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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accidental acute mercury vapor poisoning in three persons is reported. Three hours after exposure, symptomatology began by chills, vomiting, diarrhea and chest pain. Two patients, respectively 67 and 77 year old, presented severe pulmonary edema, then neurological symptoms with tremor and coma. This toxic pulmonary edema, which entailed artificial ventilation, was followed in both cases by an acute interstitial pulmonary fibrosis which led to death respectively after six and sixteen days. In the third case (a thirty eight year old patient) a skin rash, erythematous and pustuliform was observed. Analysis for total mercury by flameless atomic absorption showed very high mercury levels in blood and urine of the three patients. The effect of treatment by Dimercaptopropanol on renal excretion of mercury was studied. Optic and electron microscopy of the lung of the two patients who died showed the pulmonary changes of acute interstitial fibrosis.
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PMID:Accidental acute mercury vapor poisoning. 50 88

Besides general complications of immunosuppression such as increased susceptibility to opportunistic infections or malignancy, individual immunosuppressive agents are associated with specific side effects. Nephrotoxicity is the major side effect of cyclosporine (CsA). Various attempts have been made to minimize this toxicity, such as monitoring drug blood levels, modifying the protocol, and coadministering other agents. Other side effects caused by CsA are hepatotoxicity, hyperkalemia, hypertension, tremor, gum overgrowth, and hirsutism. Azathioprine (AZA) causes dose-related bone marrow suppression, commonly leading to leukopenia. Careful monitoring of complete blood cell count and dosage adjustment according to white blood cell count are usually adequate to prevent serious leukopenia. The side effects of corticosteroids are numerous and include slow wound healing and de novo insulin-dependent diabetes mellitus. Many complications are dose related, and with low dosage or discontinuation of steroids, their frequency rapidly decreases. Antilymphoblast and antithymocyte globulins (P-ALG) are foreign antibodies and may cause allergic-type reactions such as fever, chill, and hypotension. The initial side effect of monoclonal antibody (muromonab-CD3, OKT3) is similar to that of P-ALG. It includes high fever, shaking chills, headache, rigors, and hypotension. To prevent it, acetaminophen, an antihistamine, and a steroid usually are administered before injection. Because this agent is also associated with high frequency of pulmonary edema, it should not be given to any patient who has more than 3% body weight gain during the week prior to therapy. In rare case, it causes aseptic meningitis or encephalopathy, which is manifested by fever, severe headache, and seizure.
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PMID:Complications associated with immunosuppressive therapy and their management. 174 17

A case of fatal amniotic fluid embolism leading to hypernatremia following instillation of hypertonic saline is reported. This complication of saline-induced abortion has not been reported previously in the literature. The patient was an obese 16-year-old black female, gravida 1, para 0, whose gestational age at time of abortion was 21.5 weeks. 26 hours after the procedure, which was well tolerated by the patient, she complained of severe abdominal cramps with projectile expulsion of amniotic fluid. Generalized convulsions and shaking followed and the patient went into shock. Death occurred within 2 hours. At autopsy, microscopic examination of lungs revealed pulmonary edema with marked vascular congestion, focal areas of atelectasis, and intra-alveolar hemorrhages. Positive test results for mucin in a few pulmonary vessels and intra-alveolar capillaries confirmed a diagnosis of amniotic fluid embolism. There was marked congestion of the blood vessels of the kidneys, liver, brain, and spleen. Amniotic fluid embolism represents about 10% of the maternal mortality in the US; however, this complication generally occurs during labor, delivery, and the immediate postpartum period. Moreover, most such cases occur in older, multiparous women in the 3rd trimester of pregnancy. It is possible that hypernatremia following amniotic fluid embolism occurs more frequently than reported. Routine examination of blood during pregnancy and of the vitreous humor in cases of pregnancy-related mortality could be useful in establishing a diagnosis of amniotic fluid embolism.
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PMID:Hypernatremia due to amniotic fluid embolism during a saline-induced abortion. 335 24

