Wernicke Encephalopathy—Clinical Pearls

Sinha, Shirshendu; Kataria, Archish; Kolla, Bhanu Prakash; Thusius, Nuria J.; Loukianova, Larissa L.

doi:10.1016/j.mayocp.2019.02.018

Cited by 106 publications

(138 citation statements)

References 20 publications

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“…While the presentation of WE is highly variable, description of the symptom triad is the traditional starting point ( Table 1). Yet the complete triad is only seen in 10-33% of patients, [6][7][8] since the complete triad represents an advanced thiaminedeficient state. 9 An estimated 75-80% of WE cases are misdiagnosed based on postmortem necropsy studies.…”

Section: The Clinical Syndromementioning

confidence: 99%

“…14 Mental changes can range from apathy to more severe involvement including obtundation and, rarely, coma. 8 In approximately 80% of cases, if left untreated, WE transitions into Korsakoff Syndrome (KS), which is characterized by chronic memory impairment, retrograde or anterograde amnesia, confabulation, and mood disturbance such as indifference or mild euphoria. 15…”

Section: Encephalopathymentioning

confidence: 99%

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<p>Neuro-ophthalmic Manifestations of Wernicke Encephalopathy</p>

Isen¹,

Kline²

2020

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Wernicke encephalopathy (WE) is a life-threatening but reversible syndrome resulting from acute thiamine deficiency that is frequently overlooked and underdiagnosed. It is classically characterized by a triad of ocular dysfunction, ataxia, and altered mental status. However, less than 1/3 patients have the complete triad, so it is crucial to have a high index of suspicion. Awareness of the early signs of WE is essential to prevent clinical progression, as patients with the full triad already have a profoundly thiamine-deficient state. This review highlights the neuro-ophthalmic manifestations of WE to guide the clinician in identifying the condition. In addition, we provide an update regarding the clinical characteristics, pathophysiology, neuroimaging and laboratory findings, treatment options, and prognosis of WE.

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Section: The Clinical Syndromementioning

confidence: 99%

Section: Encephalopathymentioning

confidence: 99%

<p>Neuro-ophthalmic Manifestations of Wernicke Encephalopathy</p>

Isen¹,

Kline²

2020

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“…AMS is by far the most common presentation followed by ocular signs and then gait disturbances. Other rarer but known presenting symptoms such as: hypothermia, hypotension, and coma are worth noting [1]. A sequela which is seen in chronic thiamine deficiency is Korsakoff psychosis where there is irreversible, persistent, and severe impairment of working memory [6].…”

Section: Manifestation: History Symptoms and Medical Imagingmentioning

confidence: 99%

“…Wernicke's encephalopathy (WE) is a reversible neuropsychiatric disorder caused by thiamine deficiency. The classic triad of presenting symptoms include ataxia, ophthalmoplegia, and confusion; though other rarer presenting signs can include hypothermia, hypotension, and coma [1]. Classically associated with alcohol use disorder in the Western world, it is easily and often overlooked in nonalcoholic patients.…”

Section: Introductionmentioning

confidence: 99%

A Summertime Stupor

Mauerman

Durojaye

Sridharan

2020

Cureus

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Most commonly seen with alcohol use disorder in the developed world, Wernicke's encephalopathy (WE), a disorder caused by thiamine deficiency can be readily missed in the setting of other predisposing conditions such as malnutrition, the most common cause worldwide. We present a case of a 21-year-old female with sudden progressive decline in her level of alertness and mentation along with severe hypothermia who had clinical features and imaging findings consistent with WE in the setting of pancreatitis and chronic gastritis. WE should be suspected in all patients who present with altered mental status (AMS) and who are at an increased risk of malnutrition despite a normal or high body mass index, so that treatment with thiamine may be initiated and further neurologic sequelae can be averted.

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“…Although rapid response to therapy may be seen in heart failure, the neuropathy may take months to improve . In Wernicke‐Korsakoff syndrome, treatment should quickly improve ocular abnormalities . Gait ataxia improves gradually and often incompletely.…”

Section: Thiamine (Vitamin B1)mentioning

confidence: 99%

Nutritional neuropathies

Gwathmey

Grogan

2019

Muscle and Nerve

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Neuropathies associated with nutritional deficiencies are routinely encountered by the practicing neurologist. Although these neuropathies assume different patterns, most are length‐dependent, sensory axonopathies. Cobalamin deficiency neuropathy is the exception, often presenting with a non–length‐dependent sensory neuropathy. Patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy, whereas vitamin E deficiency is uniquely associated with a spinocerebellar syndrome. In contrast to those nutrients for which deficiencies produce neuropathies, pyridoxine toxicity results in a non–length‐dependent sensory neuronopathy. Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss (such as with dialysis), autoimmune conditions such as pernicious anemia, and with certain drugs that inhibit nutrient absorption. When promptly identified, therapeutic nutrient supplementation may result in stabilization or improvement of these neuropathies.

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Wernicke Encephalopathy—Clinical Pearls

Abstract: Abbreviations and Acronyms: AN = anorexia nervosa; MRI = magnetic resonance imaging; WE = Wernicke encephalopathy

Cited by 106 publications

References 20 publications

<p>Neuro-ophthalmic Manifestations of Wernicke Encephalopathy</p>

<p>Neuro-ophthalmic Manifestations of Wernicke Encephalopathy</p>

A Summertime Stupor

Nutritional neuropathies

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