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 » Subjects and Methods
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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 3  |  Page : 378-381

Comparative study of electrophysiological changes in snake bites

Department of Medicine, BJ Medical College and Sassoon General Hospital, Pune, Maharashtra, India

Date of Web Publication5-Jun-2015

Correspondence Address:
Patwari Panduranga
Room No. 506, Resident Quarters, BJGMC and SGH, Pune - 411 001, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.158214

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 » Abstract 

Aims: To study and compare the electrophysiological changes in neuroparalytic or vasculotoxic snakebites.
Materials and Methods: 40 patients who had a definite history of snakebite, either vasculotoxic or neuroparalytic, were selected. They were grouped as Group A, 20 patients having a neuroparalytic snakebite with definite envenomation at the time of admission, and Group B, 20 patients having a vasculotoxic snakebite with definite envenomation at the time of admission. All patients underwent a detailed clinical examination, all relevant investigations and nerve conduction studies according to protocol.
Results: In this study, we noticed that the motor nerve conduction amplitude, conduction velocity and distal latency were within normal limits in both the groups. On RNS (repetitive nerve stimulation study) of facial and median nerves, a decremental response was seen in 13 (65%) patients in facial nerve and in 7 (35%) patients in median nerve in Group A; while, the same response was seen in 8 (40%) patients in facial nerve and 3 (15%) patients in median nerve in Group B. A post exercise decremental response was seen in 13 (65%) patients in median nerve and 16 (80%) patients in facial nerve in Group A; and, in 3 (15%) patients in median nerve and 8 (40%) patients in facial nerve in Group B.
Conclusions: In our study, we noticed that the decremental response on RNS was not only present in neuroparalytic snake bite (post-synaptic neuromuscular blockade) but also in vasculotoxic snakebite [pre-synaptic neuromuscular blockade] (seen in Russel's viper).

Keywords: Facial nerve; median nerve; repetitive nerve stimulation study; snake bite

How to cite this article:
Panduranga P, Sangle S A, Mane AA, Doshi S, Kadam D B. Comparative study of electrophysiological changes in snake bites. Neurol India 2015;63:378-81

How to cite this URL:
Panduranga P, Sangle S A, Mane AA, Doshi S, Kadam D B. Comparative study of electrophysiological changes in snake bites. Neurol India [serial online] 2015 [cited 2021 Jul 27];63:378-81. Available from:

 » Introduction Top

Neurotoxicity is a well-known feature of envenoming due to elapids (family Elapidae) such as kraits (Bungarus spp.) and cobras (Naja spp). Although considered relatively less common with true vipers (family Viperidae), neurotoxicity due to beta-neurotoxins, mostly neurotoxic phospholipase A2 toxins [1] (PLA2s), is well recognized in envenoming with the Russell's viper (Daboia russelii; found in Sri Lanka and South India), the asp viper (Vipera aspis), [2] the adder (Vipera berus) [3],[4] and the nose-horned viper (Vipera ammodytes). [5]

Most of the electrophysiological studies have been performed on patients suffering from neuroparalytic snake bite (for example, krait and cobra), but the studies documenting electrophysiological abnormalities in patients with vasculotoxic snake bites (Viper) are few. Neurological manifestations (electrophysiological abnormalities) due to a viper bite are usually reported from South India and Sri Lanka but have not been reported from Western India. This study aims to document the neurological manifestations and electrophysiological abnormalities in cases of vasculotoxic snakebite from western India. The defective neuromuscular junction (NMJ) transmission can be pre-synaptic or post-synaptic. The pre-synaptically active neurotoxins (beta-neurotoxins, mainly neurotoxic phospholipase A2 toxins, bind to the motor nerve terminals, leading to the depletion of synaptic acetylcholine (Ach) vesicles, resulting in impaired release of ACh, and later, leading to degeneration of the motor nerve terminal. [6] The post-synaptically active neurotoxins (alpha-neurotoxins) bind to the post-synaptic muscle nicotinic acetyl choline receptor (nAChRs). They resemble the action of d-tubocurarine (dTC). dTC classically produces a reversible, non-depolarising post-synaptic block by competitive inhibition of ACh binding to the muscle nAChR. [6] In this type of toxicity, the antivenom may facilitate dissociation of the toxin from the ACh receptor and accelerate recovery [7] and a clinical response to acetycholineesterase inhibitors (AChEIs), similar to that seen in myasthenia gravis, is more likely. The recent insights into neuro-muscular junction (NMJ) transmission have enabled better and more comprehensive characterization of the more recently described toxins. Candoxin, a novel toxin isolated from the venom of the Malayan or blue krait (Bungarus candidus), is a non-conventional three-finger toxin (3FTX) with structural similarities to alpha-bungarotoxin. [8],[9] However, in contrast to the nearly irreversible blockade produced by alpha-bungarotoxin, candoxin produces a readily reversible block of the post-synaptic nAChR. In addition, candoxin also inhibits the pre-synaptic neuronal AChRs and produces tetany and tetanic fade on rapid repetitive stimulation. [8],[9]

