SESSION TYPE: Miscellaneous Case Report Posters I
PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION: Wernicke’s encephalopathy has historically been associated with chronic alcoholism; however, it can be related to multiple other conditions. A case of thiamine deficiency in a non-alcoholic patient is presented here.
CASE PRESENTATION: A 24 year-old white female patient with a history of depression and morbid obesity presented with complaints of generalized weakness. She had history of recent bariatric surgery. The patient had been complaining of diffuse weakness for more than 3 weeks. She saw her primary care physician who reassured her by saying, “it’s all in your head.” Unfortunately, the patient continued to deteriorate and eventually became unable to ambulate. The patient’s exam was remarkable for ophtalmoplegia, diffuse weakness with areflexia. Her sensation was intact and no tremor was noted. Upon admission, the patient had a lumbar puncture which showed benign cerebrospinal fluid. Magnetic resonance imaging of her brain showed abnormal signal through the caudate nuclei and bilateral basal ganglia in a symmetrical fashion. The patient’s laboratory values including thyroid stimulating hormone, creatine phosphokinase, vitamin B-12 levels, sedimentation rate, antinuclear antibodies and anti-acetylcholine receptor (AChR) antibody all were normal. With concern about Wernicke’s encephalopathy, the patient was started on thiamine 500 mg given intravenously every 8 hours. The next day, the patient’s ophtalmoplegia dramatically improved. Also, her weakness resolved over the next few days.
DISCUSSION: Wernicke’s encephalopathy (WE) is an acute form of thiamine deficiency caused by diminished glucose utilization in the brain. The diagnosis of Wernicke’s encephalopathy is challenging, especially in non-alcoholic patients. It is suspected clinically when patients present with symptoms of encephalopathy, ataxia, nystagmus or other forms of oculomotor dysfunction. However, patients rarely present with these classic symptoms, and a diagnosis of WE should not be discounted if patients do not fit the standard clinical picture. Normal MRI findings should not rule out or delay the treatment of suspected Wernicke’s encephalopathy. The classic finding of mammillary bodies atrophy is not always observed in non-alcoholic WE. Since absorption of thiamine through the gastrointestinal system is limited, patients with suspected WE should be treated with intravenous thiamine.
CONCLUSIONS: Thiamine deficiency remains clinically underdiagnosed. Physicians should remain vigilant for atypical presentation of WE in non-alcoholic patients.
1) The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Thomson A; Alcohol Alcohol 2002 Nov-Dec;37(6):513-21
DISCLOSURE: The following authors have nothing to disclose: Souheil Abdel Nour, Holly Abdel Nour, Jayantilal Mehta, Ryland Byrd, Thomas Roy
No Product/Research Disclosure InformationEast Tennessee State University, Johnson City, TN