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Crotalphine, a novel potent analgesic peptide from the venom of the South American rattlesnake Crotalus durissus terrificus. This is likely to be related to defective ACh transmission at parasympathetic nerve terminals, but the exact mechanisms have not been identified.
Neurotoxins have been shown to bind to nAChRs in autonomic ganglia but the significance of this in humans is not clear [] , []. In addition, a few cases of acute neuropathy have been reported following envenoming by Russell's viper Daboia russelii [72] , [74] and Eastern coral snake Micrurus fulvius [48].
There are several reports of delayed neurological manifestations after snake envenomation. Some are reports of persistence of neurological deficits which first developed during the acute stage. Distinction from critical illness neuropathy and myopathy may be difficult when symptoms are first noticed soon after recovery from the acute phase, especially with a background of ventilation, ICU care, or sepsis [28] , []. There are several other reports of neurological deficits developing at variable time points after recovery from the acute phase of envenoming.
Some of the reports are confined to reporting of prolonged symptoms [11] , and objective documentations with neurophysiological assessments are rare. In a series of patients bitten by the common krait Bungarus caeruleus , 38 patients had delayed neurological deficits. Fourteen of them had nerve conduction defects that lasted for 2 weeks to 6 months before complete recovery [10]. There are several reports suggestive of polyneuropathy after the acute phase of envenoming, with persistence of symptoms for several months [9] , [65].
One patient developed motor and sensory neuropathy 2 weeks after an unidentified snakebite and treatment with antivenom and tetanus toxoid. His clinical, biochemical, and electrophysiological features were suggestive of GBS []. Another report is of a patient who had acute neurotoxicity and respiratory arrest after a krait bite and developed quadriparesis 3 weeks later with elevated CSF protein and evidence of a sensorimotor axonal-type polyneuropathy [22].
However, GBS seems unlikely here as he had a coma with dilated pupils. Perhaps the most interesting report is by Neil et al. They have demonstrated a potential immunological basis for the syndrome, with cross-reactivity shown between glycosidic epitopes of venom proteins and neuronal GM2 ganglioside, without evidence of direct neurotoxicity of the venom [80]. There are few robust studies of long-term neurological effects.
In the first detailed clinical and neurophysiological study of long-term neurological deficits, Bell et al. Significant differences were noted in some neurophysiological parameters compared with controls. These included prolongation of sensory, motor, and F-wave latencies, and reduction of conduction velocities. The changes were more marked in the upper limbs than the lower limbs, suggesting a systemic effect related to envenoming rather than local neurological damage, as all cases in the study were bitten on the lower limb.
No abnormalities were seen on repetitive nerve stimulation, indicating lack of residual deficits in neuromuscular junction transmission. Taken together, the results were suggestive of a non-length-dependent demyelinating-type polyneuropathy.
The neurophysiological abnormalities were not typical of a toxin-mediated neuropathy, which usually would be associated with axonal damage. Interestingly, abnormalities in nerve conduction were only seen in those with presumed elapid bites []. The factors responsible for the causation of long-term neurological effects need further study. Persistent axonal damage due to neurotoxins, and delayed immune-mediated reactions to toxins or antivenom are possible explanations.
There is also some experimental evidence for delayed neuropathic effects. In their report of beta-bungarotoxin—induced toxicity in rats, Prasarnpun et al. Although the clinical manifestations of acute neuromuscular weakness with respiratory involvement are well recognised, it is surprising how many questions remain unanswered regarding neurotoxicity. This lack of clarity may at least partly be explained by the emerging evidence that has led to an increased understanding of neuromuscular transmission.
This suggests that previously held traditional models of two different types of neurotoxicity pre-synaptic or post-synaptic are inadequate to explain all of the differences seen in symptom evolution and recovery, patterns of weakness, respiratory involvement, and responses to antivenom or AChEI therapy. For example, it is becoming clear that many of the post-synaptic toxins produce nearly irreversible binding, and long-lasting effects.
This variability in toxicity may partly explain the differences in the pattern of envenomation by different species in different geographical regions, and it is highly likely that the presence of a number of different toxins in one venom also contributes. Detailed analysis of venoms from different snake species from different regions may help further elucidate these. In addition to neuromuscular failure, several other interesting acute and delayed neurological manifestations have been described after snake envenomation, and there is very little understanding of their pathophysiological basis.
These are further pointers to the diversity of the types of neurotoxicity produced by different snake species. We propose that changes be classified as acute onset within the first 2 weeks after snakebite, which may persist until late stages , delayed onset within 2—8 weeks , and late onset after 8 weeks of envenoming. Improved case definitions are the key to a better understanding of neurotoxicity from different snakes. This can only be achieved by either the identification of dead snakes or the use of laboratory or near-patient detection of venom antigen.
Further development of such techniques for developing countries where snakebites are common is vital to allow accurate and meaningful clinical descriptions of neurotoxicity. Given the high morbidity and mortality, better treatment options are clearly needed in neurotoxic envenoming.
