13 research outputs found
Current treatment options in vestibular migraine
No full textApproximately 1% of the general population in western industrialized countries suffers from vestibular migraine. However, it remains widely unknown and often under diagnosed even despite the recently published diagnostic criteria for vestibular migraine. Treatment trials that specialize on vestibular migraine are scarce and systematic randomized controlled clinical trials are only now emerging.This review summarizes the knowledge on the currently available treatment options that were tested specifically for vestibular migraine and gives an evidence-based, informed treatment recommendation with all its limitations.To date only two randomized controlled treatment trials provide limited evidence for the use of rizatriptan and zolmitriptan for the treatment of vestibular migraine attacks because of methodological shortcommings. There is an on-going a multicenter randomized placebo-controlled trial testing metoprolol 95 mg vs. placebo (PROVEMIG-trial). Therefore, the therapeutic recommendations for the prophylactic treatment of vestibular migraine are currently widely based on the guidelines of migraine with and without aura as well as expert opinion
Calretinin as a marker for premotor neurons involved in upgaze in human brainstem
No full textEye movements are generated by different premotor pathways. Damage to them can cause specific deficits of eye movements, such as saccades. For correlative clinico-anatomical post-mortem studies of cases with eye movement disorders it is essential to identify the functional cell groups of the oculomotor system in the human brain by marker proteins. Based on monkey studies, the premotor neurons of the saccadic system can be identified by the histochemical markers parvalbumin and perineuronal nets in humans. These areas involve the interstitial nucleus of Cajal (INC) and the rostral interstitial nucleus of the medial longitudinal fascicle (RIMLF), which both contain premotor neurons for upgaze and downgaze. Recent monkey and human studies revealed a selective excitatory calretinin-positive input to the motoneurons mediating upgaze, but not to those for downgaze. Three premotor regions were identified as sources of calretinin input in monkey: y-group, INC and RIMLF. These findings suggest that the expression pattern of parvalbumin and calretinin may help to identify premotor neurons involved in up- or downgaze. In a post-mortem study of five human cases without neurological diseases we investigated the y-group, INC and RIMLF for the presence of parvalbumin and calretinin positive neurons including their co-expression. Adjacent thin paraffin sections were stained for the aggrecan component of perineuronal nets, parvalbumin or calretinin and glutamate decarboxylase. The comparative analysis of scanned thin sections of INC and RIMLF revealed medium-sized parvalbumin positive neurons with and without calretinin coexpression, which were intermingled. The parvalbumin/calretinin positive neurons in both nuclei are considered as excitatory premotor upgaze neurons. Accordingly, the parvalbumin-positive neurons lacking calretinin are considered as premotor downgaze neurons in RIMLF, but may in addition include inhibitory premotor upgaze neurons in the INC as indicated by co-expression of glutamate decarboxylase in a subpopulation. Calretinin-positive neurons ensheathed by perineuronal nets in the human y-group are considered as the homologue premotor neurons described in monkey, projecting to superior rectus and inferior oblique motoneurons. In conclusion, combined immunostaining for parvalbumin, perineuronal nets and calretinin may well be suited for the specific identification and subsequent analysis of premotor upgaze pathways in clinical cases of isolated up- or downgaze deficits
Towards a concept of disorders of higher vestibular function
No full textBackground: Vestibular disorders are commonly characterized by a combination of perceptual, ocular motor, postural, and vegetative manifestations, which cause the symptoms of vertigo, nystagmus, ataxia, and nausea. Multisensory convergence and numerous polysynaptic pathways link the bilaterally organized central vestibular network with limbic, hippocampal, cerebellar, and non-vestibular cortex structures to mediate higher cognitive functions.Anatomical classification of vestibular disorders: The traditional classification of vestibular disorders is based on the anatomical site of the lesion. While it distinguishes between the peripheral and the central vestibular systems, certain weaknesses become apparent when applied clinically. There are two reasons for this: first, peripheral and central vestibular disorders cannot always be separated by the clinical syndrome; second, a third category, namely disorders of higher vestibular function, is missing. These disorders may be caused by peripheral as well as central vestibular lesions. Functional classification: Here we discuss a new concept of disorders of higher vestibular function which involve cognition and more than one sensory modality. Three conditions are described that exemplify such higher disorders: room tilt illusion, spatial hemineglect, and bilateral vestibulopathy all of which present with deficits of orientation and spatial memory.Conclusions: Further elaboration of such disorders of higher multisensory functions with respect to lesion site and symptomatology is desirable. The room tilt illusion and spatial hemineglect involve vestibular and visual function to the extent that both conditions can be classified as either disorders of higher vestibular or of higher visual functions. A possible way of separating these disorders in a first step is to determine whether the causative lesion site affects the vestibular or the visual system. For the vestibular system this lesion site may be peripheral