 » Subjects and Methods Top

This study was conducted in the Department of Medicine, from September 2011 to August 2013. A synopsis of the study protocol was submitted to the Institutional Ethical Committee and approval was obtained. Patients were selected from the ward and medical ICU of the hospital. In the study, patients having a definite history of snake bite, either vasculotoxic or neuroparalytic, were included. Patients with unknown bites and snake bites without definite envenomation were excluded from the study. The total sample size of 40 was divided into two groups of 20 each (Group A: Neuroparalytic snake bite patients, Group B: Vasculotoxic snake bite patients). The study protocol was explained in detail to all the subjects. Informed written consent was taken from the subjects willing to participate in the study. A questionnaire was designed to obtain their basic clinical information. A nerve conduction study was conducted at a fixed room temperature of 30 0 C within 6 to 10hrs after the patient's hospitalization.

 » Assessment of Patient Top

Clinical evaluation

The patients were asked questions regarding symptoms of the snake bite at the time of admission; patients with a neuroparalytic snakebite, presenting with ptosis, respiratory distress, neck muscle weakness and respiratory paralysis were included in Group A. Patients with vasculotoxic snakebite presenting with bleeding manifestations (haematuria), extensive cellulitis at the site of bite, prolonged bleeding time (BT), clotting time (CT) and 20 min whole blood clotting time (WBCT) were included in Group B. A detailed history, general examination and neurological examination were carried out in all the patients selected for the study. The offending snake was identified by examination of the dead snake brought by the patients at the time of admission, or by the photograph of the snake. The patients with a definite history of snakebite, with either neuroparalytic or vasculotoxic manifestations, who were not able to identify the snake, or did not bring the dead snake along with them, were classified as patients having an unidentified snakebite. Patients were inducted into the study regardless of whether or not the antisnake venom (ASV) had already been administered. Patients who had already received neostigmine were also included in the study. The relevant laboratory investigations were done on the day of admission.

Electrophysiological evaluation of peripheral nerve function

The methodology adopted for measurement of nerve conduction parameters was as follows:

The patients underwent nerve conduction studies. Nerve conduction parameters were measured by using the standard RMS ALERON 401 machine (Recorders and Medicare systems, India) in the Department of Medicine. Recordings were done using the standard procedure such as temperature control (32-34 o C), careful distance measurements and recording of well-defined and artefact-free responses.

Motor nerve conduction and repetitive nerve stimulation (RNS) were performed on median and facial nerves of either side. The procedure was carried out by using surface electrodes. The amplitude and latency of the motor action potential and velocity of conduction in the concerned nerve were recorded. After this motor nerve conduction, a repetitive nerve stimulation (RNS) study was performed. The nerves selected for RNS were the facial and median nerves.

In this study, the nerve was stimulated repeatedly at either 3 cycles per second [slow RNS] (5 such stimulations were given); or, at 30 cycles per second [rapid RNS] (5-100 stimuli were given). The action potentials resulting as a consequence of this repeated stimulation were sequentially recorded and a comparison was made between the amplitude of the first (s1) and the fourth (s4) action potentials to find out if decrement was present. If the results of this test were borderline, the test was repeated after voluntary muscle activity for 30 seconds, or if this was not possible (in comatose patients), the muscle was stimulated repeatedly to stimulate voluntary muscle contraction and the repetitive stimulation test was performed again. This record constituted the post-tetanic action potential study. As per the standard protocol, a decrement was considered significant if s4/s1 (i.e., the difference in the amplitude between the fourth and first stimuli during repetitive stimulation study) was more than 10% (i.e., a decrement of 10%). On testing at 30 cycles per second, a decrement of more than 20% was considered significant.

