Journal of Vestibular Research - Volume 21, issue 6

Authors: Rauch, Steven D.

Article Type: Introduction

DOI: 10.3233/VES-2012-0439

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 297-298, 2011

Authors: von Brevern, Michael | Neuhauser, Hannelore

Article Type: Research Article

Abstract: Both migraine and dizziness/vertigo rank among the most common complaints in the general population. Worldwide, the lifetime prevalence of migraine is about 14%. Approximately 20% to 30% of the general population are affected by dizziness and vertigo. Given the high prevalence of vertigo and migraine in the general population it is not surprising that many patients suffer from both symptoms. Nonetheless, in the last decade epidemiological arguments have progressively accumulated to strengthen the hypothesis that vertigo is linked to migraine beyond a mere chance concurrence. Several studies with selected patient groups have shown that the prevalence of vertigo is …increased in patients with migraine. Vice versa, patients presenting to a dizziness clinic have a history of migraine more often than would be expected by chance. The epidemiological link between vertigo and migraine has recently been confirmed on the population level. The relation between vertigo and migraine is intricate. In vestibular migraine, vertigo is conceptualized as a vestibular symptom caused by migraine. Vestibular migraine is the most common cause for recurrent spontaneous vertigo with a lifetime-prevalence in the general population of about 1%. Other vestibular disorders that display an increased prevalence of migraine are benign paroxysmal positional vertigo and Menière's disease. Furthermore, migraine is associated with motion sickness, rare ataxia disorders and psychiatric syndromes that can also manifest with vertigo and dizziness. Show more

Keywords: Migraine, vestibular, vertigo, dizziness

DOI: 10.3233/VES-2011-0423

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 299-304, 2011

Authors: Burstein, Rami | Jakubowski, Moshe | Rauch, Steven D.

Article Type: Research Article

Abstract: The cardinal symptom of migraine is headache pain. In this paper we review the neurobiology of this pain as it is currently understood. In recent years, we discovered that the network of neurons that sense pain signals from the dura changes rapidly during the course of a single migraine attack and that the treatment of an attack is a moving target. We found that if the pain is not stopped within 10–20 minutes after it starts, the first set of neurons in the network, those located in the trigeminal ganglion, undergo molecular changes that make them hypersensitive to the changing …pressure inside the head, which explains why migraine headache throbs and is worsened by bending over and sneezing. We found that if the pain is not stopped within 60–120 minutes, the second group of neurons in the network, those located in the spinal trigeminal nucleus, undergoes molecular changes that convert them from being dependent on sensory signals they receive from the dura by the first set of neurons, into an independent state in which they themselves become the pain generator of the headache. When this happens, patients notice that brushing their hair, taking a shower, touching their periorbital skin, shaving, wearing earrings, etc become painful, a condition called cutaneous allodynia. Based on this scenario, we showed recently that the success rate of rendering migraine patients pain-free increased dramatically if medication was given before the establishment of cutaneous allodynia and central sensitization. The molecular shift from activity-dependent to activity-independent central sensitization together with our recent conclusion that triptans have the ability to disrupt communications between peripheral and central trigeminovascular neurons (rather than inhibiting directly peripheral or central neurons) explain their clinical effects. Both our clinical and pre-clinical findings of the last five years point to possible short- and long-term advantages in using an early-treatment approach in the treatment of acute migraine attacks. Show more

Keywords: Migraine, headache, pain, sensitization

DOI: 10.3233/VES-2012-0433

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 305-314, 2011

Authors: Balaban, Carey D.

Article Type: Research Article

Abstract: This review develops the hypothesis that co-morbid balance disorders and migraine can be understood as additive effects of processing afferent vestibular and pain information in pre-parabrachial and pre-thalamic pathways, that have consequences on cortical mechanisms influencing perception, interoception and affect. There are remarkable parallel neurochemical phenotypes for inner ear and trigeminal ganglion cells and these afferent channels appear to converge in shared central pathways for vestibular and nociceptive information processing. These pathways share expression of receptors targeted by anti-migraine drugs. New evidence is also presented regarding the distribution of serotonin receptors in the planum semilunatum of the primate cristae ampullaris, …which may indicate involvement of inner ear ionic homeostatic mechanisms in audiovestibular symptoms that can accompany migraine. Show more

Keywords: Migraine, balance disorders, vestibular pathways, nociception

DOI: 10.3233/VES-2011-0428

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 315-321, 2011

Authors: Lewis, Richard F. | Priesol, Adrian J. | Nicoucar, Keyvan | Lim, Koeun | Merfeld, Daniel M.

Article Type: Research Article

Abstract: Vestibular symptoms caused by migraine, referred to as vestibular migraine, are a frequently diagnosed but poorly understood entity. Based on recent evidence that normal subjects generate vestibular-mediated percepts of head motion and reflexive eye movements using different mechanisms, we hypothesized that percepts of head motion may be abnormal in vestibular migraine. We therefore measured motion detection thresholds in patients with vestibular migraine, migraine patients with no history of vestibular symptoms, and normal subjects using the following paradigms: roll rotation while supine (dynamically activating the semicircular canals); quasi-static roll tilt (statically activating the otolith organs); and dynamic roll tilt (dynamically activating …the canals and otoliths). Thresholds were determined while patients were asymptomatic using a staircase paradigm, whereby the peak acceleration of the motion was decreased or increased based on correct or incorrect reports of movement direction. We found a dramatic reduction in motion thresholds in vestibular migraine compared to normal and migraine subjects in the dynamic roll tilt paradigm, but normal thresholds in the roll rotation and quasi-static roll tilt paradigms. These results suggest that patients with vestibular migraine may have enhanced perceptual sensitivity (e.g. increased signal-to-noise ratio) for head motions that dynamically modulate canal and otolith inputs together. Show more

Keywords: Vestibular, migraine, vertigo, psychophysics, thresholds

DOI: 10.3233/VES-2011-0422

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 323-330, 2011

Authors: Staab, Jeffrey P.

Article Type: Research Article

Abstract: Recent years have witnessed an upsurge of interest in migraine as a cause of vestibular symptoms. Starting with 1970s case reports linking migraine to childhood vertigo, neurotologists worldwide have increasingly diagnosed migraine. Various syndromes of vestibular migraine (VM) have been described, diagnostic criteria proposed, epidemiologic data collected, and neurophysiologic models developed. Yet, the concept that migraine causes vestibular symptoms rests on a surprisingly thin research database. Current concepts of VM are based on expert opinion, not empirical data. No general consensus exists about the definition of VM. No studies have analyzed its essential features. Just one well-controlled medication trial has …been published. No biomarkers are known. To stimulate more rigorous research, this paper poses three questions about clinical investigations into migraine and vestibular symptoms: What variables should be measured? What patients should be studied? How might clinical trials yield both clinically useful results and greater insights into pathophysiologic processes? Using these questions, the limits of current knowledge are explored. Applicable research methods from epidemiology to genetics are examined. Pilot data demonstrating pharmacologic and genetic dissection techniques are presented. Ambitious, but practical, near-term clinical research goals are enumerated, including rigorous validation of diagnostic criteria and development of empirically derived management guidelines. Show more

Keywords: Vestibular migraine, validation, epidemiology, comorbidity, treatment

DOI: 10.3233/VES-2011-0426

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 331-340, 2011

Article Type: Other

DOI: 10.3233/VES-2011-21607

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 343-344, 2011

Article Type: Other

DOI: 10.3233/VES-2011-21608

Citation: Journal of Vestibular Research, vol. 21, no. 6, pp. 343-344, 2011