The treatment for this may be to increase signage, post an advisory speed limit, apply a high-friction road surface, add crash barriers or any one of a number of other visible interventions. The immediate result may be to reduce collisions at the bend, but the subconscious relaxation on leaving the "dangerous" bend may cause drivers to act with fractionally less care on the rest of the road, resulting in an increase in collisions elsewhere on the road, and no overall improvement over the area. In the same way, increasing familiarity with the treated area will often result in a reduction over time to the previous level of care and may result in faster speeds around the bend due to perceived increased safety (risk compensation). Epidemiology
In 2004 50 million more were injured in motor vehicle collisions. In 2013, between 1.25 million and 1.4 million people were killed in traffic collisions, up from 1.1 million deaths in 1990. That number represents about 2.5% of all deaths. Approximately 50 million additional people were injured in traffic collisions, a number unchanged from 2004.India recorded 105,000 traffic deaths in a year, followed by China with over 96,000 deaths. This makes motor vehicle collisions the leading cause of injury and death among children worldwide 10–19 years old (260,000 children die a year, 10 million are injured) and the sixth leading preventable cause of death in the United States. In 2019, there were 36,096 people killed and 2.74 million people injured in motor vehicle traffic crashes on roadways in the United States.
The blood-brain barrier breakdown results in vasogenic edema, which promotes the development of RPON. Neuropeptides-induced
Alternatively, it is proposed that migraine-related release of neuropeptides from trigeminal nerve fibers terminating on the circle of Willis might be the cause. Some of the neuropeptides released are potentially toxic, and may induce blood-brain barrier breakdown that accounts for ophthalmoplegia. Neuropathic mechanism
Additional models have been proposed to explain the cause of RPON. The thickened and enhanced symptomatic nerve, as shown in recent MRI findings, might be indicative of the existence of structural nerve damage in RPON. Therefore, neuropathy is suggested as the primary cause of RPON, either induced by recurrent viral infections or immune-mediated inflammation. However, cerebrospinal fluid (CSF) analyses are normal in the vast majority of RPON cases, which is inconsistent with the findings of autoimmune or inflammatory-mediated pathomechanism. Nevertheless, several neuropathic mechanisms have been proposed. Benign viral infection
The enhancement and thickening of the oculomotor nerve can occur in a variety of infectious inflammatory conditions. However, spontaneous resolution is unlikely to occur in viral infection, except for benign viral infection that usually causes mild or no symptoms in humans. Therefore, benign viral infection could be an explanation for the development of RPON. Immune-mediated inflammation
Recent MRI findings have led to the current understanding of RPON as an inflammation-induced neuropathy. Recurrent demyelinating neuropathy is proposed as a pathophysiological pathway because similar MRI findings have been observed in both RPON and chronic inflammatory demyelinating neuropathy.