Convulsions poisons causing

Cytisine. This base belongs to the same pharmacological group as nicotine.It is a powerful poison causing nausea, convulsions and death by failure of respiration. The nicotine-like action is shared by A -methyl-cytisine but the latter, according to Scott and Chen, who have made a detailed study of its action, is weaker and has about one-fortieth the toxicity of nicotine. 

Sodium azide is a toxic as well as an explosive substance (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nd e(j New York John Wdey Sons). Although inert to shock, violent decomposition can occur when heated at 275°C. Contact of solid or solution with lead and copper must be avoided. Reactions with halogens, carbon disulfide, or chromyl chloride can be explosive. Dissolution in water produces toxic vapors of hydrazoic acid. The salt is an acute poison causing headache, hypotension, hypothermia, and convulsion. 

Strychnine-poisoned birds show clinical effects within 2h of ingesting the product. The birds become apprehensive and nervous and have violent tetanic convulsions, which cause them to become exhausted and to die of hypoxia. Sodium monofluoroacetate causes overstimulation of the CNS and myocardial depression. Cardiac failure is the cause of death and occurs within 1 h of consuming the product or contaminated carcass. 

Illicium religiosum, I. anisatum. Highly toxic Japanese variant of the safe plant, Chinese star anise (/. verum). All parts of the plant, particularly the seeds, are poisonous, causing vomiting and epileptiform convulsions of the type caused by picrotoxin, with dilated pupil and cyanosis. Kills by effects on respiratory and cardiovascular centres in medulla. Regarded as a sacred plant and found growing around Buddhist temples and graveyards. 

Strychnine, a neurotoxin, is the chief alkaloid present in nux vomica, which is derived from special species of Strychnos, particularly Strychnos nux vomica and Strychnos ignatia. Strychnine is found chiefly in the seeds of these plants, accompanied usually by brucine. Strychnine poisoning causes muscular stiffness, increased reflex reactions, tremors, involuntary twitches, sudden convulsions, and opisthotonus (see Figure 89). 

Paipunine is one of numerous alkaloids isolated from various species of the plant family Stemonaceae. Paipunine was isolated and its pharmacology studied by Lee and Chen (254). Concentrations varying from 1 400,0 0 to 1 100,000 caused contraction of the isolated guinea pig uterus. Paipunine is a convulsant poison, the chief site of action being the medulla. 

Methyl bromide (bromomelhane [CAS 74-83-9]) Causes severe Irritation and burns upon direct contact. Vapors irritating to the lung pulmonary edema may result. The CNS, liver, and kidneys are major target organs acute poisoning causes nausea, vomiting, delirium, and convulsions. Both inhalation and skin exposure may cause systemic toxicity. Chronic exposures associated with peripheral neuropathy in humans. Evidence for adverse effects on fetal development in test animals. Limited evidence of carcinogenicity in test animals (lARC 3). See also p 263, and chloropicrin in this table. 

The inhibition of AChE leads to the accumulation of the neurotransmitter ACh in synapses of the central and peripheral nervous systems and over-stimulation of post-synaptic cholinergic receptors. Exposure to even small amounts of an organophosphorus compound can be fatal as the poison causes seizures, convulsions and lesions of the central nervous system. The current standard treatment for poisoning usually consists of combined administration of anticholinergic drugs (preferably atropine) and AChE reactivators (called oximes). 

Inhibition of AChE is irreversible, preventing the substrat (ACh) from reacting with the esterase site. Consequently, accumulation of ACh results in all symptoms of acetylcholine poisoning caused by organophosphates (Santos et al. 2007). Symptoms of intoxication appear after approximately 50 % of the AChE is inhibited and the typical effects are agitation, muscle weakness, muscle fasciculations, hypersalivation and sweat. Severe poisonings may cause respiratory failure, unconsciousness, confusion, convulsions and/or death (Sogorb and Vilanova 2002 Duysen et al. 2012). 

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. 

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