Central Vestibular Lesions Research Articles

Concordant GRADE-3 Truncal Ataxia and Ocular Laterodeviation in Acute Medullary Stroke.

Background: Severe truncal ataxia associated with an inability to sit up without assistance (STA grade 3) is frequent in patients with central acute vestibular syndrome (AVS) involving the brainstem or cerebellum. When these patients have nystagmus, central HINTS excludes peripheral lesions; however, additional localization and lateralization signs are helpful, not only to resolve the peripheral versus central vestibular lesion dilemma, but to zero in on a precise lesion localization/lateralization to the lateral medulla, the most common ischemic lesion localization associated with an initially false-negative stroke MRI. Methods: This is a study of AVS patients with additional inclusion criteria: grades 2 or 3 ataxia with an eventual diagnosis of medullary stroke (MS), either involving the lateral medulla (LMS) or the medial medulla (MMS), and horizontal (h) gaze paralysis was the main exclusion criteria. All patients sat on the side of the bed or stretcher, with assistance if needed. A general neurologic examination followed in the sitting position, the testing protocol included the head impulse, spontaneous nystagmus, and skew deviation (HINTS) tests, followed by observation of the effect of brief 3-5 sec eyelid closure on ocular position, and saccade and pursuit eye movement tests. If they could sit, the protocol included the ability to stand with a wide base, then a narrow base, the Romberg test, and tandem gait. Radiographic lesion localization and horizontal gaze deviation concluded the protocol. Results: A total of 34 patients met the entry criteria, 34 MS (13 in the lateral medulla, 12 previously described, and 1 new patient), and 1 new MMS. Among them, n = 10/12 had grade 3 ataxia, and 3 (1 new patient) had grade 2 ataxia. In addition, overt ocular laterodeviation (OLD) was present in thirteen of them (35.3%). All OLD patients had gaze deviation and ipsilateral saccade and truncal lateropulsion, 1 medial medulla stroke patient had grade 3 truncal contrapulsion and contralateral hemiparesis without OLD, n = 20/21 patients with LMS without OLD had grade 3 truncal ataxia, and 1 had grade 2 truncal ataxia. Discussion: AVS patients with severe truncal ataxia (inability to sit without assistance) potentially have brainstem, cerebellum, or subcortical lesions. All patients had central HINTS; however, simultaneous direction-concordant STA 3 and OLD provided greater lateral medulla localization specificity, affecting the ipsilateral medulla. Future work to explore a practical posterior circulation stroke scale that includes HINTS, STA, and OLD will potentially select cases for thrombolysis even in the event of initially false-negative imaging.

Unique compensatory oculomotor behavior in people living with multiple sclerosis

IntroductionGlobally, there are 3 million people living with multiple sclerosis (PLW-MS). A large proportion of PLW-MS have abnormal vestibular function tests that suggest central vestibular lesions. Yet, data regarding vestibular-ocular control in PLW-MS is limited. Thus, we aimed to further characterize compensatory saccade (CS) behavior in PLW-MS. MethodsWe analyzed video head impulse data from four groups of six age- and sex-matched adults: people living with mild MS (PLW-mild-MS, people living with moderate MS (PLW-moderate-MS), people living with unilateral vestibular deafferentation (PLW-UVD), and healthy controls (HC). ResultsPLW-moderate-MS had lower lateral canal vestibulo-ocular reflex (VOR) gain bilaterally compared to PLW-mild MS (p < 0.001), HC (p < 0.001), and PLW-UVD (p < 0.001). CS frequency was higher for impulses towards the less affected side in PLW-moderate-MS versus the more (p = 0.01) and less (p < 0.001) affected sides in PLW-mild-MS. CS latency was shorter (p < 0.001) and CS peak velocity was lower (p < 0.001) with impulses towards the more affected side versus the less affected side in PLW-moderate-MS. However, CS peak velocity with impulses towards each side was similar in PLW-mild-MS (p = 0.12). Gaze position error (GPE) was larger after impulses towards the more affected side versus the less affected side in PLW-moderate-MS (p < 0.001) and PLW-mild-MS (p < 0.001). MS-related disability was moderately associated with VOR gain (p < 0.001) and GPE (p < 0.001). Additionally, we identified micro-saccades and position correcting saccades that were uniquely employed by PLW-MS as compensatory gaze stabilizing strategies. ConclusionsIn PLW-MS, the characteristics of compensatory oculomotor behavior depend on the extent of residual VOR gain.

