Absence of nystagmus during REM sleep in patients with vestibular neuritis.
Saccades, including fast phases of nystagmus, disappear during drowsiness and non-rapid eye movement (NREM) sleep, but are present during the alert state and REM sleep. The purpose of this study was to determine whether spontaneous nystagmus is present in patients with vestibular neuritis during REM sleep. Eight patients with spontaneous nystagmus due to vestibular neuritis and eight control patients without any nystagmus underwent at least one night of polysomnography. Fast phases of nystagmus were analyzed. The number of right and left horizontal saccades were counted, first during 3-5 minute samples of the awake state before sleep onset, then during the first REM episode and the last REM episode of nocturnal sleep, and finally during the alert state in the morning after nocturnal sleep. All patients with vestibular neuritis showed significantly more saccades (fast phases) towards the side contralateral to their vestibular lesion in the awake state before and after the polysomnography. This reflects their spontaneous nystagmus. By contrast, during REM sleep the patients with vestibular neuritis showed no preponderance in saccade direction. The eye movement pattern in REM was the same for patients and controls. In conclusion, peripheral vestibular imbalance producing nystagmus in vestibular neuritis in the awake state is not active at the brain stem level during REM sleep. (+info)
Caloric and search-coil head-impulse testing in patients after vestibular neuritis.
The objective of this study was to compare results of quantitative head-impulse testing using search coils with eye-movement responses to caloric irrigation in patients with unilateral vestibular hypofunction after vestibular neuritis. The study population consisted of an acute group (<3 days; N = 10; 5 male, 5 female; 26-89 years old) and a chronic group (>2 months; N = 14; 8 male, 6 female; 26-78 years old) of patients with unilateral vestibular hypofunction after vestibular neuritis. The testing battery included: (1) simultaneous measurement of eye and head rotations with search coils in a magnetic coil frame during passive Halmagyi-Curthoys head-impulse testing and (2) electronystagmography during bilateral monaural 44 degrees C-warm and 30 degrees C-cold caloric irrigation. The main outcome measures were (1) the gain of the horizontal vestibulo-ocular reflex during search-coil head-impulse testing and (2) the amount of canal paresis during caloric irrigation. All acute and chronic patients had a unilateral gain reduction during search-coil head-impulse testing. A pathological canal paresis factor was present in 100% of the acute patients but in only 64% of the chronic patients. The clinically suspected unilateral vestibular hypofunction resulting from vestibular neuritis was validated in all acute patients by both search-coil head-impulse and caloric testing. Hence, either of these tests is sufficient for diagnosis in the acute phase of vestibular neuritis. Chronic patients, however, were reliably identified only by search-coil head-impulse testing, which suggests that the low-frequency function of the labyrinths often becomes symmetrical, leading to a normal canal paresis factor. (+info)
Suppression of eye movements improves balance.
The aim of this study was to investigate the possible interaction of vestibulo-ocular and vestibulo-spinal functions. Spontaneous eye movements and anterior-posterior and lateral body sway were recorded simultaneously in 10 patients with vestibular neuritis (Experiment 1) and in 11 healthy subjects (Experiment 2) while all subjects wore a mask that allowed fixation of a head-fixed target. For the healthy subjects, there was no significant difference in postural sway for the conditions of eyes open in darkness and fixation of the head-fixed target. For the patients, the question was whether transient suppression of the spontaneous nystagmus by fixating the target affected excessive body sway or whether modulation of nystagmus and postural sway were largely independent. The mean peak slow-phase velocity of the spontaneous nystagmus decreased from 13.5 +/- 5.6 to 4.3 +/- 2.4 degrees /s during fixation. The suppression of nystagmus also reduced postural sway while standing on foam rubber. Mean value decreased from 25.2 +/- 7.6 to 16.2 +/- 7.7 mm (right-left root mean square values; ANOVA, P = 0.003). Since a head-fixed target was used to suppress spontaneous eye movements, the data cannot be explained by any stabilizing effect of afferent visual cues. Instead, ocular motor efference copy signals or reafferences may have contributed to the postural instability of patients with vestibular neuritis, which would explain the reduction of postural sway during fixation suppression of the nystagmus. Thus, ocular motor signals rather than afferent visual cues about retinal slip are used for visual control of postural sway, at least in this experimental paradigm. (+info)
Symptoms of vertigo in general practice: a prospective study of diagnosis.
BACKGROUND: There is little published evidence of the general practice experience of the diagnostic outcomes when symptoms of vertigo present. What research there is has been dominated by specialist centres. This gives a skewed view of the prevalence of the causes of such symptoms. AIM: To describe the likely diagnosis of symptoms of vertigo. DESIGN OF STUDY: Prospective cohort study METHODS: Thirteen GPs were recruited and trained to clinically assess and follow up all patients presenting with symptoms of vertigo over a six-month period Age-sex data were simultaneously gathered on those who consulted with non-vertiginous dizziness. RESULTS: The main diagnoses assigned by the GPs in 70 patients were benign positional vertigo, acute vestibular neuronitis and Meniere's disease, which together accounted for 93% (95% confidence interval = 71% to 100%) of patients' symptoms. Ninety-one per cent of patients were managed in general practice and 60% received a prescription for a vestibular sedative. CONCLUSION: This study suggests that presentations of symptoms of vertigo can be clinically diagnosed in most cases. The diagnoses recorded by GPs differ in proportion to those in specialist centres, with a larger number of patients suffering from benign positional vertigo and acute vestibular neuronitis in general practice, in contrast with specialist centres, which see more patients with Meniere's disease. (+info)
Methylprednisolone, valacyclovir, or the combination for vestibular neuritis.
