Acute Vestibular Lesions Research Articles

Abecedario del examen vestibuloespinal. Revisión bibliográfica

Introducción y objetivo: Durante las largas cuarentenas impuestas en el mundo por la pandemia de COVID-19 los médicos hemos empezado a usar con mayor asiduidad la modalidad de consulta virtual. La neurootología no ha sido una excepción en este contexto y usando el mecanismo de las videollamadas hemos podido dar atención y contención a un buen número de pacientes durante este período. Por esta razón y basados en la experiencia singular de este periodo, hemos diseñado un examen sistemático, basado en pruebas vestíbulo-espinales simples y presentadas en forma nemotécnica (abecedario). Sobre la base de nuestra experiencia y con una revisión de la literatura se intenta demostrar la etiología y topografía vestibular de los hallazgos. Método: Revisión narrativa. Para la búsqueda de la bibliografía se utilizó la metodología de revisión sistemática de documentos en metabuscadores y bases de datos. Periodo analizado del 2001 al 2019, en diversas revistas científicas. Resultados: El examen se dividió en cuatro pasos de acuerdo con las cuatro primeras letras del alfabeto: Ataxia (gradación), Bárány (desviación de los índices), Cefálico (tilt o inclinación cefálica de la cabeza en relación con el tronco) y Desviación (desviación oblicua de los ojos Test de skew). Discusión: Se plantea el uso de la mnemotecnia abecedario para ordenar el examen vestíbulo espinal en los pacientes con afección del sistema vestibular, de manera simple y práctica, permitiendo la modalidad virtual. Conclusiones: Este sencillo abecedario vestíbulo-espinal permite, asociado a un interrogatorio exhaustivo, realizar un examen vestibular eficaz por medios virtuales, separar eficazmente lesiones centrales de periféricas en cuadros vestibulares agudos con alta sensibilidad y especificidad y finalmente hacer un topodiagnóstico del lado de lesión vestibular.

Evidence for a Role of Orexin/Hypocretin System in Vestibular Lesion-Induced Locomotor Abnormalities in Rats.

Vestibular damage can induce locomotor abnormalities in both animals and humans. Rodents with bilateral vestibular loss showed vestibular deficits syndrome such as circling, opisthotonus as well as locomotor and exploratory hyperactivity. Previous studies have investigated the changes in the dopamine system after vestibular loss, but the results are inconsistent and inconclusive. Numerous evidences indicate that the orexin system is implicated in central motor control. We hypothesized that orexin may be potentially involved in vestibular loss-induced motor disorders. In this study, we examined the effects of arsanilate- or 3,3′-iminodipropionitrile (IDPN)-induced vestibular lesion (AVL or IVL) on the orexin-A (OXA) labeling in rat hypothalamus using immunohistochemistry. The vestibular lesion-induced locomotor abnormalities were recorded and verified using a histamine H4 receptor antagonist JNJ7777120 (20 mg/kg, i.p.). The effects of the orexin receptor type 1 antagonist SB334867 (16 μg, i.c.v.) on these behavior responses were also investigated. At 72 h post-AVL and IVL, animals exhibited vestibular deficit syndrome and locomotor hyperactivity in the home cages. These responses were significantly alleviated by JNJ7777120 which also eliminated AVL-induced increases in exploratory behavior in an open field. The numbers of OXA-labeled neurons in the hypothalamus were significantly increased in the AVL animals at 72 h post-AVL and in the IVL animals at 24, 48, and 72 h post-IVL. SB334867 significantly attenuated the vestibular deficit syndrome and locomotor hyperactivity at 72 h post-AVL and IVL. It also decreased exploratory behavior in the AVL animals. These results suggested that the alteration of OXA expression might contribute to locomotor abnormalities after acute vestibular lesion. The orexin receptors might be the potential therapeutic targets for vestibular disorders.

Vestibular compensation: the neuro-otologist's best friend.

