Central Vestibular Lesions Research Articles

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.

Model approach to neurological variants of visuo-spatial neglect

Neglect is a neurological disorder of spatial attention with reduced awareness of visual stimuli in the hemifield contralateral to an acute temporo-parietal lesion mainly of the right hemisphere. There is a close association of multisensory orientation centers (MSO) and vestibular tonus imbalance. A lesion of the dominant right MSO causes a left-sided neglect due to a lack of ipsilateral activation of the visual cortex, which is further enhanced by increasing inhibition from the contralateral visual cortex. The nondominant MSO in the left hemisphere might be involved in the manifestation of the less frequent and more transient right-sided neglect and in the plastic mechanisms of gradual recovery from left-sided neglect or extinction. There is evidence that a vestibular tonus inbalance due to peripheral or central vestibular pathway lesions may also induce a neglect. In a first model approach using an attractor network and assuming that there is only one MSO in the right hemisphere, it is possible to simulate attentional shifts into a visual hemifield and to induce a neglect. The neural network model consists of four layers of neurons: retina, MSO, visual cortex V1, and superior colliculus. The superior colliculus layer is modeled as a recurrent attractor network with one inhibitory interneuron and synaptic weights chosen to implement a winner-take-all network that centers the hill of activity on the strongest input. We are well aware of the simplifications used in the conceptual drawings and the computational model, but nevertheless hope that they will serve as an inspiration for further modeling and clinical studies.

Electronystagmographic analysis of caloric test parameters in vestibular disorders

The electronystagmographical analysis of the eye movements provoked by caloric stimulation is an important method in the evaluation and topical diagnostic procedure of several vestibular lesions. The aim of the study was to compare the electronystagmographical results of caloric response in several vestibular disorders. The patients were divided into five groups: right and left unilateral and bilateral peripheral lesions, central vestibular dysfunction, and normal vestibular function. In the normal vestibular system group the average caloric nystagmus SPV in normal vestibular system was 17.4 °/s. In the peripheral lesion groups the average slow phase velocities are decreased in the affected side, as we expected. In the compensated vestibular lesion the average ASPV of caloric nystagmus is also decreased on the unaffected side. This might be caused by the effect of the central adaptive mechanisms. According to our observations, in central dysfunctions the average caloric ASPV and the spontaneous nystagmus ASPV is increased (25.0 °/s). This suggests that in central vestibular lesions the central inhibiting mechanisms of the caloric response are impaired. Our results show that electronystagmographical analysis of spontaneous and caloric nystagmus is very important in the evaluation of dizzy patients.

Electronystagmography versus videonystagmography in diagnosis of vertigo

Vertigo is a very common symptom mainly caused by the lesion of vestibular system (peripheral or central) and often accompanied by some work-related diseases and occupational intoxications. The aim of this study was to assess the value of electronystagmography (ENG) and videonystagmography (VNG) for diagnosing vertigo of various origin. The study included four groups, 25 subjects each, of patients suffering from vestibular disorders of peripheral, central and mixed origin versus healthy controls. All were examined by means of ENG and VNG, using the bithermal caloric test with 30°C and 44°C air irrigations of the ears. The findings (frequency of induced nystagmus FRQ, its slow phase velocity SPV, canal paresis CP, directional preponderance DP, vestibular excitability VE) were analysed and compared. In all patients with vertigo due to vestibular neuritis, barotrauma and kinetosis, significant CP, the important sign of peripheral site of vestibular lesion was identified both in ENG and VNG. None of the patients with central origin disorders showed CP in VNG; in the majority of cases DP was observed. However, in ENG we found CP in 5 patients with central origin disorders. There were no essential differences between ENG and VNG in measurements of FRQ and SPV except for higher values in VNG in controls and patients with mixed vertigo. The results suggest that the VNG should be recommended in preference as the valuable method to assess vertigo and to discriminate between the peripheral and the central vestibular lesions.

