Muscle tremors

OtherMa.gnesium Disorders. Neuromuscular irritabHity, convulsions, muscle tremors, mental changes such as confusion, disorientation, and haHucinations, heart disease, and kidney stones have aH been attributed to magnesium deficiency. Excess Mg " can lead to intoxication exemplified by drowsiness, stupor, and eventuaHy coma. 

Contact the primary care provider if palpitations, tachycardia, chest pain, muscle tremors, dizziness, headache, flushing, or difficulty with urination or breatliing occur. 

Acute exposure to large amounts of endosulfan results in frank effects manifested as hyperactivity, muscle tremors, ataxia, and convulsions. Possible mechanisms of toxicity include (a) alteration of neurotransmitter levels in brain areas by affecting synthesis, degradation, and/or rates of release and reuptake, and/or (b) interference with the binding of those neurotransmitter to their receptors. 

Pilocarpine, arecoline and, of course, muscarine itself are naturally occurring muscarinic agonists, while oxotremorine is a synthetic one, which, as its name implies, can cause muscle tremor through a central effect. 

A 16- year-old male treated for bronchial asthma develops skeletal muscle tremors. Which of the following agents may be responsible for this finding ... 

Signs of disulfoton toxicity, such as muscle tremors, fasciculations, lacrimation, and salivation, in animals are generally observed after a few daily doses, but begin to diminish in severity as exposure to dislllfoton continues (Bombinski and DuBois 1958). This phenomenon is known as tolerance. Tolerance appears to be a reproducible phenomenon that does not depend on the organophosphate insecticide used, the route of administration, or the animal species (Costa et al. 1982b). Several possible mechanisms have been proposed /explain this phenomenon. 

Disulfoton exposure results in cholinergic signs such as salivation, diarrhea, pupil constriction, muscle tremors, and weight loss. Ataxia, convulsions, coma, respiratory distress, and death are common signs associated with a more severe toxicosis. Nervous tissue is evidently the most sensitive target organ. 

In animals, exposure to high concentrations of phenol in air for a few minutes irritates the lungs, and repeated exposure for several days produces muscle tremors and loss of coordination. Exposure to high concentrations of phenol for several weeks results in paralysis and severe injury to the heart, kidneys, liver, and lungs, followed by death in some cases. When exposures involve... 

The seriousness of the effect of a harmful substance can be expected to increase as both the level and duration of exposure increase. Repeated exposure to low levels of phenol in drinking water has been associated with diarrhea and mouth sores in humans. Ingestion of very high concentrations of phenol has resulted in death. In animals, drinking water with extremely high concentrations of phenol has caused muscle tremors and loss of coordination. 

Other Systemic Effects. Dalin and Kristoffersson (1974) reported elevated serum concentrations of potassium and magnesium in rats exposed to 26 ppm phenol vapor continuously for 15 days. While not necessarily adverse, this effect may be related to the muscle tremors and neurological effects observed following inhalation exposure to phenol (see Section 2.2.1.4). 

F (severe muscle tremors, Conning and mg/kg marked twitching, Hayes 1970... 

Muscle tremors and convulsions are characteristic effects of acute dermal phenol toxicity in laboratory animals. Tremors that developed into convulsions and prostration were reported in rats exposed to 107.1 mg/kg liquid phenol application surface areas were not reported (Conning and Hayes 1970). In pigs, application of 500 mg/kg over 35-40% of the body surface (0.44 mg/cm2/kg) resulted in muscular tremors in the head region within 3-5 minutes of exposure (Pullin et al. 1978). This was followed by dilation of the pupils, loss of coordination, and excess salivation and nasal discharge within 5 minutes of exposure. It was followed by convulsions, coma, and death 5-7 minutes after exposure in two of three pigs. Direct application of a dose of 37.5 mg/kg phenol to the inner ear resulted in a reduced threshold for auditory brainstem response (Schmidt et al. 1990). 

If you breathe bromomethane, you may develop a headache and begin to feel weak and nauseated several hours later. If you breathe a large amount, fluid may build up in your lungs and it may be hard to breathe. You may have muscle tremors, and sometimes even seizures. Your kidneys may also be injured, and urine production may slow or stop. In severe cases, these effects can lead to death. In less serious cases, most of these effects usually disappear after several weeks, but some of the effects may never go away. 

A case report of oral exposure to technical-grade chlordane reported neurological effects including irritability, salivation, dizziness, muscle tremors, and convulsions (Dadey and Kammer 1953). However, exposure measurements were not provided in the report, and technical-grade chlordane contains varying amounts of heptachlor. The effects cannot be said to have resulted from exposure to heptachlor only. 

Neurotoxicity. The only human data on neurotoxicity come from case reports of occupational exposures to chlordane in which the route was not specified, and for which the effects could not be related directly to heptachlor or heptachlor epoxide alone (Dadey and Kammer 1953). Signs of neurotoxicity, such as irritability, salivation, lethargy, dizziness, labored respiration, muscle tremors, and convulsions, were reported. No data exist describing neurologic effects in animals following inhalation exposure of any duration. Acute and intermediate oral studies in animals provide support for the supposition that the neurotoxicity of chlordane seen in humans may be due in part to heptachlor or heptachlor epoxide. Although there are no reasons to suspect that neurotoxic effects... 

Accidental ingestion has caused fatalities effects were repeated, violent, clonic convulsions, sometimes superimposed on a continuous tonic spasm. Respiratory difficulty and cyanosis, secondary to the convulsions, were common. After nonfatal accidental ingestions, symptoms have included malaise, dizziness, nausea, and vomiting. Agitation, collapse, convulsions, loss of consciousness, muscle tremor, fever, and cyanosis have commonly been observed. Most patients who survive recover completely over 1-3 days protracted illness is... 

The lethal oral dose in humans is estimated to be 0.3-0.5 g/kg. Symptoms of inhalation, absorption, or ingestion in humans (inferred mostly from animal studies) may include numbness of oral mucous membranes, nausea, vomiting, abdominal pain, muscle tremor, incoordination, clonic convulsions, and stupor. 

WARNING Long-acting p2-agonists may t risk of asthma-related death Uses COPD maint Action LA p2-agonist, relaxes airway smooth muscles Dose 15 meg neb bid, 30 meg/d max Caution [C, ] w/ CV Dz, X Contra Not for acute asthma component hyp sensitivity peds w/ phenothiazines Disp Meg neb SE Chest/back pain, D, sinusitis, leg cramps, dyspnea, rash, flu-synd, t BP, arrhythmias, heart block J-K EMS Monitor ECG for arrhythmias, heart block, and hypokalemia (flattened T waves) t risk of acute asthma attack, treat w/ shortacting p-agonist OD May cause CP, palpitations, muscle tremors and cramps, and syncope symptomatic and supportive... 

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