Why vestibular compensation (VC) after an acute unilateral vestibular loss is the neuro-otologist’s best friend is the question at the heart of this paper. The different plasticity mechanisms underlying VC are first reviewed, and the authors present thereafter the dual concept of vestibulo-centric versus distributed learning processes to explain the compensation of deficits resulting from the static versus dynamic vestibular imbalance. The main challenges for the plastic events occurring in the vestibular nuclei (VN) during a post-lesion critical period are neural protection, structural reorganization and rebalance of VN activity on both sides. Data from animal models show that modulation of the ipsilesional VN activity by the contralateral drive substitutes for the normal push–pull mechanism. On the other hand, sensory and behavioural substitutions are the main mechanisms implicated in the recovery of the dynamic functions. These newly elaborated sensorimotor reorganizations are vicarious idiosyncratic strategies implicating the VN and multisensory brain regions. Imaging studies in unilateral vestibular loss patients show the implication of a large neuronal network (VN, commissural pathways, vestibulo-cerebellum, thalamus, temporoparietal cortex, hippocampus, somatosensory and visual cortical areas). Changes in gray matter volume in these multisensory brain regions are structural changes supporting the sensory substitution mechanisms of VC. Finally, the authors summarize the two ways to improve VC in humans (neuropharmacology and vestibular rehabilitation therapy), and they conclude that VC would follow a “top-down” strategy in patients with acute vestibular lesions. Future challenges to understand VC are proposed.

Plasticity of the histamine H3 receptors after acute vestibular lesion in the adult cat

After unilateral vestibular neurectomy (UVN) many molecular and neurochemical mechanisms underlie the neurophysiological reorganizations occurring in the vestibular nuclei (VN) complex, as well as the behavioral recovery process. As a key regulator, the histaminergic system appears to be a likely candidate because drugs interfering with histamine (HA) neurotransmission facilitate behavioral recovery after vestibular lesion. This study aimed at analyzing the post-lesion changes of the histaminergic system by quantifying binding to histamine H3 receptors (H3R; mediating namely histamine autoinhibition) using a histamine H3 receptor agonist ([3H]N-α-methylhistamine). Experiments were done in brain sections of control cats (N = 6) and cats submitted to UVN and killed 1 (N = 6) or 3 (N = 6) weeks after the lesion. UVN induced a bilateral decrease in binding density of the agonist [3H]N-α-methylhistamine to H3R in the tuberomammillary nuclei (TMN) at 1 week post-lesion, with a predominant down-regulation in the ipsilateral TMN. The bilateral decrease remained at the 3 weeks survival time and became symmetric. Concerning brainstem structures, binding density in the VN, the prepositus hypoglossi, the subdivisions of the inferior olive decreased unilaterally on the ipsilateral side at 1 week and bilaterally 3 weeks after UVN. Similar changes were observed in the subdivisions of the solitary nucleus only 1 week after the lesion. These findings indicate vestibular lesion induces plasticity of the histamine H3R, which could contribute to vestibular function recovery.

Vestibular compensation in acute unilateral medullary infarction

The aim of this fluorodeoxyglucose (FDG)-PET study was to determine whether the activation pattern in patients with an acute unilateral central vestibular lesion (e.g., lesion of the vestibular nucleus) differs from that known in patients with an acute peripheral vestibular deficit. Twelve patients with circumscribed unilateral medullary brainstem infarctions (6 right, 6 left) causing acute vestibular imbalance underwent resting-state (18)F-FDG-PET. Regional cerebral glucose metabolism was measured twice without any stimulation and with eyes closed: in the acute phase after infarct onset on mean day 8 (range 4-12), and again 6 months later in 7 patients after recovery. Group subtraction analyses and comparisons with a dataset of 12 age-matched controls were done with Statistic Parametric Mapping. In the acute stage, the pattern of signal increases differed from that in peripheral vestibular lesions: whereas signals in the infratentorial areas in the contralateral medulla and cerebellum (peduncle, vermis, hemispheres) were increased, areas at the cortical level were largely spared. Signal decreases were found in similar sites in the visual cortex bilaterally. The current data provide evidence that the lesion site significantly modifies the glucose metabolism pattern in an acute vestibular lesion. Different compensation strategies seem to be apparent: after vestibular nucleus lesions, compensation occurs preferably in brainstem-cerebellar loops; after peripheral lesions, it occurs at the cortical level.

Effects of Acute Vestibular Lesions on Visual Orientation and Spatial Memory, Shown for the Visual Straight Ahead

The aim of this study was to investigate the relation between the vestibular system and orientation in space and the role of acute vestibular lesions in spatial memory. In a first step it could be shown that determining the visual straight ahead is systematically influenced by caloric irrigation: deviations up to 10 degrees appeared, which are directed to the slow phase of the simultaneously provoked nystagmus. In a second step, 20 healthy subjects and 20 patients suffering from an acute vestibular disorder were asked to adjust a luminous point visual straight ahead. Whereas the healthy subjects' visual straight ahead was in a range of +/-2 degrees, the vestibular patients showed significantly greater deviations. If healthy subjects and patients were asked to replace a luminous point, which was exposed for a short time, to its original position, young and older healthy subjects showed good performance, with an error not greater than 3 degrees, whereas the vestibular patients showed significantly greater inaccuracy. We conclude that the visual straight ahead is a vestibular-dependent parameter of visual orientation and that spatial memory is influenced by acute vestibular lesions. For the first time it is shown that acute vestibular lesions impair spatial memory. This can be explained by the close relationship between the vestibular system and the hippocampus.

