Wernicke encephalopathy (WE) is a neurologic disorder characterized by clinical symptoms, such as nystagmus, ataxia, and mental confusion. Hypothermia in patients with WE is a rare complication, and its pathogenic mechanism and therapy are yet to be ascertained. Herein, we presented a case of a 61-year-old man who was diagnosed with WE 3 months earlier. We investigated the cause of hypothermia (35.0℃) that occurred after an enema (bowel emptying). Brain magnetic resonance imaging revealed mammillary body and hypothalamus atrophy. In the autonomic function test, the sympathetic skin response (SSR) test did not evoke SSR latencies on both hands. In addition, abnormal orthostatic hypotension was observed. Laxative and stool softener medication were administered, and his diet was modified, which led to an improvement in constipation after 2 weeks. Moreover, there was no recurrence of hypothermic episode. This is the first reported case of late-onset hypothermia secondary to WE.
Ataxia ; Atrophy ; Brain ; Constipation ; Diet ; Enema ; Hand ; Humans ; Hypotension, Orthostatic ; Hypothalamus ; Hypothermia* ; Magnetic Resonance Imaging ; Mammillary Bodies ; Middle Aged ; Nervous System Diseases ; Recurrence ; Skin ; Wernicke Encephalopathy*

Wernicke's encephalopathy is an acute neurological deterioration due to a reversible brain lesion caused by thiamine deficiency. Most of the affected patients are thiamine-depleted alcoholics, and the condition usually involves the medial thalami, mammillary bodies, and periaqueductal area. However, there are rare reports of lesions in the cerebellum and cerebral cortex, especially in patients with nonalcoholic Wernicke's encephalopathy. We report a case of nonalcoholic Wernicke's encephalopathy involving atypical diffuse cortical regions, and review previously reported cases.
Alcoholics ; Brain ; Cerebellum ; Cerebral Cortex ; Humans ; Mammillary Bodies ; Thiamine Deficiency ; Wernicke Encephalopathy*

PURPOSE: We report a case of an acute incomitant esotropia with Wernike's encephalopathy. CASE SUMMARY: A 64-year-old male visited our hospital because of diplopia lasting a week. He was a chronic alcoholic drinking two bottles of makgeolli daily and eating little for a month. He showed -2 underaction of bilateral lateral rectus muscles and 45 prism diopters of esotropia at the primary position at the first visit. He had ataxia and mild cognitive impairment. There were high signal intensities in the periaqueductal area and mammillary bodies in the brain fluid attenuated inversion recovery magnetic resonance image. He was diagnosed with Wernike's encephalopathy clinically and was immediately treated with intravenous thiamine. He showed -0.5 underaction of bilateral lateral muscles and 8 prism diopters of esotropia at the primary position 3 days after thiamine treatment. CONCLUSIONS: Wernicke's encephalopathy is a medical emergency. If diagnosis and treatment are delayed, patients may have neurological sequelae that can lead to death. Esotropia and diplopia can be the presenting manifestations in Wernike's syndrome without other symptoms. In taking patient histories, physicians should ask about alcohol consumption and low food intake because of the possibility of acute incomitant esotropia associated with Wernicke's encephalopathy.
Alcohol Drinking ; Alcoholics ; Ataxia ; Brain ; Diagnosis ; Diplopia ; Drinking ; Eating ; Emergencies ; Esotropia* ; Humans ; Male ; Mamillary Bodies ; Middle Aged ; Mild Cognitive Impairment ; Muscles ; Thiamine ; Wernicke Encephalopathy

Wernicke's encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine deficiency. Traditionally, diagnosis of WE rests on a clinical symptom triad consisting of ocular signs, altered consciousness, and ataxia. However, the complete triad is only present in a fraction of cases, which means that WE tends to be under-diagnosed, especially in nonalcoholic patients. Brain MRI of WE patients usually shows symmetrical signal intensity alterations in the thalami, mammillary bodies, and periaqueductal area, because of cytotoxic edema in the same region. These typical findings are useful diagnostic leads in WE patients with atypical symptoms. However, atypical findings can occasionally be seen in the vermis of cerebellum and cerebellar nuclei. Notably, alterations of signal intensity in the cerebellar dentate nuclei, which is a typical finding of metronidazole-induced encephalopathy (MIE), need to be distinguished according to medication history and response to thiamine.
Ataxia ; Brain ; Cerebellar Nuclei ; Cerebellum ; Consciousness ; Edema ; Humans ; Mamillary Bodies ; Metronidazole ; Thiamine ; Thiamine Deficiency ; Wernicke Encephalopathy

PURPOSE: To report a case of subacute optic neuropathy caused by thiamine (vitamin B1) deficiency. CASE SUMMARY: A 44-year-old woman was referred to the ophthalmology department due to decreased vision which began 10 days prior to presentation. The patient history indicated that she had undergone chemotherapy for ovarian cancer and she had been dependent on total parenteral nutrition for 3 weeks due to nausea and vomiting. Her best corrected vision of the right and the left eyes were 0.15 and 0.2, respectively. Color vision was severely impaired in both eyes without retrobulbar pain. There was marginal blurring on the temporal side of the optic discs of both eyes. The optic nerves were unremarkable on orbital and brain magnetic resonance imaging (MRI). There was high signal intensities in both the mammillary body and periaqueductal gray matter on T2-weighted imaging. In addition, the patient exhibited ataxia along with short-term memory loss. She was diagnosed with Wernicke's encephalopathy. Thiamine was administrated based on the diagnosis, and after 2 days of administration, the patient's vision and neurologic symptoms began to improve. Two weeks later, the patient recovered her vision. CONCLUSIONS: Thiamine deficiency may cause optic neuropathy and can be recovered with early thiamine supplementation. This condition could occur due to deficient oral thiamine administration. We should keep this point in mind and try to prevent or diagnose early.
Adult ; Ataxia ; Brain ; Color Vision ; Diagnosis ; Drug Therapy ; Female ; Humans ; Magnetic Resonance Imaging ; Mamillary Bodies ; Memory, Short-Term ; Nausea ; Neurologic Manifestations ; Ophthalmology ; Optic Nerve ; Optic Nerve Diseases* ; Orbit ; Ovarian Neoplasms ; Parenteral Nutrition, Total ; Periaqueductal Gray ; Thiamine Deficiency ; Thiamine* ; Vomiting ; Wernicke Encephalopathy*

