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Seizures sarin

Symptoms Sarin exposure includes rhinorrhea, chest tightness, pinpoint pupils, shortness of breath, excessive salivation and sweating, nausea, vomiting, abdominal cramps, involuntary defecation and urination, muscle twitching, confusion, seizures, flaccid paralysis, coma, respiratory failure, and death. [Pg.268]

Chapman, S., Kadar, T., Gilat, E. (2006). Seizure duration following sarin exposure affects neuro-inflammatory markers in the rat hrain. Neurotoxicology 27 277-83. [Pg.659]

The G agents present a vapor hazard as they are very volatile. VX has a high dermal toxicity, even through intact skin, as the liquid does not evaporate quickly (Berkenstadt et al, 1991 Sidell et al, 1997). VX is 300 times more toxic than tabun on skin. A very small drop on the skin may cause sweating and fasciculations at the site. A larger dermal drop may cause loss of consciousness, seizures, apnea, and flaccid paralysis. Toxicity in descending order, on a per weight basis, is VX > soman > sarin > tabun (HSDB, 2008). [Pg.728]

Nerve - Cyclohexyl sarin (GF) - Sarin (GB) - Soman (GD) - Tabun (GA) - VX - Miosis (pinpoint pupils) - Copious secretions - Muscle twitching/ fasciculations - Miosis (pinpoint pupils) - Blurred/dim vision - Headache - Nausea, vomiting, diarrhea - Copious secretions/ sweating - Muscle twitching/ fasciculations - Breathing difficulty - Seizures... [Pg.142]

Nozaki et al. (1995) also reported on the treatment of a patient exposed to VX in an attempted murder by the same Aum Shinrikyo cult that released sarin in Matsumoto and the Tokyo subway terrorist attacks. Reportedly, VX was sprayed on the victim s back the man noted impaired vision and then experienced seizures and loss of consciousness. He arrived at the emergency room about 2 h after exposure semi-comatose... [Pg.294]

Acetylcholine levels in the neuromuscular junction are rapidly reduced by the enzyme acetylcholinesterase. A number of nerve gas poisons act to inhibit acetylcholinesterase (such as sarin and VX), such that muscles are continuously stimulated to contract. This leads to blurred vision, bronchoconstriction, seizures, respiratory arrest, and death. The poisons are covalent modifiers of acetylcholinesterase therefore, recovery from exposure to such poisons requires the synthesis of new enzyme. A new generation of acetylcholinesterase inhibitors, which act reversibly (i.e., they do not form covalent bonds with the enzyme), are now being used to treat dementia, in particular dementia as brought about by Alzheimer s disease. [Pg.866]

Acnte neurotoxic investigation using per-fnsed canine brain indicated that 400 pg of sarin caused seizure in 5.6 minntes after... [Pg.677]

Nerve agents such as tabun (GA), sarin (GB), soman (GD), and VX inhibit acetylcholinesterase enzyme throughout the body, notably in the nervous system. This causes hyperactivation of cholinergic pathways, causing convulsive seizures and respiratory failure. VX differs from its G agent counterparts in its low volatility. [Pg.118]


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See also in sourсe #XX -- [ Pg.46 ]




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