It then began to appear in adults who were unable to fend off the infection because they had never been exposed as children, and they readily spread it via sexual contact to other adults who also had limited or no resistance, causing deformity and death where before it had been only been a temporary childhood ailment. This transition is reported to have coincided temporally with the return of the Columbus expedition from the New World. The most compelling evidence for its validity is the presence of syphilitic-like damage to bones in a number of adult skeletons found in the British city of Hull who were buried over a century before Columbus made his journey to the Americas.More recent analysis of that research, however, concluded in 2012 that syphilis almost certainly had a New World origin.The causative organism, Treponema pallidum, was first identified by Fritz Schaudinn and Erich Hoffmann, in 1905. The first effective treatment for syphilis was arsphenamine, discovered by Sahachiro Hata in 1909, during a survey of hundreds of newly synthesized organic arsenical compounds led by Paul Ehrlich. It was manufactured and marketed from 1910 under the trade name Salvarsan by Hoechst AG. This organoarsenic compound was the first modern chemotherapeutic agent. During the 20th century, as both microbiology and pharmacology advanced greatly, syphilis, like many other infectious diseases, became more of a manageable burden than a scary and disfiguring mystery, at least in developed countries among those people who could afford to pay for timely diagnosis and treatment.
The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system, which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while theres piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow. The reason this issue is much more prominent for lesions at or above the T6 level is because the Splanchnic nerves emerge from the T5 level and below. Loss of brains control over T6 and below causes splanchnic arteries to reflexively vasoconstrict and since the Splanchnic arteries are the bodys largest reservoir for circulating blood, their vasocontriction dramatically affects the blood pressure of the body. Diagnosis
The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may experience headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia.