Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare case of criminal, chronic thallium poisoning is described. In spite of the general prohibition of the cosmetics, drugs and rodent exterminators containing thallium thallium intoxications are still observed occasionally. In the reported case typical symptoms as initial pain, dryness of the skin, constipation and insomnia were missing. The clinical picture was dominated by a polyneuropathy more pronounced in the lower extremities, a lesion of the optic nerve and the psychic symptoms of organic damage. A particular feature was the early loss of sensitivity of the anterior rami of the intercostal nerves.
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PMID:[Chronic thallium poisoning (author's transl)]. 46 65

According to the authors' observations, the symptoms of nervous system derangement associated with legionnaires' disease rather often enter the disease structure and can virtually be characterized as a manifestation of infectious and toxic encephalopathy and polyneuropathy (encephalopolyneuropathy). In the majority of cases, the neurological disorders develop acutely or subacutely after or simultaneously with respiratory lesions. The clinical picture of encephalopathy is marked by permanent headache, mental abnormalities, memory disturbances, insomnia, pronounced astheno-vegetative and vascular manifestations. In patients with legionellosis, polyneuropathy is manifested by paresthesias, less frequently by pains in the distal parts of the limbs and myasthenia without visible atrophies. Vegetative disorders such as vegetative polyneuropathy of the hands and legs, visceral polyneuropathies are typical symptoms of the disease whatever its gravity. Vegetovascular dystonia together with long-term AP instability is an obligate sign of the disease. Electrophysiological examinations (EEG, REG, EMG) support the clinical findings and may serve the basis for an objective evaluation of the gravity of the neurological disorders. The degree of pulmonary lesions and the intensity of vegetative disorders eventually determine the torpidity and characteristics of the disease course.
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PMID:[Nervous system involvement in legionellosis (legionnaires' disease)]. 164 36

A 31 year-old inhabitant of French Guiana was prescribed mercuric iodide per os for two and a half months. Shortly before the end of the treatment he developed fasciculations in the trunk and particularly the lower limb muscles, distal painful paresthesias with vasomotor disorders, episodes of excessive perspiration and palmoplantar erythema, moderate fluctuating hypertension, progressive loss of weight and irritability with insomnia. Clinical and electrical signs of neuropathy were lacking. The clinical picture was that of Morvan's fibrillary chorea with acrodynia, the conditions of onset strongly suggesting a mercurial intoxication. Blood and particularly urine mercury levels were elevated. Administration of dimercaprol (BAL) considerably increased urinary excretion of mercury and there was progressive improvement and finally recovery after two months of BAL treatment. This case exemplifies the possible co-existence of fibrillary chorea and acrodynia. Whereas in many cases of fibrillary chorea a precise etiology cannot be determined, the affection can be induced by mercury as by gold administration. The fact that cases of fibrillary chorea due to mercury poisoning are rarely reported may be the result of individual patient hypersensitivity or particular metabolic absorption and excretion features of mercury. This case cannot be included within the continuous activity syndrome of muscle fibers described by Isaacs, since muscle contractures were absent and there was associated acrodynia. Moreover, there was no latent polyneuropathy, in spite of the intense fasciculations. It must be concluded, therefore, that in spite of its rarity fibrillary chorea should keep its semiologic autonomy.
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PMID:[Morvan's fibrillary chorea and acrodynic syndrome following mercury treatment]. 652 13

Thirty-one adult diabetic patients with painful distal symmetrical polyneuropathy were treated with low doses of oral trazodone (50 or 100 mg/day). After 2 weeks of therapy, 19 patients (61.3%) experienced symptomatic relief, and 7 (22.6%) experienced complete relief. Although 8 patients (25.8%) discontinued the drug because of side effects, these were relatively minor (dizziness, headache, insomnia). Low-dose trazodone is recommended as an effective treatment option for painful diabetic neuropathy.
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PMID:The use of low-dose trazodone in the treatment of painful diabetic neuropathy. 1050 15

Hemodiafiltration with larger amounts of substitution fluid offers an optimal way to remove uremic substances. Hemodiafiltration could be indicated for all hemodialysis patients. Large observational studies have shown an association of a lower mortality risk with hemodiafiltration using more than 15 liters of substitution fluid. Specific indications should be considered because hemodiafiltration has been reported to be effective against hyperphospatemia, malnutrition, insomnia, irritability, restless-leg syndrome, polyneuropathy, anemia, itching and joint pain, and may prevent dialysis-associated amyloidosis. In this chapter, hemodiafiltration prescriptions concerning blood and dialysate fl ow, infusion rate, vascular access and frequency are detailed.
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PMID:Optimizing the prescription of hemodiafiltration. 1768 62

Chronic kidney disease (CKD) predisposes one to either deficiency or toxic excess of different micronutrients. The knowledge on micronutrients-specifically water-soluble vitamins and trace elements-in CKD is very limited. Consequently, current guidelines and recommendations are mostly based on expert opinions or poor-quality evidence. Abnormalities of micronutrient resources in CKD develop for several reasons. Dietary restrictions and anorexia lead to an insufficient micronutrient intake, while diuretics use and renal replacement therapy lead to their excessive losses. Absorption is unpredictable, and metabolism impaired. Better understanding of the micronutrient needs of CKD patients could have an impact on many complications linked to vitamin and trace element disorders, including high mortality, increased risk of atherosclerosis, inflammation, oxidative stress, anemia, polyneuropathy, encephalopathy, weakness and fragility, muscle cramps, bone disease, depression, or insomnia. Here, we summarize the up-to-date knowledge on micronutrient resources in different stages of CKD, and share our experience with the assessment of micronutrient status.
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PMID:Vitamins and Microelement Bioavailability in Different Stages of Chronic Kidney Disease. 2829 76

We describe the case of a 74-year-old fit and healthy man who developed a profound sleep disorder characterized by mid-day hypersomnia and debilitating insomnia. A wide range of therapies, including a large number of stimulants and hypnotics with multiple different mechanisms of action, failed to improve his condition. Trials with oral prosthetic devices and a wide range of face masks with positive pressure assistance and multiple continuous positive airway pressure (CPAP) titration studies failed to help. Along with his sleep disorder, our patient developed a slowly evolving axonal sensorimotor polyneuropathy with a subtle autonomic neuropathy. Due to the latter two conditions, a comprehensive paraneoplastic panel was obtained and revealed extremely high titer glutamic acid decarboxylase (GAD-65) autoantibodies. This was confirmed by three independent laboratories and by cerebrospinal fluid staining of rat hippocampus, revealing the classic tram-track lines along the dentate gyrus. Our patient was treated empirically with intravenous immunoglobulin. We believe that our case reveals a unique syndrome related to GAD-65 autoantibodies and adds to the growing list of GAD-65 associated diseases. This case is particularly provocative as it raises the idea to check for GAD-65 autoimmunity in patients who suffer from a profound sleep disorder resistant to conventional treatment.
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PMID:Glutamic Acid Decarboxylase (GAD-65) Autoimmunity Associated With Profound Daytime Hypersomnia, Nighttime Insomnia, Mild Autonomic Neuropathy and Axonal Sensori-Motor Polyneuropathy: A Case Report on a New Phenotype. 3324 Jul 8