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Reversible Dysphagia and Dementia in a Patient with Bromide Intoxication

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J Neurol (2004) 251 : 1282–1284 DOI 10.1007/s00415-004-0527-8 C. Y. Yu P. K. Yip Y. C. Chang M. J. Chiu

Reversible Dysphagia and

Dementia in a Patient

with Bromide Intoxication

Received: 12 January 2004

Received in revised form: 6 April 2004 Accepted: 6 May 2004

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 medica-tions [1]. However, in Asian coun-tries bromide is still available as an ingredient of many over-the-counter (OTC) medications [2–4]. A variety of neuropsychiatric and dermatological manifestations arise from bromide intoxication but dysphagia has never been re-ported as a key manifestation.

We report a 73-year-old man with bromvalyrelurea intoxication manifesting as reversible dyspha-gia, dementia and pseudo-hyper-chloremia. The patient was admit-ted after a falling accident and a delirious episode 10 days previ-ously. He had noticed a gradual mental deterioration during the past year. He had a history of im-paired recent memory, difficulty in finding his way home and occa-sional 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 dermato-logical manifestations of bromo-derma such as generalized rash or acneiform eruptions. Neurological examination showed poor

atten-tion span with fluctuating con-sciousness, 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 photoparoxys-mal responses. The peak frequency of the EEG power spectrum ob-tained from the artifact free back-ground activity was 2.3 Hz, com-patible 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 oropharyn-geal dysphagia. The patient had prominent abnormal bolus holding

in the oral phase, impaired swal-lowing trigger and mild vallecular and pyriform stasis in the pharyn-geal phase (Fig. 1a). Marked hyper-chloremia (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 over-dose to account for the hyper-chloremia.

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 aceta-minophen, 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 main-tain high daily urine output (3~4 liters). His impaired consciousness, psychotic symptoms, dysarthria, dysphagia and cerebellar ataxia

re-LETTER TO THE EDITORS

JON 1527

Table 1 Blood chemistry data

Hospitalization Day

Mmol/L Day 1 Day 7 Day 21

Sodium (serum) 142 139.6 141.2

Chloridea(serum) 179 134 103

Carbon dioxide (serum) 30.1 21.8 23.2

Anion gapb(serum) –67.1 –16.2 15

Bromidec, d(serum) 12.69±0.24 0.77±0.08

Bromidec(urine) 5.69±0.08 0.61±0.03

ameasured by an ion-selective electrode with a bromide interference ratio of 3.0 bcalculated as sodium – (chloride + carbon dioxide)

cmeasured spectrophoto metrically using the gold chloride method dtoxic level of serum > 12.5 to 18.8 mmol/L

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solved gradually while the serum bromide returned to normal limits (0.77 ± 0.08 mmol/L). The MMSE score improved by 20 points (from 8/30 to 28/30) and the EEG showed diminished slow waves with nor-malization of the background ac-tivities (peak frequency of the EEG power spectrum 8.2 Hz). Follow-up VFSS in about 4 weeks revealed only mild dysphagia (Fig. 1b). He then resumed oral feeding and gained 4 kg of body weight in 1 month.

Bromism refers to a chronic bromide intoxication characterized by neuro-psychiatric and dermato-logical disturbances [5], which usually develop after ingestion of excessive amounts over a 2–4 week or longer period. Bromvalerylurea is an organic bromide with hyp-notic-sedative effects that is still used as an ingredient in many OTC analgesics in Asian countries such as Japan, Thailand and Taiwan. The neuropsychiatric symptoms of bromism usually resolve when bromide is effectively excreted. However, irreversible cerebellar atrophy may occasionally occur [6, 7]. Pseudohyperchloremia is the result of an interaction between bromide and the reagent used to measure serum chloride by the ion-specific method yielding a false

high serum chloride level and thus a decreased or negative anion gap. Colorimetric titration may accu-rately measure the chloride level [8]. Direct measurement of the bromide level may be achieved by using the gold chloride method of spectrometry to confirm the diag-nosis [9]. In general, obvious clini-cal symptoms and signs appear when the serum level is more than 12.5 mmol/L and the condi-tion is probably lethal when level exceeds 37.5 mmol/L [10]. The serum level of our patient was 12.69 ± 0.24 mmol/L, which was almost certainly associated with the clinical toxicity.

