Jae-Hwan Choi1, Kee-Yong Cho2, Seung-Yi Cha2, Jae-Deuk Seo3, Min-Ji Kim2, Yu Ri Choi2, Sung-Hee Kim4, Ji-Soo Kim4, Kwang-Dong Choi5. 1. Department of Neurology, Pusan National University School of Medicine, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Republic of Korea. 2. Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine and Biomedical Research Institute, Busan, Republic of Korea. 3. Department of Neurology, Bonhospital, Busan, Republic of Korea. 4. Department of Neurology, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. 5. Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine and Biomedical Research Institute, Busan, Republic of Korea. Electronic address: kdchoi@medimail.co.kr.
Abstract
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.
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.