About Nystagmus Transformation in a Case of Apogeotropic Lateral Semicircular Canal Benign Paroxysmal Positional Vertigo

There are two forms of lateral semicircular canal benign paroxysmal positional vertigo: geotropic and apogeotropic. When the pathophysiological mechanism of the apogeotropic form is that of canalolithiasis, we can observe a transformation from an apogeotropic nystagmus into a geotropic one. Usually, this phenomenon happens simultaneously on both sides, thus enabling us to observe a right-beating paroxysmal positional nystagmus when the patient lies on the right side and a left-beating paroxysmal positional nystagmus on the left side. We describe a case in which the transformation occurred gradually, so that, after three head rotations from side to side in supine position, there was a right nystagmus beating toward the ground (geotropic) with the patient on the right side and a right nystagmus beating away from the ground (apogeotropic) on the left side. However, after further rotations we observed the nystagmus transformation also on the left side, with a geotropic nystagmus on both sides. The phenomenon of gradual transformation could happen because initially only a part of the debris moved from the anterior to the posterior aspect of the canal during head rotations

Epigone migraine vertigo (EMV): a late migraine equivalent.

Migrainous headache is determined by pathogenetic mechanisms that are also able to affect the peripheral and/or central vestibular system, so that vestibular symptoms may substitute and/or present with headache. We are convinced that there can be many different manifestations of vestibular disorders in migrainous patients, representing true different clinical entities due to their different characteristics and temporal relashionship with headache. Based on such considerations, we proposed a classification of vertigo and other vestibular disorders related to migraine, and believe that a particular variant of migraine-related vertigo should be introduced, namely "epigone migraine vertigo" (EMV): this could be a kind of late migraine equivalent, i.e. a kind of vertigo, migrainous in origin, starting late in the lifetime that substitutes, as an equivalent, pre-existing migraine headache. To clarify this particular clinical picture, we report three illustrative clinical cases among 28 patients collected during an observation period of 13 years (November 1991 - November 2004). For all patients, we collected complete personal clinical history. All patients underwent standard neurotological examination, looking for spontaneous-positional, gaze-evoked and caloric induced nystagmus, using an infrared video camera. We also performed a head shaking test (HST) and an head thrust test (HTT). Ocular motility was tested looking at saccades and smooth pursuit. To exclude other significant neurological pathologies, a brain magnetic resonance imaging (MRI) with gadolinium was performed. During the three months after the first visit, patients were invited to keep a diary noting frequency, intensity and duration of vertigo attacks. After that period, we suggested that they use prophylactic treatment with flunarizine (5 mg per day) and/or acetylsalicylic acid (100 mg per day), or propranolol (40 mg twice a day). All patients were again recommended to note in their diary the frequency and intensity of both headache and vertigo while taking prophylactic therapy. Control visits were programmed after 4, 12 and 24 months of therapy. All patients considerably improved symptoms with therapy: 19 subjects (68%) reported complete disappearance of vestibular symptoms, while 9 (32%) considered symptoms very improved. The subjective judgement was corroborated by data from patients diaries. We conclude that EMV is a clinical variant of typical migraine-related vertigo: a migraineassociated vertigo, headache spell independent, following a headache period, during the lifetime of a patient

Posterior Semicircular Canal Benign Paroxysmal Positional Vertigo Presenting with Torsional Downbeating Nystagmus: An Apogeotropic Variant

The aim of this study is to verify the hypothesis that free-floating particles could sometimes localize into the distal portion of the non ampullary arm of the posterior semicircular canal (PSC) so that assuming the Dix-Hallpike’s positions, the clot could move towards the ampulla eliciting a inhibitory torsional-down beating paroxysmal positional nystagmus (PPNy), instead of typical excitatory torsional-up beating PPNy. Among 45 patients with vestibular signs suggesting anterior semicircular canal paroxysmal positional vertigo (PPV), collected from February 2003 to August 2006, we detected a group of 6 subjects whose clinical findings showed a singular behaviour during follow-up. At the first check-up, all patients were submitted to different types of physical manoeuvres for ASC canalolithiasis. Patients were controlled during the same session and after one week. When we found that nystagmus was qualitatively changed we adopted the appropriate physical therapies for that sign. At a next check-up, after having performed some physical therapies, all patients had a typical PSC PPNy of the opposite side, with respect to that of the ASC initially diagnosed. Basing on these observations we conclude that PSC PPV, similarly to lateral semicircular canal PPV, could manifests in a apogeotropic variant

Apogeotropic posterior semicircular canal benign paroxysmal positional vertigo: some clinical and therapeutic considerations

We lately reported the cases of patients complaining positional vertigo whose nystagmic pattern was that of a peripheral torsional vertical positional down beating nystagmus originating from a lithiasis of the non-ampullary arm of the posterior semicircular canal (PSC). We considered this particular pathological picture the apogeotropic variant of PSC benign paroxysmal positional vertigo (BPPV). Since the description of the pilot cases we observed more than 150 patients showing the same clinical sign and course of symptoms. In this paper we describe, in detail, both nystagmus of apogeotropic PSC BPPV (A-PSC BPPV) and symptoms reported by patients trying to give a reasonable explanation for these clinical features. Moreover we developed two specific physical therapies directed to cure A-PSC BPPV. Preliminary results of these techniques are related