Vestibular and Ocular Motor Properties in Lateral Medullary Stroke Critically Depend on the Level of the Medullary Lesion (original) (raw)
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Isolated central vestibular syndrome
Annals of the New York Academy of Sciences, 2015
Isolated vestibular syndrome may occur all along the vestibular pathways from the peripheral labyrinth to the brain. By virtue of recent developments in clinical neurotology and neuroimaging, however, diagnosis of isolated central vestibulopathy is increasing. Here, we review five distinct syndromes of isolated central vestibular syndrome from lesions restricted to the vestibular nuclei, the nucleus prepositus hypoglossi, the flocculus, the tonsil, and the nodulus, and introduce a new vestibular syndrome from isolated involvement of the inferior cerebellar peduncle. Decreased responses to head impulses do not exclude a central lesion as a cause of isolated vestibular syndrome. Brain imaging, including diffusion-weighted magnetic resonance imaging (MRI), may be falsely negative during the acute phase in patients with isolated vestibular syndrome because of a stroke. Central signs should be sought carefully in patients with isolated vertigo, even when the patients show the features of...
American Journal of Otolaryngology, 1980
Quantitative analysis of electro-oculographic recordings of eye movement in response to precise visual and vestibular stimuli makes possible the differentiation of three categories of vestibular syndromes due to pathological changes in three different parts of the visual vestibule-ocular reflex arc: (1) decreased vestibule-ocular reflex gain (e.g., decrease in slow component velocity), but normal fast components and visual-vestibular interaction (labyrinth and eighth nerve); (2) normal slow component velocity but abnormal ~ast components to all stimuli (pontine or medullar reticular formation); and (3) normal slow component velocity to vestibule-ocular stimulation but abnormal visual-vestibular interaction as well as normal fast components (visual-motor pathways or cerebellum).
Background and Purpose-Acute vestibular syndrome (AVS) is often due to vestibular neuritis but can result from vertebrobasilar strokes. Misdiagnosis of posterior fossa infarcts in emergency care settings is frequent. Bedside oculomotor findings may reliably identify stroke in AVS, but prospective studies have been lacking. Methods-The authors conducted a prospective, cross-sectional study at an academic hospital. Consecutive patients with AVS (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with 1 stroke risk factor underwent structured examination, including horizontal head impulse test of vestibulo-ocular reflex function, observation of nystagmus in different gaze positions, and prism cross-cover test of ocular alignment. All underwent neuroimaging and admission (generally 72 hours after symptom onset). Strokes were diagnosed by MRI or CT. Peripheral lesions were diagnosed by normal MRI and clinical follow-up. Results-One hundred one high-risk patients with AVS included 25 peripheral and 76 central lesions (69 ischemic strokes, 4 hemorrhages, 3 other). The presence of normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, or skew deviation (vertical ocular misalignment) was 100% sensitive and 96% specific for stroke. Skew was present in 17% and associated with brainstem lesions (4% peripheral, 4% pure cerebellar, 30% brainstem involvement; 2 , P0.003). Skew correctly predicted lateral pontine stroke in 2 of 3 cases in which an abnormal horizontal head impulse test erroneously suggested peripheral localization. Initial MRI diffusion-weighted imaging was falsely negative in 12% (all 48 hours after symptom onset). Conclusions-Skew predicts brainstem involvement in AVS and can identify stroke when an abnormal horizontal head impulse test falsely suggests a peripheral lesion. A 3-step bedside oculomotor examination (HINTS: Head-ImpulseO NystagmusOTest-of-Skew) appears more sensitive for stroke than early MRI in AVS. (Stroke. 2009;40:3504-3510.)
Journal of Neurology, Neurosurgery & Psychiatry, 2005
Background: Spontaneous nystagmus caused by dorsolateral medullary infarction may be of vestibular origin. Objectives: To test if imbalance of the central pathways of the semicircular canals contributes to spontaneous nystagmus in dorsolateral medullary syndrome. Methods: We examined four patients with dorsolateral medullary syndrome and recorded spontaneous nystagmus binocularly at gaze straight ahead with the three-dimensional search coil technique. The median slow phase velocity of the nystagmus was analysed in the light and in the dark, and the normalised velocity axes were compared with the rotation axes as predicted from anatomical data of the semicircular canal. Results: The slow phase rotation axes of all patients aligned best with the rotation axes resulting from stimulation of the contralesional posterior and horizontal semicircular canals. This alignment cannot be explained by pure otolith imbalance. Conclusion: We propose that vestibular imbalance caused by an ipsilesional lesion of the central semicircular canal pathways of the horizontal and anterior semicircular canals largely accounts for spontaneous nystagmus in dorsolateral medullary syndrome.
