Left Ponto-Mesencephalic Infarcts Causing an Ocular Tilt Reaction With Ipsilesional Torsional Nystagmus [TN] and Lateral Alternating Skew Deviation [LASD]
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ABSTRACT:
SUBMITTER: Maramattom B
PROVIDER: S-EPMC8061496 | biostudies-literature | 2020 Jun
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND/AIMS: Few studies have investigated normal response characteristics of torsional optokinetic nystagmus (tOKN). The authors have investigated the effect of stimulus velocity and central/peripheral stimulation on tOKN. METHODS: Torsional OKN was elicited using a sinusoidal grating rotating at velocities of 3 degrees /s to 1000 degrees /s in clockwise and anticlockwise directions. To investigate the effect of central stimulation, stimulus size was varied from 2.86 degrees to 50.8 degrees. An artificial scotoma placed over a 50.8 degrees stimulus was varied from 2.86 degrees to 43.2 degrees to investigate peripheral stimulation. Eight subjects participated in each experiment and torsional eye movements were recorded using video-oculography. The mean slow phase velocity (MSPV) and gain were calculated. RESULTS: The maximum gain occurred in response to 8 degrees /s stimulation. The MSPV increased up to a stimulus velocity of 200 degrees /s achieving a maximum of 3 degrees /s in both directions. MSPV was linearly correlated with the log of stimulus velocity. The smallest field size, rotating at 40 degrees /s, evoked 10% of the gain elicited by the largest display. When the most peripheral stimulus was used, the gain was maintained at 50% of the gain evoked when the full display was used. CONCLUSIONS: A wide range of stimulus velocities can elicit tOKN and peripheral field stimulation contributes significantly to its response.
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Project description:ObjectiveSkew deviation results from a dysfunction of the graviceptive pathways in patients with an acute vestibular syndrome (AVS) leading to vertical diplopia due to vertical ocular misalignment. It is considered as a central sign, however, the prevalence of skew and the accuracy of its test is not well known .MethodsWe performed a prospective study from February 2015 until September 2020 of all patients presenting at our emergency department (ED) with signs of AVS. All patients underwent clinical HINTS and video test of skew (vTS) followed by a delayed MRI, which served as a gold standard for vestibular stroke confirmation.ResultsWe assessed 58 healthy subjects, 53 acute unilateral vestibulopathy patients (AUVP) and 24 stroke patients. Skew deviation prevalence was 24% in AUVP and 29% in strokes. For a positive clinical test of skew, the cut-off of vertical misalignment was 3 deg with a very low sensitivity of 15% and specificity of 98.2%. The sensitivity of vTS was 29.2% with a specificity of 75.5%.ConclusionsContrary to prior knowledge, skew deviation proved to be more prevalent in patients with AVS and occurred in every forth patient with AUVP. Large skew deviations (> 3.3 deg), were pointing toward a central lesion. Clinical and video test of skew offered little additional diagnostic value compared to other diagnostic tests such as the head impulse test and nystagmus test. Video test of skew could aid to quantify skew in the ED setting in which neurotological expertise is not always readily available.
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Project description:The linear vestibulo-ocular reflex (LVOR) is mediated primarily by the otolith organs in the inner ear. Skew deviation is a vertical strabismus believed to be caused by imbalance of otolithic projections to ocular motor neurons (disynaptically through the medial longitudinal fasciculus in the brain stem or polysynaptically through the cerebellum). The authors postulated that if skew deviation is indeed caused by damage to these projections, patients with skew deviation would show abnormal LVOR responses.Six patients with skew deviation caused by brain stem or cerebellar lesions and 10 healthy subjects were recruited. All subjects underwent brief, sudden, interaural translations of the head (head heaves) using a head-sled device at an average peak acceleration of 0.42g (range, 0.1-1.1g) while continuously viewing an earth-fixed target monocularly at 15 and 20 cm. LVOR sensitivity (peak rotational eye velocity to peak linear head velocity) and velocity gain (peak actual-to-ideal rotational eye velocities) were calculated for the responses within the first 100 ms after onset of head movements.LVOR sensitivities and velocity gains in patients were decreased by 56% to 62% in both eyes compared with healthy subjects. This binocular reduction in LVOR responses was asymmetric--the magnitude of reduction differed between eyes by 37% to 143% for sensitivities and by 36% to 94% for velocity gains. There were no differences in response between right and left heaves.The binocular, asymmetric reduction in LVOR sensitivity and velocity gain provides support that imbalance in the otolith-ocular pathway is a mechanism of skew deviation.
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Project description:A 16-year-old boy with rotatory positional vertigo and nausea, particularly when lying down, visited our clinic. Initially, we observed vertical/torsional (downward/leftward) nystagmus in the supine position, and it did not diminish. In the sitting position, nystagmus was not provoked. Neurological examinations were normal. We speculated that persistent torsional down-beating nystagmus was caused by the light cupula of the posterior semicircular canal. This case provides novel insights into the light cupula pathophysiology.
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Project description:Evaluating the patient with acute constant vertigo or diplopia can be a daunting task for clinicians, who recognize that such symptoms can be the manifestation of potentially devastating disorders like stroke but may be uncomfortable eliciting and interpreting the key symptoms and subtle signs that distinguish dangerous from benign causes. We present a novel and highly instructive case of a patient with acute vertigo and binocular diplopia from a large skew deviation due to vestibular neuritis. As the case unfolds, text and video commentary guide the clinician through the important elements of the history, bedside examination, and laboratory evaluation necessary for accurate diagnosis in the acute vestibular syndrome. We demonstrate how to interpret nystagmus and properly perform the head impulse test and test of skew deviation and discuss the pitfalls of overreliance on imaging when evaluating patients with acute vertigo.
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