Patterns of spontaneous and head-shaking nystagmus in cerebellar infarction: imaging correlations

Horizontal head-shaking may induce nystagmus in peripheral as well as central vestibular lesions. While the patterns and mechanism of head-shaking nystagmus are well established in peripheral vestibulopathy, they require further exploration in central vestibular disorders. To define the characteristics and mechanism of head-shaking nystagmus in central vestibulopathies, we investigated spontaneous nystagmus and head-shaking nystagmus in 72 patients with isolated cerebellar infarction. Spontaneous nystagmus was observed in 28 (39%) patients, and was mostly ipsilesional when observed in unilateral infarction (15/18, 83%). Head-shaking nystagmus developed in 37 (51%) patients, and the horizontal component of head-shaking nystagmus was uniformly ipsilesional when induced in patients with unilateral infarction. Perverted head-shaking nystagmus occurred in 23 (23/37, 62%) patients and was mostly downbeat (22/23, 96%). Lesion subtraction analyses revealed that damage to the uvula, nodulus and inferior tonsil was mostly responsible for generation of head-shaking nystagmus in patients with unilateral posterior inferior cerebellar artery infarction. Ipsilesional head-shaking nystagmus in patients with unilateral cerebellar infarction may be explained by unilateral disruption of uvulonodular inhibition over the velocity storage. Perverted (downbeat) head-shaking nystagmus may be ascribed to impaired control over the spatial orientation of the angular vestibulo-ocular reflex due to uvulonodular lesions or a build-up of vertical vestibular asymmetry favouring upward bias due to lesions involving the inferior tonsil.

Presumptive meningoencephalitis secondary to extension of otitis media/interna caused by Streptococcus equi subspecies zooepidemicus in a cat

A 5-year-old castrated male domestic longhair cat was presented with neurological signs consistent with a central vestibular lesion and left Horner’s syndrome. Computed tomography images revealed hyperattenuating, moderately contrast-enhancing material within the left tympanic bulla, most consistent with left otitis media/interna. Marked neutrophilic pleocytosis was identified on cerebrospinal fluid analysis. Streptococcus equi subspecies zooepidemicus (SEZ) was isolated from the cerebrospinal fluid. Intracranial extension of otitis media/interna is relatively infrequent in small animals. There are no reports of otitis media/interna caused by SEZ in dogs or cats. This is the first report of otitis media/interna and presumptive secondary meningoencephalitis caused by SEZ in a cat.

Comparative Study on Cases of Vertigo and Dizziness in the Emergency Room and Otorhinolaryngological Clinic

We recently studied the characteristics of vertigo and dizziness in 197 patients who first visited the emergency room (ER group) and in 288 patients who first visited the otorhinolaryngological clinic of Minoh City Hospital (ENT group) between January 1 and December 31 of 2009. The ER group can be regarded as representing the hyperacute phase and the ENT group as representing the acute to chronic phase. These two groups were completely distinct. We also subdivided these groups into the high risk subgroup (H subgroup) for cases with the underlying diseases of diabetes mellitus, hypertension, cerebrovascular disease and hyperlipidemia, and the normal subgroup (N subgroup). Comparison of the two groups showed that, in the ER group, a significantly larger numbers of patients had symptoms of peripheral vestibular origin except for BPPV and Meniere's disease, and a significantly larger number of patients had symptoms of unknown origin in the ENT group. Half of this group may be accounted for by patients with symptoms of peripheral vestibular origin except for BPPV and Meniere's disease in the ER group. In 8 out of 158 patients of the ER group and 1 out of 122 patients of the ENT group, cerebral lesions were not found on CT images but were found with MRI. Careful investigation is necessary in the patients with normal CT findings. Central vestibular lesions were found in 7 out of 197 patients (3.5%) of the ER group and 5 out of 288 patients (1.7%) of the ENT group. The incidence of central lesions tended to be higher in the ER group than in the ENT group. There was no significant difference in the incidence of central lesion among the H and N subgroups of both groups. Careful investigation of the central vestibular lesion is also necessary in the N subgroup.