MRI findings of ependymoma in a 12‐month‐old cat

AbstractA 12‐month‐old domestic shorthair cat was presented for a progressive 2‐week history of behavioural changes, difficulties in jumping, falling, leaning towards the right side and right‐sided head tilt. Neurological examination revealed a right‐sided head tilt, leaning to the right and vestibular ataxia. Hopping was reduced on the right thoracic and right pelvic limbs. The rest of the neurological and the physical examinations were unremarkable. The neuroanatomic localisation was consistent with a right central vestibular lesion. On MRI an intraventricular mass, causing mass effect was identified in the fourth ventricle. In T1‐weighted post‐contrast images, the lesion showed peripheral ring contrast enhancement, causing obstructive hydrocephalus and ventriculomegaly, creating a similar appearance to that previously described in feline infectious peritonitis. The mass was found to be ependymoma on the histopathological examination.

What happens to vertiginous population after emission from the Emergency Department?

Background - Dizziness is one of the most frequent complaints when a patient is searching for medical care and resolution. This can be a problematic presentation in the emergency department, both from a diagnostic and a management standpoint. Purpose - The aim of our study is to clarify what happens to patients after leaving the emergency department. Methods - 879 patients were examined at the Semmel-weis University Emergency Department with vertigo and dizziness. We sent a questionnaire to these patients and we had 308 completed papers back (110 male, 198 female patients, mean age 61.8 ± 12.31 SD), which we further analyzed. Results - Based on the emergency department diagnosis we had the following results: central vestibular lesion (n = 71), dizziness or giddiness (n = 64) and BPPV (n = 51) were among the most frequent diagnosis. Clarification of the final post-examination diagnosis took several days (28.8%), and weeks (24.2%). It was also noticed that 24.02% of this population never received a proper diagnosis. Among the population only 80 patients (25.8%) got proper diagnosis of their complaints, which was supported by qualitative statistical analysis (Cohen Kappa test) result (κ = 0.560). Discussion - The correlation between our emergency department diagnosis and final diagnosis given to patients is low, a phenomenon that is also observable in other countries. Therefore, patient follow-up is an important issue, including the importance of neurotology and possibly neurological examination. Conclusion - Emergency diagnosis of vertigo is a great challenge, but despite of difficulties the targeted and quick case history and exact examination can evaluate the central or peripheral cause of the balance disorder. Therefore, to prevent declination of the quality of life the importance of further investigation is high.

Vestibular disease in dogs: association between neurological examination, MRI lesion localisation and outcome.

To determine whether the neurological examination correctly distinguishes between central and peripheral vestibular lesions in dogs. Retrospective study on dogs with vestibular disease presenting to two referral clinics in Germany. Ninety-three dogs were included; neurological examination suggested central vestibular disease in 62 and a peripheral lesion in 31. MRI diagnosis was central vestibular disease in 68 dogs and peripheral in 25. Of the 62 dogs with a lesion localisation diagnosed as central vestibular by neurological exam, 61 were correctly identified (98.4%). Twenty-four of the 31 dogs diagnosed with a peripheral lesion by neurological exam had a consistent lesion on MRI (77.4%). The neurological examination is efficient at identifying lesions in the central vestibular system but less so for peripheral lesions. Therefore it is prudent to recommend imaging in dogs that show signs of peripheral vestibular syndrome but do not rapidly respond to treatment.

57-Year-Old Man With Vertigo

57-Year-Old Man With Vertigo

Peripheral vestibular disorders: an update.

