Thiamine Deficiency Masquerading As Guillain-Barré Syndrome

Abstract

Thiamine (vitamin B1) deficiency may be associated with serious neurological manifestations, including peripheral neuropathy, paralysis, confusion, paresthesia, pain, dysarthria, and nystagmus. The primary etiology of thiamine deficiency is consumption of a diet deficient in thiamine. In the United States, the most common cause of thiamine deficiency is alcohol use disorder due to the poor dietary intake that is often associated with this diagnosis. Thiamine deficiency also develops at an increased frequency in patients who have had gastric bypass surgery. Other medical conditions less commonly associated with thiamine deficiency include hyperemesis gravidarum, diabetes, and malnutrition outside of alcohol use disorder. Prompt recognition of thiamine deficiency is important since it is readily treatable, and prompt treatment increases the likelihood of favorable clinical outcomes. On the other hand, delayed diagnosis and treatment of severe thiamine deficiency can lead to permanent neurological deficits or may even be fatal. Since clinicians often do not consider thiamine deficiency in patients without a history of alcohol use disorder, this diagnosis is often either delayed or missed altogether. This case series presents four patients with acute neuropathy due to thiamine deficiency (normal range >70-180 nmol/L) and with corresponding neurophysiological and electromyographical data. It highlights the need to consider thiamine deficiency in all patients with acute to subacute lower extremity weakness or numbness.