present an unusual case of a patient with a positive Tullio phenomenon, brief Valsalva-induced transient horizontal nystagmus, reduced left caloric response, and bilateral vestibulo-ocular reflex loss. This study discusses the pathophysiology and differential diagnosis concerning the suspected pathology for the phenomenon of utricular hydrops or vestibular atelectasis and presents a literature review.
Project description:Vestibular schwannoma (VS) is commonly accompanied by hearing loss, tinnitus, and dizziness and tends to be chronically progressive in nature. We report a case of VS presenting as left vestibular neuritis (VN) in a previously healthy 57-year-old patient. Right-beating horizontal-torsional spontaneous nystagmus was observed, and the bedside head impulse test revealed a left catch-up saccade. The bithermal caloric test showed left canal paresis, and pure-tone audiometry revealed an average threshold of 22.5 dB bilaterally. Brain magnetic resonance imaging (MRI) demonstrated a 0.7-cm enhancing mass in the left internal auditory canal, consistent with VS. The patient was administered with high-dose systemic corticosteroids and vestibular suppressants with antiemetic, which relieved acute vertigo. Although dizziness in VS is chronically progressive in nature, VS may present as an acute vestibular syndrome that mimics VN. VS should be considered a potential cause of acute vestibular syndrome, and thorough neurological examination with MRI may be helpful for accurate diagnosis.
Project description:RationaleVestibular paroxysmia (VP) is characterized by spontaneous, recurrent, short, paroxysmal attacks of vertigo with or without tinnitus.Patient concernsWe report a case of paroxysmal recurrent vertigo accompanying clicking tinnitus on the left side in a 61-year-old patient. He had undergone microvascular decompression to treat the left-side hemifacial spasm 6 years prior. The patient first developed vertigo attacks about 3 years after microvascular decompression, and the attacks increased in frequency over the last 4 months. Video-nystagmography revealed a background right-beating nystagmus which was reversed every 55 seconds, to left-beating nystagmus for 17 seconds.DiagnosisBrain magnetic resonance imaging and angiography demonstrated a compression of the cisternal segment of the left vestibulocochlear nerve between the tortuous right vertebral artery and the posterior wall of the left porus acusticus internus.Interventions and outcomesUnder the diagnosis of VP, 300 mg oxcarbazepine was administered daily, which relieved the symptoms dramatically.LessonThe neurovascular cross-compression of the vestibulocochlear nerve by the contralateral vertebral artery tortuosity can cause VP. Periodic paroxysms of right-beating nystagmus accompanying the left-side tinnitus during vertigo attacks in our patient can be explained by secondary central hyperactivity in both vestibular and cochlear nuclei following long-standing neurovascular cross-compression.
Project description:Vestibular paroxysmia (VP) is a disorder encountered in the pediatric population that etiology has been attributed to neurovascular cross-compression syndrome (NVCC). The purpose of this study was to report a new probable pathological condition, the narrowed internal auditory canal (IAC), which appears to be involved in the development of a clinical picture of VP in the pediatric population. A retrospective descriptive comparative study was conducted to compare clinical, electrophysiological, radiological, and therapeutic outcomes in both etiologies. Overall, 16 pediatric patients suffering from VP were included and divided into two groups: patients with narrowed internal auditory (Group 1) were compared to those with NVCC syndrome (Group 2). Patients in both groups were similar in terms of auditory complaints, as well as hearing, vestibular, and electrophysiological status. A narrowed IAC was encountered in the adolescent age category and females, especially those with rapid growth. The diagnosis requires a careful analysis of the shape and diameters of the IAC. Radiologic measurements in the axial plane do not seem to be sufficient to confirm the diagnosis, and, therefore, an analysis of diameters in the coronal plane is required. Treatment with sodium-channel blockers drugs showed promising results not only by relieving vertigo but also by normalizing the electrophysiological findings. In conclusion, a narrowed IAC can be considered in patients suffering from VP.
Project description:We present recent advances in the genetics of recurrent vertigo, including familial episodic ataxias, migraneous vertigo, bilateral vestibular hypofunction and Meniere's disease.Although several vestibular disorders are more common within families, the genetics of vestibulopathies is largely not known. Genetic loci and clinical features of familial episodic ataxias have been defined in linkage disequilibrium studies with mutations in neuronal genes KCNA1 and CACNA1A. Migrainous vertigo is a clinical disorder with a high comorbidity within families much more common in females with overlapping features with episodic ataxia and migraine. Bilateral vestibular hypofunction is a heterogeneous clinical group defined by episodes of vertigo leading to progressive loss of vestibular function which also can include migraine. Meniere's disease is a clinical syndrome characterized by spontaneous episodes of recurrent vertigo, sensorineural hearing loss, tinnitus and aural fullness and familial Meniere's disease in around 10-20% of cases. An international collaborative effort to define the clinical phenotype and recruiting patients with migrainous vertigo and Meniere's disease is ongoing for genome-wide association studies.
Project description:The authors describe two patients suffering from demyelinating central nervous system disease who developed intense vertigo and downbeat nystagmus upon tilting their heads relative to gravity. Brain MRI revealed in both cases a single, small active lesion in the right brachium conjunctivum. The disruption of otolithic signals carried in brachium conjunctivum fibres connecting the fastigial nucleus with the vestibular nuclei is thought to be causatively involved, in agreement with a recently formulated model simulating central positional nystagmus. Insufficient otolithic information results in erroneous adjustment of the Listing's plane in off-vertical head positions, thus producing nystagmic eye movements.