Acute Vestibular Nucleus Lesion Affects Cortical Activation Pattern during Caloric Irrigation in PET

Acute Vestibular Nucleus Lesion Affects Cortical Activation Pattern during Caloric Irrigation in PET

Acute Vestibular Nucleus Lesion Affects Cortical Activation Pattern during Caloric Irrigation in PET

Acute Vestibular Nucleus Lesion Affects Cortical Activation Pattern during Caloric Irrigation in PET

Autonomic Function Interferes in Cardiovascular Reflexes

Background. Experimental work indicates that the vestibular system participates in autonomic reflexes during body movement and postural changes. However, there are no studies of cardiovascular reflexes during vertigo due to human acute vestibular lesions. Methods. We assessed the response to active change of posture and hand immersion in cold water in seven patients with unilateral peripheral vestibular failure (vestibular neuritis) and seven age/sex-matched healthy subjects in acute phase (72 h from vertigo onset) and at 2 weeks of follow-up. Results. During acute phase, patients showed decreased blood pressure response during cold hand test ( p<0.05). Upright stance induced deficient decrease of the respiratory component of heart rate variability ( p<0.05) with lack of increase in low frequency/high frequency (LF/HF) ratio. At 2 weeks of follow-up, these abnormalities improved. Conclusions. Results suggest that acute vestibular lesions can interfere with cardiovascular autonomic responses in humans. This may reflect disruption of normal vestibulo-autonomic reflexes.

Acute vestibulopathy.

Acute vestibulopathy is characterized by the acute or subacute onset of vertigo, dizziness or imbalance with or without ocular motor, sensory, postural or autonomic symptoms and signs, and can last for seconds to up to several days. Acute vestibular lesions may result from a hypofunction or from pathological excitation of various peripheral or central vestibular structures (labyrinth, vestibular nerve, vestibular nuclei, cerebellum or ascending pathways to the thalamus and the cortex). This update focuses on new aspects of the aetiology, pathophysiology, epidemiology, and treatment of (i) acute peripheral disorders (benign paroxysmal positioning vertigo, vestibular neuritis, Menière's disease, perilymph fistula, especially 'superior canal dehiscence syndrome', vestibular paroxysmia); and (ii) acute central vestibular disorders (especially 'vestibular migraine'). Finally, the clinical relevance of recent diagnostic tools (three-dimensional analysis of eye movement, imaging techniques) is discussed.

Three-dimensional human VOR in acute vestibular lesions.

Three-dimensional human VOR in acute vestibular lesions.

Perceptual studies in patients with vestibular neurectomy.

Twelve patients undergoing unilateral vestibular neurectomy for the treatment of refractory vertigo were investigated. Vestibular motion perception was assessed using a self-rotational task and "vestibular remembered saccades". Cervical perception was also measured with remembered saccades. The tests were performed pre- and post-operatively to examine changes in vestibular and cervical perception following an acute vestibular lesion, and to monitor the progress of vestibular compensation. These perception tests were carried out in conjunction with a conventional evaluation of the vestibular ocular reflex (VOR), using electro-oculography. The patients' subjective symptoms at each stage of testing were also quantified with questionnaires. Generally, in the vestibular tests, for stimulation to the operated side, responses became strongly hypometric directly after the neurectomy, with a partial recovery during convalescence. In the cervical test, responses were bilaterally reduced immediately after operation. Results from both of the vestibular perception tests were significantly correlated with the VOR assessment of vestibular function. Scores for the patients' subjective symptoms of "vertigo" were only significantly correlated with the vestibular perception tests, and not with the conventional measures of vestibular function. Perceptual measurements afford useful complementary information in the assessment of vestibular patients.

Dynamic, Properties of Feed Back Control of Human Posture in Subjects with Vestibular Neuritis

Postural control was studied in 22 subjects with vestibular neruitis within 14 days after the onset of symptoms. Dynamic feed back control of posture were evaluated by analyzing the postural responses to vibration toward calf muscles applied according to a PRBS schedule. Properties of the dynamic control was normalized as swiftness, stiffness and damping of the responses. There was no prominent group differences between the 22 subjects with vestibular neuritis and 17 normal subjects. However, when studying the change in parameters evoked by presence or absence of visual information it was found that the abundant changes of control parameters, especially in stiffness, met in normal subjects had declined in subjects with vestibular neuritis. The present finding suggests that although subjects after an acute vestibular lesion may achieve a sufficient postural control by utilizing information from other somatosensory receptors, this is concomitant with changes of the feed back control.

