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)

Thirthy-three alcoholics, aged between 31 and 82 years, were treated for 7 to 30 days with tiapride. The dosage was 600 mg/day (200 mg 3 times daily) by mouth or 100 to 800 mg/day I.M. Out of 27 cases of tremor treated, there were 25 favourable results, one average result and one nil result. Insomnia and character disorders, e.g. anguish, depression, nightmares, hallucinations, were improved during the first few days of treatment in 27 cases out of 30. Out of 12 cases of algo-paresthesia of the lower limb treated, the were 9 good or excellent results, 2 average results and 1 nil result. A favourable result was observed in 7 cases out of nine in vomiting, water brash (3 cases out of 4), and in 16 cases out of 20 in anorexia. No clinical or laboratory disturbance attributable to tiapride was noted in our patients whose general health was often very poor.
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PMID:[Tiapride and alcoholic disorders of central origin. Apropos of 33 cases]. 21 35

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

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. The development of the syndrome may result from a confluence of several factors, including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25

1. The authors review the literature describing acute symptomatology produced by the gradual or abrupt withdrawal of heterocyclic antidepressants, monoamine oxidase inhibitors (MAOI) and neuroleptics. 2. Withdrawal of heterocyclic antidepressants and antipsychotic agents causes similar symptomatology. Symptoms produced by the discontinuation of these drugs include nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. 3. Psychotic relapse is often presaged by anxiety, agitation, restlessness, and insomnia. Prodromal symptoms are distinguished from the effects of neuroleptic withdrawal by a temporal relationship of the latter to reductions in the dosage or discontinuation of antipsychotic agents. 4. Withdrawal of MAOIs can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium, and paranoid psychosis. 5. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. 6. The capacity of MAOIs to exert amphetamine-like effects presynaptically and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines provide a basis for the development of psychotic symptoms upon the withdrawal of MAOI. Evidence for this hypothesis is reviewed.
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PMID:Heterocyclic antidepressant, monoamine oxidase inhibitor and neuroleptic withdrawal phenomena. 196 71

The authors review the literature discribing non-dyskinetic antipsychotic withdrawal phenomena. Withdrawal of these agents can cause nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgia, paresthesia, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness and insomnia, but the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.
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PMID:Antipsychotic withdrawal symptoms: phenomenology and pathophysiology. 289 77

The literature describing nondyskinetic antipsychotic withdrawal symptoms is reviewed. The withdrawal of antipsychotic agents can result in nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. Psychotic relapse is often presaged by increased anxiety, agitation, restlessness, and insomnia. However, the temporal relationship of these prodromal symptoms to reduction in the dosage or discontinuation of neuroleptics distinguishes them from the effects of abrupt withdrawal.
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PMID:Antipsychotic withdrawal phenomena in the medical-surgical setting. 290 18

American trypanosomiasis (Chagas' disease) is an endemic parasitic disease afflicting more than 20 million persons in Latin America. Two drugs are currently being used for treatment of the acute phase of Chagas' disease: 4-[(5-nitrofurfurylidene)amino-3-methylthiomorpholine-1,1-di oxide] (Nifurtimox; Nfx) and (N-benzl-2-nitro-1-imidazole acetamide) (Benznidazole; Bz). Nfx and Bz have serious undesirable effects, which have been reported during their clinical use, including anorexia and weight loss, nausea and vomiting, nervous excitation, insomnia, psyche depressions, convulsions, vertigo, headache, sleepiness, myalgias, arthralgias, loss of balance, disorientation, forgetfulness, paresthesias, adynamia, acoustic phenomena, peripheral neuropathies, gastralgia, mucosal edema, hepatic intolerance, skin manifestations, and intolerance to drinking alcohol. Effects in the central and peripheral nervous system of Nfx were also reproduced in animals. Signs of testicular and ovarian injury were reported for both Nfx and Bz, the effects of Bz being in general less intense than those of Nfx. Both drugs evidenced mutagenicity. In light of the present knowledge about the toxicity of Nfx and Bz, further studies on the mutagenic, teratogenic, carcinogenic, and reproductive effects of both drugs are recommended. Lack of information is particularly serious for Bz. Studies on Nfx and Bz biotransformation, activation to reactive metabolites, and potential mechanisms for their toxic effects were analyzed. Risk-benefit considerations of the use of Nfx and Bz were made and an analysis of the need for research on Chagas' disease chemotherapy was also performed.
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PMID:Toxic effects of nifurtimox and benznidazole, two drugs used against American trypanosomiasis (Chagas' disease). 315 55

An epidemic of urinary retention among workers in a polyurethane manufacturing plant was discovered in the spring of 1978. The most severely affected workers had neurogenic bladders confirmed by cystometrograms and mild sensory peripheral neuropathy. A survey of the plant disclosed increased incidence of urinary retention, muscle weakness, paresthesia, insomnia, and sexual dysfunction in exposed workers. A catalyst containing dimethylaminopropionitrile was identified as the probable causative agent, and after its removal no new cases occurred.
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PMID:An epidemic of urinary retention caused by dimethylaminopropionitrile. 624 74

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

The effects of estrogen/gestagen (e/g) treatment given in a 28-day cycle (Trisequens forteR, Novo) on menopausal symptoms and plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were studied in a placebo trial. 119 normal women in the early postmenopausal period with mild to moderate climacteric complaints were included. At 3-month intervals for 2 years the participants were examined and filled in questionnaires containing the 11 symptoms of the Kupperman index (10). For each symptom a score was given. In the e/g group 77% (43/56) completed the trial compared with 83% (54/63) in the control group. A total of 61% of the women complained of hot flushes and from 9% to 44% complained of the remaining 10 Kupperman symptoms. At all eight examinations e/g treatment was found to have reduced the symptom score as well as the proportion of women with hot flushes, paresthesia, insomnia, nervousness, vertigo and formication. The symptom score of hot flushes and insomnia declined significantly (p less than 0.01). In the 24 women with hot flushes and in the 19 without, e/g caused similar reduction in the mean score of the other 10 symptoms. No placebo effect was seen. E/g caused a significant (p less than 0.01) fall in the elevated plasma concentrations of FSH and LH. Vaginal bleeding was regular in 38/43 and irregular in 4/43 women during hormone treatment. No serious side effects were attributed to e/g therapy. It is concluded that e/g treatment, in addition to its beneficial effects on hot flushes and insomnia, also alleviates several other climacteric symptoms.
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PMID:Effects of two years' estrogen-gestagen replacement on climacteric symptoms and gonadotropins in the early postmenopausal period. 681 85


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