Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.
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PMID:Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans. 402 52

The case of an alcoholic man is reported who survived a suicidal hanging attempt, and subsequently suffered of amnesia, dementia, apathy and behavioural abnormalities. A clinical diagnosis of hypoxic brain damage was made, but upon autopsy six years later, extensive pseudosystematic thalamic degeneration and mammillary body atrophy were found, indicating a status post Wernicke encephalopathy. Precipitation of the disease is attributed to the synergetic effect of cerebral hypoxia/ischemia and thiamine deficiency.
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PMID:Wernicke-Korsakoff syndrome following attempted hanging. 823 15

An 18-year-old woman in her first pregnancy with hyperemesis gravidarum, presented dehydration, without hyponatremia. She was confused with profound disorientation, apathy, and drowsiness. She presented upbeating nistagmus on upward gaze and gate ataxia recognised as Wernicke's encephalopathy. Laboratory tests demonstrated hypokalemia, hypernatremia and aminotransferase elevation. The serum osmolality was 319 mOsm/kg and the water deficiency 2.73 l. The patient developed weakness in the four limbs, with hypotonicity, absence of tendon reflexes and showed bilateral Babinski signs. A T2 weighted sagittal cranial-magnetic resonance imaging revealed a high signal within mid-pons suggesting central pontine myelinolysis. In this case we highlight the absence of hyponatremia. Furthermore, the central pontine myelinolysis was probably secondary to hypokalemia, hypernatremia and hyperosmolality.
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PMID:[Central pontine myelinolysis induced by hyperemesis gravidarum]. 1041 97

Wernicke's encephalopathy (WE) is a severe brain disorder, first described in 1881, and is caused by a nutritional deficiency of thiamine (vitamin B1) found mostly in patients suffering from chronic alcoholism. In addition, WE can also complicate bariatric surgery if adequate vitamin supplementation is not insured. Without immediate treatment, the prognosis is poor and the mortality rate is high. Most patients present with atypical neurological symptoms, which hampers rapid diagnosis. We present a 40-year-old woman who underwent gastroplasty combined with gastric banding for severe obesity. She experienced repetitive vomiting and her diet was without vitamin supplementation. After three months she developed convergent strabismus, apathy and urinary incontinence, which was diagnosed as WE and treated as such. Six months later her recovery was incomplete, still showing gait difficulties and nystagmus. We aim to show that adequate vitamin supplementation in patients undergoing gastroplasty is necessary, especially considering the risk of permanent neurological deficits.
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PMID:Vitamin B1 in the treatment of Wernicke's encephalopathy due to hyperemesis after gastroplasty. 2272 4

In this review, we present a survey on Korsakoff's syndrome (KS), a residual syndrome in patients who suffered from a Wernicke encephalopathy (WE) that is predominantly characterized by global amnesia, and in more severe cases also by cognitive and behavioral dysfunction. We describe the history of KS and its definition, its epidemiology, and the lack of consensus criteria for its diagnosis. The cognitive and behavioral symptoms of KS, which include anterograde and retrograde amnesia, executive dysfunction, confabulation, apathy, as well as affective and social-cognitive impairments, are discussed. Moreover, recent insights into the underlying neurocognitive mechanisms of these symptoms are presented. In addition, the evidence so far on the etiology of KS is examined, highlighting the role of thiamine and alcohol and discussing the continuity hypothesis. Furthermore, the neuropathology of KS is reviewed, focusing on abnormalities in the diencephalon, including the mammillary bodies and thalamic nuclei. Pharmacological treatment options and nonpharmacological interventions, such as those based on cognitive rehabilitation, are discussed. Our review shows that thiamine deficiency (TD) is a crucial factor in the etiology of KS. Although alcohol abuse is by far the most important context in which TD occurs, there is no convincing evidence for an essential contribution of ethanol neurotoxicity (EN) to the development of WE or to the progression of WE to KS. Future research on the postmortem histopathological analysis of brain tissues of KS patients is crucial for the advancement of our knowledge of KS, especially for associating its symptoms with lesions in various thalamic nuclei. A necessary requirement for the advancement of studies on KS is the broad acceptance of a comprehensive definition and definite diagnostic criteria. Therefore, in this review, we propose such a definition of KS and draft outlines for prospective diagnostic criteria.
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PMID:Korsakoff's syndrome: a critical review. 2922 66

We report a rare case of Wernicke encephalopathy (WE) in a 35-year-old woman with hyperemesis gravidarum (HG). Initially, the disease manifested as passivity, a loss of interest, sleeping too much, apathy and disorientation. The correct diagnosis was established after the detection of typical pathological findings of WE in the thalamus by magnetic resonance imaging (MRI), which was indicated for the appearance of eye symptomatology in the form of nystagmus. Subsequent treatment with thiamine led to rapid improvement in the patient's clinical status and a favorable course of pregnancy.
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PMID:Wernicke encephalopathy-a rare complication of hyperemesis gravidarum. 3212 44

A 55-year-old woman developed acute promyelocytic leukaemia during treatment with all-trans-retinoic acid and arsenic trioxide. Initially, she presented with symptoms of epigastric pain, vomiting, and nausea, and she developed acute pancreatitis. She was treated with parenteral nutritional supplementation for 20 days. However, the patient continued to develop refractory hyponatraemia, hypotension, and apathy. Finally, the patient was diagnosed with Wernicke encephalopathy (WE) using head magnetic resonance imaging. The patient underwent high-dose intravenous thiamine administration, and her symptoms were alleviated. WE is a rare adverse event during acute pancreatitis therapy. Acute pancreatitis that is caused by all-trans-retinoic acid and arsenic trioxide is a rare complication of acute promyelocytic leukaemia during chemotherapy. Further study is essential to improve our comprehension of the risk factors for complications in patients with acute promyelocytic leukaemia, considering that the associated complications were potentially caused by multiple etiological factors. A better understanding of these risk factors may help to improve the prognosis of patients with acute promyelocytic leukaemia at an early stage.
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PMID:Severe Wernicke encephalopathy and acute pancreatitis due to all-trans-retinoic acid and arsenic trioxide during treatment of acute promyelocytic leukaemia: a case report. 3299 92