Atypical neurological manifestations in Wernicke’s encephalopathy due to hyperemesis gravidarum

Divya, M. B.; Kubera, N S; Jha, Nivedita; Jha, Ajay Kumar; Thabah, Molly Mary

doi:10.1080/1028415x.2021.1931781

Cited by 9 publications

(8 citation statements)

References 15 publications

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“…Ironside noted uncertainty that death from severe HG with advancing deterioration would be averted by vitamin B 1 therapy 57 . Similar to findings by Sheehan and Ironside in 1939, incomplete recovery from thiamin administration was evident in our series, with prolonged ataxia, which included wheelchair dependence, psychosis/delirium, and loss of short‐term and long‐term memory 26,31,32,34,36,37 . Whereas there were no maternal fatalities in our series, there were four cases of IUFD and one neonatal demise, a pregnancy wastage rate of 18.5%.…”

Section: Discussionsupporting

confidence: 90%

“…Administering thiamin in insufficient doses, <500 mg of intravenous thiamin three times per day until acute symptoms resolve is considered suboptimal treatment, which continues in current times 38 . In our series of 27 women with HG‐WE, 8 (29.8%) were undertreated with thiamin (24,25,27,28,32: cases 2,3,6; 37). We highlight the role of minerals in thiamin metabolism as critical, and whereas magnesium was assessed in many of these 18 reports, phosphorus was not.…”

Section: Discussionmentioning

confidence: 91%

“…We present our findings, representing 27 women, in Table 1. [20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37] T A B L E 1 Description of pregnant women with HG deteriorating into WE…”

Section: Resultsmentioning

confidence: 99%

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Gestational malnutrition, hyperemesis gravidarum, and Wernicke's encephalopathy: What is missing?

Erick

2022

Nut in Clin Prac

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Hyperemesis gravidarum (HG), or the severe nausea and vomiting of pregnancy, is one of the most dreaded complications of gestation, affecting between 1.5% and 3.0% of pregnant women. From the late 1800s to the mid-1980s, the etiology was frequently cited to have psychological and/or-laterperhaps hormonal origins, which have numbered at least 10. Current research has unearthed a genetic basis for HG that implicates growth differentiation factor 15, insulin-like growth factor binding protein 7, and hormone receptors (namely, glial cell line-derived neurogenic factor family receptor alpha-like and the progesterone receptor). Whatever the origins of this disease, it has caused immeasurable physiological and psychological damage to women, their fetuses, and their families. The psychological trauma includes a high rate of suicidal ideation as well as posttraumatic stress disorder. Whereas the healthcare costs are substantial for the mother with HG, the lifetime costs to the neonate include that which accompanies reduced employment earnings related to cognitive compromise. Another devastating outcome of severe HG can be Wernicke's encephalopathy (WE), which has a high fetal and maternal mortality rate. Our study explored 18 current reports of HG and WE. We highlighted additional presenting features we believe also accompany, and sometimes replace, the classically taught triad components of WE: ataxia, confabulation, and nystagmus. We agree with the conclusion made by Sheehan and Ironside in 1939 that thiamin alone may not reverse WE, and we offer possible explanations. Lastly, we offer suggestions for remediation.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 91%

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Gestational malnutrition, hyperemesis gravidarum, and Wernicke's encephalopathy: What is missing?

Erick

2022

Nut in Clin Prac

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“…This misattribution has long obscured the fact that alcohol abuse usually only provides the context in which thiamine depletion develops, and that alcohol neurotoxicity does not contribute to the development of KS or other residual syndromes in any essential way [ 5 , 8 , 12 ]. In line with this, WE and KS have been reported in cases with non-alcoholic thiamine deficiency, such as bariatric surgery [ 13 ], cancer [ 14 ], anorexia nervosa [ 15 ], or hyperemesis gravidarum [ 16 ]. At present, the most reliable clinical diagnosis of WE is achieved with the Caine criteria.…”