To provide an update on the most frequent peripheral vestibular disorders. The on-going classification of vestibular disorders by the Bárány Society represents major progress. The diagnosis of bilateral vestibulopathy (BVP) requires quantitative testing of vestibular function. 'Acute unilateral peripheral vestibulopathy' (AUPVP) is now preferred over 'vestibular neuritis.' Menière's disease is a set of disorders with a significant genetic contribution. The apogeotropic variant of horizontal canal benign paroxysmal positional vertigo (hcBPPV) and anterior canal BPPV (acBPPV) can be distinguished from a central vestibular lesion. Vestibular paroxysmia is now an internationally accepted clinical entity. The diagnosis of SCDS is based on conclusive findings. Diagnosis of BVP requires significantly reduced vestibular function. The clinical picture of AUPVP depends on how much the vestibular end organs or their innervation are affected. Menière's disease phenotype is a constellation of symptoms. Although diagnostic and therapeutic criteria for pc and hcBPPV are well defined, a number of less frequent and controversial are increasingly diagnosed and can be treated. Diagnosis of vestibular paroxysmia requires that a patient responds to treatment with a sodium channel blocker. The diagnosis of SCDS requires conclusive findings with various methods. There is still a great need for state-of-the-art randomized controlled treatment trials in most peripheral vestibular disorders.

Canine and feline vestibular syndrome

Signs of vestibular dysfunction (head tilt, asymmetric ataxia, spontaneous nystagmus, unilateral falling and rolling) are characteristic enough to be easily recognized without difficulty, even by inexperienced clinicians. Further differentiation between the peripheral (inner ear, vestibular nerve) and the central (vestibular nuclei, cerebellar peduncles, fastigial nucleus and flocculonodular lobe of the cerebellum) vestibular system should be based on a thorough history and an astute neurological examination. Affected animals should be reevaluated by serial neurological reexaminations to improve the accuracy of the initial assessment. Concomitant neurological signs, such as spastic hemiparesis or tetraparesis, proprioceptive déficits, other cranial nerve dysfunction and/or behavioral changes are indicative of central than peripheral vestibular syndrome. Apart from the minimum data base (complete blood count, serum biochemistry, urinalysis), the diagnostic evaluation should also include otoscopy, plain radiography of tympanic bullae (peripheral vestibular lesions), ear CT, brain MRI and cererebrospinal fluid analysis (central vestibular lesions). The present review first describes the clinical features of the vestibular syndrome from a differential point of view, regarding its neuroanatomical origin and secondly the most common conditions primarily characterized by vestibular dysfunction in the dog and cat.

Diagnosis, treatment, and rehabilitation in patients with dizziness and cognitive impairment

Complaints of dizziness and instability are the common reason for seeking a neurologist's advice at an outpatient visit and can be the frequent reason for emergency hospitalization. Difficulty in diagnosing the causes of dizziness and instability is due to a diversity of diseases manifested by these symptoms. The list of etiological factors includes peripheral and central vestibular lesions and unrelated nervous system diseases. In a number of cases, dizziness and instability are concurrent with cognitive impairment. Complaints of poor concentration and memory, dizziness and instability can often be associated with brain degenerative and/or vascular lesions, as well as with pathological mood changes and anxiety disorder. The diagnosis of these diseases requires neurovestibular examination, cognitive testing, and assessment of the emotional status of patients. Early detection of the causes of dizziness and memory disorders ensures better treatment results. There are different approaches to therapy for dizziness and cognitive impairment: drug and non-drug correction techniques (vestibular rehabilitation and cognitive training). Biofeedback procedures were shown to be highly effective. The effect of tanakan in treating patients with involvement of the peripheral vestibular system and brain structures is discussed

Peripheral vestibular syndrome. Etiologic differential diagnosis algorithm and therapeutic recommendations

Peripheral vestibular syndrome is frequently met in daily ENT practice (30% of patients). History and bedside exa­mination are crucial un differentiating peripheral and central vestibular lesions, as in establishing the ae­tio­logy whenever possible. This paper presents a dif­ferential diagnostic algorithm for vertiginous syn­drome, a specific category of the vestibular lesions, in which clinical presentation is dominated by VERTIGO. It also presents appropriate treatment options for each aetiology. Bimodal treatment - medication (betahystine) and customised vestibular rehabilitation programs - aims to facilitate the physiologic vestibular central com­pen­sation process. This will enable more rapid and more complete recovery of the unilateral vestibular lesion.

