Sirs: Bromide intoxication is nowadays rarely seen in Western society because its medical use was to a large extent replaced by much safer and more effective medications [1]. However, in Asian countries bromide is still available as an ingredient of many over-thecounter (OTC) medications [2–4]. A variety of neuropsychiatric and dermatological manifestations arise from bromide intoxication but dysphagia has never been reported as a key manifestation. We report a 73-year-old man with bromvalyrelurea intoxication manifesting as reversible dysphagia, dementia and pseudo-hyperchloremia. The patient was admitted after a falling accident and a delirious episode 10 days previously. He had noticed a gradual mental deterioration during the past year. He had a history of impaired recent memory, difficulty in finding his way home and occasional incoherent speech. He had become partially dependent for activities of daily living for 6 months. During the same period, dysarthria and dysphagia were also noticed, and he lost about 15 kg of his body weight. On examination, the patient did not have dermatological manifestations of bromoderma such as generalized rash or acneiform eruptions. Neurological examination showed poor attention span with fluctuating consciousness, dysarthria with staccato speech and dysphagia, particularly choking on liquids. Bilateral gag reflexes were preserved. Both limb and trunk ataxia with a wide-based gait were noted. He scored 8/30 on the Mini Mental State Examination (MMSE). No weakness, rigidity or abnormal reflexes were detected. He was given nasogastric tube feeding soon after the admission. During the hospitalization, he also had psychotic symptoms with visual and auditory hallucinations and persecutory delusions so that a low dose quetiapine 12.5 mg per day was given. Brain computed tomography was unremarkable. An electroencephalogram (EEG) on the day of admission showed nearly continuous slow waves with intermittent generalized delta waves and positive photoparoxysmal responses. The peak frequency of the EEG power spectrum obtained from the artifact free background activity was 2.3 Hz, compatible with a moderate to severe diffuse cortical dysfunction. The findings of video fluoroscopic swallowing study (VFSS), that was recorded after swallowing 5 ml barium of various consistencies, disclosed a moderate oropharyngeal dysphagia. The patient had prominent abnormal bolus holding in the oral phase, impaired swallowing trigger and mild vallecular and pyriform stasis in the pharyngeal phase (Fig. 1a). Marked hyperchloremia (179 mmol/L) with a significant negative anion gap (–67.1 mmol/L) was found in his biochemistry studies, but there was no evidence of hyperlipidemia, multiple myeloma or lithium overdose to account for the hyperchloremia. Reviewed his drug history, we found that he habitually used an OTC analgesic, the Ming-Ton Pain Killer, for more than a decade. Each gram of the analgesic consists of 200 mg bromvalerylurea, 350 mg ethoxybenzamide, 200 mg acetaminophen, and 50 mg caffeine anhydrous. He had taken up to 15 packs a day (bromvalerylurea 3 g/day) in the past six months in order to relieve his intractable chronic headache. His bromide levels were 12.69 ± 0.24 mmol/L in serum and 5.69 ± 0.08 mmol/L in urine on the admission day (Table 1). Forced diuresis was achieved with intravenous saline and intermittent boluses of furosemide (20 mg/ampoule). These were administered to maintain high daily urine output (3~4 liters). His impaired consciousness, psychotic symptoms, dysarthria, dysphagia and cerebellar ataxia reLETTER TO THE EDITORS