Section: Introductionmentioning

confidence: 73%

Coordination and Cognition in Pure Nutritional Wernicke’s Encephalopathy with Cerebellar Degeneration after COVID-19 Infection: A Unique Case Report

Arts

Dorst

Vos

et al. 2023

JCM

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Background: Alcoholic cerebellar degeneration is a restricted form of cerebellar degeneration, clinically leading to an ataxia of stance and gait and occurring in the context of alcohol misuse in combination with malnutrition and thiamine depletion. However, a similar degeneration may also develop after non-alcoholic malnutrition, but evidence for a lasting ataxia of stance and gait and lasting abnormalities in the cerebellum is lacking in the few patients described with purely nutritional cerebellar degeneration (NCD). Methods: We present a case of a 46-year-old woman who developed NCD and Wernicke’s encephalopathy (WE) due to COVID-19 and protracted vomiting, resulting in thiamine depletion. We present her clinical course over the first 6 months after the diagnosis of NCD and WE, with thorough neuropsychological and neurological examinations, standardized clinical observations, laboratory investigations, and repeated MRIs. Results: We found a persistent ataxia of stance and gait and evidence for an irreversible restricted cerebellar degeneration. However, the initial cognitive impairments resolved. Conclusions: Our study shows that NCD without involvement of alcohol neurotoxicity and with a characteristic ataxia of stance and gait exists and may be irreversible. We did not find any evidence for lasting cognitive abnormalities or a cerebellar cognitive-affective syndrome (CCAS) in this patient.

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“…30 While the classic triad for Wernicke encephalopathy is gait ataxia, ophthalmoplegia, and encephalopathy, the caveat for diagnosis is that with incomplete presentations of the triad, varying degrees of oculomotor dysfunction and atypical manifestations such as a stroke mimic have been frequently reported. 31 32 33 Similarly, while Wernicke encephalopathy typically affects midline structures such as thalamus, mammillary bodies, and periaqueductal gray matter, in addition to the cerebellar hemisphere and superior anterior vermis, 30 34 a wide range of radiographic findings have been reported, including stroke-like cortical T2 hyperintensity or the absence of an overt imaging abnormality. 33 35 36 Given that ataxia associated with thiamine deficiency is treatable, patients with ataxia and risk factors for nutritional deficiency should be treated empirically with high-dose intravenous thiamine to avoid devastating brain hemorrhage, 37 preferably after sending a test of whole blood thiamine level.…”

Section: Nutritional Deficiency Cerebellar Ataxiamentioning

confidence: 99%

Ataxias: Hereditary, Acquired, and Reversible Etiologies

Lin

Kuo

2023

Semin Neurol

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A variety of etiologies can cause cerebellar dysfunction, leading to ataxia symptoms. Therefore, the accurate diagnosis of the cause for cerebellar ataxia can be challenging. A step-wise investigation will reveal underlying causes, including nutritional, toxin, immune-mediated, genetic, and degenerative disorders. Recent advances in genetics have identified new genes for both autosomal dominant and autosomal recessive ataxias, and new therapies are on the horizon for targeting specific biological pathways. New diagnostic criteria for degenerative ataxias have been proposed, specifically for multiple system atrophy, which will have a broad impact on the future clinical research in ataxia. In this article, we aim to provide a review focus on symptoms, laboratory testing, neuroimaging, and genetic testing for the diagnosis of cerebellar ataxia causes, with a special emphasis on recent advances. Strategies for the management of cerebellar ataxia is also discussed.

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Atypical neurological manifestations in Wernicke’s encephalopathy due to hyperemesis gravidarum

Cited by 9 publications

References 15 publications

Gestational malnutrition, hyperemesis gravidarum, and Wernicke's encephalopathy: What is missing?

Gestational malnutrition, hyperemesis gravidarum, and Wernicke's encephalopathy: What is missing?

Coordination and Cognition in Pure Nutritional Wernicke’s Encephalopathy with Cerebellar Degeneration after COVID-19 Infection: A Unique Case Report

Ataxias: Hereditary, Acquired, and Reversible Etiologies

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