Adolfo M. Bronstein

Migraine and Ménière's disease: is there a link?

Background: A possible link between Ménière’s disease (MD) and migraine was originally suggested by Prosper Ménière. Subsequent studies of the prevalence of migraine in MD produced conflicting results. Objective: To determine the lifetime prevalence of migraine in patients with MD compared to sex- and age-matched controls. Methods: The authors studied 78 patients (40 women, 38 men; age range 29 to 81 years) with idiopathic unilateral or bilateral MD according to the criteria of the American Academy of Otolaryngology. Diagnosis of migraine with and without aura was made via telephone interviews according to the criteria of the International Headache Society. Additional information was obtained concerning the concurrence of vertigo and migrainous symptoms during Ménière attacks. The authors interviewed sex- and age-matched orthopedic patients (n = 78) as controls. Results: The lifetime prevalence of migraine with and without aura was higher in the MD group (56%) compared to controls (25%; p < 0.001). Forty-five percent of the patients with MD always experienced at least one migrainous symptom (migrainous headache, photophobia, aura symptoms) with Ménière attacks. Conclusions: The lifetime prevalence of migraine is increased in patients with MD when strict diagnostic criteria for both conditions are applied. The frequent occurrence of migrainous symptoms during Ménière attacks suggests a pathophysiologic link between the two diseases. Alternatively, because migraine itself is a frequent cause of audio-vestibular symptoms, current diagnostic criteria may not differentiate between MD and migrainous vertigo.

Visual influences on balance

This paper discusses the impact of vision on balance and orientation in patients with vestibular disorders and in anxiety patients with space and motion discomfort (SMD). When the vestibular system is impaired, vision has a greater influence on standing postural control, resulting in greater sway when individuals are presented with erroneous or conflicting visual cues. Studies have shown that individuals with other motion sensitivities, such as motion sickness, also tend to rely on vision for balance and do not disregard erroneous visual cues. Recently, patients with anxiety disorders that include SMD also have been shown to have increased postural sway in conflicting visual environments, similar to patients with vestibular disorders. Thus, while specific vestibular deficits are not always directly associated with SMD, data regarding the impact of vision on balance suggest that some patients with SMD may have an underlying balance disorder.

Positional down beating nystagmus in 50 patients: cerebellar disorders and possible anterior semicircular canalithiasis

Objectives: To clarify the clinical significance of positional down beat nystagmus (pDBN). Methods: A discussion of the neuro-otological findings in 50 consecutive patients with pDBN. Results: In 38 patients there was evidence of CNS disease (central group) but in 12 there was not (idiopathic group). In the CNS group, presenting symptoms were gait, speech, and autonomic dysfunction whereas in the idiopathic group patients mostly reported positional vertigo. The main neurological and oculomotor signs in the CNS group were explained by cerebellar dysfunction, including 13 patients with multiple system atrophy. In patients with multiple system atrophy with a prominent extrapyramidal component, the presence of pDBN was helpful in the differential diagnosis of atypical parkinsonism. No patient with pDBN had the Arnold-Chiari malformation, a common cause of constant down beat nystagmus (DBN). In the idiopathic group, the pDBN had characteristics which suggested a peripheral labyrinthine disorder: vertigo, adaptation, and habituation. In six patients an additional torsional component was found (concurrently with the pDBN in three). Features unusual for peripheral disorder were: bilateral positive Dix-Hallpike manoeuvre in nine of 12 patients and selective provocation by the straight head-hanging manoeuvre in two Conclusion: It is argued that some patients with idiopathic pDBN have benign paroxysmal positional vertigo (BPPV) with lithiasis of the anterior canal. The torsional component may be weak, because of the predominantly sagittal orientation of the anterior canal, and may not be readily seen clinically. Nystagmus provocation by bilateral Dix-Hallpike and straight head-hanging may be explained by the vertical upwards orientation of the ampullary segment of the anterior canal in the normal upright head position. Such orientation makes right-left specificity with the Dix-Hallpike manoeuvre less important than for posterior canal BPPV. This orientation requires a further downwards movement of the head, often achieved with the straight head-hanging position, to provoke migration of the canaliths. The straight head-hanging manoeuvre should be carried out in all patients with a history of positional vertigo and a negative Dix-Hallpike manoeuvre.