Necrotizing Cerebellitis and Cerebellar Atrophy Caused by Neospora caninum Infection: Magnetic Resonance Imaging and Clinicopathologic Findings in Seven Dogs

Adult dogs with neosporosis can develop a variety of neurologic signs. No area of predilection within the nervous system so far has been identified in adult dogs. To document neosporosis as a cause of progressive cerebellar ataxia and cerebellar atrophy in dogs. Seven client-owned dogs. Retrospective, descriptive study. Age at diagnosis ranged from 1 year 6 months to 9 years 11 months. Neuroanatomic localization indicated cerebellar and brainstem disease in 6 dogs and a central vestibular lesion in 1 dog. In all 7 dogs, there was moderate to marked bilaterally symmetrical cerebellar atrophy, with the atrophied cerebellum being surrounded by a region of T2-weighted hyperintense and T1-weighted hypointense signal. Cerebrospinal fluid (CSF) analysis in all but 1 dog showed mononuclear pleocytosis and high protein concentration. Polymerase chain reaction testing for Neospora caninum performed on the CSF was positive in 4/5 dogs tested and there was a high titer of serum antibodies to N. caninum (> or = 1 : 800) in all 6 dogs tested. Postmortem examination in 1 dog confirmed cerebellar atrophy and multifocal nonsuppurative encephalitis with areas of malacia and leptomeningitis. All of the remaining 6 dogs were treated with some combination of clindamycin, trimethoprim, sulfadiazine, and pyrimethamine. Two dogs were euthanized because of deterioration or relapse of neurologic signs, but treatment of the remaining 4 dogs resulted in improvement (3 dogs) or resolution (1 dog) of neurologic signs. Neosporosis is an important cause of progressive cerebellar ataxia and cerebellar atrophy in adult dogs.

Imaging cortical activity after vestibular lesions

In this article we will discuss our current knowledge of multisensory vestibular structures and their functions in the human cortex. Most of it derives from brain activation studies with PET and fMRI in humans conducted over the last decade. They have confirmed the existence of several separate and distinct cortical areas that were identified earlier by tracer and electrophysiological studies in animals, especially in monkeys. The patterns of activations and deactivations during vestibular stimulations in healthy subjects have been compared with those in patients with acute and chronic peripheral and central vestibular disorders. The following reviews what is presently known about the interconnections of vestibular structures, their activations and interactions with other sensory modalities, the correlations of perceptual and motor functions in normal humans, and the changes that result from strategic unilateral peripheral and central vestibular lesions such as vestibular neuritis and bilateral vestibular failure, on the one hand, and central vestibular nucleus lesions due to ischemic infarctions of the lateral medulla (Wallenberg's syndrome), on the other.

