OBSERVATION Epilepsy Due to a Destructive Brain Lesion Caused by a Scorpion Sting Leonardo Bonilha, MD, PhD; Fernando Cendes, MD, PhD; Enrico Ghizoni, MD; Ronan José Vieira, MD, PhD; Li Min Li, MD, PhD Background: Symptomatic acute epileptic seizures may Approximately 24 hours after the sting, she began to occur in up to 5% of individuals, especially children, with convulse. She was then taken to a hospital where she scorpion stings. The occurrence of a long-lasting brain achieved suboptimal seizure control, with daily tonic- lesion or the development of epilepsy after a scorpion sting clonic seizures and left hemiplegia during the follow- has never been observed. ing week. During our clinical investigation, her rou- tine electroencephalogram showed the presence of Objective: To describe the development of epilepsy sec- interictal spikes and diffuse slowing in the right brain ondary to an extensive hemispheric destructive brain le- hemisphere. Magnetic resonance imaging showed a sion after a scorpion sting. widespread destructive lesion of her right cerebral hemisphere affecting both the cortical and subcortical Patient: A 15-year-old with a moderate global cogni- structures. tive impairment and a mild left hemiparesis, with sei- zures occurring approximately once monthly. Conclusion: This is a rare illustration of the biological effects of the toxin of T serrulatus concerning its excito- Results: The mother reported that the patient at the toxicity and the potential to induce a brain lesion of an age of 4 years was stung by a brown scorpion, Tityus epileptogenic nature. serrulatus. The patient soon developed local pain and paresthesias followed by diaphoresis and somnolence. Arch Neurol. 2004;61:1294-1296 CORPION STINGS ARE A FRE- We report a case of a child who devel- quent cause of emergency oped epilepsy because of a destructive medical consultations in brain lesion after a sting by T serrulatus. tropical countries.1 The We review the biological effects of the scor- symptoms presented by pa- pion toxin and discuss the neurotoxicity Stients with scorpion stings are usually re- of the venom in the setting of the devel- lated to the neurotoxic effects of scor- opment of a brain lesion and recurrent pion venom.2 Scorpion stings are rarely nonprovoked seizures. fatal, but cardiopulmonary fatalities have been reported, especially when the pa- tients are children. REPORT OF A CASE Tityus serrulatus is a brown-colored scorpion encountered in the northwest- A healthy 4-year-old child, living in the ern region of Brazil. It has a unique mor- state of Bahia in the northwestern phological feature, a saw-toothed forma- region of Brazil, was stung in her left tion in the third bead of its tail. This makes middle finger by a brown scorpion. Her possible the straightforward visual iden- mother witnessed the event and later tification of the species. The usual effects described the features of T serrulatus. of T serrulatus stings are local pain and The child soon developed local pain and Author Affiliations: mild somatic sensation features, such as paresthesias followed by diaphoresis Neuroimaging Laboratory, paresthesias and numbness. However, the and somnolence. Approximately 24 Department of Neurology (Drs Bonilha, Cendes, Ghizoni, worst effects of the T serrulatus toxins com- hours after the sting, she began to con- and Li) and Department of prise somnolence, tremors, confusion, and vulse. She was then taken to a hospital Emergency Medicine arrhythmia. Acute symptomatic seizures where she achieved suboptimal seizure (Dr Vieira), State University of have been reported to occur in up to 5% control, with daily tonic-clonic seizures Campinas, Campinas, Brazil. of all cases.1 during the following week. During this (REPRINTED) ARCH NEUROL / VOL 61, AUG 2004 WWW.ARCHNEUROL.COM 1294 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/26/2021 A B C Figure. A, T1-weighted magnetic resonance imaging of the axial plane showing diffuse right cortical and subcortical destruction. B, T1-weighted magnetic resonance imaging of the coronal plane showing a cortical and subcortical atrophy of the right frontal and temporal lobes. C, Fluid-attenuated inversion recovery sequence magnetic resonance imaging of the axial plane showing ex vacuo lateral ventricle enlargement and widespread increased signal intensity in the subcortical portion of the right hemisphere, indicating gliosis. period, and between the seizures, she stayed alert and slows down or blocks the channel inactivation and sta- conscious, with left hemiplegia. When the seizures bilizes the channel in its open state.3 Conversely, the began to abate, 1 week after the sting, she was dis- ␤-neurotoxin binds to site 4 of the sodium