Neural Correlates of Visual-Motion Perception as Object- or Self-motion

Both self-motion and objects moving in our visual field generate visual motion by displacing images on the retina. Resolving this ambiguity may seem effortless but large-field visual-motion stimuli can yield perceptual rivalry between the real percept of object-motion and the illusory percept of self-motion (vection). We used functional magnetic resonance imaging to record brain activity in human observers exposed to constant-velocity roll-motion. This stimulus induced responses in areas reaching from calcarine to parieto-occipital and to ventral and lateral temporo-occipital cortex and the anterior insula. During vection, early motion-sensitive visual areas and vestibular parieto-insular cortex deactivated, whereas higher-order parieto- and temporo-occipital areas known to respond to optical flow retained identical activity levels. Within this sustained response, these latter areas displayed transient activations in response to each perceptual switch as identified in event-related analyses. Our results thus show that these areas are responsive to the type of visual motion stimulus and highly sensitive to its perceptual bistability. The only region to be more active during perceived self-motion was in, or close to, the cerebellar nodulus. This activation may correspond to the gain increase of torsional optokinetic nystagmus during vection and/or to changes in sensory processing related to the rotational percept. In conclusion, we identified neural correlates of perceiving self-motion from vision alone, i.e., in the absence of confirmatory vestibular or proprioceptive input. These functional properties preserve the organisms ability to move accurately in its environment by relying on visual cues under conditions when the other spatial senses fail to provide such information.

Interference between postural control and mental task performance in patients with vestibular disorder and healthy controls

OBJECTIVES To determine whether interference between postural control and mental task performance in patients with balance system impairment and healthy subjects is due to general capacity limitations, motor control interference, competition for spatial processing resources, or a combination of these. METHOD Postural stability was assessed in 48 patients with vestibular disorder and 24 healthy controls while they were standing with eyes closed on (a) a stable and (b) a moving platform. Mental task performance was measured by accuracy and reaction time on mental tasks, comprising high and low load, spatial and non-spatial tasks. Interference between balancing and performing mental tasks was assessed by comparing baseline (single task) levels of sway and mental task performance with levels while concurrently balancing and carrying out mental tasks. RESULTS As the balancing task increased in difficulty, reaction times on both low load mental tasks grew progressively longer and accuracy on both high load tasks declined in patients and controls. Postural sway was essentially unaffected by mental activity in patients and controls. CONCLUSIONS It is unlikely that dual task interference between balancing and mental activity is due to competition for spatial processing resources, as levels of interference were similar in patients with vestibular disorder and healthy controls, and were also similar for spatial and non-spatial tasks. Moreover, the finding that accuracy declined on the high load tasks when balancing cannot be attributed to motor control interference, as no motor control processing is involved in maintaining accuracy of responses. Therefore, interference between mental activity and postural control can be attributed principally to general capacity limitations, and is hence proportional to the attentional demands of both tasks.

Visual vertigo syndrome: clinical and posturography findings.

Neuro-otological and posturography findings in 15 patients with visually induced vertiginous symptoms (visual vertigo) are reported. Thirteen patients were considered to have a peripheral vestibular disorder; seven had abnormal caloric or rotational test results. Two patients had CNS disorder--a cerebellar degeneration and a brainstem stroke. Posturography testing showed that five patients showed abnormally large body sway induced by full field visual motion stimulation. This group included the two patients with CNS disease and four with strabismic symptoms (diplopia, squint surgery, and ocular muscle weakness). It is concluded that visual vertigo is a heterogeneous syndrome with peripheral or central aetiologies and may occur if patients with balance disorders show high visual field dependence. In patients with visual vertigo, the presence of additional CNS or strabismic symptoms may cause inappropriate postural reactions in environments with conflicting or disorienting visual stimuli, probably by reducing the ability to resolve the sensory conflict.

Bilateral loss of vestibular function: clinical findings in 53 patients.

Abstract The clinical presentations and aetiologies of a series of 53 cases of bilateral vestibular failure (BVF) seen by the authors over a decade were evaluated by retrospective review of the medical records. Thirty-nine per cent of patients had associated neurological disease; 13% had a progressive cerebellar syndrome with disabling gait ataxia, abnormal eye movements and cerebellar atrophy on neuro-imaging. BVF was usually unsuspected. Nine per cent had cranial or peripheral neuropathies and in this group there was no abnormality of brain stem/cerebellar oculomotor function, but hearing loss was common. Eleven per cent revealed BVF and hearing loss secondary to meningitis, and 6% had other neurological disorders. Idiopathic BVF was found in 21% of cases, characterised by paroxysmal vertigo and/or oscillopsia, but no abnormal clinical signs. Gentamicin ototoxicity accounted for a further 17%, while autoimmune disease was present in 9% of patients. Otological or neoplastic disease was diagnosed in the remaining 13% of patients. It was concluded that neurological, audiological and ocular motor assessments allow the probable cause of BVF to be defined in approximately 80% of cases. A group of BVF related to autoimmune pathologies is reported for the first time, indicating the need for immunological screening. Idiopathic BVF may present with only minor visual or vestibular symptoms, while in patients with cerebellar degeneration, BVF may be unsuspected and, thus, underdiagnosed.