Poliovirus and enterovirus 71 (EV71) are both neurotropic enteroviruses that cause serious neurological diseases, such as poliomyelitis and encephalitis. The neurovirulence of EV71 in cynomolgus monkeys was demonstrated previously by intraspinal inoculation. In this study, an improved simian model of EV71 infection was established by using intravenous inoculation, which revealed clinical and neuropathological similarities between this model and human cases of encephalitis. Experimental EV71 infection induced direct neurological manifestations, such as tremor, ataxia and brain oedema, but not non-neurological complications, such as pulmonary oedema and cardiac failure. Using this model of EV71 infection, the neurotropic characteristics of the prototype strains of EV71 and poliovirus type 1 (PV1) were compared. Three monkeys were inoculated intravenously with 10(5.5) TCID50 EV71 and all developed neurological disease signs within 4-6 days of inoculation. However, after inoculation with 10(5.5) TCID50 PV1 strain OM1 (PV1-OM1), the major manifestation was flaccid paralysis, starting from the lower limbs 6-9 days post-inoculation. Histopathological and virological analyses of moribund monkeys revealed that disseminated EV71 infection was characterized by severe panencephalitis involving both the pyramidal and extrapyramidal systems. In contrast, the lesions induced by PV1-OM1 were mainly restricted to the pyramidal tract, particularly the spinal motor neurons, thalamus and motor cortex. In conclusion, neuropathological involvement in this model correlated well with the apparent differences in neurological disease induced by EV71 and PV1-OM1. Thus, intravenous inoculation with EV71 is an excellent model to study the neuropathology of EV71 and to evaluate candidate vaccines and potential antiviral agents.
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PMID:Differential localization of neurons susceptible to enterovirus 71 and poliovirus type 1 in the central nervous system of cynomolgus monkeys after intravenous inoculation. 1544 61

(1) When people who are physically dependent on alcohol stop drinking, they experience an alcohol withdrawal syndrome. The symptoms generally resolve spontaneously within a week, but more severe forms may be associated with generalised seizures, hallucinations and delirium tremens, which can be fatal. (2) We carried out a literature review in order to obtain answers to the following questions: how to predict or rapidly diagnose a severe alcohol withdrawal syndrome; how to prevent and treat this syndrome; how to manage severe forms; and how to deal with the risk of vitamin B1 deficiency. (3) The main risk factors for severe withdrawal syndrome are: chronic heavy drinking; a history of generalised seizures; and a history of delirium tremens. (4) Anxiety, agitation, tremor, excessive sweating, altered consciousness and hallucinations are signs of a severe withdrawal syndrome. (5) Individual support and effective communication seem to reduce the risk of severe withdrawal syndrome. (6) Oral benzodiazepines are the best-assessed drugs for preventing a severe alcohol withdrawal syndrome, particularly the risk of seizures. When given for a maximum of 7 days, the adverse effects are usually mild. (7) Clinical trials of other antiepileptics suggest they are less effective than benzodiazepines, and their addition to benzodiazepine therapy offers no tangible advantage. (8) Betablockers increase the risk of hallucinations, and clonidine increases the risk of nightmares, and the efficacy of these two drugs is not well documented. Neuroleptics increase the risk of seizures. There are no convincing data to support the use of magnesium sulphate or meprobamate (the latter carries a risk of serious adverse effects). Acamprosate, naltrexone and disulfiram are not beneficial in alcohol withdrawal. (9) Gradual withdrawal, i.e. ingestion of decreasing amounts of alcohol, has not been compared with other methods but is generally not recommended. (10) There are no specific recommendations on hydration. Note that excessive water-sodium intake carries a risk of pulmonary oedema in patients with heart disease. (11) As vitamin B1 deficiency is frequent and can lead to serious complications in alcohol-dependent patients, oral vitamin B1 supplementation is widely recommended, despite the absence of comparative trials. High doses must be used to compensate for poor absorption. Intravenous administration is best if patients have very poor nutritional status or severe complications such as Gayet-Wernicke encephalopathy (a medical emergency), even though rare anaphylactic reactions have been reported after vitamin B1 injection. (12) Planned alcohol withdrawal in specialised hospital units has been extensively studied. Outpatient withdrawal may be more appropriate for patients who are at low risk of developing severe withdrawal syndrome. (13) A large proportion of alcohol-dependent patients were excluded from trials of withdrawal strategies. These include elderly patients, patients with serious psychiatric or somatic disorders, and patients who are also dependent on other substances. (14) An oral benzodiazepine is the best-assessed treatment for a single episode of generalised seizures or hallucinations during alcohol withdrawal. (15) In randomised comparative trials benzodiazepines were more effective than neuroleptics in preventing delirium-related mortality. Currently, with appropriate fluid-electrolyte support, continuous monitoring of vital signs, and respiratory support if necessary, the mortality rate for delirium tremens is under 3%. (16) In practice, patients who are attempting to stop drinking alcohol need close personal support and communication, and a reassuring environment, as well as regular monitoring for early signs of a withdrawal syndrome; the latter may require benzodiazepine therapy.
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PMID:Alcohol withdrawal syndrome: how to predict, prevent, diagnose and treat it. 1732 38