Diagnosis and current therapy of vestibular syndromes

Vertigo and dizziness are with an annual incidence of more than 10% and a lifetime prevalence of more than 30% among the most frequent symptoms. The keys to the diagnosis are the patient history and the bedside examination: a) for the patient history the time course, type and triggers of symptoms and accompanying symptoms, b) for the clinical examination of the vestibular system the head-impulse test (HIT), the examination for a spontaneous nystagmus, a displacement of subjective visual vertical, a positional nystagmus and the Romberg test, and c) for the differentiation between an acute peripheral and central vestibular lesion the skew deviation, central fixation nystagmus, gaze-evoked nystagmus, saccadic smooth pursuit and a normal HIT. The various forms of vertigo are treated with pharmacological therapy, physical therapy, psychotherapeutic measures and, rarely, surgery. For pharmacotherapy there are basically eight groups of drugs that can be used: anti-emetics, -inflammatory, -menières, -migraineous medications, anti-depressants, -convulsants, aminopyridines and acetyl-DL-leucine, however, with a currently often low level of evidence.

Predictors of central vestibular disorders from videonystagmography tests

Abstract The diagnosis of central vestibular lesion is challenging and sometimes there is an overlap in symptoms and signs with a peripheral vestibular lesion. In some selected cases, dizziness is the only presenting symptom and in other patients, mild neurological symptoms as numbness are ignored. Videonystagmography (VNG) is considered a useful method for diagnosing vertigo of peripheral origin; however, not all the patients with central vertigo can be diagnosed easily. Benign paroxysmal positional vertigo and central positional vertigo share common criteria. The aim of the present study is to assess the usefulness of different VNG tests as predictors of central vestibular disorders, to determine the criteria that differentiate central positional nystagmus from the peripheral type, and to attempt to relate the abnormality in different VNG tests to certain central nervous system (CNS) levels. A retrospective study was carried out on 51 patients with possible central vestibular disorders from VNG tests battery and were referred for an MRI for further assessment. According to MRI results, the patients were divided into group A (31 patients), the group with manifest MRI findings, and group B, the group with free MRI (20 patients). Different VNG tests were compared between both groups. Three predictors of CNS lesion by VNG were determined: fixation index (FI), oculomotor tests, and central positional nystagmus; there was a statistically significant difference between both groups in FI, oculomotor tests, and central positional nystagmus, and apogeotropic criteria or nystagmus in multiple plains. There was no relation between any of those predictors and specific levels in the CNS. VNG tests are a good diagnostic tool to differentiate between peripheral and central vestibular lesions. The inclusion of FI and positional tests to the oculomotor tests increases the sensitivity of the VNG. In some cases, it is difficult to distinguish between benign paroxysmal positional vertigo and central positional vertigo; apogeotropic nystagmus and nystagmus in multiple plains should raise the suspicion of CNS lesion. Anterior circulation ischemia may lead to chronic vertigo symptoms. Central vestibular vertigo could be caused by dysfunction or excitation of various structures in the CNS including the vestibular cortex.

Chapter 8 - Eye movements in vestibular disorders

The differential diagnosis of patients with vestibular symptoms usually begins with the question: is the lesion central or is it peripheral? The answer commonly emerges from a careful examination of eye movements, especially when the lesion is located in otherwise clinically silent areas of the brain such as the vestibular portions of the cerebellum (flocculus, paraflocculus which is called the tonsils in humans, nodulus, and uvula) and the vestibular nuclei as well as immediately adjacent areas (the perihypoglossal nuclei and the paramedian nuclei and tracts). The neural circuitry that controls vestibular eye movements is intertwined with a larger network within the brainstem and cerebellum that also controls other types of conjugate eye movements. These include saccades and pursuit as well as the mechanisms that enable steady fixation, both straight ahead and in eccentric gaze positions. Navigating through this complex network requires a thorough knowledge about all classes of eye movements to help localize lesions causing a vestibular disorder. Here we review the different classes of eye movements and how to examine them, and then describe common ocular motor findings associated with central vestibular lesions from both a topographic and functional perspective.

Subjective visual vertical testing in children and adolescents.

