Scorpion envenomation can result in distinct clinical syndromes. Most scorpion species' stings cause only local pain and inflammation that respond well to minimal supportive therapy and wound care. These scorpions pose no significant management issues and, with few exceptions, are not discussed here in further detail. The truly dangerous scorpions of the world, typified by Tityus species in the Caribbean region and in South America, Androctonus species and Buthus occitanus in North Africa, Leiurus quinquestriatus in the Near East, and Mesobuthus tamulus in India, cause an "autonomic storm" with prominent cardiopulmonary effects. A third clinical syndrome occurs from stings of Centruroides species in the southwestern United States and Mexico and from Parabuthus species in southern Africa. These produce prominent neurologic effects associated with excess cholinergic tone. Children are typically more severely affected than adults and often require prompt medical management to avoid morbidity and mortality. The ideal treatment of scorpion envenomation remains controversial, primarily because controlled clinical trials are lacking. Although anecdotal experience and comparisons of historic cohorts demonstrate a benefit from aggressive symptomatic and supportive care, the proper use of antivenins has not been fully resolved.
[...] Many scorpion specimens reveal a broken stinger that does not penetrate human skin well. Scorpions grasp prey in their pedipalps and then rapidly thrust the tail overhead to sting. The chelicerae tear the food apart. Scorpions feed primarily on ground-dwelling arthropods and small lizards. The scorpion consumes only the juices and liquefied tissues of its prey, discarding the solid parts. Scorpions envenom by stinging; although stings may be reported as bites, true scorpion bites have not been documented and would be inconsequential if they did occur. [...]
[...] Each scorpion species' venom contains several neurotoxins, but they all share a similar structure and homologous sequences. In neuronal membranes, these toxins cause two effects with regard to fast sodium channels involved in action potential transmission: incomplete inactivation of sodium channels during depolarization, resulting in a widening of the action potential, and a slowly developing, inward sodium current after repolarization, leading to membrane hyperexcitability. The net result is repetitive firing of axons. enhancing release of neurotransmitters (acetylcholine, norepinephrine, dopamine, glutamate, aspartate, ?-aminobutyric acid [GABA]) at synapses and at neuromuscular junctions. [...]
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