Marcello Cherchi

Bilateral vestibular loss.

Bilateral vestibular loss is a rare cause of visual disturbance (oscillopsia) and imbalance. When severe, the most common cause is iatrogenic-gentamicin ototoxicity. Bilateral loss is easily diagnosed at the bedside with the dynamic illegible E test. If this test is omitted, it can easily be misdiagnosed as a cerebellar syndrome. Treatment is largely supportive. Care should be taken to avoid medications that suppress vestibular function, and to encourage activity.

Sound evoked triceps myogenic potentials

Objective: To determine if a sound evoked myogenic potential could be obtained from the triceps with the recording and stimulus parameters routinely used to obtain a vestibular evoked myogenic potential (VEMP) from the sternocleidomastoid. Study Design: Prospective study of myogenic potentials recorded from the triceps in healthy subjects. We used a monaural acoustic stimulus and measured the unrectified myogenic potential using surface electromyography electrodes, using response-triggered averaging, on the triceps of 18 subjects. Setting: University-affiliated otoneurology clinic. Patients: Eighteen healthy adult volunteers (11 women and 7 men), age ranging between 27 and 36 years. Main Outcome Measures: Latencies and amplitudes of the first two waves of the evoked response. Results: The P1 latency was 36.83 ± 8.42 ms (range, 26.34-57.99 ms; 95% confidence interval [CI], 33.53-40.14 ms), the N1 latency was 43.74 ± 8.80 ms (range, 34.67-66.32 ms; 95% CI, 40.29-47.19 ms), the P1-N1 interlatency was 6.90 ± 1.23 ms (range, 5.21-9.79 ms; 95% CI, 6.42-7.39 ms), and the P1-N1 interamplitude was 93.23 ± 51.25 &mgr;V (range, 16.33-206.62 &mgr;V; 95% CI, 73.14-113.32 V). Conclusion: A monaural sound stimulus elicits a robust and reproducible surface myogenic potential in triceps muscles.

Mal de débarquement syndrome.

Mal de débarquement syndrome (MdDS) is typified by a prolonged rocking sensation - for a month or longer - that begins immediately following a lengthy exposure to motion. The provoking motion is usually a sea voyage. About 80% of MdDS sufferers are women, and most of them are middle-aged. MdDS patients are troubled by more migraine headaches than controls. Unlike dizziness caused by vestibular disorders or motion sickness, the symptoms of MdDS usually improve with re-exposure to motion. The long duration of symptoms - a month or more - distinguishes MdDS from land-sickness. Treatment of MdDS with common vestibular suppressants is nearly always ineffective. Benzodiazepines can be helpful, but their usefulness is limited by the potential for addiction. Studies are ongoing regarding treatment with visual habituation and transcranial magnetic stimulation.

Infrequent Causes of Disequilibrium in the Adult

This content focuses on some of the less common causes of dizziness in the adult. The diseases have been divided into the 2 broad categories of those causing chronic symptoms and those causing episodic symptoms. Presented here are the unusual causes of chronic disequilibrium in the adult, including bilateral vestibular loss, progressive supranuclear palsy, spinocerebellar ataxias, and mal de debarquement. Also discussed are the unusual causes of episodic disequilibrium in the adult, including psychogenic disequilibrium, vestibular paroxysmia, episodic ataxia, vestibular seizures, and cervicogenic vertigo.

Gradual hearing loss with bilateral labyrinthine hemorrhage in chronic myelogenous leukemia

Abrupt onset of hearing loss in chronic myelogenous leukemia has been reported. We report a patient in whom hearing loss and dizziness developed subacutely, and MRI revealed bilateral labyrinthine hemorrhage. A previously healthy 55-year-old woman experienced 6 weeks of fatigue and headache. She was treated with two courses of oral antibiotics for a presumed sinus infection without improvement. She then developed progressive left-sided hearing loss over 4 days followed by progressive right-sided hearing loss, resulting in complete bilateral deafness. The hearing loss was associated with increasing dizziness that prompted hospitalization. On admission she had a white blood cell count of 800,000/μL with myelocytes, promyelocytes, and mature neutrophilic predominance. The diagnosis of chronic myelogenous leukemia in chronic phase was confirmed by the cytogenetic studies and reverse transcription PCR specific for the BCR-ABL fusion transcript (confirming the presence of the Philadelphia chromosome [a t(9;22) translocation containing the BCR-AL fusion gene which encodes a 210-kd protein with deregulated tyrosine kinase …

