Is the Auditory Brainstem Response Diagnostic for Vestibular Paroxysmia? / 대한평형의학회지

OBJECTIVES: Vestibular paroxysmia (VP) of the eighth cranial nerve is characterized by recurrent auditory and vestibular disturbances when a proximal part of the eighth cranial nerve is continuously pressed by a vessel. A detailed history and several ancillary diagnostic tools, such as tinnitogram, caloric test, auditory brainstem response (ABR) and magnetic resonance imaging, are used for diagnosis of VP. Among them, although Møller criteria using ABR is a simple method, the previous study is insufficient. Therefore, this study aimed to evaluate ABR's diagnostic value of VP. METHODS: ABR records of the 14 patients (patient group) who were diagnosed with VP and 45 patients (as control) who were diagnosed with only tinnitus were reviewed retrospectively. We analyzed the differences in Møller criteria between 2 groups. RESULTS: Mean age of the patient group was 52.9 years old and the control group was 55.4 years old. As compared with the control group, there were no significant differences of Møller 3 criteria contents (peak II wave amplitude < 33% [35.7% vs. 15.5%, p=0.133], interpeak latency I–III ≥2.3 msec [42.8% vs. 35.5%, p=0.622]), Contralateral interpeak latency III–V ≥2.2 msec (0% vs. 4.4%, p=1.000) in patient group. CONCLUSION: There was no significant difference of ABR parameters according to the Møller criteria between patient and control groups.

Paroxismia vestibular: reporte de un caso / Vestibular paroxysmia: case report

Presentamos el caso de un paciente joven quien presenta 4 a 5 crisis diarias de vértigo espontáneo de segundos de duración, todos o casi todos los días desde hace 9 meses. Estas crisis no tienen gatillo posicional, y hay completa ausencia de sintomatologia entre crisis. Como discutimos en el artículo, este cuadro coíncide con los recientemente publicados criterios para una paroxismia vestibular, entidad supuestamente secundaria a la compresión neurovascular del nervio vestibular. El paciente respondió de forma inmediata y completa a carbamazepina a dosis bajas, el tratamiento de elección en la paroxismia vestibular.

We present the case of a young patient, with a 9-month long history of 4 to 5 daily spells of spontaneous vertigo, each lasting only seconds. There is no positional trigger, and there is a complete lack of symptoms between attacks. As is discussed in the article, this matches the recently published criteria for Vestibular Paroxysmia, an entity allegedly secondary to neurovascular compression of the vestibular nerve. The patient responded immediately and completely to carbamazepine at low dosage, the preferred treatment for vestibular paroxysmia.

Vestibular Paroxysmia and Hemifacial Spasm by Vascular Compression / 대한평형의학회지

Vestibular Paroxysmia and facial spasm may be caused by vascular compression of the vestibular and facial root entry zone. We report a case of paroxysmal nystagmus accompanied by facial spasm and which is well visualized by three-dimensional reconstruction images. The 3-dimensional reconstruction image supports the view that vestibular paroxysmia may occur with hemifacial spasm simultaneously due to vascular compression.

Clinical Features and Therapeutic Effects of Vestibular Paroxysmia / 听力学及言语疾病杂志

Objective To investigate the clinical features and the therapeutic effects in patients with vestibu-lar paroxysmia(VP) .Methods A total of 32 patients with VP were analyzed retrospectively through pure -tone au-diometry (PTA) ,auditory brainstem response(ABR) ,magnetic resonance imaging (MRI) ,and vestibular function . The effects were assessed after 3 months treatment of carbamazepine (CBZ) or oxcarbazepine (OXA) .Results The main clinical symptom of 32 patients was a brief spell of vertigo ,and 75% of patient's attacks were regularly precipi-tated by certain head positions or position changes .The most common accompanying symptom was unsteadiness of stance or gait (75 .00% ) .The PTA thresholds were elevated in 11 patients (34 .38% ) .MRI in all patients showed neurovascular cross -compression(NVCC) .Among 30 patients who performed ABR tests ,24 (80 .00% ) were ab-normal and 19 patients (63 .33% )were found that the interpeak latency (IPL) of wave I-III( IPL I-III) prolonged more than 2 .2 ms .The course of the patients with IPL I -III prolonged was relatively longer (P=0 .231) ,but there was no significantly difference .All patients received carbamazepine (CBZ) or oxcarbazepine (OXA) for one month .One case was lost to follow -up ,4 had no symptom improvement and 27 had a significant reduction in the attack frequency and intensity respectively after treatment of one month ,two months ,three months and 6 months of the drug withdrawal ,compared with the previous (P<0 .05) .The level of vertigo was significantly improved(P<0 .05) .Conclusion Episodic spells of vertigo are the main clinical symptom of VP ,regularly caused by certain head positions or position changes .The NVCC can be found by MRI in all patients .The IPL I -III in ABR was pro-longed in most patients ,some of them have hearing loss .CBZ and OXA are effective with VP and also significant in the experimental treatment of diagnosis .

Vestibular Paroxysmia Mimicking Benign Parxysmal Positional Vertigo / 대한평형의학회지

Vestibular paroxysmia is the name given to the syndrome caused by vascular compression of the vestibulocochlear nerve. The main symptoms of vestibular paroxysmia are recurrent, spontaneous, brief attacks of spinning, non-spinning vertigo or positional vertigo that generally last less than one minute, with or without ear symptoms (tinnitus and hypoacusis). Prior to attributing a patient's symptoms to vestibular paroxysmia, however, clinicians must exclude common conditions like benign paroxysmal positional vertigo, Menière's disease, vestibular neuritis and vestibular migraine. This is usually possible with a thorough history and bedside vestibular/ocular motor examination. Herein, we describe a patient with vestibular paroxysmia that mimicked resolved BPPV with a literature review.

Clinical observation of keyhole neurovascular decompression on diagnosis and treatment of vestibular paroxysmia / 中国耳鼻咽喉头颈外科

[ABSTRACT]OBJECTIVETo evaluate the diagnostic value and curative effect of keyhole neurovascular decompression with local anesthesia for vestibular paroxysmia.METHODSOf 40 patients with trigeminal neuralgia, hemifacial spasm and glossopharyngeal neuralgia, 8 of them combined with vestibular paroxysmia underwent keyhole neurovascular decompression under local anesthesia to explore the vascular compression of acoustic nerve root and have the neurovascular decompression. The evaluation of the vertigo after operation was performed with symptom report card. The patients were followed-up for 36 to 61 months. RESULTSThe vessels compressing the root zone of the vestibular nerve were found in 8 patients with vestibular paroxysmia, of whom 7 patients had the vascular compression vertigo induced during operation and the vertigo was disappeared after operation, moreover, one patient had no vascular compression vertigo induced during operation and the vertigo was not changed after operation. With the average follow-up of 57 months, of 8 patients with vestibular paroxysmia, 7 patients had no recurrence of the vertigo, and the effective control rate was 87.5%.CONCLUSION Local anesthesia keyhole neurovascular decompression was not only an effective way for treating vestibular paroxysmia and controlling the vertigo, but also had certain clinical significance in the diagnosis of vestibular paroxysmia.