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Objective: To evaluate how often the positive sign of HINTS (Head-Impulse, Gaze Evoked Nystagmus, Test of Skew) appears in patients with acute peripheral vestibular lesion, HINTS findings were quantitatively measured and analyzed in patients with peripheral vestibulopathy accompanying spontaneous nystagmus.Methods: HINTS was evaluated in 14 vertigo patients with spontaneous nystagmus. Horizontal vestibulo-ocular reflex (VOR) gain was measured using the video head impulse test (vHIT). To evaluate gaze-evoked nystagmus (GEN), slow-phase velocities at different points of lateral gaze were measured and plotted, then the slope and its inverse value, the neural integrator time constant, were calculated. Skew deviation was tested using anaglyph filters to simulate the alternate cover test, and the degree and latency of vertical eyeball deviation were measured. The ABCD2 score was calculated to evaluate the risk of stroke.Results: Among 13 patients of peripheral vestibulopathy, 7 showed positive signs in HINTS (normal vHIT: 5, direction-changing GEN: 0, skew deviation: 3). One patient with a cerebellopontine angle tumor presented with both a peripheral and central pattern and showed positive HINTS findings (presence of direction-changing GEN). The mean VOR gain of patients with abnormal vHIT was 0.58±0.29 and 1.10±0.11 in the affected and contralateral side, respectively, while those in patients with normal vHIT were 1.04±0.21 and 1.13±0.12, respectively. The neural integrator time constant calculated from the mean slope of horizontal slow-phase velocity according to horizontal eye position was 42.9 s. The mean vertical eyeball deviation of patients with positive skew was 2.14±1.18° while uncovering the eye on the affected side, and -1.97±1.59° while uncovering the eye on the unaffected side. The median ABCD2 score of 14 patients was 2 (range, 1-3).Conclusions: HINTS findings were objectively measured in vertigo patients with spontaneous nystagmus. Although positive findings of HINTS have been recognized as a central sign, 54% (7/13) of cases with peripheral vestibulopathy showed positive HINTS signs. HINTS results should be interpreted carefully considering that a substantial proportion of peripheral vestibulopathy shows a positive HINTS sign. [ABSTRACT FROM AUTHOR]

Objective To investigate the patterns and mechanisms of audiovestibular impairments associated with intracranial hypotension. Methods We had consecutively recruited 16 patients with intracranial hypotension at the Neurology Center of Pusan National University Hospital for two years. Spontaneous, gaze-evoked, and positional nystagmus were recorded using 3D video-oculography in all patients, and the majority of them also had pure tone audiometry and bithermal caloric tests. Results Of the 16 patients, five (31.3%) reported neuro-otological symptoms along with the orthostatic headache while laboratory evaluation demonstrated audiovestibular impairments in ten (62.5%). Oculographic analyses documented spontaneous and/or positional nystagmus in six patients (37.5%) including weak spontaneous vertical nystagmus with positional modulation (n = 4) and pure positional nystagmus (n = 2). One patient presented with recurrent spontaneous vertigo and tinnitus mimicking Meniere's disease, and showed unidirectional horizontal and torsional nystagmus with normal head impulse tests during the attacks. Bithermal caloric tests were normal in all nine patients tested. Audiometry showed unilateral (n = 6) or bilateral (n = 1) sensorineural hearing loss in seven (53.8%) of the 13 patients tested. Conclusions Intracranial hypotension frequently induces audiovestibular impairments. In addition to endolymphatic hydrops and irritation of the vestibulocochlear nerve, compression or traction of the brainstem or cerebellum due to loss of CSF buoyancy may be considered as a mechanism of frequent spontaneous or positional vertical nystagmus in patients with intracranial hypotension. [ABSTRACT FROM AUTHOR]

Abstract: A 51-year-old man developed sudden vertigo, right hearing loss and dysphagia. Examination revealed right Horner syndrome, spontaneous torsional-horizontal nystagmus, right central type facial palsy, dysarthria, reduced soft palate elevation without gag reflex, left hypesthesia, right dysmetria and imbalance. Audiometry and bithermal caloric tests documented right sensorineural hearing loss and canal paresis. Brain MRI and cerebral angiography documented right lateral medullary infarction from vertebral artery dissection, without involvement of other parts of the brainstem supplied by the anterior inferior cerebellar artery (AICA). This case suggests artery-to-artery embolism as a possible mechanism of isolated vertigo or hearing loss from labyrinthine infarction. [Copyright &y& Elsevier]

Abstract: Although several papers have been published on perverted head shaking nystagmus (PHSN) associated with focal brainstem or cerebellar lesion, there are no reports of a focal pontine infarct that causes PHSN. We report a patient with focal pontine infarction who presented with sustained dizziness, limb dysmetria on the left extremity, decreased sensations to position and vibration of the left extremity, and gait imbalance. Only vestibular abnormality was downbeat nystagmus after vigorous head shakings. The maximum slow phase velocity of PHSN was 26°/s, and its duration was about 20s. This is the first report of PHSN associated with focal pontine infarction. Crossed ventral tegmental tract and velocity storage mechanism of vestibulocerebellum might be related on PHSN in this case. [ABSTRACT FROM AUTHOR]