To the best of our knowledge, dysphagia caused by bromism has never been reported as a key fea-ture of bromism. The three phases of deglutition, including oral, pha-ryngeal and esophageal phases, require the neural integrity from supranuclear, nuclear to peripheral neuromuscular levels. Clinical ob-servations and cortical mapping using magnetic stimulation [11, 12] demonstrate the role of the inferior frontal gyrus in modulating swal-lowing. Dysphagia is also fre-quently seen in basal ganglia and cerebellar lesions which attest the involvement of these systems in normal deglutition [13]. In terms

of bromism, high cortical as well as cerebellar functions are impaired, and this is probably the basis for the observed dysphagia. In our patient, the gag reflexes were pre-served and the stasis in vallecular and pyriform sinuses disclosed by VFSS was mild, which further sug-gests that brainstem dysfunction did not contribute much to the symptoms.

In conclusion, bromide intoxica-tion should be considered as a differential diagnosis of dysphagia and dementia especially in the face of an unexplained hyperchloremia.

References

1. Bowers GN Jr, Onoroski M (1990) Hy-perchloremia and the incidence of Bromism in 1990. Clin Chem 36: 1399–1403

2. Rothenberg DM, Berns AS, Barkin R, et al. (1990) Bromide intoxication sec-ondary to pyridostigmine bromide therapy. JAMA 263:1121–1122 3. Vasuyattakul S, Lertpattanasuwan N,

Vareesangthip K, et al. (1995) A nega-tive anion gap as a clue to diagnose bromide intoxication. Nephron 69: 311–313

4. Ng YY, Lin WL, Chen TW, et al. (1992) Spurious hyperchloremia and de-creased anion gap in a patient with dextromethorphan bromide. Am J Nephrol 12:268–270

Fig. 1 (A) Video fluoroscopic swallowing study (VFSS) on day 3 of the hospitalization shows markedly abnormal bolus holding, piecemeal swallowing and abnormal oral mucosa coating; (B) Follow-up VFSS at about 4 weeks shows near normal swallowing except mildly abnormal bolus holding

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5. Hanes F, Yates A (1938) An analysis of four hundred instances of chronic bro-mide intoxication. South Med J 31: 667–671

6. Kawakami T, Takiyama Y, Yanaka I, et al. (1998) Dystonic posture and cere-bellar ataxia due to nonsteroidal anti-inflammatory drug abuse. Intern Med 37:788–791

7. Su CF, Wu CC, Yeh JC, et al. (2002) Spu-rious hyperchloremia and cerebellar ataxia: clue to suggest chronic brom-valerylurea intoxication. Clin Nephrol 57:93–94

8. Elin RJ, Robertson EA Johnson E (1981) Bromide interferes with deter-mination of chloride by each of four methods. Clin Chem 27:778–779

9. Gray MG, Moore M (1942) Blood bro-mide determinations: their use and in-terpretation. J Lab Clin Med 27: 680–686

10. Matthew J Ellenhorn (1997) Ellen-horn’s Medical Toxicology, diagnosis and treatment of human poisoning. 2nd

ed., pp 979–980

11. Hamdy S, Aziz Q, Rothwell JC, et al. (1996) The cortical topography of hu-man swallowing musculature in health and disease. Nat Med 2:1217–1224 12. Urban PP, Hopf HC, Connemann B, et

al. (1996) The course of corticohy-poglossal projections in the human brainstem. Brain 119:1031–1038 13. Hughes TAT, Wiles CM (1998)

Neuro-genic dysphagia: the role of the neurol-ogist. J Neurol Neurosurg Psychiatry 64:569–572

C. Y. Yu · P. K. Yip, MD · Ming-Jang Chiu, MD, PhD ()

Department of Neurology

National Taiwan University Hospital 7, Chun-Shan S Rd Taipei, 100, Taiwan Tel.: +886-2/23123456-5339 Fax: +886-2/23418395 E-Mail: mjchiu@ntumc.org mjchiu@ha.mc.ntu.edu.tw Y. C. Chang, MD

Department of Medical Imaging National Taiwan University Hospital College of Medicine

National Taiwan University Taipei, Taiwan

數據

Table 1 Blood chemistry data
Fig. 1 (A) Video fluoroscopic swallowing study (VFSS) on day 3 of the hospitalization shows markedly abnormal bolus holding, piecemeal swallowing and abnormal oral mucosa coating; (B) Follow-up VFSS at about 4 weeks shows near normal swallowing except mild

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