Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not.
The cause of BV remains unclear in about half of all patients despite intensive examinations. A large subgroup of these patients have associated cerebellar dysfunction and peripheral polyneuropathy. This suggests a new syndrome that may be caused by neurodegenerative or autoimmune processes.
A reliable and reproducible method for precisely predicting the neurological outcome of patients with hypoxic-ischemic encephalopathy after cardiac arrest is urgently needed in neurological intensive care units. We prospectively investigated the predictive power of serum concentrations of neuron-specific enolase (NSE) and protein S-100B (S-100B) measured on days 1, 2, 3 and 7 as well as somatosensory-evoked potentials (SEPs) recorded within 48 h and on day 7 after cardiopulmonary resuscitation (CPR) in 27 patients (14 females, 13 males; mean age 61.3 ± 17.3 years) with hypoxic-ischemic encephalopathy. During the first 7 days after CPR, median values of NSE and S-100B were increased in patients who remained unconscious after CPR compared to those patients who regained consciousness (significance up to ≤0.001). The best predictor of negative outcome was an NSE cutoff point ≧43 µg/l on day 2; this had a sensitivity of 90.9% and a specificity of 100%. Additional use of S-100B on day 2 did not increase sensitivity, but this could be markedly increased by combining NSE and S-100B on days 1, 3 and 7. SEPs showing bilateral loss of cortical responses identified patients who did not regain consciousness with a specificity of 100%.
Bilateral vestibulopathy (BV) is characterized by impaired or lost function of both peripheral labyrinths or of the eighth nerves. In a review of 255 patients (mean age +/- SD, 62 +/- 16 years) with BV diagnosed in the authors' dizziness unit between 1988 and 2005, 62% of the patients were male. Previous vertigo attacks had occurred in 36%, indicating a sequential manifestation. The definite cause of BV was determined in 24% and the probable cause in 25%. The most common causes were ototoxic aminoglycosides (13%), Ménière's disease (7%), and meningitis (5%). Strikingly, 25% exhibited cerebellar signs. Cerebellar dysfunction was associated with peripheral polyneuropathy in 32% compared with 18% in BV patients without cerebellar signs. In a follow-up study on 82 BV-patients (mean age at the time of diagnosis 56.3 +/- 17.6 years), the frequency and degree of recovery or worsening of vestibular function over time were determined. The patients were reexamined 51 +/- 6 months after the first examination. Electronystagmography with bithermal caloric irrigation was analyzed by measurement of the mean peak slow-phase velocity (SPV) of the induced nystagmus. Statistical analysis of the mean peak SPV revealed a nonsignificant worsening over time (initial mean peak SPV 3.0 +/- 3.5 degrees/s vs. 2.1 +/- 2.8 degrees/s). Only patients with BV due to meningitis exhibited an increasing, but nonsignificant SPV (1.0 +/- 1.4 degrees/s vs. 1.9 +/- 1.6 degrees/s). Forty-three percent of patients subjectively rated the course of their disease as stable, 28% as worsened, and 29% as improved.
Bilateral vestibulopathy (BV) is characterized by impaired or lost function of both labyrinths or eighth nerves. The diagnosis is routinely established by the head-thrust test, caloric irrigation and rotational testing with electronystagmography to determine the high- and low-frequency deficit of the vestibulo-ocular reflex. All three methods evaluate semicircular canal function only. Vestibular-evoked myogenic potentials (VEMPs) provide a measure of saccular otolith function. The aim of this study was to evaluate the frequency and extent of saccular dysfunction in patients with BV and to correlate saccular with horizontal semicircular canal dysfunction. A total of 84 BV-patients (23 females, mean age 62 +/- 15 (SD) years at the time of diagnosis assessment) were examined with VEMPs, electronystagmography with caloric irrigation and a standardized neuro-ophthalmological and -otological examination; 47 healthy subjects (18 females, mean 56 +/- 19 years) served as controls. Amplitudes P1-N1 were significantly lower in patients with BV compared to controls (mean P1-N1 of all ears 82.1 +/- 50.7 microV in the patients vs. 130.8 +/- 85.9 microV in healthy volunteers). VEMPs were absent unilaterally in four patients with BV and in none bilaterally. In contrast, caloric responses were absent bilaterally in 40 patients. There was no correlation between amplitude P1-N1 and caloric-induced nystagmus. The latencies P1 and N1 were not significantly different between patients and controls. Thus, in our study population saccular function appeared to be less affected than horizontal semicircular canal function.
