Abstract

Stroke presenting with acute vestibular syndrome remains a diagnostic challenge. It could be possible to diagnose the hyperacute/acute stroke with an introduction of brain imaging such as diffusion-weighted images. In this scenario, however, the importance of neurological examination has been underestimated in clinical field, especially in acute vestibular syndrome not accompanied by focal neurological deficits. Herein, we present a pontine infarction presenting with acute vestibular syndrome showing negative finding on initial diffusion-weighted image and try to emphasize the importance of neurotological examination in managing the patients with isolated vertigo. An 84-year-old man presented with acute vertigo, imbalance, tinnitus in the left ear, and motion intolerance of 2 h duration. Intermittent spontaneous dizziness and visual blurring for several minutes preceded this acute vestibular event by about 20 days. He reported no history of ear disease or ear symptoms. Past medical history included hypertension. His vital signs were stable, except for high blood pressure (171/99). A spontaneous right, upward, clockwise beat was noted, which increased without fixation (Fig. 1a). This nystagmus increased at the rightward gaze, which was converted to a leftward beat at the opposite gaze. The nystagmus was not increased by any induced maneuver, such as vibration or head shaking. A prominent catch-up saccade was noted during the leftward horizontal head impulse test. The patient veered leftward and could not walk in tandem. However, the diffusionweighted image (DWI)s taken 4 h after symptom onset were normal (Fig. 1b). Severe stenosis of the basilar artery was noted (Fig. 1c). Pure tone audiometry showed a linear decrement in the left ear at 50 dB. There was 78 % canal paresis in the left ear. In our patient, rightward horizontotorsional nystagmus with a leftward positive head impulse test suggested left peripheral vestibulopathy, whereas there were also characteristics of central vestibulopathy, including gaze-evoked nystagmus, no increment in spontaneous nystagmus induced by maneuvers, and a strong tendency to veer leftward. Although the patient was admitted to the stroke intensive-care unit and treated with an antiplatelet agent and intravenous hydration, the patient’s symptoms and sign did not improve. A follow-up DWI showed high signal intensity in the vestibular nerve root entry zone of the pons (Fig. 1d). Our patient had normal brain DWIs at the time of his isolated audiovestibular loss, but subsequently displayed acute infarct in the anterior inferior cerebellar artery (AICA) territory on follow-up brain MRI when his imbalance continued for 4 days. This case supports the proposition that labyrinthine infarction may be a warning sign of impending pontocerebellar infarction in the AICA territory [1]. Our patient also demonstrates that bedside eye movement findings (such normal head impulse test, skew deviation, and direction-changing nystagmus; ‘‘HINTS’’) can differentiate central from peripheral causes of acute vestibular syndrome (AVS), even outperforming early DWIs [2–5]. Therefore, it is helpful for clinicians to keep S.-H. Jeong (&) S. Kim H. J. Song H. Jo Department of Neurology, Chungnam National University Hospital, 640, Daesa–dong, Joong-ku, Daejeon 301-721, Korea e-mail: mseaj@hanmail.net

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