False-positive head-impulse test in cerebellar ataxia
No full textAbstract:The objective of this study was to compare the findings of the bedside head impulse test (HIT), passive head rotation gain, and caloric irrigation in patients with cerebellar ataxia (CA). In 16 patients with CA and bilaterally pathological bedside HIT, VOR gains were measured during HIT and passive head rotation by scleral search coil technique. Eight of the patients had pathologically reduced caloric responsiveness, while the other eight had normal caloric responses. Those with normal calorics showed a slightly reduced HIT gain (mean±SD: 0.73±0.15). In those with pathological calorics, gains 80ms and 100 ms after the HIT as well as the passive rotation VOR gains were significantly lower. The corrective saccade after head turn occurred earlier in patients with pathological calorics (111±62 ms after onset of the HIT) than in those with normal calorics. (191±17 ms, p=0.0064) We indentified two groups of patients with CA: those with an isolated moderate HIT deficit only, probably due to floccular dysfunction, and those with combined HIT, passive rotation and caloric deficit, probably due to a peripheral vestibular deficit. From a clinical point of view, these results show that the bedside HIT alone can be false positive for establishing a diagnosis of a bilateral peripheral vestibular deficit in patients with CA
Beyond dizziness: virtual navigation, spatial anxiety and hippocampal volume in bilateral vestibulopathy
No full textBilateral vestibulopathy (BVP) is defined as the impairment or loss of function of either the labyrinths or the eighth nerves. Patients with total BVP due to bilateral vestibular nerve section exhibit difficulties in spatial memory and navigation and show a loss of hippocampal volume. In clinical practice, most patients do not have a complete loss of function but rather an asymmetrical residual functioning of the vestibular system. The purpose of the current study was to investigate navigational ability and hippocampal atrophy in BVP patients with residual vestibular function. Fifteen patients with BVP and a group of age- and gender- matched healthy controls were examined. Self-reported questionnaires on spatial anxiety and wayfinding were used to assess the applied strategy of wayfinding and quality of life. Spatial memory and navigation were tested directly using a virtual Morris Water Maze Task. The hippocampal volume of these two groups was evaluated by voxel-based morphometry. In the patients, the questionnaire showed a higher spatial anxiety and the Morris Water Maze Task a delayed spatial learning performance. MRI revealed a significant decrease in the gray matter mid-hippocampal volume (Left: p = 0.006, Z = 4.58, Right: p < 0.001, Z = 3.63) and posterior parahippocampal volume (Right: p = 0.005, Z = 4.65, Left: p < 0.001, Z = 3.87) compared to those of healthy controls. In addition, a decrease in hippocampal formation volume correlated with a more dominant route-finding strategy. Our current findings demonstrate that even partial bilateral vestibular loss leads to anatomical and functiona
Vestibular function and quality of life in vestibular schwannoma: does size matter?
No full textObjectives. Patients with vestibular schwannoma (VS) frequently suffer from disabling vestibular symptoms. This prospective follow-up study evaluates vestibular and auditory function and impairment of quality of life due to vertigo, dizziness and imbalance in patients with unilateral vestibular schwannoma of different sizes before/ after microsurgical or radiosurgical treatment. Methods. 38 patients with unilateral vestibular schwannoma were included. 22 received microsurgery, 16 cyberknife radiosurgery. Two follow-ups took place after a median of 50 and 186.5 days. Patients received a standardized neuro-ophthalmological examination, electronystagmography with bithermal caloric testing, and pure-tone audiometry. Quality of life was evaluated with the Dizziness Handicap Inventory (DHI). Patient data was grouped and analyzed according to the size of the VS (group 1: < 20mm vs group 2: ≥ 20mm). Results. In group 1, the median loss of vestibular function was +10.5% as calculated by Jongkees Formula (range –43;+52; group 2: median + 36%, range –56; +90). The median change of DHI scores was –9 in group 1 (range –68;30) and +2 in group 2 (–54;+20). Median loss of hearing was 4dB (-42;93) in group 1 and 12dB in group 2 (5;42).Conclusions. Loss of vestibular function in vestibular schwannoma clearly correlates with tumor size. However, loss of vestibular function was not strictly associated with a long-term deterioration of quality of life. This may be due to central compensation of vestibular deficits in long-standing large tumors. Loss of hearing before treatment was significantly influenced by the age of the patient but not by tumor size. At follow-up 1 and 2, hearing was significantly worse in those patients with a large VS and after microsurgical treatment