Isolated vestibular nuclear infarction: report of two cases and review of the literature
Journal of Neurology, 2013
Cerebral infarction presenting with isolated vertigo remains a diagnostic challenge. To define the clinical characteristics of unilateral infarctions restricted to the vestibular nuclei, two patients with isolated unilateral vestibular nuclear infarction had bedside and laboratory evaluation of the ocular motor and vestibular function, including videooculography, bithermal caloric irrigation, the head impulse test (HIT) using magnetic scleral coils, and cervical and ocular vestibular-evoked myogenic potentials (VEMPs). We also reviewed the literature on isolated vertigo from lesions restricted to the vestibular nuclei, and analyzed the clinical features of seven additional patients. Both patients showed spontaneous torsional-horizontal nystagmus that beat away from the lesion side, and direction-changing gaze-evoked nystagmus. Recording of HIT using a magnetic search coil system documented decreased gains of the vestibular-ocular reflex for the horizontal and posterior semicircular canals on both sides, but more for the ipsilesional canals. Bithermal caloric tests showed ipsilesional canal paresis in both patients. Cervical and ocular VEMPs showed decreased or absent responses during stimulation of the ipsilesional ear. Initial MRIs including diffusion-weighted images were normal or equivocal, but follow-up imaging disclosed a circumscribed acute infarction in the area of the vestibular nuclei. Infarctions restricted to the vestibular nuclei may present with isolated vertigo with features of both peripheral and central vestibulopathies. Central signs should be sought even in patients with spontaneous horizontal-torsional nystagmus and positive HIT. In patients with combined peripheral and central vestibulopathy, a vestibular nuclear lesion should be considered especially when hearing is preserved. Keywords Vestibulopathy Á Vestibular nucleus Á Lateral medullary infarction Á Vertigo H.-J. Kim and S.-H. Lee equally contributed to this study.
Journal of Neurology, 2020
Objective: Ocular lateral deviation (OLD) is a conjugate, ipsilesional, horizontal ocular deviation associated with brief (3-5 sec) closing of the eyes, commonly linked to the lateral medullary syndrome (LMS). There is limited information regarding OLD in patients with the acute vestibular syndrome (AVS). In one case series 40 years ago OLD was suggested to be a central sign. Recently, horizontal ocular deviation on imaging (RadOLD) was frequently associated with anterior circulation stroke and horizontal gaze palsy. Similarly, RadOLD has been associated with posterior circulation stroke, e.g., LMS and cerebellar stroke, but without clinical correlation with OLD. Methods: This is a prospective, cross-sectional diagnostic study of 151 acute AVS patients. Patients had spontaneous nystagmus. Horizontal gaze deviation was an exclusion criterion. We noted the effect of brief 3-5 sec eyelid closure on eye position, and then used the HINTS algorithm (the head impulse test, nystagmus characteristics and skew deviation) and RadOLD, to establish a correlation between clinical and radiologic findings
Acute Vestibular Syndrome in Cerebellar Infarction: A Case Report
https://www.ijrrjournal.com/IJRR\_Vol.8\_Issue.9\_Sep2021/IJRR-Abstract06.html, 2021
Introduction: Acute vestibular syndrome (AVS) is characterized by rapid onset of vertigo, nausea and vomiting, and gait unsteadiness in association with head motion intolerance and nystagmus, lasting days to weeks. Although the majority of AVS patients have acute peripheral vestibulopathy, some may also have brainstem or cerebellar strokes. Cerebellar infarctions sometimes only cause vertigo. The Head Impulse Test, skew deviation, and nystagmus testing provide for great sensitivity and specificity in distinguishing between peripheral vestibular impairment and stroke. Case: A 41-year-old male patient suffered from acute-onset vertigo and dizziness about 5 hours before admission, which started when he started doing his morning routine. Patients also feel gait unsteadiness and almost fall to the left side. There was no weakness in extremities, skew face or slurred speech. Patient's neurological status showed the cerebellar examination was positive left dysmetria, left dysdiadochokinesia, the Romberg test open eye fell to the left, normal Head Impulse Test (HIT), with horizontal bidirectional nystagmus and negative skew deviation test. Cerebellum infarction was discovered using computed tomography imaging. After passing through the acute stroke period, patients are offered symptomatic therapy in the form of betahistine, antiplatelet medication, and vestibular rehabilitation planning. On the tenth day after the onset, the patient's symptoms began to improve. Conclusion: Proper diagnosis of acute vestibular syndrome will guide the necessary tests. The HINTS oculomotor test at the bedside can detect acute vestibular stroke.
