Nervous system toxicity

Oral poisoning after accidental phenol ingestion has caused fulminant central nervous system depression, hepatorenal and cardiopulmonary failure [20]. No hepatorenal or central nervous system toxicities with properly performed chemical peels have been reported in the literature [21]. 

NSAIDs are associated with gastrointestinal, renal, hepatic, and central nervous system toxicity and may increase blood pressure. NSAIDs that are selective for the cyclooxygenase-2 (COX-2) isozyme are less likely to cause gastrointestinal complications but may increase the risk of cardiovascular events. They are no more effective than nonselective NSAIDs. Selective agents should be reserved for patients at high risk of gastrointestinal complications and low risk for cardiovascular events. 

K. Arulanantham and M. Genel, Central nervous system toxicity associated with ingestion of propylene glycol, J. Pediatr, 93, 515 (1978). 

Rimantadine, amantadine Central nervous system toxicity... 

Peripheral neuropathy has also occurred in humans as the result of solvent abuse of products containing -hexane (Altenkirch et al. 1977 Chang et al. 1998 Spencer et al. 1980). Clinical signs were very similar to those seen after occupational exposure however, signs of central nervous system toxicity may also be present due to other components in the inhaled mixtures, e.g., toluene (Spencer et al. 1980). 

Neurological examinations of humans with M-hexanc-induced peripheral neuropathy have not shown clinical signs of central nervous system toxicity (Herskowitz et al. 1971 Yamamura 1969). There have been reports of altered evoked potentials recorded in the brain (increased latency, decreased amplitude) in humans occupationally exposed to -hexane (Mutti et al. 1982c Seppalainen et al. 1979). There has been one report of an individual occupationally exposed to -hexane for 38 years who developed Parkinsonism (Pezzoli et al. 1995), although the etiology of this case is complicated by the fact that the patient had a sister who was probably affected by Parkinsonism. Further studies, particularly prospective... 

An outbreak of acute human endrin poisoning associated with central nervous system toxicity and 19 deaths in 194 known cases occurred in Pakistan in 1984 (Rowley et al. 1987). The vector for exposure was not identified, but contamination of a food item was the likely cause of poisoning. 

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... 

Respiratory Effects. Breathing irregularities including Cheyne-Stokes respiration developed in two persons who fell into cisterns containing copper cyanide or potassium cyanide (Dodds and McKnight 1985 Trapp 1970) or whose hands were exposed to hydrogen cyanide (Potter 1950). The effects reflect the central nervous system toxicity of cyanide. 

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. 

Albrecht WN. 1987. Central nervous system toxicity of some conunon environmental residues in the mouse. J Toxicol Environ Health 21 (4) 405-421. 

Two additional features of the nervous system are particularly important to a discussion of neurotoxicity. The blood—brain barrier and the blood-nerve barrier act as protective devices for the nervous system, and are effective at preventing movement of certain chemicals from the blood to the brain and nerves. Unfortunately neither barrier is effective against all types of molecule, and there are plenty of examples of brain and nervous system toxicants that can penetrate the barriers. ... 

Evidence of central nervous system toxicity in animals includes disturbed equilibrium in cats exposed to 7,200 ppm chloroform for 5 minutes, deep narcosis in cats exposed to 21,500 ppm for 13 minutes, deep narcosis in mice exposed to 4,000 ppm for 30 minutes, slight narcosis in mice exposed to 3,100 ppm for 1 hour, and no obvious effects in mice exposed to 2,500 ppm for 2 hours (Lehmann and Flury 1943). Memory retrieval was affected in mice exposed to chloroform via anesthesia (concentration not specified) (Valzelli et al. 1988). The amnesic effect was not long-lasting. 

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). 

Neurotoxicity. No clinical signs of central nervous system toxicity or histological alterations of nervous system organs and tissues were observed in rats or mice in the NCI (1978) chronic oral bioassay. Tests for neurotoxicity in animals may be appropriate if there is clinical evidence of neurological dysfunction in general oral or dermal toxicity studies of I 2-diphenylhydrazine. 

Tramadol is an opioid analgesic and when given to patients who are also receiving imipramine (a tricyclic antidepressant), there is an increased risk of central nervous system toxicity. The risk of occurrence of sedation is increased. 

Toxicology. Chlorinated dibenzo-p-dioxins (CDDs) cause chloracne, may cause hepato-toxicity, immunotoxicity, reproductive toxicity, developmental toxicity, and central nervous system toxicity, and are considered to be a human carcinogen. 

Central nervous system toxicity from either social abuse of nitrous oxide or extremely heavy occupational exposure has been characterized by symptoms of numbness, paresthesias, impairment of equilibrium, and difficulty in concentration. In severe cases, the patient becomes incontinent, impotent, and unable to walk. Neurological signs include ataxic gait, muscle weakness, impaired sensation, and diminished reflexes. 

Toxicology. Phenol is an irritant of the eyes, mucous membranes, and skin systemic absorption causes nervous system toxicity as well as liver and kidney damage. 

Boekelheide K. 1987. 2,5-Hexanedione alters microtubule assembly. I. Testicular atrophy, not nervous system toxicity, correlates with enhanced tubulin polymerization. Toxicol AppI Pharmacol 88 370-382. 

Lignocaine s clearance by the liver is flow dependent. In heart failure cardiac output may be very low and therefore hepatic blood flow through both the hepatic artery and the portal venous system is also low. This meant a lower extraction of the drug from the blood and accumulation of lignocaine until the high plasma concentration produced the central nervous system toxicity. 

A variety of adverse effects have been reported following the use of antacids. If sodium bicarbonate is absorbed, it can cause systemic alkalization and sodium overload. Calcium carbonate may induce hypercalcemia and a rebound increase in gastric secretion secondary to the elevation in circulating calcium levels. Magnesium hydroxide may produce osmotic diarrhea, and the excessive absorption of Mg++ in patients with renal failure may result in central nervous system toxicity. Aluminum hydroxide is associated with constipation serum phosphate levels also may become depressed because of phosphate binding within the gut. The use of antacids in general may interfere with the absorption of a number of antibiotics and other medications. 

Lobelia Nervous system toxicity, respiratory paralysis... 

Preskorn SH, Jerkovich GS. Central nervous system toxicity of tricyclic antidepressants phenomenology, course, risk factors and role of therapeutic drug monitoring. J Clin Psychopharmacol 1990 10 88-95. 

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