Vision Loss As a Presenting Feature of Wernicke Encephalopathy

Sura, Amol; Curé, Joel K.; Kline, Lanning B.

doi:10.1097/wno.0000000000000771

Cited by 3 publications

(3 citation statements)

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“…35 If it occurs, vision loss is typically severe and bilateral with acuity worse than 20/200 and may lead to loss of light perception. 40,41 Vision loss in WE is often due to optic neuropathy with disc edema or associated retinal hemorrhage. However, a few cases of vision loss have been reported even in patients with normal-appearing discs.…”

Section: Neuro-ophthalmic Findingsmentioning

confidence: 99%

“…6,8 Similarly, when managing cases of suspected WE, the clinician should be aware of refeeding syndrome, which can occur when replenishing nutrition in the chronically malnourished. 41 This typically occurs within four to seven days of refeeding and results in increased glycogen, fat, and protein synthesis. 83 With increased metabolic demand, thiamine and magnesium levels may fall, leading to WE.…”

Section: Treatmentmentioning

confidence: 99%

“…20 The prognosis for visual recovery in WE is also favorable, but there are reports of permanent visual impairment. 35,36,41 Improvement in gait ataxia is common, but in contrast to ophthalmic abnormalities, the recovery is delayed and typically incomplete. 8 Most patients are left with residual gait impairment.…”

Section: Prognosismentioning

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: Neuro-ophthalmic Findingsmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

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

Isen¹,

Kline²

2020

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Reversible Bilateral Vision Loss: An Unusual Presentation of Wernicke-Korsakoff Syndrome

Guagliardo,

Singh,

Thakkar

et al. 2024

Cureus

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Neuro-ophthalmic manifestations of Wernicke encephalopathy (WE) are uncommon and vary from nystagmus, oculomotor palsies, anisocoria, and optic disc edema to vision loss. We describe a case of a 53year-old woman presenting with subacute bilateral painless vision decline, lower-extremities weakness with impaired ambulation, headache, and abdominal pain. Neurological examination was pertinent for confabulation, bilateral decreased visual acuity with an absent blink to threat, absent afferent pupillary defect and fundus abnormalities, and significant allodynia in bilateral lower extremities. Besides elevated inflammatory marker with an erythrocyte sedimentation rate (ESR) of 130 mm/hr, her infectious, autoimmune, paraneoplastic, and neuromyelitis optica work-up was overall unremarkable. Brain MRI showed abnormal fluid-attenuated inversion recovery (FLAIR) signaling in bilateral mammillary bodies and around periaqueductal gray matter concerning WE. Due to concerns of Wernicke-Korsakoff syndrome (WKS), parenteral high-dose thiamine was initiated with significant clinical improvement. The patient was also later found to have a positive anti-myelin oligodendrocyte glycoprotein (MOG) antibody, which was deemed false positive given the atypical phenotype and symptomatic improvement with thiamine supplementation. This case encourages the consideration of vision loss as a manifestation of WKS, especially in patients who have risk factors. Testing serum levels of thiamine is strongly encouraged; however, initiating empiric treatment is advocated for high clinical suspicion due to its reversible nature and minimal risk for side effects.

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