Subjective visual vertical (SVV) is a vestibular test commonly used in adults that has not been well studied in children. In this test, the patient aligns a projected line with the perceived true vertical. Deviation of >2° is usually associated with utricular dysfunction and may also be seen with central vestibular lesions. The goal of this study was to determine the efficacy of SVV in children. Prospective, controlled study. Thirty-three children aged 7 to 18 years with (n = 21) and without (n = 12) dizziness underwent static SVV. History, exam, rotary chair, and caloric testing were used to categorize subjects with dizziness into groups with peripheral vestibular loss (PVL), benign paroxysmal positioning vertigo (BPPV), central vertigo (CV), and nonvestibular dizziness (NVD). Mean SVV deviation was significantly higher in the peripheral vestibular loss group (n = 4; 2.1 ± 1.5) compared to BPPV (n = 5; 0.5 ± 0.3), CV (n = 7; 0.4 ± 0.3), NVD (n = 5; 0.6 ± 0.4), and control (n = 12; 0.7 ± 0.5) groups by one-way analysis of variance (P = .002). SVV deviation >2° demonstrated a sensitivity of 100%, specificity of 75%, positive predictive value of 100%, and negative predictive value of 97% for PVL. SVV is a simple, noninvasive test that provides a valuable contribution to the assessment of peripheral vestibular function in children. 3b Laryngoscope, 126:727-731, 2016.

CHRONIC SYMPTOMS FROM MULTIPLE CONCUSSIONS IMPROVED THROUGH FUNCTIONAL BRAIN-BASED STRATEGIES.

Event Abstract Back to Event CHRONIC SYMPTOMS FROM MULTIPLE CONCUSSIONS IMPROVED THROUGH FUNCTIONAL BRAIN-BASED STRATEGIES. Susan Esposito1* and David Koentop2 1 Life University, United States 2 Atlantic Medicine and Wellness, United States Background: A male graduate student in his mid-twenties presented to a functional neurology clinic for assessment of tremors, head fogginess, impaired reading comprehension, and inability to focus. Examination revealed a right hypertropia and a 6Hz tremor of his hands bilaterally. The patient showed decreased ability of gaze stabilization in all visual planes with aberrant saccades and pursuits. The patient’s history included numerous concussions and cranial impacts over years of playing hockey. Methods: A thorough neurological exam including Computerized Dynamic Posturography (CDP) and video nystagmography (VNG) testing confirmed a central vestibular lesion, cortical desynchronization, and inability to gaze fixate. He underwent a two month long program of functional neurological treatment that included complex passive movements of upper and lower extremities, brain-based therapeutic eye exercises, somatosensory evoked potential stimulations, and whole-body multiaxis vestibular rehabilitation. Results: The tremors in his hands completely disappeared immediately after treatment, but subsequently re-emerged with reduced amplitude and frequency. Head fogginess, inability of reading comprehension, decreased mental focus, and aberrant eye motions have reduced substantially. CDP scores improved drastically with eyes closed, head in extension on a perturbed surface from 0 to 46.5% stability. Square wave jerks and other eye movement aberrations were markedly diminished on VNG testing. Conclusion: Functional neurological treatments including vestibular rehabilitation strategies were used with positive outcomes in this case of tremors, head fogginess, impaired reading comprehension and mental focus. Further research in of the use of these strategies is suggested. Keywords: Functional Neurology, Tremor, brain fog, vestibular therapy, Chiropractic Conference: International Symposium on Clinical Neuroscience: TBI and Neurodegeneration, Orlando, Florida, United States, 10 Dec - 14 Dec, 2015. Presentation Type: Poster Presentation Topic: Case Reports for Poster Presentation Citation: Esposito S and Koentop D (2015). CHRONIC SYMPTOMS FROM MULTIPLE CONCUSSIONS IMPROVED THROUGH FUNCTIONAL BRAIN-BASED STRATEGIES.. Front. Neurol. Conference Abstract: International Symposium on Clinical Neuroscience: TBI and Neurodegeneration. doi: 10.3389/conf.fneur.2015.58.00037 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 31 Oct 2015; Published Online: 02 Nov 2015. * Correspondence: Dr. Susan Esposito, Life University, Marietta, Georgia, 30060, United States, susan.esposito@life.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Susan Esposito David Koentop Google Susan Esposito David Koentop Google Scholar Susan Esposito David Koentop PubMed Susan Esposito David Koentop Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Towards a concept of disorders of "higher vestibular function".

