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In 1988, we introduced impulsive testing of semicircular canal (SCC) function measured with scleral search coils and showed that it could accurately and reliably detect impaired function even of a single lateral canal. Later we showed that it was also possible to test individual vertical canal function in peripheral and also in central vestibular disorders and proposed a physiological mechanism for why this might be so. For the next 20 years, between 1988 and 2008, impulsive testing of individual SCC function could only be accurately done by a few aficionados with the time and money to support scleral search-coil systems--an expensive, complicated and cumbersome, semi-invasive technique that never made the transition from the research lab to the dizzy clinic. Then, in 2009 and 2013, we introduced a video method of testing function of each of the six canals individually. Since 2009, the method has been taken up by most dizzy clinics around the world, with now close to 100 refereed articles in PubMed. In many dizzy clinics around the world, video Head Impulse Testing has supplanted caloric testing as the initial and in some cases the final test of choice in patients with suspected vestibular disorders. Here, we consider seven current, interesting, and controversial aspects of video Head Impulse Testing: (1) introduction to the test; (2) the progress from the head impulse protocol (HIMPs) to the new variant--suppression head impulse protocol (SHIMPs); (3) the physiological basis for head impulse testing; (4) practical aspects and potential pitfalls of video head impulse testing; (5) problems of vestibulo-ocular reflex gain calculations; (6) head impulse testing in central vestibular disorders; and (7) to stay right up-to-date--new clinical disease patterns emerging from video head impulse testing. With thanks and appreciation we dedicate this article to our friend, colleague, and mentor, Dr Bernard Cohen of Mount Sinai Medical School, New York, who since his first article 55 years ago on compensatory eye movements induced by vertical SCC stimulation has become one of the giants of the vestibular world. [ABSTRACT FROM AUTHOR]

In 1991 we proposed that while the syndrome of isolated intracranial hypertension might have many definite and probable causes, it has nonetheless a single unifying pathophysiological mechanism: namely, impairment of cerebrospinal fluid (CSF) reabsorption. For that reason, we also proposed then that it is best described by a single, unifying, inclusive term, namely, pseudotumor cerebri syndrome. Although it appears that there is, as far as nomenclature is concerned, now international agreement, there is as yet no agreement on pathophysiology and classification. Herein we outline our views on these matters and give our reasons. [ABSTRACT FROM AUTHOR]

Objective:To report the outcome of posterior semicircular canal occlusion surgery for intractable benign positional vertigo, regarding vertigo cure rate and hearing and balance outcomes.Methods:Retrospective review of 53 patients presenting with benign positional vertigo, unresponsive to repositioning manoeuvres, who eventually underwent posterior canal occlusion, over a 20 year period.Results:From 1991 to 2011, 5364 benign positional vertigo patients were treated in our balance disorders clinic; 53 of those who failed to respond to repositioning underwent posterior canal occlusion. All 53 were cured of their benign positional vertigo. Nine suffered some symptomatic permanent hearing loss (>20 dB at low and >25 dB at high frequencies). Ten patients suffered caloric vestibular function deterioration, with mild but permanent subjective imbalance in five; a further 10 patients with no post-operative caloric test changes also had some permanent imbalance. Benign positional vertigo later developed in the operated ear lateral canal in two patients and in the opposite ear posterior canal in eight patients. Two patients needed bilateral sequential posterior canal occlusion.Conclusion:Posterior canal occlusion is a highly effective treatment for intractable benign positional vertigo, with what is probably an acceptable risk to hearing and balance: five of six patients will have no hearing problem and nine of 10 no balance problem after surgery. [ABSTRACT FROM PUBLISHER]

Purpose: To review the extent and mechanism of the recovery of vestibular function after sudden, isolated, spontaneous, unilateral loss of most or all peripheral vestibular function – usually called acute vestibular neuritis. Methods: Critical review of published literature and personal experience. Results: The symptoms and signs of acute vestibular neuritis are vertigo, vomiting, nystagmus with ipsiversive slow-phases, ipsiversive lateropulsion and ocular tilt reaction (the static symptoms) and impairment of vestibulo-ocular reflexes from the ipsilesional semicircular canals on impulsive testing (the dynamic symptoms). Peripheral vestibular function might not improve and while static symptoms invariably resolve, albeit often not totally, dynamic symptoms only improve slightly if at all. Conclusions: The persistent loss of balance that some patients experience after acute vestibular neuritis can be due to inadequate central compensation or to incomplete peripheral recovery and vestibular rehabilitation has a role in the treatment of both. [ABSTRACT FROM AUTHOR]