Provocative maneuvers for vestibular disorders

Publisher Summary This chapter discussses maneuvers that are employed during physical examination to provoke nystagmus and, thereby diagnose compensated or episodic vestibular disorders. Maneuvers are divided into four broad categories: (1) those used primarily in diagnosing unilateral vestibular loss; (2) those used in diagnosing pressure sensitivity; (3) those used in diagnosing central conditions; and (4) those used in diagnosing cervical vertigo. The chapter reviews that these techniques require a general understanding of how to provoke the nystagmus as well as an appreciation of what to expect in a positive maneuver. This chapter describes each maneuver that provides a “trace” type output and provides a link to an online movie on the authors web site that shows a positive response. Other bedside tests that provoke nystagmus and instrumented procedures for nystagmus are also discussed in this chapter.

PULSE-SYNCHRONOUS TORSIONAL PENDULAR NYSTAGMUS IN UNILATERAL SUPERIOR CANAL DEHISCENCE

A physically active 62-year-old man experienced the gradual onset of intermittent positional dizziness, occurring primarily on inclining his head upwards or downwards. Dizziness also appeared less commonly with abrupt turns of the head or while bearing down during a bowel movement. He denied tinnitus. He had no significant family history, he had never sustained head or neck trauma, and he was on no medications. Treatment with meclizine had not alleviated his symptoms. On physical examination with video Frenzel goggles (Micromedical Technology, Chatham, IL), there was a primary position torsional nystagmus, of approximately 1 Hz. There was also a low-amplitude downbeating nystagmus, greater on lateral gaze, and with no positional modulation. By watching the nystagmus while palpating the pulse, it was appreciated that the torsional nystagmus was pulse-synchronous, with the clockwise component corresponding to the pulse upswing. The torsional nystagmus was present when the patient was sitting or standing, but was suppressible in those positions with the Valsalva maneuver, and was absent when supine (see video on the Neurology ® Web site at www.neurology.org). Laboratory investigation revealed vestibular evoked myogenic potentials to be fourfold enlarged on the right, and the responses could be obtained at a lower threshold on the …

Amplitude of Sound Evoked Triceps Myogenic Potential Scales with Force

Objective: To determine whether the amplitude of the sound evoked triceps myogenic potential (SETMP) scales with the tonic force exerted by the muscle. Study design: A prospective study of myogenic potentials was conducted in 16 normal subjects. A monaural acoustic stimulus was presented to subjects while they while they exerted varying degrees of force with the triceps muscles. Subjects were required to activate the triceps by leaning into pressure transducers placed at shoulder height thereby supporting their body weight. The unrectified myogenic potential was collected using response triggered averaging of the signal from surface electromyogram (EMG) electrodes placed over the triceps bilaterally.

Paraneoplastic Upbeat Nystagmus in Renal Cell Carcinoma

Received date: February 10, 2015; Accepted date: April 23, 2015; Published date: April 27, 2015Copyright: ©2015 Cherchi M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use,distribution, and reproduction in any medium, provided the original author and source are credited.

The Gain-Time Constant Product Quantifies Total Vestibular Output in Bilateral Vestibular Loss

Patients with inner ear damage associated with bilateral vestibular impairment often ask “how much damage do I have.” Although there are presently three clinical methods of measuring semicircular canal vestibular function; electronystagmography (ENG or VENG), rotatory chair and video head-impulse (VHIT) testing; none of these methods provides a method of measuring total vestibular output. Theory suggests that the slow cumulative eye position can be derived from the rotatory chair test by multiplying the high frequency gain by the time constant, or the “GainTc product.” In this retrospective study, we compared the GainTc in three groups, 30 normal subjects, 25 patients with surgically induced unilateral vestibular loss, and 24 patients with absent or nearly absent vestibular responses due to gentamicin exposure. We found that the GainTc product correlated better with remaining vestibular function than either the gain or the time constant alone. The fraction of remaining vestibular function was predicted by the equation R = (GainTc/11.3) – 0.6. We suggest that the GainTc product answers the question “how much damage do I have,” and is a better measure than other clinical tests of vestibular function.