And convulsions

NMD A, kainic acid, and AMPA, are stimulants and convulsants (14). These agents are used only experimentally. 

Sulfolane causes minimal and transient eye and skin irritation (19,20). Inhalation of sulfolane vapors in a saturated atmosphere is not considered biologically significant. However, when aerosol dispersions have been used to elevate atmospheric concentration, blood changes and convulsions have been observed in laboratory animals (22,31). Convulsions caused by sulfolane injected intraperitoneaHy have also been studied (32). 

Symptoms of deficiency in animals include poor appetite, stunted growth, and weight loss increased incidence of irritabihty and convulsions (tetany) some growth abnormahties decreased egg production in poultry with reduced hatchabihty and thin eggsheU quahty and birth of weak, dead, or deformed offspring in other animals. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

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. 

Health Hazards Information - Recommended Personal Protective Equipment Eye protection Symptoms Following Exposure Vapors from very hot material may irritate eyes and produce headache, drowsiness, and convulsions General Treatment for Exposure Remove fresh air. Wash affected skin areas with water. Flush eyes with water Toxicity by Inhalation (ThresholdLimit Value) 5 mg/m Short-Term Exposure limits Not pertinent Toxicity by Ingestion Grade 1 LDjq 5 to 15 g/kg Late Toxicity Birth defects in rats polyneuritis in humans Vapor (Gas) Irritant Characteristics Not pertinent liquid or Solid Irritant Characteristics No appreciable hazard. Practically harmless to the skin Odor Threshold Data not available. 

Reynolds and Waud found that capaurine produced paralysis on injection into the lymph sac of frogs, and convulsions when injected into mice or rabbits in doses of 100-200 mgm./kilo. It depressed the activity of the heart, intestine and uterus. The methyl ether caused convulsions in frogs, but otherwise acted like capaurine. 

Symptoms of ergotism that must be reported immediately in dude coolness , numbness and tingling of extremities dyspnea, nausea, confusion, tachycardia or bradycardia, chest pain, hallucinations and convulsions If these reactions occur, the nurse immediately reportsthem to the primary health care provider because use of the drug must be discontinued. 

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. 

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. 

Acute clinical signs of neurotoxicity, manifested by hyperexcitability, dyspnea, decreased respiration, tremors, and convulsions, were identified in the available literature as effects caused by high doses of endosulfan. Exposure to high levels of endosulfan in humans may possibly be associated with permanent brain damage as manifested by cognitive and emotional deterioration, memory impairment, and... 

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