Statistical analysis

The data was managed in a Microsoft excel spreadsheet. General informative tables were prepared with mean and standard deviation. Scatter plot was used to observe correlation between the parameters. Demographics and general information like the count, average and percentage figures for various parameters, with all permutations and combinations, were calculated on Microsoft Excel sheets. A P < 0.05 was considered statistically significant. Chi-Square test, Fisher exact test and Student's t-test were used to investigate and model the impact of various parameters. All statistical analysis was done using SPSS and Minitab 16.

 » Results Top

In this study, the mean motor nerve conduction amplitudes (mv) were within normal limits. In the median nerve, it was 9.54 ± 3.75 mv and10.6 ± 4.49 mv (P = 0.425) in Group A and B respectively. In the facial nerve, the amplitude in group A was 1.45 ± 0.609mv and in Group B, 1.25 ± 0.586 mv (P = 0.291). The mean distal latency in the median nerve was 3.05 ± 1.1 ms and 3.47 ± 1.6 ms (P = 0.349); and, the mean distal latency in the facial nerve, 3.02 ± 1.2 ms and 2.987 ± 1.093 ms (P = 0.931) in Group A and B respectively, which was within normal limits. The mean conduction velocity in the median nerve was 60.82 ± 11.53m/s in Group A and 57.78 ± 11.19 m/s in Group B (P = 0.931) which was within normal limits. There was no statistical significant difference in amplitude, distal latency and conduction velocity between Group A and Group B [Table 1]. On repetitive nerve stimulation study (RNS) [Table 2], a decremental response was noted frequently, seen in 13 (65%) patients in facial nerve (P = 0.2049) and 7 (35%) in median nerve (P = 0.2733) of Group A, and in 8 (40%) patients in facial nerve and 3 (15%) patients in median nerve of Group B. However, this was not statistically significant. Post exercise RNS decremental response was seen in 13 (65%) patients in median nerve and 16 (80%) patients in facial nerve of Group A, and in 3 (15%) patients in median nerve and 8 (40%) patients in facial nerve of Group B (median nerve, P = 0.0031; facial nerve, P = 0.0225), which was highly significant. The decremental response in RNS [Table 3] in Group A was seen in 5 (38.46%), 4 (30.76%) and 4 (30.76%) patients of cobra, krait and unknown snake bite, respectively; and, in Group B in 1 (12.5%), 3 (37.5%), and 4 (50.00%) patients of cobra, unknown snake, and viper bite, respectively.
Table 1: Nerve conduction parameters

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Table 2: Repetitive nerve stimulation study (RNS) in facial and median nerve

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Table 3: Comparison of the incidence of the decremental response in RNS of facial nerve in different types of snake bites between the two groups

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 » Discussion Top

As has already been pointed out in the introduction, the electrophysiology of patients who have suffered a snake bite has been sparsely documented. In the present study, the electrophysiological changes between neuroparalytic and vasculotoxic snake bites were compared. There was no statistically significant difference between the mean motor nerve conduction amplitudes (mv), distal latency and conduction velocity (which were within normal limits), in both the groups. A decremental response in Group A patients with neuroparalytic snake bites was seen in 13 (65%) patients in the facial nerve, and 7 (35%) in the median nerve; and, in Group B, in 8 (40%) patients in the facial nerve, and 3 (15%) patients in the median nerve. There was no statistically significant difference in the decremental response to RNS in the facial and median nerves in either Group A or Group B. In Thailand, a decremental response was found in the nerve conduction studies done by Aksarnugraha et al. [10] on 20 subjects following a neurotoxic (cobra) bite. Similar findings were found on post exercise RNS, with a decremental response [Table 2] seen in 13 (65%) and 16 (80%) patients in the median and facial nerves, respectively, in Group A; and, in 3 (15%) and 8 (40%) patients in the median and facial nerves, respectively in Group B. This was found to be highly statistically significant. Rastogi et al., [11] studied five patients with a neurotoxic snake bite caused by the Indian krait, and found neither decrement after RNS nor post-tetanic fatigue. In a study done by Watt et al., [12] a decremental response was seen on nerve conduction studies in two of the ten cases of neurotoxic bite due to a cobra (Najanaja philippinensis). In our study, we found that 4 (50%) patients of viper bite had a decremental response on RNS [Table 3]. Trevett et al., [13] found a decremental response with post tetanic potentiation followed by post tetanic exhaustion in patients following the bite of a Papuan taipan snake.