Challenges in Neuro-Otology

This article provides an overview of the current methods of diagnosis and treatment of patients with vertigo, dizziness, or imbalance, as well as an analysis of ongoing problems besetting the field of neuro-otology. Aims and challenges are also described with the hope of stimulating basic and clinical research on these very frequent symptoms. Vertigo and dizziness are among the most frequent symptoms that patients experience at some time in their lives. With a lifetime prevalence of about 30% and an annual incidence that increases with age, vertigo and dizziness will become even more important in the future. Despite this high prevalence and burden of disease, considerable challenges remain. Most patients with acute vertigo and dizziness are uncertain who to consult, because their problem lies inbetween the specializations of ear, nose, and throat (ENT) and neurology, and in some cases, ophthalmology, internal medicine, or psychiatry. While neurologists are very familiar with the anatomy, physiology, and pathophysiology of the central nervous system (central vestibular and ocular motor systems), ENT physicians specialize in the peripheral vestibular and audiological systems. However, very few have detailed knowledge of both the central and peripheral systems. Moreover, most ENT physicians practice mainly as ENT surgeons, and therefore, they are not necessarily specialists on vertigo and dizziness. With a few exceptions (South Korea, and some centers in the USA, UK, and Australia) cooperation between neurology and ENT as well as neuro-otology and oto-neurology is far from perfect. The underlying diseases resulting in vertigo and dizziness cover a broad spectrum of anatomical structures. Possible etiologies include ischemia, infection, autoimmune disorders, mechanical inner ear disorders, psychosomatic, and somatoform disorders. Therefore, the approach to patients requires a broad-based knowledge of anatomy, physiology, pathophysiology, and pharmacology as well as in-depth practical experience with the different methods available for evaluating the vestibular and ocular motor systems. Medical education in neuro-otology is also less than optimal. The problem begins in Medical School, where the vestibular and ocular motor systems are assumed to be among the most complicated anatomical and physiological systems of humans. Therefore, most medical students are not attracted to this field, which may also explain their limited knowledge of the subject. This downward trend continues during post-graduate training for most neurologists and ENT physicians, and is further exacerbated by the above-mentioned overlapping of the two disciplines. Moreover, to establish a correct diagnosis, physicians must examine the vestibular, audiological, and ocular motor systems. Furthermore, many physicians have difficulties examining the ocular motor system and ultimately interpreting their findings. What is pathological and what do the findings mean? Thus, topographical anatomical diagnosis remains a challenge: it is imperative to be able to discriminate between peripheral and central vestibular lesions is imperative. The link between basic physiology and the modeling of the vestibular and the ocular motor systems, on the one hand, and their clinical implications and applications, on the other, are far from ideal. While we know the detailed workings of the vestibular and ocular motor systems and can model their function and dysfunction, this knowledge has not yet been fully integrated in clinical practice. Conversely, clinical findings have to be linked with basic knowledge in order to stimulate the knowledge of physiology and the modeling of these systems. State-of-the-art randomized controlled clinical trials on the frequent causes of vertigo and dizziness as well as their underlying disorders are still lacking. This is true for phobic postural vertigo, vestibular migraine, Meniere's disease, vestibular paroxysmia, downbeat and upbeat nystagmus, episodic ataxia, and perilymphatic fistula. The number of studies available on the impact of vertigo and dizziness, as well as impaired vestibular function on patients’ quality of life and functioning are limited. Long-term studies on the natural course of the different forms of vertigo, their recurrence rates, or the long-term efficacy of available treatments are non-existent. This is true for most forms of vertigo and dizziness. In brief our growing knowledge of the anatomy and physiology of the vestibular and related ocular motor systems, as well as basic and clinical research must still overcome a number of shortcomings and limitations to improve diagnosis, develop new diagnostic criteria, and better understand the pathophysiology of these disorders. Hopefully, new treatment strategies and state-of-the-art prospective clinical trials will improve the quality of life and functioning in patients with vertigo and dizziness.

A bucket of static vestibular function

Validation of a bedside test to measure the monocular and binocular subjective visual vertical (SVV). Monocular and binocular measurements of the SVV were made in 30 healthy subjects (mean age 46.1 +/- 16.4 years) and 30 patients with acute peripheral or central vestibular lesions (mean age 51.3 +/- 17.1 years). The established method uses a hemispheric dome (adjustment of a bar to the vertical without spatial orientation clues in a motor-driven, hemispheric dome randomly covered with colored dots). It was compared to a simple, self-made bucket method, in which the subject estimates true verticality by attempting to properly align a straight line visible on the bottom of a bucket that is rotated at random by the examiner. Comparative measurements of the whole group (n = 60) showed no difference in the distribution of monocular or binocular SVV values while using the hemispheric dome or the bucket method. Intertest reliability was 89% for monocular and 90% for binocular SVV measurements. Intratest reliability of the bucket method in 10 repetitions was 92% for binocular and monocular SVV determinations. With the bucket method, the range of absolute deviations of SVV values from true verticality in healthy subjects was 1.1 +/- 0.7 degrees for monocular and 0.9 +/- 0.7 degrees for binocular measurements (mean +/- SD). There was no significant effect of age or gender. The bucket method is an easily performed and reliable bedside test for determining monocular and binocular subjective visual vertical. The bucket can be modified within 1 hour and costs less than $5.