BACKGROUND: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Therefore, corticosteroids, antiviral agents, or a combination of the two might improve the outcome in patients with vestibular neuritis. METHODS: We performed a prospective, randomized, double-blind, two-by-two factorial trial in which patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir, or methylprednisolone plus valacyclovir. Vestibular function was determined by caloric irrigation, with the use of the vestibular paresis formula (to measure the extent of unilateral caloric paresis) within 3 days after the onset of symptoms and 12 months afterward. RESULTS: Of a total of 141 patients who underwent randomization, 38 received placebo, 35 methylprednisolone, 33 valacyclovir, and 35 methylprednisolone plus valacyclovir. At the onset of symptoms there was no difference among the groups in the severity of vestibular paresis. The mean (+/-SD) improvement in peripheral vestibular function at the 12-month follow-up was 39.6+/-28.1 percentage points in the placebo group, 62.4+/-16.9 percentage points in the methylprednisolone group, 36.0+/-26.7 percentage points in the valacyclovir group, and 59.2+/-24.1 percentage points in the methylprednisolone-plus-valacyclovir group. Analysis of variance showed a significant effect of methylprednisolone (P<0.001) but not of valacyclovir (P=0.43). The combination of methylprednisolone and valacyclovir was not superior to corticosteroid monotherapy. CONCLUSIONS: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not. (+info)
Recovery of the high-acceleration vestibulo-ocular reflex after vestibular neuritis.
Vestibular neuritis (VN) usually leads to a sudden gain asymmetry of the high-acceleration horizontal vestibulo-ocular reflex (VOR). We asked whether this asymmetry decreases over time indicating peripheral recovery and/or central compensation. The horizontal VOR during rapid rotational head impulses to both sides was recorded with search coils in 37 patients at different time periods (1-240 weeks) after the onset of VN. In ten patients, sequential measurements were performed. Gains of the VOR during head impulses toward the ipsilesional side significantly increased after the initial drop (average gains: < 1 week: 0.35; 1-4 weeks: 0.33; 4-40 weeks: 0.55; 40-240 weeks: 0.50). Gains on the contralesional side, however, were only slightly reduced and showed no significant change. We conclude that, in contrast to patients after hemilabyrinthectomy or unilateral vestibular neurectomy, the ocular response to ipsilesional rotations in patients after VN improves over time. This finding suggests that ipsilesional recovery is peripheral or, if central, depends on spared peripheral function. The physiology of linear and nonlinear VOR pathways predicts a considerable gain reduction for contralesional head impulses if central compensation mechanisms are not engaged. Thus, the relatively preserved gain on the contralesional side can be explained only by central "upregulation". Apparently, for high accelerations of the head, effective central compensation after VN does not aim to balance the gains of the VOR but tries to boost the contralesional gain close to normal. (+info)
Head-shaking nystagmus depends on gravity.
In acute unilateral peripheral vestibular deficit, horizontal spontaneous nystagmus (SN) increases when patients lie on their affected ear. This phenomenon indicates an ipsilesional reduction of otolith function that normally suppresses asymmetric semicircular canal signals. We asked whether head-shaking nystagmus (HSN) in patients with chronic unilateral vestibular deficit following vestibular neuritis is influenced by gravity in the same way as SN in acute patients. Using a three-dimensional (3-D) turntable, patients (N = 7) were placed in different whole-body positions along the roll plane and oscillated (1 Hz, +/-10 degrees ) about their head-fixed vertical axis. Eye movements were recorded with 3-D magnetic search coils. HSN was modulated by gravity: When patients lay on their affected ear, slow-phase eye velocity significantly increased upon head shaking and consisted of a horizontal drift toward the affected ear (average: 1.2 degrees /s +/-0.5 SD), which was added to the gravity-independent and directionally nonspecific SN. In conclusion, HSN in patients with chronic unilateral peripheral vestibular deficit is best elicited when they are lying on their affected ear. This suggests a gravity-dependent mechanism similar to the one observed for SN in acute patients, i.e., an asymmetric suppression of vestibular nystagmus by the unilaterally impaired otolith organs. (+info)
A genome-wide linkage scan of familial benign recurrent vertigo: linkage to 22q12 with evidence of heterogeneity.
Benign recurrent vertigo (BRV) is a common disorder affecting up to 2% of the adult population and may be etiologically related to migraine because of similarities in the clinical spectrum of the phenotypes and a high co-morbidity within families. Many families have multiple-affected genetically related individuals suggesting familial transmission of the disorder with moderate to high penetrance. While clinically similar to episodic ataxias, there are currently no genes identified that contribute to BRV and no systematic linkage studies performed. In an initial effort to genetically define BRV, we have selected from our Neurology Clinic population a subset of 20 multigenerational families with apparent autosomal dominant transmission, and performed genetic linkage mapping using both parametric and non-parametric linkage (NPL) approaches. The Affymetrix 10K SNP Mapping Assay was used for the genotyping. Heterogeneity LOD (HLOD) analysis reveals the evidence of genetic heterogeneity for BRV and evidence of linkage in a subset of the families to 22q12 (HLOD = 4.02). An additional region was identified by NPL analysis at 5p15 (LOD = 2.63). As migraine is observed substantially more commonly both within the BRV-affected individuals and the related family members, it is possible that a form of migraine is allelic to the BRV locus at 22q12. However, testing linkage or the chromosome 22q12 region to a broader migraine/vertigo phenotype by defining affectation status as either migrainous headaches or BRV greatly weakened the linkage signal, and no significant other peaks were detected. Thus, BRV and migraine does not appear to be allelic disorders within these families. We conclude that BRV is a heterogeneous genetic disorder, appears genetically distinct from migraine with aura and is linked to 22q12. Additional family and population-based linkage and association studies will be needed to determine the causative alleles. (+info)