Suppression of visually evoked postural responses

SummaryNormal subjects standing on an earth-fixed force platform inside a movable room displaced at velocities comparable to those accompanying spontaneous body sway, exhibit a visually evoked postural response (VEPR) some 600 ms after the start of the room movement. It consists of a displacement of the centre of force of the body in the direction of the stimulus (primary component), followed shortly by a corrective displacement in the opposite (secondary component). On second presentation of the stimulus VEPR is markedly reduced, but only if full proprioceptive information from the lower limbs is available to the subjects. A patient deprived of this information showed much enhanced VEPR which he was unable to suppress, in contrast to a patient with absent vestibular function who presented normal VEPR. The results show that in the presence of conflict between different sensory clues, vision is initially dominant in sway control, although adaptive processes can quickly rearrange this hierarchy.

Simulator based rehabilitation in refractory dizziness

Abstract.Patients with chronic vestibular symptoms are common in neurological practice but the most effective treatment remains an open question. The purpose of our study was to conduct a controlled, between–group comparison of patients’ responses to a customised exercise regime (Group C, for customised) versus treatment additionally incorporating simulator based desensitisation exposure (Group S, for simulator) integrating whole–body or visual environment rotators. Forty chronic peripheral vestibular patients who had previously undergone conventional vestibular rehabilitation without notable improvement were randomly assigned into Group C or S. Individuals attended therapy sessions twice weekly for eight weeks and were provided with a customised home programme. Response to treatment was assessed at four–week intervals with dynamic posturography, vestibular time constants, and questionnaires concerning symptoms, symptom–triggers and emotional status. At final assessment posturography and subjective scores had significantly improved for both groups, although Group S showed greater improvement. A statistically significant improvement for visual vertigo symptom scores was noted only for Group S (p < 0.01; total improvement 53.5 %). Anxiety and depression levels significantly decreased for both groups; improvements were significantly correlated particularly to improvements in visual vertigo (SCQ) (p < 0.01; r = 0.53 and r = 0.57, respectively). Significant differences were noted between groups (p = 0.02) for posturography scores. Vestibular time constants showed no notable change in either group. Conclusions: Both groups improved but exposure to simulator motion gave overall better results. These effects were also observed in psychological symptoms and partly relate to simulator effects on visual vertigo symptoms. Visual motion and visuo–vestibular conflict situations should be incorporated in the rehabilitation of patients with refractory dizziness.

Vision and vertigo: Some visual aspects of vestibular disorders

This review deals with two syndromes, oscillopsia and visual vertigo. Oscillopsia is the illusion of oscillation of the visual surroundings. For diagnosis purposes one should ask, when does the oscillopsia occur? If oscillopsia is only present during head (or whole body) movements, the likely underlying cause is a bilateral defect in the vestibulo-ocular reflex (VOR). The more common causes are post meningitic vestibular damage, gentamicin ototoxicity or bilateral idiopathic vestibular failure. When oscillopsia develops after specific head positions, it is usually due to a positional nystagmus, usually the result of brainstem-cerebellar disease. When the oscillopsia is largely unrelated to head movements, one should ask, is it fairly constant or is it in attacks (paroxysmal)? If the oscillopsia is constant it is usually due to the presence of a clinically observable nystagmus; the most common is downbeat nystagmus but the most visually disabling is pendular nystagmus. If the oscillopsia comes in brief attacks it is usually due to a paroxysmal nystagmus as observed in irritative VIII nerve and brainstem lesions. However, the most common cause of paroxysmal oscillopsia is a non organic condition called voluntary nystagmus. Treatment of oscillopsia is often pharmacological but disappointing; the best chance of success is carbamazepine for paroxysmal disorders secondary to structural vestibular nerve/nuclear lesions. Visual vertigo should not be confused with oscillopsia. It can be defined as dizziness provoked by visual environments with large size (full field) repetitive or moving visual patterns. Patients with visual vertigo report discomfort in supermarkets and when viewing movement of large visual objects, eg crowds, traffic, clouds or foliage. Visual vertigo is present in many patients with a history of a peripheral vestibular disorder, particularly those who are visually dependent (ie subjects who use vision preferentially for postural and space orientation control). Patients with visual vertigo benefit from the addition to their standard vestibular rehabilitation of optic flow (optokinetic) stimuli and exercises involving visuo-vestibular conflict.