Neurological complications of venomous snake bites: a review

Abstract

Snake bite envenoming is a neglected tropical disease affecting millions of people living in the developing world. According to the offending snake species, the clinical picture may be dominated by swelling and soft tissue necrosis in the bitten limb, or by systemic or neurological manifestations. Serious neurological complications, including stroke and muscle paralysis, are related to the toxic effects of the venom, which contains a complex mixture of toxins affecting the coagulation cascade, the neuromuscular transmission, or both. Metalloproteinases, serine proteases, and C-type lentins (common in viper and colubrid venoms) have anticoagulant or procoagulant activity and may be either agonists or antagonists of platelet aggregation; as a result, ischemic or hemorrhagic strokes may occur. In contrast, the venom of elapids is rich in phospholipase A(2) and three-finger proteins, which are potent neurotoxins affecting the neuromuscular transmission at either presynaptic or post-synaptic levels. Presynaptic-acting neurotoxins (called β-neurotoxins) inhibit the release of acetylcholine, while post-synaptic-acting neurotoxins (called α-neurotoxins) cause a reversible blockage of acetylcholine receptors. Proper management of the envenomed patient, including prompt transport to the hospital, correction of the hemostatic disorder, ventilatory support, and administration of antivenom, significantly reduces the risk of neurological complications which, in turn, reduce the mortality and improve the functional outcome of survivors.