LAUSR

Positional vertigo and nystagmus may occur in association with central as well as peripheral vestibular lesions. Differentiation of central from benign paroxysmal positional vertigo (BPPV) is important due to its potentially grave underlying pathology in central positional nystagmus (CPN) [1, 2]. Herein, we report a patient with apogeotropic CPN due to tuberculous granuloma involving the cerebellar nodulus who had been misdiagnosed as having BPPV initially even with brain MRIs twice and showed a progression into severe imbalance over the following years. This report emphasizes the importance of scrutinized evaluation of the brain using gadolinium-enhanced MRIs in patients with a suspicion of CPN. A 72-year-old man had worsening vertigo and unsteadiness for about 2 years. Initially, the patient was diagnosed as apogeotropic horizontal canal BPPV (HC-BPPV) based on the observed positional nystagmus. Since the positional nystagmus did not respond to repeated canalith-repositioning maneuvers (CRMs), he took brain MRIs without gadolinium-enhancement twice, both reported as normal (Fig. 1a). At presentation to our dizziness center, the patient showed left beating spontaneous nystagmus only without visual fixation (Fig. 1d). During straight head hanging, he showed transient downbeat nystagmus along with the preexisting left beating nystagmus. He showed perverted head-shakingnystagmus (pHSN). Apogeotropic nystagmus was induced during supine roll test, and the left beating nystagmus in the rightward head-turned position was greater than the right beating apogeotropic nystagmus (Fig. 1e). The apogeotropic nystagmus had no latency, peaked initially, and lasted more than one minute. Repeated CRMs for left apogeotropic HCBPPV were in vain without fatigability of the nystagmus. He could not walk without a cane. Findings of other neurological examination were normal. With a suspicion of CPN, we reviewed his previous MRIs and found a suspicious lesion involving the area of nodulus. Repeated brain MRIs with gadolinium-enhancement confirmed a ring-enhancing lesion involving the nodulus with an increased cerebral blood volume (Fig. 1b, c). Whole body and brain positron emission tomography (PET) revealed multiple hypermetabolic nodules in the right lung. Chest CT and bronchoscopy finally confirmed pulmonary tuberculosis. With a suspicion of tuberculous granuloma involving the lung and brain, the patient was placed on anti-tuberculous medications for 1 year. Follow-up MRIs documented a gradual resolution of the brain lesions. He also showed a marked improvement of gait ataxia, and became able to walk unaided. Even with the initial suspicion of CPN based on refractoriness to repeated CRMs, improper protocols of repeated brain MRIs without a gadolinium-enhancement delayed the diagnosis in our patient. Central positional nystagmus may be paroxysmal or persistent. Paroxysmal forms of CPN are ascribed to enhanced responses of the vestibular afferents during positioning due to lesions involving the nodulus and uvula [3]. In * Ji-Soo Kim [email protected]