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Show ORIGINAL CONTRIBUTION Room Tilt Illusion Influenced by Head Position Chen Zhao, MD, PhD, Shasha Lu, MD, PhD, Nadja Tajouri, MD, Konstantinos Aliferis, MD, Theodor Landis, MD, and Avinoam B. Safran, MD Abstract: After a low brainstem stroke, a 73- year-old man experienced episodes of 90° tilting of the visual environment in the sagittal plane evoked or terminated by voluntarily changing his head position. The episodes ceased 10 days after the stroke. This provocation by head position supports the idea that pathologic visual- vestibular interaction is at the basis of the room tilt illusion. (/ Neuro- Ophthalmol 2007; 27: 297- 299) R oom tilt illusion is a perception characterized by transient 90° or 180° rotation of the visual surroundings ( 1). This phenomenon can occur in the frontal, sagittal, or horizontal planes and is usually associated with vertebrobasilar ischemia. This perceptual phenomenon may result from impairment of visuospatial inputs and their cortical integration ( 1,2). We are not aware of reports indicating whether and how it can be induced or stopped voluntarily. Herein we report a patient who, after a pontocerebellar ischemic event, experienced episodes of 90° tilting of the visual environment in the sagittal plane. The patient could control the occurrence of illusion by changing the position of his head. CASE REPORT A 73- year- old man with hypertension and atrial fibrillation experienced the sudden onset of dizziness accompanied by diplopia, ataxia, dysarthria, and bilateral hyper-acusis. On the day of hospitalization, physical examination had shown saccadic pursuit, small rapid nystagmus on upgaze, and coarse nystagmus evoked by lateral gaze, as Ophthalmology Clinic ( CZ, SL, NT, KA, ABS) and Neurology Clinic ( TL), Department of Clinical Neurosciences, Geneva University Hospitals, Geneva, Switzerland; Tianjin Eye Hospital ( CZ), Tianjin Medical University, Tianjin, People's Republic of China; and JiangSu Province Hospital ( SL), Nanjing, JiangSu, People's Republic of China. Chen Zhao and Shasha Lu have contributed equally to this study. Address correspondence to Avinoam B. Safran, MD, Ophthalmology Clinic, Department of Clinical Neurosciences, Geneva University Hospitals, 22 rue Alcide Jentzer, 1211 Geneva 14, Switzerland; E- mail: a. b. safran @ hcuge. ch well as ataxia of speech, extremities ( left more than right), and gait. Mental status was normal. Neuro- ophthalmologic examination disclosed a best-corrected visual acuity of 20/ 25 in both eyes and normal visual fields. The patient displayed a slight head tilt to the left and a 2- degree right hypertropia in primary gaze position, upgaze, and downgaze. Subjective visual vertical measurements consistently showed a tilt to the left of 3- 5 degrees with right eye fixating and 6- 7 degrees with left eye fixating, as measured on the screen described by Safran et al ( 3). Left internuclear ophthalmoplegia and left Horner syndrome were also noted. Brain MRI performed 1 day after hospitalization revealed ischemia in cerebellar and pontine areas in the territory of the left superior cerebellar artery ( Fig. 1). Cerebral digital subtraction angiography demonstrated arterial stenoses at several levels, including the left vertebral artery at its junction with the basilar artery and in the initial part of the left superior cerebellar artery ( Fig. 2). The ataxic manifestations regressed gradually. From the 4th to the 10th day after the stroke, the patient described episodes of static misperception of the visual environment. The episodes occurred 3- 4 times per day. During them, he would perceive the visual environment as suddenly tilted 90° backward in the sagittal plane. In his hospital bedroom, when looking at a bed positioned in front of him, he suddenly perceived it as turned vertically. The man lying in that bed now appeared upright, hanging in front of the bed and facing him directly. ( The patient was so amazed by this distorted perception that he did not explore the rest of the room.) This illusion was instantaneous, static, and disappeared completely within approximately 30 seconds. The patient noted that he was able to induce or stop the perceptual phenomenon by changing the position of his head. Thus, he could provoke the illusion by extending his neck or lying horizontally in the bed. In contrast, the illusion disappeared immediately when he closed his eyes, tilted his head forward, and opened his eyes. DISCUSSION The first description of room tilt illusion appeared in 1805 when Bishopp ( 4) reported a complete upside- down visual inversion and considered it a manifestation of hysteria. J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 297 J Neuro- Ophthalmol, Vol. 27, No. 4, 2007 Zhao et al FIG. 1. Diffusion MRI shows restricted diffusion in the left cerebellum and pons, consistent with infarction in the domain of the left superior cerebellar artery ( arrows). Since then, most of the cases of transient misperception of visual surroundings have been reported in association with brainstem ( 1,5), cerebellar ( 6), cortical ( 7), or labyrinthine disorders ( 8). In our patient, there was clinical and imaging evidence of brain stem ischemia. Ophthalmic examination showed persisting symptoms of otolithic dysfunction, manifested by an ocular tilt reaction. Left internuclear ophthalmoplegia and left Horner syndrome were also present. These findings were consistent with the hypothesis that lower brainstem ischemia can generate room tilt illusion ( 9,10). It has been proposed that room tilt illusion is caused by disturbed coordination of visual and vestibular- otolith pathways ( 1,2,11). The integration of visual and otolithic inputs might be influenced either directly at the level of the medulla or indirectly at the site of integration in the posterior parietal cortex ( 1). It has been shown that to create a neural image of visual surroundings, the posterior parietal cortex integrates three kinds of signals: visual information, vestibular information originating from otolithic inputs, and eye- position information ( 12- 14). We should also consider the possibility that signals originating from changes in head position may affect the process of visual-vestibular integration, one coming from neck proprioception and the other from the integration of head velocity signals ( 15,16). In our patient, the illusion could be evoked by abruptly facing upward and stopped by forcibly bowing the head forward. This phenomenon indicates an indirect influence of peripheral vestibular inputs on central perceptual FIG. 2. Digital subtraction cerebral angiography shows stenosis in the left vertebral artery at its junction with the basilar artery ( arrow) and at the basilar- left superior cerebellar artery junction ( arrowhead). pathways ( 8). Thus, our patient provides evidence of a visual- vestibular interactive mechanism participating in the room tilt illusion. 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