Background: 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 or central. The criterion of “higher function” is fulfilled if cognition or senses other than the primarily affected one come into play.

Geotropic Central Paroxysmal Positional Nystagmus in a Patient With Human Immunodeficiency Virus Encephalopathy

Central vestibular lesions may cause paroxysmal positional nystagmus (PPN) or paroxysmal positional vertigo as a result of lesions involving the brainstem dorsolateral to the fourth ventricle or the cerebellar nodulus/uvular region. PPN usually presents as persistent downbeating nystagmus during head hanging or as apogeotropic horizontal nystagmus during head turning in the supine position. Geotropic PPN during head turning in the supine position has not been previously reported. We report such a case in a patient with HIV encephalopathy.

Central vestibular dysfunction in an otorhinolaryngological vestibular unit: incidence and diagnostic strategy.

Introduction Vertigo can be due to a variety of central and peripheral causes. The relative incidence of central causes is underestimated. This may have an important impact of the patients' management and prognosis. Objective The objective of this work is to determine the incidence of central vestibular disorders in patients presenting to a vestibular unit in a tertiary referral academic center. It also aims at determining the best strategy to increase the diagnostic yield of the patients' visit. Methods This is a prospective observational study on 100 consecutive patients with symptoms suggestive of vestibular dysfunction. All patients completed a structured questionnaire and received bedside and vestibular examination and neuroimaging as required. Results There were 69 women and 31 men. Their ages ranged between 28 and 73 (mean 42.48 years). Provisional videonystagmography (VNG) results were: 40% benign paroxysmal positional vertigo (BPPV), 23% suspicious of central causes, 18% undiagnosed, 15% Meniere disease, and 4% vestibular neuronitis. Patients with an unclear diagnosis or central features (41) had magnetic resonance imaging (MRI) and Doppler studies. Combining data from history, VNG, and imaging studies, 23 patients (23%) were diagnosed as having a central vestibular lesion (10 with generalized ischemia/vertebra basilar insufficiency, 4 with multiple sclerosis, 4 with migraine vestibulopathy, 4 with phobic postural vertigo, and 1 with hyperventilation-induced nystagmus). Conclusions Combining a careful history with clinical examination, VNG, MRI, and Doppler studies decreases the number of undiagnosed cases and increases the detection of possible central lesions.

Early and Phasic Cortical Metabolic Changes in Vestibular Neuritis Onset

Functional brain activation studies described the presence of separate cortical areas responsible for central processing of peripheral vestibular information and reported their activation and interactions with other sensory modalities and the changes of this network associated to strategic peripheral or central vestibular lesions. It is already known that cortical changes induced by acute unilateral vestibular failure (UVF) are various and undergo variations over time, revealing different cortical involved areas at the onset and recovery from symptoms. The present study aimed at reporting the earliest change in cortical metabolic activity during a paradigmatic form of UVF such as vestibular neuritis (VN), that is, a purely peripheral lesion of the vestibular system, that offers the opportunity to study the cortical response to altered vestibular processing. This research reports [18F]fluorodeoxyglucose positron emission tomography brain scan data concerning the early cortical metabolic activity associated to symptoms onset in a group of eight patients suffering from VN. VN patients’ cortical metabolic activity during the first two days from symptoms onset was compared to that recorded one month later and to a control healthy group. Beside the known cortical response in the sensorimotor network associated to vestibular deafferentation, we show for the first time the involvement of Entorhinal (BAs 28, 34) and Temporal (BA 38) cortices in early phases of symptomatology onset. We interpret these findings as the cortical counterparts of the attempt to reorient oneself in space counteracting the vertigo symptom (Bas 28, 34) and of the emotional response to the new pathologic condition (BA 38) respectively. These interpretations were further supported by changes in patients’ subjective ratings in balance, anxiety, and depersonalization/derealization scores when tested at illness onset and one month later. The present findings contribute in expanding knowledge about early, fast-changing, and complex cortical responses to pathological vestibular unbalanced processing.

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.