This prolonged activity of sodium channels results in an erection. There may be nerve damage due to the stabilization of voltage-dependent sodium channels in the open conformation. This position leads to the prolonged and continuous firing of neurons in the somatic, sympathetic, and parasympathetic nervous systems. Continuous firing of neurons causes over excitation and prevents the transmission of normal nerve impulses down the axon.The venom composition of the deathstalker scorpion contains neurotoxins which are almost completely responsible for this symptom. The poison from this scorpion contain 4 components: chlorotoxin, charybdotoxin, scyllatoxin, and agitoxins. Upon injection with the venom, sacral parasympathetic nerve are stimulated causing a change in the neuronal transmission in vascular and nonvascular smooth muscles. The compound known as the vasoactive intestinal polypeptide (VIP) is the main transmitter. This polypeptide is realized from nerves found long the erectile tissue of the corpus calosum. VIP is the strongest relaxant of penile smooth muscle structure, resulting in an erection upon envenomation. This is the proposed mechanics for all scorpion of the family Buthidae, whose venom composition contains these compounds. Epidemiology
Overview
Scorpions are nocturnal animals that typically live in deserts, mountains, caves, and under rocks. It is when they are disturbed that they attack. Scorpions that possess the ability to inject toxic venom with their sting belong to the family Buthidae. The Middle East and North Africa are home to the deadliest scorpions, belonging to the genus Buthus, Leiurus, Androctonus, and Hottentotta. In South America, the deadliest scorpion belongs to genus Tityus.
Pathophysiology
The etiology of RPON is still unknown and remains controversial - some scientists believe that RPON is a subtype of migraine, while others believe that it is a neuropathic disorder. As such, different potential etiologic mechanisms have been proposed based on case reports, including migrainous and neuropathic mechanisms. Yet, the renaming of RPON from OM indicates that the neuropathic cause may play a more important role than the migrainous cause in the pathophysiology of RPON. Migrainous mechanism
RPON was previously thought to be having a migrainous origin since it shares some common characteristics with migraine, and their only differences are the intensity and duration of headaches. Therefore, it was postulated that migraine caused ophthalmoplegia in RPON. However, the major argument against a migrainous origin is the long latency period between the onset of headache and ophthalmoplegia (up to 14 days), which is not consistent with a typical migraine. Nevertheless, several migrainous mechanisms have been proposed. Nerve compression
Compression mechanism is the first theory postulated regarding the pathophysiology of RPON. It is proposed that headache is caused by direct pressure on CNIII (compression neuropathy) within the cavernous sinus due to edema of the walls of the internal carotid artery (ICA) or posterior cerebral artery (PCA) during migraine episodes. Ischemia
Cavernous section of the ICA and a perforating vessel from the proximal PCA are responsible for supplying CNIII, CNIV, and CNVI. During migraine attacks, vasoconstriction of the ICA and PCA may lead to a reversible and ischemic breakdown of the blood-brain barrier.