CONTINUUM: Lifelong Learning in Neurology, 2021
PURPOSE OF REVIEW: This article provides a practical approach to acute vestibular syndrome while highlighting recent research advances. RECENT FINDINGS: Acute vestibular syndrome is defined as sudden-onset, continuous vertigo lasting longer than 24 hours with associated nausea and vomiting, all of which are worsened with head movement. Acute vestibular syndrome is provoked by a variety of central and peripheral causes, the most common of which are vestibular neuritis and acute stroke (posterior circulation). A clinical approach focusing on timing, associated history, and ocular motor findings can improve diagnostic accuracy and is more sensitive and specific than early neuroimaging. Because of the shared neurovascular supply, both peripheral and central vestibular disorders can manifest overlapping signs previously considered solely peripheral or central, including vertical skew, nystagmus, abnormal vestibular ocular reflex, hearing loss, and gait instability. Although acute vestibular syndrome is typically benign, stroke should be considered in every person with acute vestibular syndrome because it can act as a harbinger of stroke or impending cerebellar herniation. Treatment is focused on physical therapy because the evidence is minimal for the long-term use of medication. SUMMARY: The diagnosis of acute vestibular syndrome first requires the elimination of common medical causes for dizziness. Next, underlying pathology must be determined by distinguishing between the most common causes of acute vestibular syndrome: central and peripheral vestibular disorders. Central vestibular disorders are most often the result of ischemic stroke affecting the cerebellar arteries. Peripheral vestibular disorders are assumed to be caused mostly by inflammatory sources, but ischemia of the peripheral vestibular apparatus may be underappreciated. By using the HINTS Plus (Head Impulse test, Nystagmus, Test of Skew with Plus referring to hearing loss assessment) examination in addition to a comprehensive neurologic examination, strokes are unlikely to be missed. For nearly all acute vestibular disorders, vestibular physical therapy contributes to recovery.
Vestibular function in severe bilateral vestibulopathy
Journal of Neurology Neurosurgery and Psychiatry, 2001
Objectives-To assess residual vestibular function in patients with severe bilateral vestibulopathy comparing low frequency sinusoidal rotation with the novel technique of random, high acceleration rotation of the whole body. Methods-Eye movements were recorded by electro-oculography in darkness during passive, whole body sinusoidal yaw rotations at frequencies between 0.05 and 1.6 Hz in four patients who had absent caloric vestibular responses. These were compared with recordings using magnetic search coils during the first 100 ms after onset of whole body yaw rotation at peak accelerations of 2800°/s 2 . OV centre rotations added novel information about otolithic function. Results-Sinusoidal yaw rotations at 0.05 Hz, peak veocity 240°/s yielded minimal responses, with gain (eye velocity/head velocity)<0.02, but gain increased and phase decreased at frequencies between 0.2 and 1.6 Hz in a manner resembling the vestibulo-ocular reflex. By contrast, the patients had profoundly attenuated responses to both centred and eccentric high acceleration transients, representing virtually absent responses to this powerful vestibular stimulus. Conclusion-The analysis of the early ocular response to random, high acceleration rotation of the whole body disclosed a profound deficit of semicircular canal and otolith function in patients for whom higher frequency sinusoidal testing was only modestly abnormal. This suggests that the high frequency responses during sinusoidal rotation were of extravestibular origin. Contributions from the somatosensory or central predictor mechanisms, might account for the generation of these responses. Random, transient rotation is better suited than steady state rotation for quantifying vestibular function in vestibulopathic patients. (J Neurol Neurosurg Psychiatry 2001;71:53-57)