Any object with force and/or speed, typically a ball, fist or vehicle accidents, can result in orbital floor and/or medial wall fractures. These disruptions permit air entry into the orbital subcutaneous from the sinus, with a one-way check valve mechanism that forbids the air from exiting. Victims are often found in sport-related concussion, automobile vehicle accidents, or snowboarding accidents. Traumatic injuries do not cause onset swelling unless there is a forceful injection of air from vigorous sneezing, nose-blowing, or coughing. These generate an acute increase in intraorbital pressure, compromising the intraorbital neurovascular structures, which subsequently trigger the development of orbital emphysema. Postoperative complications
Orbital emphysema is a common result of certain types of surgery, in particular the ones that involve orbital medial wall. It may also occur in other oral, nasal, and maxillofacial surgical interventions, in which the occurrence is unexpected. They can weaken sinuses, bony structure, induce deep orbital tissue damages, or globe perforation that cause air leakage into the periorbital soft tissues and superiorly into the supraorbital fat. These surgical procedures may possibly introduce staphylococci, streptococci, and anaerobic bacteria via a compromised bony wall that can cause periorbital infection. The corresponding weakened or degenerated tissues cannot withstand the sudden increase in intraocular pressure and impaired ocular perfusion, driven by severe coughing or sneezing. It subsequently results in air trapped in the periorbital subcutaneous tissue and the development of orbital emphysema, which is often mistaken as allergic reactions.
1970: Mary F. Lyon and Susan Hawkes reported that a gene on the X chromosome caused complete insensitivity to androgens in mice. 1981: Barbara Migeon et al. narrowed down the locus of the human androgen receptor gene (or a factor controlling the androgen receptor gene) to somewhere between Xq11 and Xq13. 1988: The human androgen receptor gene is first cloned and partially analyzed by multiple parties. Terry Brown et al. reported the first mutations proven to cause AIS. 1989: Terry Brown et al. reported the exact locus of the AR gene (Xq11-Xq12), and Dennis Lubahn et al. published its intron-exon boundaries. 1994: The androgen receptor gene mutations database was created to provide a comprehensive listing of mutations published in medical journals and conference proceedings. Early terminology
The first descriptions of the effects of AIS appeared in the medical literature as individual case reports or as part of a comprehensive description of intersex physicalities. In 1839, Scottish obstetrician Sir James Young Simpson published one such description in an exhaustive study of intersexuality that has been credited with advancing the medical communitys understanding of the subject. Simpsons system of taxonomy, however, was far from the first; taxonomies or descriptions for the classification of intersexuality were developed by Italian physician and physicist Fortuné Affaitati in 1549, French surgeon Ambroise Paré in 1573, French physician and sexology pioneer Nicolas Venette in 1687 (under the pseudonym Vénitien Salocini), and French zoologist Isidore Geoffroy Saint-Hilaire in 1832.