Arachnid Science: Article Reviews

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Bonilha, L., Cendes, F., Ghizoni, E., Vieira, R.J. & L.M. Li, 2004. Epilepsy due to a destructive brain lesion caused by a scorpion sting. Archives of Neurology, 61: 1294-1296.

Scorpion stings typically result in local pain or numbness and edema (swelling) around the sting area. However, it is possible that symptoms may be much more severe, as illustrated by the case report here, the first documentation of sustained brain damage due to scorpion venom. A young girl (age 4, healthy otherwise) was stung on the hand by a brown scorpion later identified as Tityus serrulatus, a native of northwestern Brazil commonly referred to as the Brazilian yellow scorpion. The girl immediately developed local pain around the sting area. In the following hours she became extremely tired and her body produced excessive sweat. Approximately 24 hours post-sting, she was taken to the hospital after having her first convulsive seizure; these seizures were to continue daily for the next week. For two years following the sting, she suffered several seizures per week and no anticonvulsive medications proved effective. Now age 15, she has mild paralysis and general intellectual impairment. Her rate of seizures has decreased to about one per month. MRI images of her brain reveal severe scarring; expansion of the lateral ventricle (a hollow space centrally located in the brain that contains the cerebrospinal fluid) has led to tissue damage and/or loss due to compression of her cerebral cortex. An EEG test confirmed abnormal activity in the right hemisphere of the brain, which is consistent with the paralysis and other movement difficulties now confined to the left half of her body.

Scorpion toxins are species-specific and are comprised of various proteins, which each are made up of chains of peptides. The clustering arrangement of these peptides ensures a high degree of specialization for the type of cell membranes with which they can bind and cause changes in the prey organism. When venom molecules enter the brain of the scorpionÕs prey, they attach themselves to the channels of neurons (brain cells) and thereby change the functioning of those cells. Channels are gate-like openings in the cell membrane that actively filter what ions (atoms with electrical charge) are allowed to enter the cell by monitoring intra- and extracellular electrical charges. When venom binds to the channel of a cell it causes changes in the working properties of that cell. This often means that the cell dramatically increases its activity. The venom-induced seizures reported in this paper are likely due to this type of sustained hyperactivity. The "kindling" explanation of epilepsy suggests that, much like a fire that starts to rage out of control, some epileptic seizures result from the activity of a small group of brain cells that become overactive. As cells increase their activity, they stimulate neighboring cells to become active too. The wave of hyperactivity spreads over an increasing area, eventually leading to convulsions produced by chronic activity in the area of the brain that controls body movements.

Based on how they affect the one class of cell channels that are regulated by sodium ions, scorpion toxins are categorized into alpha- or beta-toxin subfamilies. (The venom of T. serrulatus contains both alpha and beta toxins.) Scientists have mostly studied how scorpion venoms attack the sodium channels of brain cells, but what happens to calcium and potassium channels is still not well understood.

For more information: www.archneurol.com

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