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<p>Wernicke’s encephalopathy (WE), a neurological disorder caused by thiamine deficiency, often presents with atypical symptoms that mimic Guillain-Barré syndrome (GBS) or its Miller Fisher variant (MFS), leading to diagnostic delays. This diagnostic overlap can result in inappropriate treatments and poor outcomes if not promptly recognized. We present two cases where WE was initially misdiagnosed as GBS, highlighting the importance of early thiamine therapy in suspected cases. The first case involved a 37-year-old primigravida with hyperemesis gravidarum, presenting with ascending areflexic quadriparesis, ataxia, nystagmus, and psychiatric symptoms. Initially suspected to be MFS, she received intravenous immunoglobulin (IVIG) without improvement. Magnetic resonance imaging (MRI) revealed T2 hyperintensities in the dorsomedial thalami, mammillary bodies, and periaqueductal grey matter, confirming WE. Thiamine supplementation led to significant recovery. The second case involved a 30-year-old post-caesarean female with a history of antral gastrectomy, presenting with ascending paralysis, sensory ataxia, and ophthalmoplegia. Diagnosed initially as the acute motor sensory axonal neuropathy (AMSAN) variant of GBS, she showed no response to IVIG. MRI findings confirmed WE, and thiamine therapy resulted in gradual neurological improvement. Both cases underscore the diagnostic challenges and the critical need for early recognition of WE in patients with risk factors such as vomiting or malabsorption. These cases illustrate the diagnostic overlap between WE and GBS, emphasizing the importance of considering WE in patients presenting with acute neurological deficits, particularly in non-alcoholic individuals with predisposing factors. Early MRI and thiamine therapy are essential to prevent irreversible neurological damage and improve outcomes. Clinicians should maintain a high index of suspicion for WE in atypical presentations of GBS, especially in the presence of risk factors for thiamine deficiency.</p>

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The Thiamine Deception: When Wernicke’s Encephalopathy Disguises as Guillain-Barré Syndrome and a Brief Review of Thiamine Deficiency–Related Peripheral Neuropathy (TDRPN)—A Case Series

  • 期刊论文

  • 发表日期：

    2025年6月7日

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  • Aneesha Chatterjee,
  • Sibi S.,
  • Jayaram Saibaba,
  • Keerti Priya S. B.,
  • D. K. S. Subrahmanyam

摘要

Wernicke’s encephalopathy (WE), a neurological disorder caused by thiamine deficiency, often presents with atypical symptoms that mimic Guillain-Barré syndrome (GBS) or its Miller Fisher variant (MFS), leading to diagnostic delays. This diagnostic overlap can result in inappropriate treatments and poor outcomes if not promptly recognized. We present two cases where WE was initially misdiagnosed as GBS, highlighting the importance of early thiamine therapy in suspected cases. The first case involved a 37-year-old primigravida with hyperemesis gravidarum, presenting with ascending areflexic quadriparesis, ataxia, nystagmus, and psychiatric symptoms. Initially suspected to be MFS, she received intravenous immunoglobulin (IVIG) without improvement. Magnetic resonance imaging (MRI) revealed T2 hyperintensities in the dorsomedial thalami, mammillary bodies, and periaqueductal grey matter, confirming WE. Thiamine supplementation led to significant recovery. The second case involved a 30-year-old post-caesarean female with a history of antral gastrectomy, presenting with ascending paralysis, sensory ataxia, and ophthalmoplegia. Diagnosed initially as the acute motor sensory axonal neuropathy (AMSAN) variant of GBS, she showed no response to IVIG. MRI findings confirmed WE, and thiamine therapy resulted in gradual neurological improvement. Both cases underscore the diagnostic challenges and the critical need for early recognition of WE in patients with risk factors such as vomiting or malabsorption. These cases illustrate the diagnostic overlap between WE and GBS, emphasizing the importance of considering WE in patients presenting with acute neurological deficits, particularly in non-alcoholic individuals with predisposing factors. Early MRI and thiamine therapy are essential to prevent irreversible neurological damage and improve outcomes. Clinicians should maintain a high index of suspicion for WE in atypical presentations of GBS, especially in the presence of risk factors for thiamine deficiency.