Wernicke’s Encephalopathy: An Underrecognized and Reversible Cause of Confusional State in Cancer Patients

Kuo, Sheng‐Han; Debnam, J. Mathew; Fuller, Gregory N.; Groot, John de

doi:10.1159/000174951

Cited by 60 publications

(39 citation statements)

References 65 publications

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“…In non-alcoholic patients, the major conditions associated are AIDS, malignancies, hyperemesis gravidarum, surgery (particularly surgical patients who underwent gastric bypass), prolonged total parenteral nutrition and iatrogenic glucose loading in any predisposed patient [13,14]. The recommended dose of thiamine (in an average and healthy adult) is 0.5 mg/1000 kcal consumed or 1.4 mg/die, and, in patients receiving a strict thiamine-free diet, 2-3 weeks are needed to determine a depletion [12,[15][16][17][18]. Furthermore, WE seems to appear more quickly when TPN is administered in hypoalbuminemic patients [13].…”

Section: Discussionmentioning

confidence: 99%

“…Clinicians should consider WE in the differential diagnosis of oncology and haematology patients affected by malignancies who develop neurological symptoms while in remission after intensive chemotherapy, especially if their nutrition is unbalanced. Nevertheless, this syndrome continues to be unrecognised and misunderstood [17]. Even if neuroimaging can have a role of confirmation showing lesions and signal alterations in typical sites, the diagnosis remains clinical.…”

Section: Discussionmentioning

confidence: 99%

“…Laboratory analysis such as blood thiamine concentration and measurement of red blood cell transketolase activity are limited by a lack of sensitivity and specificity. No specific diagnostic abnormalities have been recognized in cerebrospinal fluid, electroencephalogram and evoked potentials [17]. Moreover, rarely the whole triad (altered mental status, ophthalmoplegia and gait ataxia) occurs in the same patient and occasionally arises simultaneously.…”

Section: Discussionmentioning

confidence: 99%

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Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Becilli¹,

Pagano²,

Mallio³

et al. 2017

J Blood Lymph

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Wernicke-Korsackoff Syndrome is a potentially fatal neurological complication caused by a deficiency of thiamine. The clinical diagnosis is a challenge and the syndrome is frequently misdiagnosed. In this paper we describe the case of a young man affected by T-ALL and ileotyphlitis who developed Wernicke's Encephalopathy after a month of total parenteral nutrition. Neurological symptomatology, consisting of confusion, nystagmus on lateral gaze, impairment of consciousness state, prosopagnosia and weakness in the four limbs, appeared progressively. An MRI of brain permitted to confirm the diagnosis and high-dose thiamine reintegrating therapy was started obtaining complete resolution of the syndrome.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Becilli¹,

Pagano²,

Mallio³

et al. 2017

J Blood Lymph

View full text Add to dashboard Cite

show abstract

“…His brain MRI was unremarkable, and it did not show typical signs of WE, such as T2 hyperintensity lesions over mammillary bodies, dorsomedial thalami, tectal plate, or periaqueductal area. 2 His dopamine transporters scan revealed decreased uptake in bilateral striatum and his bradykinesia and rigidity responded to levodopa, suggesting levodopa-responsive parkinsonism.…”

Section: Sectionmentioning

confidence: 99%

Clinical Reasoning: A 58-year-old man with progressive ptosis and walking difficulty

Kuo

Tanji

et al. 2017

Neurology

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A 58-year-old man developed progressive walking difficulty over 10 years. He had normal development and an unremarkable birth history. At age 30, he developed bilateral drooping eyelids with double vision. At age 48, he developed progressive gait unsteadiness, slurred speech, and swallowing difficulty. At age 55, he needed to walk with a cane. He did not have seizures, hearing loss, or memory impairment. He did not have any history of alcohol abuse or exposures to anticonvulsants. His mother has congenital cardiac disease and diabetes mellitus, and his sister has had epilepsy since childhood. His daughter is healthy.On examination, the patient had left exotropia and bilateral ptosis without fatigability. His pupillary reflex to light was normal. He had partial horizontal gaze palsy and lack of upward gaze, which was not overcome by vestibulo-ocular reflex. His saccadic eye movements were slow without nystagmus or square wave jerks. He had scanning speech. He had normal muscle power but decreased vibratory sensation and proprioception in his legs, and his deep tendon reflexes were absent. He had mild bradykinesia and arm rigidity without rest tremor. He had mild dysmetria in bilateral finger-nose-finger, finger chase, and heel-shin slide examinations and he had impaired rapid alternating movements. He had wide-base gait with variable stride length but good heel strike, and he could not perform tandem gait (video at Neurology.org).

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“…1 Other lesion sites, including the frontal cortex, lentiform nucleus, cerebellar cortex, and superior vermis of the cerebellum, were also reported in a study retrospectively reviewing autopsy-proven WE. 2 Because the sensitivity of head CT and brain MRI in diagnosing WE is only approximately 10% and 50%, respectively, 2 negative or atypical neuroimaging findings should not exclude the diagnosis of WE.…”

Section: Sectionmentioning

confidence: 99%

Clinical Reasoning: A 61-year-old man with conjugate gaze deviation, hemiparesis, and asymmetric reflexes

et al. 2017

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A 61-year-old man with a history of alcoholic cirrhosis was transferred from an outside hospital for spontaneous bacterial peritonitis, septic shock, and respiratory failure after intubation. The patient was initially on sedation; however, more than 48 hours after the sedative was discontinued, his mental status remained depressed and he also developed new onset of conjugate rightward gaze deviation. On neurologic examination, the patient was unresponsive to verbal stimuli and sternal rub. He could not follow any command, including closing or opening eyes and squeezing hands. He had remarkable conjugate, forced eye deviation that could not be corrected to cross the midline using the vestibulo-ocular reflex. Corneal and gag reflexes were preserved. He blinked to visual threat less on the left side, had no clear facial asymmetry, and withdrew on his right arm and knees but had a flaccid left arm. His reflexes were brisker on the left biceps and brachioradialis, and the other deep tendon reflexes were absent. His plantar reflex was upgoing on the left side and downgoing on the right side. CT of the head had no significant findings.

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Wernicke’s Encephalopathy: An Underrecognized and Reversible Cause of Confusional State in Cancer Patients

Cited by 60 publications

References 65 publications

Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Wernicke’s Encephalopathy in A Young Adult Affected by T Cell Acute Lymphoblastic Leukemia and Ileotiphlytis with Review of the Literature

Clinical Reasoning: A 58-year-old man with progressive ptosis and walking difficulty

Clinical Reasoning: A 61-year-old man with conjugate gaze deviation, hemiparesis, and asymmetric reflexes

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