The temporal course of nystagmus reactions after rotational stimulation (modified Veits long rotational method). Part II. Recommendations for the simplification of nystagmus evaluation in the rotational test

In this study, on the basis of the graphics showing the time course of the nystagmus reactions following rotatory stimuli (Part I), some practical proposals are made on how the nystagmus responses following the rotatory test can be routinely analysed more quickly. The recommendations are oriented to the requirement that the selection of defined 30-second-intervals during the per- and postrotatory phase for the nystagmus analysis should reflect the total reaction in healthy subjects as well as in patients with acute vestibular lesions in a representative manner. It is also shown that reducing the analysis intervals to only 15 seconds or selecting unfavourable segments, can lead to an unacceptable falsification of the results.

Time course of nystagmus reactions after rotational stimulation (modified Veits long rotation method). I. Comparison of the nystagmus reactions of probands with normal equilibrium with those of patients with vestibular disorders

In the present study, all the nystagmus reactions following the rotatory test are represented graphically after being split up into successive time intervals of 5 seconds each. The range of reactions is illustrated by comparing healthy subjects with patients with acute lesions of the vestibular system. It has been shown that during the rotatory test no signs of habituation were to be seen. The use of the parameter "fast phase velocity" (FPV) of the nystagmus to analyze the nystagmus reactions did not prove meaningful. In particular the findings in patients with acute vestibular lesions show that the nystagmus reactions following rotatory stimuli of appropriate intensity increase only to a limited extent. When interpreting the results, the influence of spontaneous nystagmus which usually underlies acute vestibular disease, is discussed in detail.

Zum Verlauf der vestibulären Frühkompensation nach akuter Labyrinthschädigung

This study discusses early vestibular compensation in man. Fifty-five patients suffering from acute vestibular lesions were clinically followed up over six months. More than 450 examinations were carried out, using several subtests such as observation of spontaneous, position, and positional nystagmus with Frenzel's glasses, and registrations of pendular rotation test and bilateral bithermal calories using electrooculography. The results were calculated and recorded on graphs to permit estimation of the influence of vestibular compensation on the features examined. In 71%, i.e., in 39 of the 55 patients, the side of hypoexcitability, the direction of spontaneous nystagmus, direction of preponderance, and deviation in Unterberger's stepping test changed from left to right and vice versa during compensation. It was not possible to discover a homogeneous time-course of compensation. The results have to be considered with respect to the evaluation of vestibular findings, especially in preoperative examinations to locate vestibular disturbances. The article proposes a graduated time schedule for follow-up examinations.

Reduction of the time constant in the VOR as a protective mechanism in acute vestibular lesions.

Fourteen patients with vestibular neuritis were examined at onset of symptoms and after one year. Postrotatory time constant and gain in the vestibulo-ocular reflex (VOR) were measured after rotation with a velocity step of 150 deg/s. There was no significant difference in gain towards the healthy side at onset of the disease compared to recordings after one year. The time constant towards the healthy side was significantly shorter at onset compared to measurements after one year. The results reflect the loss of unilateral vestibular function on the velocity storage mechanism, both in the acute situation and after compensation. The findings indicate that reduction of the time constant in the VOR is not only due to unilaterally vestibular impairment but it is also an effect of the generally reduced activity in the vestibular system after a lesion and may act as protective mechanism in acute vertigo.

Clinical Significance of the Velocity of Bodily Sway of the Center of Gravity

An attempt was made to evaluate the compensation process in patients with vestibular lesions by studying the velocity of bodily sway of the center of gravity.Patients with vestibular neuronitis, Meniere's disease and bilateral vestibular hypofunction were teasted. The data of the body sway test were analyed by micro-computer to obtain the velocity of body sway. The analysis time was 60sec and the sampling time 0.1sec.1) In patients with acute vestibular lesions whose vergigo had persisted for a relatively long time, the velocity difference between swaying to the right and to the left disappeared earlier than did nystagmus under non-gaze conditions.2) The velocity difference or the abnormal high velocity of the center of body sway recovered relatively early when tested with the eyes open in patients with bilateral vestibular lesions. However, abnormal high velocity persisted longer in the non-gaze state, which seems to reflect delayed compensation of the posture.