Nervous system toxicity convulsions

Epileptic seizures in overdosed patients may indicate a degree of nervous system toxicity. Convulsions in poisoned patients are reported to be more hkely with mefenamic acid than with other compounds (1). Other nervous system reactions (such as headache) are less frequent than with the arylcarboxylic acid derivatives. Coma has also been described as a consequence of mefenamic acid overdosage (2). 

Poisoning episodes in humans show that the central nervous system is the primary target system of orally administered endrin. Acute human poisonings by endrin-contaminated food caused symptoms of central nervous system toxicity such as jerking of arms and legs, tonic-clonic contractions, convulsions, and sudden collapse and death (Carbajal-Rodriquez et al. 1990 Coble et al. 1967 Davies and Lewis 1956 Rowley etal. 1987 Waller et al. 1992 Weeks 1967). 

Death. Clinical reports in humans and studies in animals demonstrate that death due to central nervous system toxicity is the primary acute lethal effect associated with endrin exposure. A lethal dose of endrin in humans has not been identified, but 0.2-0.25 mg endrin/kg body weight is sufficient to cause convulsions (Davies and Lewis 1956). Liver, kidney, heart, and brain damage were reported following oral and inhalation exposures. Since endrin is no longer used commercially, the general public is not... 

In addition to binding to cytochrome c oxidase, cyanide inhibits catalase, peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, and succinic dehydrogenase activities. These reactions may make contributions to the signs of cyanide toxicity (Ardelt et al. 1989 Rieders 1971). Signs of cyanide intoxication include an initial hyperpnea followed by dyspnea and then convulsions (Rieders 1971 Way 1984). These effects are due to initial stimulation of carotid and aortic bodies and effects on the central nervous system. Death is caused by respiratory collapse resulting from central nervous system toxicity. 

Neurological Effects. Neurological effects in hrnnans after acute inhalation exposure to chloroform are well documented because chloroform has been used as an anesthetic for surgery. Inhaled chloroform acts as a depressant on the central nervous system. Chronic inhalation exposure to chloroform resulted in exhaustion, lack of concentration, depression, and irritability in occupationally exposed people (Challen et al. 1958). In a case study, chloroform inhalation for 12 years resulted in psychotic episodes, hallucinations, and convulsions (Heilbmnn et al. 1945). Central nervous system toxicity was observed in humans after oral exposure to chloroform, which suggests that the effects of inhalation and oral exposure are similar. In case reports of patients who intentionally or accidentally ingested several ounces of chloroform, deep coma with abolished reflexes occurred within a few minutes (Piersol et al. 1933 Schroeder 1965 Storms 1973). 

Cycloserine causes serious dose-related central nervous system toxicity with headaches, tremors, acute psychosis, and convulsions. If oral dosages are maintained below 0.75 g/d, such effects can usually be avoided. 

Signs of methyl bromide toxicity following acute exposure include irritation of the eyes and respiratory tract, tremor, incoordination, depression of the central nervous system and convulsions. Long-term exposure induces pulmonary congestion, central nervous system effects, and renal and hepatic lesions. After oral administration to rats, hyperplasia and hyperkeratosis (and squamous-cell carcinomas) of the forestomach were observed (lARC, 1986). 

Central nervous system toxicity is rarely observed with catecholamines or drugs such as phenylephrine. In moderate doses, amphetamines commonly cause restlessness, tremor, insomnia, and anxiety in high doses, a paranoid state may be induced. Cocaine may precipitate convulsions, cerebral hemorrhage, arrhythmias, or myocardial infarction. Therapy is discussed in Chapter 59 Management of the Poisoned Patient. 

Nervous system toxicity is most often seen with rapid intravenous infusion (3,25,26). The effects include headache, dizziness, tremor, confusion, tinnitus, dysarthria, paresthesia, respiratory depression, altered level of consciousness (from drowsiness to coma), and convulsions. 

Melarsoprol is the drug of choice for the treatment of late-stage meningoencephalitic trypanosomiasis caused by the west and east African strains of the disease. Because the drug has the potential for serious nervous system toxicities (e.g., convulsions, acute cerebral edema, and coma), the drug usually is administered in a hospital setting with supervision. An additional problem with melarsoprol is the development of resistance by the parasite. 

Highly toxic exhibits acute, delayed, and chronic toxicity symptoms include nausea, vomiting, weakness, somnolence, excitement, and muscle contraction causes dermatitis and irritation on skin contact a stimulant to central nervous system, producing convulsions can cause adverse reproductive effects no evidence of carcinogenicity in rats and mice oral LD50 value (mice) 7.5 mg/kg exposure limit PEL/TLV-TWA (skin) 0.1 mg/m (OSHA ACGlH) RCRA Waste Number P050 US EPA listed extremely hazardous substance. 

The authors hypothesized that the history of febrile convulsions in this patient might have been a susceptibility factor for seizures provoked by local anesthetics. However, this is contradicted by the study quoted above, which showed that a history of seizure disorder is only a minor susceptibility factor for postoperative seizures after regional blockade, even if there was recent seizure activity [5 ]. Since the febrile convulsions were very long ago in the case reported here, the seizure might have been due to nervous system toxicity after a rather high dose of 5 mg/kg ropivacaine, despite the low concentration later found [84. ... 

The Class I agents have many similar side effects and toxicities. The anticholinergic side effects include dry mouth, constipation, and urinary hesitancy and retention. Common gastrointestinal (GI) side effects include nausea, vomiting, diarrhea, and anorexia. Cardiovascular adverse effects are hypotension, tachycardia, arrhythmias, and myocardial depression, especially in patients with congestive heart failure. Common central nervous system (CNS) side effects are headache, dizziness, mental confusion, hallucinations, CNS stimulation, paraesthesias, and convulsions. 

Neurotoxicity (damage to the nervous system by a toxic substance) may also be seen with the administration of the aminoglycosides. Signs and symptoms of neurotoxicity include numbness, skin tingling, circum-oral (around the mouth) paresthesia, peripheral paresthesia, tremors, muscle twitching, convulsions, muscle weakness, and neuromuscular blockade (acute muscular paralysis and apnea). 

The effects of endosulfan have not been studied in children, but they would likely experience the same health effects seen in adults exposed to endosulfan. Data in adults, mostly derived from cases of accidental or intentional acute exposure (ingestion) to large amounts of endosulfan, indicate that the primary target of endosulfan toxicity is the nervous system. The effects are manifested as hyperactivity and convulsions and in some cases have resulted in death (Aleksandrowicz 1979 Blanco-Coronado et al. 1992 Boereboom et al. 1998 Cable and Doherty 1999 Lo et al. 1995 Terziev et al. 1974). These effects have been reproduced in experimental animals. 

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