Enterovirus type 71 (EV71) is a causative agent of large outbreaks of hand, foot, and mouth disease (HFMD) in Europe (Bulgaria, 1975; Hungary, 1978) and South-East Asia (Malaysia, 1977; Taiwan, 1998; Singapore, 2000-2007; People's Republic of China, 2007-2009). HFMD afflicted children less than 10 years of age and resulted in recovery within 3-7 days. In a small percentage of infants (aged 6 months to 3 years), HFMD was accompanied by acute neurological complications, such as serous meningitis, poliomyelitis-like syndrome (extremity pareses and muscle paralyses); brain stem encephalitis (myoclonic jerks, tremor, lethargy, swallowing and speech disorders, cardiopulmonary failure, pulmonary edema, shock, coma, death). X-ray study revealed pulmonary hemorrhages and edema. Mortality rates were as high as 82-94% in severe cases. Incapacitating motor, respiratory, and psychoemotional disorders persisted in some surviving children. Pathomorphologically, patients with central nervous system disease and cardiopulmonary failure were found to have acute inflammation of the grey matter of the brain stem (medulla oblongata, pons) and spinal cord. Inflammatory changes in the lung and myocardial tissues were negligible or absent. Fatal pulmonary edema was neurogenic in origin and resulted from damage to the respiratory and vasomotor centers of the brain stem.
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PMID:[Encephalomyelitis caused by enterovirus type 71 in children]. 2138 32

Snake and spider bites, as well as scorpion sting envenoming, are neglected diseases affecting millions of people all over the world. Neurological complications vary according to the offending animal, and are often directly related to toxic effects of the venom, affecting the central nervous system, the neuromuscular transmission, the cardiovascular system, or the coagulation cascade. Snake bite envenoming may result in stroke or muscle paralysis. Metalloproteinases and other substances (common in vipers and colubrids) have anticoagulant or procoagulant activity, and may induce ischemic or hemorrhagic strokes. The venom of elapids is rich in neurotoxins affecting the neuromuscular transmission at either presynaptic or postsynaptic levels. The clinical picture of scorpion sting envenoming is dominated by muscle weakness associated with arterial hypertension, cardiac arrythmias, myocarditis, or pulmonary edema. These manifestations occur as the result of release of catecholamines into the bloodstream or due to direct cardiac toxicity of the venom. Cerebrovascular complications have been reported after the sting of the Indian red scorpion. Intracranial hemorrhages occur in the setting of acute increases in arterial blood pressure related to sympathetic overstimulation, and cerebral infarctions are related to either cerebral hypoperfusion, consumption coagulopathy, vasculitis, or cardiogenic brain embolism. Three main syndromes result from spider bite envenoming: latrodectism, loxoscelism, and funnel-web spider envenoming. Latrodectism is related to neurotoxins present in the venom of widow spiders. Most cases present with headache, lethargy, irritability, myalgia, tremor, fasciculation, or ataxia. Loxoscelism is caused by envenoming by spiders of the family Sicariidae. It may present with a stroke due to a severe coagulopathy. The venom of funnel-web spiders also has neurotoxins that stimulate neurotransmitter release, resulting in sensory disturbances and muscle paralysis. Proper management of the envenomed patient, including prompt transport to the hospital, correction of the hemostatic disorder, ventilatory support, and administration of antivenom, significantly reduce the risk of neurological complications which, in turn, reduce the mortality and improve the functional outcome of survivors.
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PMID:Neurological effects of venomous bites and stings: snakes, spiders, and scorpions. 2382 24