Testing a new intervention to enhance road safety

By 2020, it is estimated that road accidents will have moved from ninth to third in the worldwide ranking of burden of disease, as assessed in the disability adjusted life years (DALY)^1,2^. Therefore, it is vital to find effective methods to enhance road safety. Speed limits and traffic calming have the potential to reduce injuries due to road accidents^3,4^. Many drivers, however, do not adhere to speed limits^1-7^. Several studies have shown that adherence to speed limits can be explained by the theory of planned behaviour ^5-7^ and that it is possible to focus on drivers' intentions via self-report questionnaires. It is often difficult, however, to reach the majority of drivers on accident-prone locations with self-report questionnaires. This paper demonstrates an intervention that can be interpreted in the light of two of the theory's key variables^8^. It also has the potential to reach a large number of drivers on such locations. It is a speed-displaying device mounted next to the road (especially in villages). It tells drivers their actual speed (which is publicly visible). The measurement takes place continuously, giving the driver the chance to adjust speed and see the new speed shortly thereafter. The results show that the feedback about the current speed is associated with a significant speed reduction relative to a Control condition

Downbeat nystagmus: aetiology and comorbidity in 117 patients

Objectives: Downbeat nystagmus (DBN) is the most common form of acquired involuntary ocular oscillation overriding fixation. According to previous studies, the cause of DBN is unsolved in up to 44% of cases. We reviewed 117 patients to establish whether analysis of a large collective and improved diagnostic means would reduce the number of cases with ``idiopathic DBN'' and thus change the aetiological spectrum.Methods: The medical records of all patients diagnosed with DBN in our Neurological Dizziness Unit between 1992 and 2006 were reviewed. In the final analysis, only those with documented cranial MRI were included. Their workup comprised a detailed history, standardised neurological, neuro-otological and neuro-ophthalmological examination, and further laboratory tests.Results: In 62% (n = 72) of patients the aetiology was identified (``secondary DBN''), the most frequent causes being cerebellar degeneration (n = 23) and cerebellar ischaemia (n = 10). In 38% (n = 45), no cause was found (``idiopathic DBN''). A major finding was the high comorbidity of both idiopathic and secondary DBN with bilateral vestibulopathy (36%) and the association with polyneuropathy and cerebellar ataxia even without cerebellar pathology on MRI.Conclusions: Idiopathic DBN remains common despite improved diagnostic techniques. Our findings allow the classification of ``idiopathic DBN'' into three subgroups: ``pure'' DBN (n = 17); ``cerebellar'' DBN (ie, DBN plus further cerebellar signs in the absence of cerebellar pathology on MRI; n = 6); and a ``syndromatic'' form of DBN associated with at least two of the following: bilateral vestibulopathy, cerebellar signs and peripheral neuropathy (n = 16). The latter may be caused by multisystem neurodegeneration

Peripheral vestibular disorders

Purpose of review First, to update the diagnosis, pathophysiology, and treatment of the most frequent peripheral vestibular disorders. Second, to identify those disorders for which the diagnostic criteria are still deficient and treatment trials are still lacking. Recent findings Bilateral vestibulopathy can be reliably diagnosed by the head-impulse test, caloric irrigation, and vestibular-evoked myogenic potentials. A new frequent subtype has been described: cerebellar ataxia, neuropathy, and vestibular areflexia syndrome. Benign paroxysmal positioning vertigo can be easily diagnosed and effectively treated. Vestibular neuritis is most likely caused by the reactivation of a herpes simplex type 1 infection; the inferior vestibular nerve subtype is now well established. More evidence is needed that the recovery can be improved by corticosteroids. Endolymphatic hydrops in Meniere's disease can be depicted by high-resolution MRI after transtympanic gadolinium injection; a high-dosage and long-term prophylactic treatment with betahistine is evidently effective. Its mechanism of action is most likely an increase in the inner-ear blood flow. Vestibular paroxysmia is now a well established entity; carbamazepine is the treatment of first choice. Superior canal dehiscence syndrome can be reliably diagnosed; the best current treatment option is canal plugging. Summary Although progress has been made in the diagnosis and treatment of most peripheral vestibular disorders, more state-of-the-art trials are needed on the treatment of bilateral vestibulopathy to prove the efficacy of balance training, of vestibular neuritis (in terms of recovery of peripheral vestibular function and central compensation), of vestibular paroxysmia to prove the effects of carbamazepine, and of Meniere's disease to find the optimal dosage of betahistine

HSV-1 not only in human vestibular ganglia but also in the vestibular labyrinth

Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis. Copyright (C) 2001 S. Karger AG, Basel

Bedside differentiation of vestibular neuritis from central "vestibular pseudoneuritis".

Acute unilateral peripheral and central vestibular lesions can cause similar signs and symptoms, but they require different diagnostics and management. We therefore correlated clinical signs to differentiate vestibular neuritis (40 patients) from central ‘‘vestibular pseudoneuritis’’ (43 patients) in the acute situation with the final diagnosis assessed by neuroimaging. Skew deviation was the only specific but non-sensitive (40%) sign for pseudoneuritis. None of the other isolated signs (head thrust test, saccadic pursuit, gaze evoked nystagmus, subjective visual vertical) were reliable; however, multivariate logistic regression increased their sensitivity and specificity to 92%

Betahistine exerts a dose-dependent effect on cochlear stria vascularis blood flow in guinea pigs in vivo

Objective: Betahistine is a histamine H1-receptor agonist and H3-receptor antagonist that is administered to treat Menière’s disease. Despite widespread use, its pharmacological mode of action has not been entirely elucidated. This study investigated the effect of betahistine on guinea pigs at dosages corresponding to clinically used doses for cochlear microcirculation. Methods: Thirty healthy Dunkin-Hartley guinea pigs were randomly assigned to five groups to receive betahistine dihydrochloride in a dose of 1,000 mg/kg b. w. (milligram per kilogram body weight), 0.100 mg/kg b. w., 0.010 mg/kg b. w., 0.001 mg/kg b. w. in NaCl 0.9% or NaCl 0.9% alone as placebo. Cochlear blood flow and mean arterial pressure were continuously monitored by intravital fluorescence microscopy and invasive blood pressure measurements 3 minutes before and 15 minutes after administration of betahistine. Results: When betahistine was administered in a dose of 1.000 mg/kg b. w. cochlear blood flow was increased to a peak value of 1.340 arbitrary units (SD: 0.246; range: 0.933–1.546 arb. units) compared to baseline (p<0.05; Two Way Repeated Measures ANOVA/Bonferroni t-test). The lowest dosage of 0.001 mg/kg b. w. betahistine or NaCl 0.9% had the same effect as placebo. Nonlinear regression revealed that there was a sigmoid correlation between increase in blood flow and dosages. Conclusions: Betahistine has a dose-dependent effect on the increase of blood flow in cochlear capillaries. The effects of the dosage range of betahistine on cochlear microcirculation corresponded well to clinically used single dosages to treat Menière’s disease. Our data suggest that the improved effects of higher doses of betahistine in the treatment of Menière’s disease might be due to a corresponding increase of cochlear blood flow