Central Vertigo and Dizziness

Dizziness is a common complaint among patients seen by primary care physicians, neurologists, and otolaryngologists. The most common causes of dizziness are peripheral vestibular disorders, but central nervous system disorders must be excluded. This article provides an overview of the epidemiology of dizziness, differentiating between central and peripheral vertigo, and central causes of dizziness. Dizziness is among the most common complaints in medicine, affecting approximately 20% to 30% of persons in the general population. Dizziness is a general term for a sense of disequilibrium. Vertigo is a subtype of dizziness, defined as an illusion of movement caused by asymmetric involvement of the vestibular system. Central vestibular lesions affecting the pons, medulla, or cerebellum cause vertigo, nausea, vomiting, severe ataxia, multidirectional nystagmus that is not suppressed by optic fixation, and other neurologic signs. The other types of dizziness are dysequilibrium without vertigo, presyncope, and psychophysiologic dizziness, which is often associated with anxiety, depression, and panic disorder. Epidemiologic studies indicate that central causes are responsible for almost one-fourth of the dizziness experience by patients. The patient's history, neurologic examination, and imaging studies are usually the key to differentiation of peripheral and central causes of vertigo. The most common central causes of dizziness and vertigo are cerebrovascular disorders related to the vertebrobasilar circulation, migraine, multiple sclerosis, tumors of the posterior fossa, neurodegenerative disorders, some drugs, and psychiatric disorders.

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...

Evaluation of patients with acute vestibular syndrome

Acute vestibular syndrome is characterized by a rapid unilateral injury to either peripheral or central vestibular structures. It consists of severe vertigo, nausea and vomiting, spontaneous nystagmus, and postural instability. In many cases, a peripheral etiology is considered although it may be due to an underlying serious central pathology. The present study was designed to investigate the feasibility of differentiating the cause of acute vestibular syndrome in such patients using clinical, audiovestibular and radiologic tools. We performed a case series study of patients complaining of acute vertigo at a university referring center for hearing and balance disorders. Thirty patients with history of acute vertigo within 3 days onset with no history of previous otological or neurological disorders. Eighteen patients were due to acute peripheral vestibular lesion, 1 due to psychiatric illness under antidepressant drugs and 11 were of central vestibular lesion. The most important step in the diagnosis of acute vertigo is a thorough and detailed history. The common error of carrying out investigations in place of a detailed history is to be avoided. The clinical evaluation has the highest sensitivity and specificity in differentiating central from peripheral vestibular lesions.

Central compensation of central vestibular lesions

Central compensation of central vestibular lesions

USING CONSTRUCTIVE NEURAL NETWORKS FOR DETECTING CENTRAL VESTIBULAR SYSTEM LESION

Traditional neural network algorithms such as Backpropagation, require the definition of the network architecture prior to training. Generally these methods work well only when the network architecture is chosen appropriately. It is well known that there is no general answer to the problem of defining a neural network architecture for a given application. This fact has been one of the main motivations for the proposal of constructive neural network algorithms, which try to solve the problem by building the architecture of the neural network during its training. In this paper, we explore the use of three constructive supervised neural network algorithms in learning to identify the possibility of an existing problem in the central vestibular system of a patient, using data from optokinetic tests. The constructive neural network algorithms used are two perceptron-based algorithms, namely, Tower and Pyramid and the DistAl algorithm. The goal of the experiments, aside from creating a good classifier for detecting the presence of a central vestibular system lesion, is also to compare and contrast the performance of the recently proposed DistAl against two well-known constructive algorithms in a medical domain that has not been greatly explored with these types of experiments. In addition, results obtained with Backpropagation are presented for comparison.

Diagnostic value of vestibular evoked myogenic potentials in cerebellar and lower-brainstem strokes

Background Vestibular evoked myogenic potentials (VEMPs) provide assessment of vestibular function. They consist in picking up compound muscle action potentials in the sternocleidomastoid (SCM) muscles in response to auditory stimulation of the vestibulum. VEMP testing has found application mainly in peripheral vestibular disorders, whereas reports about VEMPs in central vestibular lesions are rather scarce. Aims of the study Based on the physiological connections between the cerebellum and the vestibular nuclei, we investigated the influence on VEMPs of cerebellar and lower-brainstem strokes. We examined whether or not this method may be suitable as a clinical tool for the evaluation of the extent of cerebellar strokes. Patients and methods Nineteen patients with cerebellar ischemic stroke and 15 patients with lower-brainstem ischemic stroke (11 in the pons, four in the medulla) were included. The latencies and amplitudes of P13 and N23 in both groups of patients were compared with those obtained in a control group of 53 normal individuals. Results VEMP responses were obtained in all patients and controls. At the group level, mean peak latencies and amplitudes, and the number of subjects with significantly deviant values did not differ between patients and controls. There were no latency or amplitude differences ipsilaterally or contralaterally to the lesion. At the individual level, there was no correlation between laterality of lesion and that of P13 or N23 abnormalities in patients with cerebellar strokes; however, there were two patients (one pontine, one medullar stroke) who presented P13 and N23 latency abnormalities ipsilaterally to the lesion. Conclusion Cerebellar strokes do not influence VEMPs. Moreover, despite previous reports, we were unable to find at a group level any statistically significant VEMP changes in patients with lower-brainstem strokes as compared with controls. Therefore, VEMPs do not appear a suitable tool for assessment of brainstem integrity in patients with posterior fossa strokes. However, they could constitute a sensitive method for documentation of involvement of the central vestibular pathways in patients with brainstem stroke.