In conclusion, electrophysiological changes were noted despite performing nerve conduction studies after several hours (6 to 10 hours) of the snake bite, irrespective of the treatment (anti-snake venom, neostigmine, etc) administered. In our study, the vasculotoxic snake bite (viper) patients had electrophysiological changes, despite not having any neuroparalytic manifestations like ptosis, neck muscle weakness, respiratory muscle involvement or areflexia. Neuroparalysis due to a viper bite, unlike in South India and Sri Lanka, has not been reported from Western India. This is the first study, to the best of our knowledge, to report electrophysiological changes following a viper bite from Western Maharashtra. However, the findings of our study cannot be generalized due to the limitation of a small sample size.

 » References Top

Dixon RW, Harris JB. Nerve terminal damage by B-bungarotoxin: Its clinical significance. Am J Pathol 1999;154:447-55.  Back to cited text no. 1
González D. Clinical aspects of bites by viper in Spain. Toxicon 1982;20:349-53.  Back to cited text no. 2
Weinelt W, Sattler RW, Mebs D. Persistent paresis of the facialis muscle after European adder (Vipera berus) bite on the forehead. Toxicon 2002;40:1627-9.  Back to cited text no. 3
Malina T, Krecsak L, Warrell DA. Neurotoxicity and hypertension following European adder (Vipera berus berus) bites in Hungary: Case report and review. QJM 2008;101:801-6.  Back to cited text no. 4
Chippaux J-P. Epidemiology of snakebites in Europe: A systematic review of the literature. Toxicon 2012;59:86-99.  Back to cited text no. 5
Bowman WC. Neuromuscular block. Br J Pharmacol 2006; 147 Suppl 1: S277-86.  Back to cited text no. 6
Harris JB, Goonetilleke A. Animal poisons and the nervous system: What the neurologist needs to know. J Neurol Neurosurg Psychiatry 2004;75 Suppl 3:iii40-46.  Back to cited text no. 7
Nirthanan S, Charpantier E, Gopalakrishnakone P, Gwee MC, Khoo HE, Cheah LS, et al. Neuromuscular effects of candoxin, a novel toxin from the venom of the Malayan krait (Bungarus candidus). Br J Pharmacol 2003;139:832-44.  Back to cited text no. 8
Nirthanan S, Gwee MC. Three-finger alpha-neurotoxins and the nicotinic acetylcholine receptor, forty years on. J Pharmacol Sci 2004;94:1-17.  Back to cited text no. 9
Aksaranguraha S, Penchart C, Pipatankul V. Electrodiagnostic studies in cobra bites patients. J Ind Assoc Phy Thailand 1980;63:148-53.  Back to cited text no. 10
Rastogi JK, Sethi PK, Neurological aspects of ophitoximia (Indian krait). A clinico- electromyographic study. Indian J Med Res 1981;73:269-79.  Back to cited text no. 11
Watt G, Theakston RDG, Hayes C G, Yambao M I, Sangalong R, Ranona CP et al. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja Najaphilippinesis). N Engl J Med 1986;315:1444-8.  Back to cited text no. 12
Trevett AJ, Lalloo DG, Nwokolo NC, Naraqi S, Kevau IH, Theakston RD, et al. Electrophysiological findings in patients envenomed following the bite of a Papuantaipan (Oxyuranus scutellatus canni). Trans R Soc Trop Med Hyg 1995;89:415-7.  Back to cited text no. 13


  [Table 1], [Table 2], [Table 3]


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