Horizontal, direction changing apogeotropic positional nystagmus (HAPN) is known to be associated with cerebellar lesions [1]. However, the pathophysiologic mechanism of cerebellar HAPN is unknown. We encountered a patient with a metastatic cerebellar tumor who presented with HAPN that disappeared after tumorectomy. Hyperactive vestibular reflexes, indicated by the results of electrophysiologic examinations, might have been the mechanism underlying the HAPN in this patient. A 70-year-old woman with a 2-month history of progressive dizziness and difficulty in walking was admitted to our hospital. She presented with truncal ataxia and HAPN but no other neurologic or neuroophthalmologic abnormalities. Contrast brain MRI revealed a well-enhanced cerebellar tumor. Because chest X-ray and CT showed a left lung tumor suggestive of lung cancer, a cerebellar metastasis was diagnosed. The cerebellar tumor was removed surgically 10 days after the patient’s admission. Pathologic examination of the surgical specimen revealed adenocarcinoma. After the tumorectomy, the HAPN was fully resolved, and the truncal ataxia was improved. The horizontal angular vestibulo-ocular reflex (A-VOR), cervical vestibular-evoked myogenic potential (C-VEMP), and ocular vestibular-evoked myogenic potential (O-VEMP) were evaluated before (when the HAPN was present) and 10 days after tumorectomy (when the HAPN had disappeared). A-VORs were recorded in darkness by means of a video-oculography-basedVORrecording and analysis system (IRN-2, Morita Mfg. Corp., Kyoto, Japan), with the patient seated on a rotating armchair with a headrest [2]. The chair was rotatedmanually in sinusoidal fashion for 20 s (frequency 0.5–0.75 Hz, amplitude 20 ) [2]. VOR gain, i.e., the eye velocity to head velocity ratio, was analyzed. C-VEMP was recorded from the tonically contracting ipsilateral sternocleidomastoid muscle during monaural stimulation with 105-dB clicks or short tone bursts (MEB 2312 testing system, Nihon Kohden, Tokyo, Japan; bandwidth 20–2,000 Hz, 200 averaged signals). Latencies of the first positive wave (p13) and second negative wave (n23) and peak-to-peak p13–n23 amplitude were measured. O-VEMP was recorded from the lower eyelids (inferior oblique muscles) during stimulation with 105 dB clicks or short tone bursts (MEB 2312, Nihon Kohden, Tokyo, Japan; bandwidth 20–2,000 Hz, 200 averaged signals). The patient was instructed to continue looking straight ahead and upward 30 . Because O-VEMP was not adequately elicited by monaural stimulation, binaural sound stimulation was applied. Latencies of the first negative wave (n1) and second positive wave (p1) and peak-to-peak n1–p1 amplitude were measured. Absolute A-VOR gains were reduced in both directions after the tumorectomy (Table 1). Cand O-VEMP amplitudes were also reduced on almost all recordings after tumorectomy (Table 1). Latencies of Cand O-VEMPs did not change. A-VOR is mediated by a semicircular-ocular pathway. C-VEMP reflects the vertical linear vestibulo-ocular reflex Electronic supplementary material The online version of this article (doi:10.1007/s10072-015-2086-4) contains supplementary material, which is available to authorized users.