Objective: Bilateral vestibulopathy (BV) leads to a bilateral deficit of the vestibulo-ocular reflex and has various aetiologies. The main goal of this study was to determine the frequency and degree of recovery or worsening of vestibular function over time. Methods: 82 patients (59 males, 23 females; mean age at the time of diagnosis 56.3 (SD 17.6) years) were reexamined 51 (36) months after the first examination. All patients underwent a standardised neuro-ophthalmological and neuro-otological examination. Electronystagmography with bithermal caloric irrigation was analysed by measurement of the mean peak slow phase velocity (SPV) of the induced nystagmus. Patients evaluated the course of their disease in terms of balance, gait unsteadiness and health related quality of life. Results: Statistical analysis of the mean peak SPV of caloric induced nystagmus revealed a non-significant worsening over time (initial mean peak SPV 3.0 (3.5)u/s vs 2.1 (2.8)u/s). With respect to subgroups of aetiology, only patients with BV due to meningitis exhibited an increasing, but non-significant SPV (1.0 (1.4)u/s vs 1.9 (1.6)u/s). Vestibular outcome was independent of age, gender, time course of manifestation and severity of BV. Single analysis of all patients showed that a substantial improvement >5u/s occurred in two patients on both sides (idiopathic n = 1, Sjögren's syndrome n = 1) and in eight patients on one side (idiopathic n = 6, meningitis n = 1, Menière's disease n = 1). In 84% of patients there was impairment of their health related quality of life (42% slight, 24% moderate, 18% severe). Forty-three per cent of patients rated the course of their disease as stable, 28% as worsened and 29% as improved. Conclusions: Our data support the view that more than 80% of patients with BV do not improve. Thus the prognosis of BV is less favourable than assumed.
Objective: Bilateral vestibulopathy (BV) leads to a bilateral deficit of the vestibulo-ocular reflex and has various aetiologies. The main goal of this study was to determine the frequency and degree of recovery or worsening of vestibular function over time. Methods: 82 patients (59 males, 23 females; mean age at the time of diagnosis 56.3 (SD 17.6) years) were reexamined 51 (36) months after the first examination. All patients underwent a standardised neuro-ophthalmological and neuro-otological examination. Electronystagmography with bithermal caloric irrigation was analysed by measurement of the mean peak slow phase velocity (SPV) of the induced nystagmus. Patients evaluated the course of their disease in terms of balance, gait unsteadiness and health related quality of life. Results: Statistical analysis of the mean peak SPV of caloric induced nystagmus revealed a non-significant worsening over time (initial mean peak SPV 3.0 (3.5)u/s vs 2.1 (2.8)u/s). With respect to subgroups of aetiology, only patients with BV due to meningitis exhibited an increasing, but non-significant SPV (1.0 (1.4)u/s vs 1.9 (1.6)u/s). Vestibular outcome was independent of age, gender, time course of manifestation and severity of BV. Single analysis of all patients showed that a substantial improvement >5u/s occurred in two patients on both sides (idiopathic n = 1, Sjögren's syndrome n = 1) and in eight patients on one side (idiopathic n = 6, meningitis n = 1, Menière's disease n = 1). In 84% of patients there was impairment of their health related quality of life (42% slight, 24% moderate, 18% severe). Forty-three per cent of patients rated the course of their disease as stable, 28% as worsened and 29% as improved. Conclusions: Our data support the view that more than 80% of patients with BV do not improve. Thus the prognosis of BV is less favourable than assumed.
The long-term course and the frequency of relapses for various peripheral vestibular disorders and somatoform phobic postural vertigo are discussed with respect to the clinically most important questions for thus afflicted patients. This review is mainly based on our own long-term follow-up studies and takes into consideration the most relevant literature. The following syndromes are discussed in detail. Vestibular neuritis: the recovery rate of peripheral vestibular function lies between 40-63% depending on early-onset treatment with corticosteroids; the recurrence rate within 10 years is 2%. Menière's disease: loss of auditory and vestibular function occurs mainly in the first 5 to 10 years; frequency of vertigo attacks may decline after 5 to 10 years; bilateral involvement increases with increasing duration of the condition in up to 30-50%; vestibular drop attacks may occur early or late within the course, mostly with spontaneous remission; high-dose and long-term treatment with betahistine significantly reduces attack frequency in Menière's disease, Benign paroxysmal positioning vertigo: the recurrence rate is 50% within 10 years (in females 58%, in males 39%), most recurrences (80%) being observed within the first year after initial relief; recurrence rate in the seventh decade is half of that in the sixth decade. Vestibular paroxysmia: medical treatment with carbamazepine or oxcarbazepine leads to a continuous significant reduction in attack frequency, intensity, and duration of 10-15% of baseline. Bilateral vestibulopathy: recovery of vestibular function is limited to single cases depending on their etiology. Phobic postural vertigo: within 5 to 16 years 27% of the patients are symptom-free, 48% improve, 22% remain unchanged, and 3% worsen; a detailed explanation of the mechanisms that cause and the factors that provoke attacks is imperative, as well as instructions for self-controlled desensitization within the context of behavioral therapy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.