channel and charged home. She continued to have almost daily does not change the channel inactivation, but it shifts the tonic-clonic seizures for 2 years after the hospitaliza- channel voltage dependence in the positive direction.7 tion, despite antiepileptic drugs. The toxin purified from the South American scor- She is now 15 years old, and her mother states that pion T serrulatus shifts the voltage-dependent activa- after the accident the patient had learning difficulties and tion of the sodium channel, leading to repetitive firing. was not able to attend elementary school. She currently Actually, the so-called Tityus toxin is a mixture of a mi- has a moderate global cognitive impairment and a mild nor fraction and a major fraction named ␥-toxin. The left hemiparesis, and her seizures occur approximately ␥-toxin binds close to binding site 4 of the Na+ channel once monthly. and blocks the channel. The same effect of delay of in- She underwent neurophysiologic and image investi- activation of the Na+ channel is produced by the major gation. Routine electroencephalogram showed the pres- component of the toxin. There are additional effects of ence of interictal spikes and diffuse slowing in the right the Tityus venom concerning blockage of delayed recti- brain hemisphere. Magnetic resonance imaging showed fier K+ channel, binding to the Ca+2–activated K+ chan- a widespread destructive lesion of her right cerebral hemi- nel of high conductance, and binding of small conduc- sphere affecting both the cortical and subcortical struc- tance Ca+2 channels.8 The biological effect of these actions, tures (Figure). however, is yet to be clarified. The clinical effects of scorpion venom intoxication COMMENT consist of local reactions such as pain, edema, pares- thesia, numbness, and somnolence. These reactions Scorpion venom is formed by mucopolysaccharides, hy- are considered to be a consequence of neurotransmit- aluronidase, phospholipase, serotonin, histamine, and pro- ter release. The systemic symptomatology is mainly tease inhibitors. The clinical manifestations of scorpion due to the catecholaminergic release, leading to tachy- venom intoxication exclusively result from the action of cardia, increased blood pressure, restlessness, muscle ␣- and ␤-toxins.3 The ␣-toxin is present in the venom of cramps, and fasciculation. Serious and fatal cases, Androctonus australis Hector, Androctonus mauretanicu especially involving children, are the consequence of mauretanicus, Buthus eupeus, Buthus occitanus tunetanus, secondary complications such as shock and pulmo- Leiurus quinquestriatus, and T serrulatus, whereas the nary edema, convulsions, brain edema, muscular ␤-toxin can be found in the venom of Centruroides sculp- paralysis, and respiratory failure.9 turatus, Centruroides suffusus suffusus, and T serrulatus.4 The present case may be a rare illustration of a brain Both ␣- and ␤-toxins are 7-kDa molecular weight poly- lesion induced by the excitotoxic effects of the scorpion peptides of 64 amino acids and 4 intramolecular disul- toxin. The persistent hyperactivation state generated by fide bridges.5 the scorpion toxin is possibly the cause of the wide- The scorpion toxins exert their in vivo effects by the spread functional and structural lesion with ischemic fea- disturbance of ion transportation through the neuronal tures. Interestingly, the lateralization of the seizures, and cell membranes both presynaptic and postsynaptic.6 The the right hemispheric brain destruction, followed a simi- ␣-neurotoxin binds to site 3 of the sodium channel and lar pattern of patients with HHE syndrome (hemicon- (REPRINTED) ARCH NEUROL / VOL 61, AUG 2004 WWW.ARCHNEUROL.COM 1295 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/26/2021 vulsion, hemiplegia, and epilepsy).10 Rasmussen syn- istrative, technical, and material support: Cendes, Vieira, drome is a possible differential diagnosis; however, we and Li. Study supervision: Ghizoni, Vieira, and Li. have not witnessed continuous epileptic activity in the Acknowledgment: We thank the patient for her kind co- patient’s electrophysiological studies or evidence of pro- operation. gression in her disease. The recurrent nonprovoked seizures in this patient sug- REFERENCES gest the development of a stable epileptogenic region in the area that was continuously activated by the scor- 1. Freire-Maia L, Campos JA, Amaral CF. Approaches to the treatment of scorpion pion toxin. Our case report suggests biological effects of envenoming. Toxicon. 1994;32:1009-1014. the toxin of T serrulatus concerning its excitotoxicity and 2. Arantes EC, Sampaio SV, Vieira CA, Giglio JR. What is tityustoxin? Toxicon. 1992; the potential to induce a brain lesion of