Nervous system toxicity tremors

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. 

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. 

Trichloroethylene is acutely toxic, primarily because of its anesthetic effect on the central nervous system. Exposure to high vapor concentrations is likely to cause headache, vertigo, tremors, nausea and vomiting, fatigue, intoxication, unconsciousness, and even death. Because it is widely used, its physiological effects have been extensively studied. 

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 central nervous system is a major target of endosulfan-induced toxicity in both humans and animals (Blanco-Coronado et al. 1992 Boyd and Dobos 1969 Boyd et al. 1970 Garg et al. 1980 Kiran and Varma 1988 Terziev et al. 1974). Therefore, individuals with seizure disorders, such as epilepsy, may be particularly susceptible because exposure to endosulfan may reduce the threshold for tremors, seizures, and other forms of neurotoxicity, as demonstrated in studies in rats (Gilbert and Mack 1995 Gilbert 1992). 

The ammonia produced by enteric bacteria and absorbed into portal venous blood and the ammonia produced by tissues are rapidly removed from circulation by the liver and converted to urea. Only traces (10—20 Ig/dL) thus normally are present in peripheral blood. This is essential, since ammonia is toxic to the central nervous system. Should portal blood bypass the liver, systemic blood ammonia levels may rise to toxic levels. This occurs in severely impaired hepatic function or the development of collateral links between the portal and systemic veins in cirrhosis. Symptoms of ammonia intoxication include tremor, slurred speech, blurred vision, coma, and ultimately death. Ammonia may be toxic to the brain in part because it reacts with a-ketoglutarate to form glutamate. The resulting depleted levels of a-ketoglutarate then impair function of the tricarboxylic acid (TCA) cycle in neurons. 

The precise mechanism of monomethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute toxicity of dimethylhydrazine exposure probably involves the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Additionally, renal and hepatic toxicity and hemolytic effects imply alternate mechanisms of toxicity. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Cases of toxic encephalopathy and macro-qAic anemia have been reported from industrial exposures that may have been as low as 60 ppm. Symptoms were headache, drowsiness, lethargy, and weakness. Manifestations of central nervous system instability included ataxia, dysarthria, tremor, and somnolence. These effects were usually reversible. In acute exposures, the central nervous system effects were the more pronounced, whereas prolonged exposure to lower concentrations primarily produced evidence of depression of erythrocyte formation. When exposure was reduced to 20 ppm, no further cases occurred. 

Toxicity/symptoms nervous system, irritability, drowsiness, depression, incoordination, and tremors ( mad as a hatter )... 

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