OBJECTIVE: The secondary verification of Leksell Gamma Knife treatment planning system (LGP) (which is the primary verification system) is extremely important in order to minimize the risk of treatment errors. Although prior methods have been developed to verify maximum dose and treatment time, none have studied maximum dose coordinates and treatment volume. METHODS: We simulated the skull shape as an ellipsoid with its center at the junction between the mammillary bodies and the brain stem. The radiation depths of the beamlets emitted from 201 collimators were calculated based on the relationship between this ellipsoid and a single beamlet expressed as a straight line. A computer program was coded to execute the algorithm. A database system was adopted to log the doses for 31x31x31 or 29,791 matrix points allowing for future queries to be made of the matrix of interest. RESULTS: When we compared the parameters in seven patients, all parameters showed good correlation. The number of matrix points with a dose higher than 30% of the maximal dose was within +/- 2% of LGP. The 50% dose volume, which is generally the target volume, differs maximally by 4.2%. The difference of the maximal dose ranges from 0.7% to 7%. CONCLUSION: Based on the results, the variable ellipsoid modeling technique or variable ellipsoid modeling technique (VEMT) can be a useful and independent tool to verify the important parameters of LGP and make up for LGP.
Brain Stem ; Enzyme Multiplied Immunoassay Technique ; Humans ; Mamillary Bodies ; Radiosurgery ; Skull ; Software

Animals ; Fatigue ; enzymology ; Male ; Mammillary Bodies ; metabolism ; Nitric Oxide Synthase Type I ; genetics ; metabolism ; Physical Exertion ; physiology ; Random Allocation ; Rats ; Rats, Wistar ; Stress, Physiological ; physiology

Wernicke encephalopathy is an acute neurologic disorder attributable to thiamine (vitamin B1) deficiency. We report the case of a 61-year-old female patient who presented Wernicke encephalopathy after surgery for pancreatic head cancer. From the ninth postoperative day, she had suffered from nausea and vomiting and had difficulties ingesting food, she was given total parenteral nutrition (TPN), but lacked adequate vitamin (thiamine) supplementation. After 28 days, she developed ataxia, ophthalmoplegia, and mental confusion. The magnetic resonance image showed pathologic changes in the medial thalamus, periaqueductal gray matter, medulla and mamillary bodies. The blood level of thiamine was very low. After intravenous and oral supplementation of thiamine (200 mg/day), consciousness was soon normalized and neurologic symptoms have gradually been improving. Nausea and vomiting disappeared after administration of a low dose of mirtazapine (7.5 mg/day). We emphasize the importance of thiamine supplementation to the patients who suffer from vomiting which hinders them from taking food and who require prolonged TPN.
Ataxia ; Consciousness ; Female ; Head and Neck Neoplasms ; Humans ; Mamillary Bodies ; Middle Aged ; Nausea ; Nervous System Diseases ; Neurologic Manifestations ; Ophthalmoplegia ; Pancreaticoduodenectomy* ; Parenteral Nutrition, Total ; Periaqueductal Gray ; Thalamus ; Thiamine ; Vitamins ; Vomiting* ; Wernicke Encephalopathy*

It is controversial whether isolated lesions of mammillothalamic tract (MTT) produce significant amnesia. Since the MTT is small and adjacent to several important structures for memory, amnesia associated with isolated MTT infarction has been rarely reported. We report a patient who developed amnesia following an infarction of the left MTT that spared adjacent memory-related structures including the anterior thalamic nucleus. The patient s memory deficit was characterized by a severe anterograde encoding deficit and retrograde amnesia with a temporal gradient. In contrast, he did not show either frontal executive dysfunction or personality change that is frequently recognized in the anterior or medial thalamic lesion. We postulate that an amnesic syndrome can develop following discrete lesions of the MTT.
Aged ; Amnesia/*etiology ; Cerebral Infarction/*complications ; Humans ; Male ; Mamillary Bodies/*physiopathology ; Neuropsychological Tests ; Thalamus/*physiopathology

A 41-year-old man was admitted due to altered mentality and confusion. He had showed progressive cerebellar ataxia, dysarthria, gait disturbance from his age of 33 years old. Brain MRI revealed high signal lesions in periaqueductal gray matter, mammillary bodies, median thalami and postcentral gyri bilaterally on T2-weighted images. Severe cerebellar atrophy was noted, too. We report a case of Wernicke's encephalopathy in a patient with probable multiple system atrophy. As far as we know, there have been no published report on this kind of case.
Adult ; Atrophy ; Brain ; Cerebellar Ataxia ; Dysarthria ; Gait ; Humans ; Magnetic Resonance Imaging ; Mamillary Bodies ; Multiple System Atrophy* ; Periaqueductal Gray ; Wernicke Encephalopathy*