• Journal of Yeungnam Medical Science
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• v.21 no.1
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• pp.91-95
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• 2004

Wernicke's encephalopathy is an acute-onset illness characterized by mental confusion, ataxia and ophthalmoplegia due to a thiamine deficiency. Immediate administration of thiamine prevents progression of the disease and reverses brain lesions. We have experienced a case of Wernicke's encephalopathy associated with hyperemesis gravidarum. As Wernicke's encephalopathy is mostly associated with chronic alcoholism, the possibility of Wernicke's encephalopathy may be ignored in young women. We emphasize the need for thiamine supplementation in the patient requiring intravenous alimentation such as hyperemesis gravidarum.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.27-31
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• 2014

Thiamine deficiency can cause peripheral polyneuropathy and Wernicke's encephalopathy. Wernicke's encephalopathy is characterized by ataxia, ophthalmoplegia, nystagmus, and confusion, and typically presents acute and rapidly progressive course, whereas peripheral neuropathy associated with thiamine deficiency manifests chronic and slowly progressive one. However, acute and rapidly progressive axonal polyneuropathy combined with Wernicke's encephalopathy is quite rare and unusual. Here, we describe a patient with Wernicke's encephalopathy who presented with acute bilateral axonal neuropathy.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.42 no.2
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• pp.120-122
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• 2016

Wernicke's encephalopathy is a fatal neurological disease caused by thiamine deficiency. Many reports indicate that Wernicke's encephalopathy is caused by malnutrition. We report the case of a 79-year-old female patient who had a left masticator space and parapharyngeal space abscess who was diagnosed with Wernicke's encephalopathy. She reported problems while eating due to the presence of the abscess, but the true quantities of food she was ingesting were never assessed. Clinicians have a responsibility to provide adequate nutritional support by ensuring that patients receive adequate nutrition. Clinicians should also keep in mind that Wernicke's encephalopathy may occur in patients who experienced prolonged periods of malnutrition.

• Investigative Magnetic Resonance Imaging
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• v.20 no.1
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• pp.71-74
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• 2016

Wernicke's encephalopathy (WE) is an acute neurological disorder resulting from thiamine deficiency. Early diagnosis and treatment of WE is important to avoid persistent brain damage. Although histopathologic examination usually demonstrates pin-point hemorrhages in affected brain parenchyma, secondary hemorrhage is a rare but serious complication of WE. We experienced a rare case of intracranial hemorrhage related to WE in a 56-year-old male patient with malnourishment.

• Clinical and Experimental Pediatrics
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• v.57 no.11
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• pp.496-499
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• 2014

Wernicke's encephalopathy is an acute neurological disorder characterized by mental confusion, oculomotor dysfunction, and ataxia. It has been reported in individuals with alcohol dependence, hyperemesis gravidarum, and prolonged parenteral nutrition without vitamin supplementation. Here we present the case of a 13-year-old male patient with neuroblastoma and a history of poor oral intake and nausea for 3 months. After admission, he showed gait disturbances, nystagmus, and excessive dizziness; his mental state, however, indicated he was alert, which did not fit the classical triad of Wernicke's encephalopathy. A diagnosis of Wernicke's encephalopathy was made only after brain magnetic resonance imaging and serum thiamine level analyses were performed. The patient's symptoms remained after 5 days of treatment with 100-mg thiamine once daily; thus, we increased the dosage to 500 mg 3 times daily, 1,500 mg per day. His symptoms then improved after 20 days of replacement therapy. This case report describes a pediatric patient who was promptly diagnosed with Wernicke's encephalopathy, despite only 2 suspicious symptoms, and who completely recovered after high doses of thiamine were given intravenously.

• The Journal of Internal Korean Medicine
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• v.41 no.5
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• pp.777-786
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• 2020

Background: This study is a report on a case of a Wernicke's encephalopathy with quadriplegia, ataxia, and impaired cognition, whose condition was improved by Korean medicine treatment. Case report: A 51-year-old man diagnosed with Wernicke's encephalopathy was treated with acupuncture, Banhabakchulchunma-tang mixed with Ondam-tang-gami (半夏白朮天麻湯合溫膽湯加味), cupping, moxibustion, and rehabilitation. Clinical symptoms were measured with the Manual Muscle Test (MMT), Berg Balance Scale (BBS), Korean Mini Mental Status Exam (K-MMSE), Functional Independence Measure (FIM), Modified Barthel Index (MBI), and a numeric rating scale (NRS). After 22 days of treatment, his clinical symptoms showed improvement. The motor function improved (MMT Rt. side Gr. 4+G/4+G, Lt. side Gr. 4G/4+G → Rt. side Gr. 5-N/4+G, Lt. side Gr. 5-N/4+G), Ataxia was relieved (BBS 3→33), cognition improved (K-MMSE 15→27), ADL scores showed improvement (FIM 58→90, MBI 40→75), and the NRS score decreased for headache (3→0). Conclusion: Korean medicine treatment could be effective in the treatment of patients with Wernicke's encephalopathy.

• Annals of Clinical Neurophysiology
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• v.11 no.2
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• pp.78-80
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• 2009

• Molecules and Cells
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• v.25 no.1
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• pp.7-19
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• 2008

Complexins play a critical role in the control of fast synchronous neurotransmitter release. They operate by binding to trimeric SNARE complexes consisting of the vesicle protein Synaptobrevin and the plasma membrane proteins Syntaxin and SNAP-25, which are key executors of membrane fusion reactions. SNARE complex binding by Complexins is thought to stabilize and clamp the SNARE complex in a highly fusogenic state, thereby providing a pool of readily releasable synaptic vesicles that can be released quickly and synchronously in response to an action potential and the concomitant increase in intra-synaptic $Ca^{2+}$ levels. Genetic elimination of Complexins from mammalian neurons causes a strong reduction in evoked neurotransmitter release, and altered Complexin expression levels with consequent deficits in synaptic transmission were suggested to contribute to the etiology or pathogenesis of schizophrenia, Huntington's disease, depression, bipolar disorder, Parkinson's disease, Alzheimer's disease, traumatic brain injury, Wernicke's encephalopathy, and fetal alcohol syndrome. In the present review I provide a summary of available data on the role of altered Complexin expression in brain diseases. On aggregate, the available information indicates that altered Complexin expression levels are unlikely to have a causal role in the etiology of the disorders that they have been implicated in, but that they may contribute to the corresponding symptoms.

• Journal of The Korean Society of Clinical Toxicology
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• v.11 no.1
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• pp.28-30
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• 2013

A 66-year-old male with chronic alcoholism presented with tremor, gait disturbance, memory impairment, insomnia, decreased appetite, and confusion. The patient had been taking lithium daily for treatment of bipolar disorder. Brain CT showed no specific abnormality, and serum lithium and ammonia levels were 3.63 mEq/L (therapeutic range, 0.6~1.2 mEq/L) and $85{\mu}g/dL$ (reference range: $19{\sim}54{\mu}g/dL$), respectively. Therefore, the initial differential diagnosis included chronic lithium intoxication, hepatic encephalopathy, Wernicke encephalopathy, or alcohol withdrawal syndrome. Even with the provision of adequate hydration, the patient's neurologic status did not show improvement, so that lactulose enema, thiamine replacement, and continuous venovenous hemodiafiltration (CVVHDF) were started on the third admission day. By the fifth admission day he had made a rapid neurologic recovery, and was discharged on the 20th admission day. Therefore, CVVHDF might be a treatment for patients with chronic lithium intoxication, because, even if serum lithium concentration is normal, lithium concentration in the brain may be different from that of the serum.