Cases reported "wernicke encephalopathy"

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1/198. Downbeat nystagmus caused by thiamine deficiency: an unusual presentation of CNS localization of large cell anaplastic CD 30-positive non-Hodgkin's lymphoma.

    A 24-year-old woman with a large cell anaplastic CD 30-positive T-cell non-Hodgkin's lymphoma (NHL) developed downbeat nystagmus, anisocoria, and oscillopsia. Prior to overt cerebral invasion by NHL, she had a thiamine deficiency with very low thiamine concentrations in the CSF, probably caused by protracted vomiting and increased vitamin B1 consumption by intrathecal tumor cells. We believe that her neurologic symptoms were caused -- at least partly -- by thiamine deficiency, as she reacted well to thiamine supplementation at the beginning of treatment. ( info)

2/198. Wernicke's encephalopathy induced by hyperemesis gravidarum.

    A report is presented on a patient with Wernicke's encephalopathy secondary to hyperemesis gravidarum. The 25-year-old female presented 11 weeks into pregnancy with prolonged vomiting. Neurological examination 8 weeks later demonstrated obtunded sensations, nystagmus and ataxia of gait. MR imaging revealed bilateral lesions in the mediodorsal nuclei of thalami, in the hypothalamus and in the periaqueductal gray matter (1). The neurological signs and the MRI findings pointed to a diagnosis of Wernicke's encephalopathy. The patient was treated with intramuscular vitamin B1 followed by oral thiamine until the end of pregnancy. The subsequent course of the pregnancy was uncomplicated, and resulted in the delivery of a healthy 2970 g male infant. A review of the literature published during the last 30 years revealed an additional 20 cases of Wernicke's encephalopathy induced by hyperemesis gravidarum. Only half of these pregnancies resulted in the birth of a normal infant. ( info)

3/198. early diagnosis of pediatric Wernicke's encephalopathy.

    Wernicke's encephalopathy may be fatal if untreated. Because Wernicke's encephalopathy is suspected to be underdiagnosed in children, the authors wished to assess the frequency of overlooked diagnosis and to establish pertinent findings that could lead to early identification of pediatric Wernicke's encephalopathy. The authors performed multiple literature searches seeking pediatric patients with Wernicke's encephalopathy (age = 20 years or younger). A total of 30 patients was found, and the authors added a new patient. Each case report had its clinical, radiologic, and laboratory data, diagnostic method, and outcome analyzed. Of 31 patients, 16 were female and 15 male; the median age /- S.D. was 11 /- 6.5 years. The most frequent underlying disorder was malignancy in 11. Thirteen patients died undiagnosed, 16 recovered with thiamine therapy (eight with sequelae), and two died of infection soon after thiamine replacement was initiated. Only six presented with the Wernicke's encephalopathy clinical triad (mental status changes, ocular signs, and ataxia) at neurologic onset; nine eventually demonstrated this triad. The high rate of patients diagnosed only at postmortem examination (41.9%) confirms that Wernicke's encephalopathy is underdiagnosed in children. Thiamine therapy is warranted if any component of the Wernicke's encephalopathy triad is present in an appropriate clinical setting. ( info)

4/198. Do acute lesions of Wernicke's encephalopathy show contrast enhancement? Report of three cases and review of the literature.

    Contrast medium was given intravenously to three nonalcoholic patients who underwent MRI or CT in the acute stage of Wernicke's encephalopathy. Lesions enhancement was not seen in one patient examined within 4 days of clinical onset, was mild in a another 3 days after clinical deterioration and marked in a patient examined 12 days after admission. Contrast enhancement of lesions was present in half of 12 cases of acute disease reported previously. There was a substantial overlap in the time interval between clinical onset and contrast-enhanced CT or MRI in the groups of enhancing and nonenhancing lesions. Since contrast enhancement may be absent in acute WE, proton-density and T2-weighted images are more useful for diagnosis of this reversible but potentially fatal condition. ( info)

5/198. wernicke encephalopathy-like symptoms as an early manifestation of Creutzfeldt-Jakob disease in a chronic alcoholic.

