Howard et al. Journal of Medical Case Reports 2010, 4:409 http://www.jmedicalcasereports.com/content/4/1/409 absent in his lower limbs, and were depressed in his upper limbs, although triceps jerks were easily elicited bilaterally. Discussion The rates of chronic and acute alcohol abuse are increasing, with 4.6% of all ill-health and premature deaths worldwide due to alcohol [3]. For individuals who chronically consume high levels of alcohol, there is often associated liver disease which impairs storage and phosphorylation of thiamine in the liver. This inade- quate liver function and low thiamine level is exagger- ated by poor diet and the increased requirement for thiamine due to the continued alcohol consumption. The lack of thiamine impairs aerobic glucose metabo- lism which in turn causes nervous system dysfunction, given its need for glucose as an energy source [4]. The neuropathy seen in most alcoholics is usually chronic, with insidious onset, is length-dependent, and is predominantly sensory. However, the physician needs to remember that in alcoholics with dry beriberi, neuro- pathy can present as an acute non-length-dependent process mimicking GBS. The acute denervation changes on EMG can be profuse and widespread, mimicking motor neurone disease. The thoraco-lumbar and cranial segments are often involved and this may be deceptive to the unsuspecting mind. Anti-GM1 antibodies have previously been found in the sera of patients with polyneuropathy and either insulin-dependent or non-insulin-dependent diabetes [5]. There are a number of possible explanations, includ- ing the independent occurrence of polyneuropathy and raised anti-GM1 antibody titre in diabetic patients, anti- GM1 antibody as an epiphenomenon associated with motor nerve damage (without direct pathogenecity), and anti-GM1 antibody mediated motor nerve destruction in some patients. Taking into account the temporal profile of our patient’s clinical deterioration and the overall clinical context, it seems unlikely that anti-GM1 anti- body contributed substantially to his rapid deterioration. Whilst a trial of treatment with intravenous immunoglo- bulin was given prior to the result of the vitamin B1 assay being available, we do not consider intravenous immunoglobulin treatment to have modified his clinical course. It is likely that this man’s background history of DM, alcohol abuse and associated nutritional deficiencies all contributed to a multifactorial initial presentation, with dry beriberi as the cause of his subsequent rapid clinical deterioration. A recent case of dry beriberi mimicking GBS [2] has been reported, although hypovitaminosis B1 had not been confirmed in that case. Although thought to be rare, we feel dry beriberi may represent an under- recognized and increasingly common cause of acute Page 3 of 4 polyneuropathy, particularly against a backdrop of increasing alcohol abuse. An increasingly high index of suspicion is likely to be needed especially given that this is a treatable condition. The clinical spectrum of beriberi encompasses dry beriberi with predominant neurological involvement and wet beriberi which mainly affects the cardiovascular sys- tem, with presentations including unexplained conges- tive cardiac failure [6] and lactic acidosis [7]. Bariatric surgery patients represent another group at risk of micronutrient deficiency, including B1 deficiency [8,9]. Thiamine deficiency can also occur in re-feeding syn- drome [10], and in patients on parenteral nutritional support [11]. Conclusion A greater index of suspicion is required for nutritional hypovitaminosis B1 as a cause of rapidly worsening polyneuropathy, particularly in view of rising alcohol abuse in the western world. Confirmation of hypovita- minosis B1 by requesting the assay prior to vitamin replacement ensures accurate diagnosis and appropriate ongoing treatment. Consent Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Acknowledgements Drs Ranjith Ramdass and Caroline Ross also undertook neurophysiological examinations on this patient and contributed to the discussion of differential diagnosis. Author details 1Department of Neurology, Royal Preston Hospital, Sharoe Green Lane, Preston, PR2 9HT, UK. 2Department of Neurophysiology, Royal Preston Hospital, Sharoe Green Lane, Preston, PR2 9HT, UK. Authors’ contributions HE and AH jointly drafted the manuscript, with OK and GL contributing. GL also undertook neurophysiological examination and contributed to the discussion of differential diagnosis. All authors read and approved the manuscript. Competing interests The authors declare that they have no competing interests. Received: 15 February 2010 Accepted: 21 December 2010 Published: 21 December 2010 References 1. Wöhrle JC, Spengos K, Steinke W, Goebel HH, Hennerici M: Alcohol-related acute axonal polyneuropathy: a differential diagnosis of Guillain-Barré syndrome. Arch Neurol 1998, 55(10):1329-1334. 2. Murphy C, Bangash IH, Varma A: Dry beriberi mimicking the Guillain-Barre syndrome. Pract Neurol 2009, 9(4):221-224.