Superior Canal Dehiscence Syndrome.

Braz J Otorhinolaryngol. 2006 May-Jun;72(3):414-8.

da Cunha Ferreira S, de Melo Tavares de Lima MA.

Department of Otorhinolaryngology and Opththalmology, Federal University of Rio de Janeiro, and the Hospital da Lagoa, Brazil. suzane.ferreira@gmail.com

Abstract

The Superior Canal Dehiscence Syndrome (SCDS) was first reported by Minor at. Al. (1998), and has been characterized by vertigo and vertical-torsional eye movements related to loud sounds or stimuli that change middle ear or intracranial pressure. Hearing loss, for the most part with conductive patterns on audiometry, may be present in this syndrome.

We performed a literature survey in order to to present symptoms, signs, diagnostic and therapeutic approaches to the SCDS, also aiming at stressing the great importance of including this syndrome among the tractable cause of vertigo. We should emphasize that this is a recent issue, still unknown by some specialists.

The Correct SCDS diagnosis, besides enabling patient treatment, precludes misdiagnosis and inadequate therapeutic approaches.

PMID: 17119781 [PubMed - indexed for MEDLINE]Free Article

Superior canal dehiscence: review of a new condition.

Clin Otolaryngol. 2005 Feb;30(1):9-15.

Banerjee A, Whyte A, Atlas MD.

Department of ENT, James Cook University Hospital, Middlesbrough, UK. anirvan.banerjee@stees.nhs.uk

Abstract

A new cause of sound and pressure induced vertigo, superior canal dehisence, is described. Auditory manifestations include hyperacusis to bone-conducted sounds and conductive hearing loss with normal acoustic reflexes.

The diagnosis is reached by a directed history, documentation of upward and torsional nystagmus evoked by sound and pressure, and radiology. Acoustic reflexes and VEMP (vestibular evoked myogenic potentials) aid in the identification of patients with an apparent conductive loss with normal acoustic reflexes or have an asymptomatic dehiscense on radiology.
Treatment involves avoidance of the precipitating stimuli. Surgical treatment, by resurfacing the dehiscence, is considered in patients with more severe symptoms.

PMID: 15748182 [PubMed - indexed for MEDLINE]

Migraine-Associated Vertigo: Diagnosis and Treatment

Seminars in Neurology 2010; 30(2): 167-174 DOI: 10.1055/s-0030-1249225

© Thieme Medical Publishers

Yoon-Hee Cha1

1 Department of Neurology, University of California Los Angeles, Los Angeles, California

ABSTRACT

Migraine-associated vertigo has become a well-recognized disease entity diagnosed based on a clinical history of recurrent vertigo attacks unexplained by other central or peripheral otologic abnormalities, which occurs in the patient with a history of migraine headaches.

There is no international agreement on what spectrum of symptoms should be covered under this diagnosis, or what terminology should be used.

The headaches and vestibular symptoms of migraine-associated vertigo may not be temporally associated, which often obscures the association.

Diagnostic tests usually show nonspecific abnormalities that are also seen in patients with migraine who do not experience vestibular symptoms.

Management generally follows the recommended treatment of migraine headaches, and includes
dietary and lifestyle modifications and
medical treatment
       with β blockers, calcium channel blockers, and tricyclic amines.

Small case series show that acetazolamide and lamotrigine appear to be more effective for the vertigo attacks than headaches.

Vestibular rehabilitation has also been shown to be helpful in several studies.

In this review, the epidemiologic and clinical features of the disorder, as well as the current state of knowledge on pathophysiology, diagnostic testing, and treatment are described.

Vestibular effects on cerebral blood flow

BMC Neuroscience 2009, 10:119doi:10.1186/1471-2202-10-119
Jorge M Serrador1,5 , Todd T Schlegel2 , F Owen Black3 and Scott J Wood2,4
1 Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA, USA
2 NASA Johnson Space Center, Houston, TX, USA
3 Neurotology Research, Legacy Health System, Portland, OR, USA
4 Universities Space Research Association, Houston, TX, USA
5 National University of Ireland Galway, Galway, Ireland


Abstract

Background
Humans demonstrate a number of unique adaptations that allow for the maintenance of blood pressure and brain blood flow when upright. While several physiological systems, including cerebral autoregulation, are involved in this adaptation the unique role the vestibular system plays in helping to maintain brain blood flow is just beginning to be elucidated. In this study, we tested the hypothesis that stimulation of the vestibular system, specifically the otoliths organs, would result in changes in cerebral blood flow.

Results
To test our hypothesis, we stimulated the vestibular organs of 25 healthy subjects by pitch tilt (stimulates both canals and otoliths) and by translation on a centrifuge (stimulates otoliths and not the canals) at five frequencies: 0.5, 0.25, 0.125 and 0.0625 Hz for 80 sec and 0.03125 Hz for 160 sec. Changes in cerebral flow velocity (by transcranial Doppler) and blood pressure (by Finapres) were similar during both stimuli and dependent on frequency of stimulation (P < 0.01). However, changes in cerebral blood flow were in opposition to changes in blood pressure and not fully dependent on changes in end tidal CO2.
Conclusion
The experimental results support our hypothesis and provide evidence that activation of the vestibular apparatus, specifically the otolith organs, directly affects cerebral blood flow regulation, independent of blood pressure and end tidal CO2 changes.

The electronic version of this article is the complete one and can be found online at:
http://www.biomedcentral.com/1471-2202/10/119