Central Compensation of Central Vestibular Lesions

Background: Peripheral and central vestibular lesions cause a vestibular tone imbalance, that is centrally compensated. Whereas the central compensation of peripheral vestibular lesions has been studied in detail, little is known about central compensation of central lesions. The subjective visual vertical (SVV) – as a component of the ocular tilt reaction – is a useful psychophysical parameter to measure central compensation for two reasons: first, it deviates in most acute peripheral and central vestibular lesions and, second, it normalizes over time despite persisting vestibular deficits. Objective: To determine the time course and degree of central compensation of central vestibular lesions by measuring the deviation of the SVV and to compare these values with those of peripheral lesions in a retrospective study. Methods: 50 patients with Wallenberg's syndrome (as a model for a central vestibular lesion) and 39 patients with vestibular neuritis (as a model for an isolated peripheral vestibular lesion) were examined. SVV was determined during at least two points of time within the first month after symptom onset. Results: The mean displacement of SVV was 10.6° in Wallenberg's syndrome and 10.5° in vestibular neuritis within the first days after onset of symptoms. SVV deviation within the last days of the observation period was averaged at 4° in the former and 3.1° in the latter group. Wilcoxon's rank sum test for matched pairs revealed a significant decrease of the deviation over time in both groups. Although the regression had an exponential character in both groups, the statistical power of individually fitted regression curves (ANOVA) was too low to perform a statistical comparison. Conclusions: We demonstrated that central compensation of a central vestibular lesion has a degree and time course similar to that of a peripheral vestibular lesion. These data provide the basis for a prospective study, which will determine the SVV and ocular torsion over a period of three months.

Initial evaluation of vertigo

Dizziness is one of the most common reasons patients visit their physicians. Balance control depends on receiving afferent sensory information from several sensory systems: vestibular, optical and proprioceptive. Bioelectric signals, generated by body movements in the semicircular canals and in the otolithic apparatus, are transported via the vestibular nerve to the vestibular nucleus. All four vestibular nuclei, located bilaterally in medial longitudinal fasciculus, are linked with central nervous system structures. These central nervous system structures are involved in maintaining visual stability, spatial orientation and balance control. Nystagmus is a result of afferent signals balance disorders. Nystagmus due to peripheral lesions is conjugate nystagmus, because there is a bilateral central connection. Lesions above the vestibular nuclei induce deficits in synchronization and conjugation of eye movements, thus the nystagmus is dissociated. This paper shows that in peripheral vestibular disorders spontaneous nystagmus is rhythmic, associated, horizontal-rotatory or horizontal, with subjective sensation of dizziness which decreases with time and harmonic signs whose direction coincides with the slow phase of nystagmus and it is associated with mild disorders during pendular stimulation with statistically significant vestibular hypofunction. Spontaneous nystagmus in central vestibular lesions is severe, dissociated, horizontal, rotatory or vertical, without changes related to optical suppression; if vestibular symptoms are present, they are non-harmonic. In central disorders, findings after thermal stimulation are either normal or pathological, with dysrhythmias and inhibition in pendular stimulation. This paper deals with differential diagnosis of vertigo based on anamnesis and clinical examination, as well as objective diagnostic tests.

Central compensation of central vestibular lesions

Central compensation of central vestibular lesions