There are several exciting reports of the use of plant extracts in the treatment of neurotoxicity [] — []. Although promising, much more research is needed before these may become therapeutic options. Until such innovative treatments are available, much can be achieved by public health measures such as better education with emphasis on early hospitalization, improved availability of antivenom and intensive care facilities in areas where snakebite is common, and international collaborative efforts to develop such strategies in these resource-limited settings.
Development of more effective and safer antivenoms including monospecific antivenoms and Fab fragments, and a better understanding of the cross-neutralisations possible with available antivenom, may help to optimize the use of antivenom in neurotoxicity [] , [] — []. Given the lack of clarity over mechanisms of neurotoxicity, the lack of consensus on the value of antivenom or AChEI therapy in snake envenoming is not surprising. Conflicting reports of their efficacy are likely to reflect different mechanisms of neurotoxicity produced by different snake species, and potentially, variations in antivenom efficacy and time of administration.
Models to predict type of toxicity, and a better understanding of the type of toxicity produced by different species, would perhaps enable better use of these treatment strategies. More data are needed on their efficacy, and may be obtained only from clinical trials in envenomation by different snake species.
Electrophysiological studies may also be valuable in helping us to understand the complex processes in human neurological envenoming. Snake neurotoxins have contributed significantly to our understanding of neuromuscular transmission and receptor function, and recent studies have highlighted many of their other properties, e.
More research into these fascinating molecules and their diverse actions would not only help us improve management of neurotoxic envenoming, but may also enable their use as potential treatments for infections, cancer, and various neurological disorders.
We gratefully acknowledge the contributions of Prof. Kularatne providing the clinical photographs and Dr. Udara drawing the diagram on neuromuscular transmission. We thank the following for their help in accessing articles: Ms. Madumi Kumarage, Ms. Purnima Jayawardena, Dr. Madeena Shahib, Dr. Abstract Snakebite is classified by the WHO as a neglected tropical disease.
Funding: The authors have indicated that no funding was received for this work. Introduction Snakebite is a neglected tropical disease of global importance [1]. Pathophysiological Basis of Neuromuscular Paralysis The peripheral neuromuscular weakness after snakebite results from defective neuromuscular junction NMJ transmission. Download: PPT. Figure 1. Sites of action of snake neurotoxins and other substances on the neuromuscular junction. Neuromuscular Transmission and Neuromuscular Block At the pre-synaptic level, the motor nerve axon terminal is responsible for the synthesis, packaging, transport, and release of the neurotransmitter acetylcholine ACh.
Table 1. Summary of some key animal studies with individual snake neurotoxins. Snake Venom and Neuromuscular Block Snake venoms do not contain a homogenous single toxin, but are complex cocktails of enzymes, polypeptides, non-enzymatic proteins, nucleotides, and other substances, many of which may have different neurotoxic properties [91] , [] , [] , [] , [] , [] , [] Table 2.
Figure 3. Bilateral ptosis and facial weakness in neurotoxic envenoming. Table 3. Summary table of some key studies with descriptions of neurotoxicity.
Respiratory Muscle Weakness Many patients with neurotoxicity develop ptosis and extraocular muscle weakness, but only a few will develop respiratory muscle weakness. Neurotoxicity, Type of Snake, and Possible Geographical Variation There is a clear variation in the propensity of similar species of snakes to produce different patterns of neuromuscular weakness in different geographical locations.
Neurophysiological Changes in Neuromuscular Paralysis Surprisingly few human data are available on the acute neurophysiological changes after snakebite. Table 4. Some human studies with neurophysiological findings in snake neurotoxicity.
Table 5. Summary of studies on interventions in neurotoxic envenoming. Acetylcholinesterase Inhibitors AChEIs, Anticholinesterases in Neurotoxicity Neuromuscular weakness, especially due to non-depolarising post-synaptic blockade, has similarities to myasthenia in pathophysiology, and it is theoretically plausible that AChEIs are effective in this type of neurotoxic envenoming.
Acute Neurotoxicity—Other Neurological Manifestations Several other interesting acute neurological features have been reported after snake envenomation, which are likely to be direct neurotoxic effects. Delayed Neurological Manifestations There are several reports of delayed neurological manifestations after snake envenomation. Discussion Although the clinical manifestations of acute neuromuscular weakness with respiratory involvement are well recognised, it is surprising how many questions remain unanswered regarding neurotoxicity.
Key Learning Points Snake venoms are complex mixtures of different toxins, and each neurotoxin has diverse neurotoxic effects. There is considerable geographical, interspecies, intraspecies, as well as possibly ontogenetic variation in neurotoxicity with snake envenoming. Accurate identification of envenoming snakes and uniform case definitions are needed to improve comparability of different reports of neurotoxic envenoming.
There are many interesting acute and delayed neurotoxic manifestations other than neuromuscular weakness, and these may reveal valuable information that may lead to a better understanding of other neurological diseases. The evidence for antivenom and AChEIs in treatment of neurotoxic envenoming is not strong, and large randomized trials are urgently needed.
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