Clinical and demographic features of vertigo: findings from the REVERT registry
No full textIntroductionDespite being a common disease, data on vertigo management in a real-world setting are scarce. AimsTo provide information on the vertigo and its management in a real-world setting.Materials and MethodsData were collected from 4,294 patients with vertigo in 13 countries over 28 months via a multi-national, non-interventional observational study (the so-called REVERT registry). Data included medical history and details of anti-vertigo therapy. ‘Clinical global impression’ (CGI) of severity (CGI-S) was assessed at baseline (V1) and then at 6 months follow-up (V2) along with CGI change (CGI-C). All variables were analysed descriptively. ResultsThe majority of patients were female, >40 years of age, and almost half had co-morbid cardiovascular disease. Diagnoses were split into 4 categories: 37.2% ‘other vertigo of peripheral vestibular origin’, 26.9% benign paroxysmal positional vertigo (BPPV), 20.5% ‘peripheral vestibular vertigo of unknown origin’ and 15.4% Menière’s disease (MD). Betahistine was the most commonly prescribed therapy prior to and after enrolment, and was followed by piracetam, ginkgo biloba and diuretics. MD had the highest proportion of betahistine treated patients. Almost half of patients were ‘moderately ill’ at V1 based on CGI-S. At V2, patient distribution moved towards ‘less severe illness’ (91.0% improved).The greatest improvements were in the more severely ill, and those with BPPV or ‘other vertigo of peripheral origin’. ConclusionsThere was a reduction in illness severity over the course of the study, some of which is likely to be due to pharmacological intervention. Further studies are needed to confirm these results
Cerebellar and visual gray matter brain volume increases in congenital nystagmus
No full textStructural brain abnormalities associated with congenital nystagmus are still unknown. In some patients with congenital nystagmus additional sensory, metabolic or gross structural alterations can be detected. In the present study voxel-based morphometry was used to compare the gray matter brain volumes of 14 individuals with congenital nystagmus without associated sensory, metabolic or obvious structural alterations (i.e. idiopathic congenital nystagmus) to those of a group of controls. Further, gray matter brain volumes were correlated with nystagmus severity as measured by sway path. Intergroup comparison exhibited significant volume increases in the human motion sensitive complex V5/MT+, the fusiform gyrus and the middle occipital gyrus bilaterally in congenital nystagmus. These volume increases may be associated with excess visual motion stimulation due to involuntary retinal slip of the visual scene. A positive correlation (linear model) of nystagmus sway path with cerebellar gray matter volume was seen in the following areas: vermal parts VIII-X as well as hemisphere lobule II, hemisphere VI, crus I, crus II, and lobule VII-IX bilaterally. There is evidence that the reported gray matter volume changes in the vestibulo-cerebellum, which correlated with nystagmus sway path, might be related to the subjects` attempt to maintain fixation, rather than be due to the generation of nystagmus
Comparison of the bedside head impulse test with the video head impulse test in a clinical practice setting: a prospective study of 500 outpatients.
No full textObjectives: The primary aim was to determine the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the bedside head impulse test (bHIT) using the video HIT (vHIT) as the gold standard for quantifying the function of the vestibulo-ocular reflex (VOR). Secondary aims were to determine the bHIT inter-rater reliability, and sensitivity in detecting unilateral and bilateral vestibulopathy.Methods: In this prospective study, 500 consecutive outpatients presenting to a tertiary neuro-otology clinic with vertigo or dizziness of various vestibular etiologies who did not have any of the pre-defined exclusion criteria were recruited. Bedside HITs were done by three experienced neuro-otology clinicians masked to the diagnosis, and the results were compared with the vHIT. The patients were likewise blinded to the bHIT and vHIT findings. Patients with VOR deficits were identified on the vHIT by referencing to the pre-selected pathological gain of 40%, the bHIT sensitivity = 51.7% and 83%, respectively. For bilateral vestibulopathy, overall bHIT sensitivity = 66.3%, reaching 86.84% for severely reduced bidirectional gains.Conclusions: For the primary outcome, the bHIT had moderate sensitivity and low PPV. While the study did not elucidate the best choice for vHIT reference, it demonstrated how the bHIT test properties varied with vHIT thresholds: selecting a lower threshold improved the sensitivity but diminished the PPV, while a higher threshold had the opposite effect. The VOR was most likely normal if the bHIT was negative due to its high NPV. The bHIT was moderately sensitive for detecting unilateral and bilateral vestibulopathy overall, but better for certain subgroups