    A case of Creutzfeldt-Jakob disease (CJD) with presenting wernicke encephalopathy (WE)-like symptoms and severe insomnia is presented. An 80-year-old alcoholic man with a 6 month history of tremors, ataxia, memory loss and confabulation, developed profound insomnia, confusion, and delirium with vivid hallucinations. polysomnography revealed a marked reduction of sleep time, with central-type sleep apnea. Neither myoclonus nor periodic synchronous discharge (PSD) was observed. An autopsy revealed diffuse spongiform changes and astrocytosis throughout the cerebral gray matter, with severe involvement of the mammillary bodies and thalamus. Prion protein (PrP) immunostaining was positive in kuru plaques in the cerebellum, PrP polymorphism at codon 129 was heterozygous Met/Val, and proteinase K resistant PrP (PrP(res)) was demonstrated by Western blotting. The lack of necrotizing lesions in the mammillary bodies, thalamus, and periaqueductal gray matter could rule out WE. The data suggest that the present case of CJD is consistent with PrP(res) type 2 (CJD M/V 2), but was unique in the lack of some typical CJD signs and the presence of signs of WE and sleep abnormalities. ( info)

6/198. Reversible MRI abnormalities in an unusual paediatric presentation of Wernicke's encephalopathy.

    BACKGROUND: We report an unusual paediatric presentation of acute Wernicke's encephalopathy in a 12-year-old boy affected by chronic gastrointestinal disease. MRI demonstrated, in addition to the typical diencephalic and mesencephalic signal abnormalities on T2-weighted images, enhancement of the mammillary bodies and the floor of the hypothalamus. MATERIALS AND methods: Following parenteral administration of thiamine for 4 days, the patient recovered from his neurological deficits and on follow-up enhanced MRI 1 month later, no signal abnormalities were found nor was there diencephalic or mesencephalic atrophy, as is usual in the chronic phase of the disease. RESULTS: MRI provides crucial information in the diagnosis of Wernicke's encephalopathy, either in the acute or chronic phases of the disease. CONCLUSION: Our report provides an additional clue for recognition of the acute phase of the disease; enhancement of the floor of the hypothalamus has not previously been described despite its recorded involvement at autopsy. ( info)

7/198. Wernicke's encephalopathy associated with hemodialysis: report of two cases and review of the literature.

    Two rare cases of Wernicke's encephalopathy (WE) in non-alcoholic patients on hemodialysis (HD) are reported. They presented with the clinical triad of WE (ophthalmoplegia, ataxia and disturbance of consciousness) and intravenous administration of thiamine led to complete elimination of these manifestations. Reduced plasma thiamine levels prior to the administration confirmed the diagnosis of WE. Interestingly, a reduction in plasma thiamine levels by about half was seen in one of the patients on HD, suggesting that thiamine, a water-soluble vitamin, can be depleted with HD. In the literature, nine HD-dependent patients have been reported to develop WE, seven of whom were diagnosed postmortem. Their premortem diagnoses included uremic encephalopathy, dysequilibrium syndrome and dialysis dementia, which can often complicate HD and present symptoms similar to those of WE. We therefore emphasize that WE, even though a rare complication, should be suspected in all patients on HD who present with at least one of the clinical triad of WE. ( info)

8/198. wernicke encephalopathy: MR findings in two patients.

    wernicke encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency. In the literature the characteristic symmetric paraventricular lesions of wernicke encephalopathy are hyperintense on T2-weighted sequences spin-echo (SE) and enhance on T1-weighted SE sequences after intravenous gadolinium administration in the acute phase. We present two patients in the acute phase of wernicke encephalopathy with special reference to the MR imaging. One of our reported cases is special because of the MR demonstration of a hemorrhagic focus in the caput of the right nucleus caudatus. The other case demonstrates no enhancement on SE T1-weighted sequences after intravenous gadolinium administration. ( info)

9/198. Gestational thyrotoxicosis with acute wernicke encephalopathy: a case report.

    A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute wernicke encephalopathy from Graves' thyroid storm, and that wernicke encephalopathy should be treated as soon as possible to improve the prognosis. ( info)

10/198. A common cause of altered mental status occurring at an uncommon age.

    Wernicke's encephalopathy is a neurologic disorder due to a nutritional deficiency of thiamine, characterized by ocular palsies, ataxia, and altered mental activity. While Wernicke's encephalopathy is commonly attributed to alcoholism in the adult population, it has been described in children receiving prolonged parenteral nutrition and those with malignancies and AIDS. The disease, however, is rarely diagnosed in the pediatric population during life. We report a case of Wernicke's encephalopathy in a child with prolonged starvation and aim to improve awareness of a potentially fatal but treatable disease. ( info)
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