Neurological Manifestations of Snakebite Envenoming

Dear Editor, We read the articles entitled "A Rare Case of Central Retinal Artery Occlusion Following Snakebite Leading to Vision Loss" and "A Study on the Clinical Profile and Complications of Snake Bite among Patients at a Tertiary Care Centre in Western Odisha" in the esteemed "Medical Journal of Dr. D.Y. Patil Vidyapeeth" with great interest. Panigrahi et al. reported a rare central retinal artery occlusion case after a snakebite.1 Pradhan et al. assessed the clinical profile and complications of hospitalized patients with snakebites in western Odisha.2 Snakebite envenomation is a neglected tropical disease and is a significant public health burden in the developing world. About five million people worldwide are bitten by snakes every year, resulting in more than two million cases of envenomation. The venom of many elapids and some viperid snakes contains neurotoxins that induce descending flaccid neuromuscular paralysis. α-neurotoxins, β-neurotoxins, dendrotoxins, and fasciculins are the main neurotoxins found in snake venoms Figure 1.3 Also, there are the three-finger toxins that form an abundant family of nonenzymatic proteins found in snake venoms, which are characteristically identified by their spatial structure, in which three loops (fingers) protrude from the central core, stabilized by four conserved disulfide bonds. The different neurotoxins are found in various percentages among other snake families. Herein, we would like to discuss the neurological manifestation of snakebite envenomation. The most common neurological presentations of snakebites are cerebrovascular events and neuromuscular paralysis.Figure 1: Snakebite and neurotoxins. PLA2 = phospholipase A2Cerebrovascular events caused by toxic snake proteins are ischemic and hemorrhagic strokes. Ischemic stroke is the most frequent central nervous system complication following viper envenomation due to abnormal activation of thrombocytes. Serine proteases and L-amino acid oxidases may be the toxins associated with ischemic stroke. A hemorrhagic stroke is a usual presentation of Viperidae snakebite envenomation due to hemorrhagins, which can cause endothelial damage and increase vascular permeability. Metalloproteinases, phospholipase A2, and C-type lectin-like proteins are toxins related to hemorrhagic stroke.4 The first signs of descending flaccid neuromuscular paralysis are ptosis and external ophthalmoplegia since ocular muscles are more susceptible to this neuromuscular blockage. Generalized myokymia is related to dendrotoxins and fasciculins, which can act in voltage-gated potassium channels and inhibit acetylcholinesterase, leading to increased nerve excitability.5 Interestingly, there are reports of polyneuropathy, including cases of typical Guillain–Barré syndrome. It is believed that some neurotoxins could lead to direct damage of nerve endings or demyelination. Optic neuritis was already reported to be associated with snakebite envenomation. The immediate effect of neurotoxin could be vasoconstriction of the optic nerve vascular supply.6 Some authors assumed that the antivenom administration might explain some neurological complications. One supporting finding of this immune-mediated damage is the delayed cerebellar ataxia and disseminated encephalomyelitis, which were only associated with antivenom administration.3,4 Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.