Blackwell Science, LtdOxford, UKPCNPsychiatry and Clinical Neurosciences1323-13162004 Blackwell Science Pty LtdJune 2004583338339CorrespondenceLetter to the EditorH-Y. Tsai et al.
Psychiatry and Clinical Neurosciences (2004), 58, 338–339
Letter to the Editor Starvation-induced Wernicke’s encephalopathy in schizophrenia Wernicke’s encephalopathy (WE) is an acute brain disease resulting from thiamine deficiency. Although one of the first reported cases occurred in a non-alcoholic patient who developed the disease, WE was subsequently regarded as a strictly alcohol-associated condition.1 There is a risk that it may be overlooked when prolonged malnutrition is associated with other psychiatric conditions not involving alcohol.2 We report a non-alcoholic schizophrenic patient who developed WE due to his hallucinatory behavior. A 41-year-old male patient made moderate grades until his high school graduation. He had few friends and was introverted. He gradually became hostile at the age of 30. He told his family that he was persecuted and monitored. His auditory hallucinations consisted of the voices of his friends. He had no history of substance or alcohol abuse and was diagnosed as having schizophrenia with irregular medication. The patient lived alone and was jobless. At 41 years of age, he told his older brother that some voices asked him to stop eating. He was brought to a general hospital because of dysarthria and general weakness after 48 days of starvation. Brain magnetic resonance imaging (MRI) showed multiple white matter change. He was transferred to National Cheng Kung University Hospital in Taiwan due to general tremors, truncal ataxia, vertical nystagmus, and shortterm memory impairment, which was discovered only after oral and parenteral nutrition for 10 days. The patient was immediately treated for Wernicke’s encephalopathy with thiamine 500 mg i.v. daily. On the following days, the patient was able to recall more and more of the events that happened before his starvation although he still could not describe in detail the voice that told him to stop eating, and what happened during his hospitalization. He could sit up by himself and had improvement in his articulation. He also took risperidone 1.5 mg everyday for the auditory hallucination. There was incomplete recovery in terms of his shortterm memory, nystagmus, and ataxia. He has lived dependently in a nursing home during the subsequent 6 months. Alcohol interferes with the active gastrointestinal transport of thiamine. For many years, WE was thought
to be associated with chronic alcoholism.3 However, the only prerequisite for the development of WE is a poor nutritional state. Wernicke’s encephalopathy may also be seen in association with rapid carbohydrate loading in the present marginal thiamine stores. This happens after nasogastric, but more often after intravenous, carbohydrate application.4 Several reasons can be found to explain the similar pathologic findings observed in schizophrenia. One possibility is that certain characteristics such as poor self-care, housing instability, and homelessness predispose patients to poor dietary habits.5 Another possibility may be the increased prevalence of alcoholism among schizophrenia patients.6 Also, some evidence shows that WE occurs more often in patients with schizophrenia.7 Furthermore, disturbance of carbohydrate metabolism may be peculiar to the schizophrenic process itself. Henneman et al. found an abnormal accumulation of lactic acid in both alcoholic and schizophrenic patients.8 Casanova described the autopsy of a schizophrenic patient who did not have a history of malabsorption or alcoholism, and who had been well taken care of by her family. The autopsy showed a similar pathology to WE.7 In the present case, symptoms started after starvation for 48 days and before the nutritional supply was initiated in the hospital. The patient may have been neglecting his physical health and regular food intake due to his psychotic symptoms. It is likely that thiamine deficiency was caused by a combination of several factors, such as a chronic state of malnutrition, acute starvation, infusion of glucose solutions, and schizophrenia itself. and 6 months later, he lived dependently in a nursing home. The prevention of WE is dependent on adequate thiamine supplementation. A poor nutritional state often occurs in the severely psychotic patient, such that clinicians must maintain a high index of suspicion, even when there is no previous history of alcohol abuse.
REFERENCES 1. Zubaran C, Fernandes JG, Rodnight R. Wernicke– Korsakoff syndrome. Postgrad. Med. J. 1997; 73: 27–31. 2. Lindboe CF, Loberg EM. Wernicke’s encephalopathy in non-alcoholics. An autopsy study. J. Neurol. Sci. 1989; 90: 125–129. 3. Hoyumpa AM Jr,, Nichols S, Henderson GI, Schenker S. Intestinal thiamin transport: effect of chronic ethanol administration in rats. Am. J. Clin. Nutr. 1978; 31: 938– 945. 4. Reuler JB, Girard DE, Cooney TG. Current concepts. Wernicke’s encephalopathy. N. Engl. J. Med. 1985; 312: 1035–1039.
Letter to the Editor
5. Torvik A. Topographic distribution and severity of brain lesions in Wernicke’s encephalopathy. Clin. Neuropathol. 1987; 6: 25–29. 6. Drake RE, Osher FC, Noordsy DL, Hurlbut SC, Teague GB, Beaudett MS. Diagnosis of alcohol use disorders in schizophrenia. Schizophr. Bull. 1990; 16: 57–67. 7. Casanova MF. Wernicke’s disease and schizophrenia: a case report and review of the literature. Int. J. Psychiatry Med. 1996; 26: 319–328. 8. Henneman DHAM, Goncz RM, Alexander L. Carbohydrate metabolism in brain disease. II. Glucose metabolism in schizophrenic, manic-depressive and involutional psychoses. Arch. Intern. Med. 1954; 94: 402–416.
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HSIANG-YI TSAI, md TZUNG LIEH YEH, md SHEEI-MEEI WANG, md PO SEE CHEN, md YEN KUANG YANG, md Department of Psychiatry, College of Medicine, National Cheng Kung University and Hospital, Taiwan Correspondence address: Dr Hsiang-Yi Tsai, Department of Psychiatry, National Cheng Kung University Hospital, 138 Sheng Li Road, Tainan 70428, Taiwan. Email:
[email protected] Received 1 September 2003; accepted 12 October 2003.
