Ocular hypertension is the presence of elevated fluid pressure inside the eye (intraocular pressure), usually with no optic nerve damage or visual field loss.For most individuals, the normal range of intraocular pressure is between 10 mmHg and 21 mmHg. Elevated intraocular pressure is an important risk factor for glaucoma. One study found that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Accordingly, most individuals with consistently elevated intraocular pressures of greater than 21mmHg, particularly if they have other risk factors, are treated in an effort to prevent vision loss from glaucoma. Pathophysiology
The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork. Diagnosis
The condition is diagnosed using ocular tonometry and glaucoma evaluation. Increased IOP without glaucomatous changes (in optic disc or visual field) is considered as ocular hypertension. Treatment
Ocular hypertension is treated with either medications or laser. Medications that lower intraocular pressure work by decreasing aqueous humor production and/or increasing aqueous humor outflow. Laser trabeculoplasty works by increasing outflow. The cannabinoids found in cannabis sativa and indica (marijuana) have been shown to reduce intraocular pressure, by up to 50% for approximately four to five hours. But due to the duration of effect, significant side-effect profile, and lack of research proving efficacy,  the American Glaucoma Society issued a position statement in 2009 regarding the use of marijuana as a treatment for glaucoma.
Theories include too early ossification of the lower wings of the sphenoid, an increased space between the orbita, due to increasing width of the ethmoid sinuses, field defects during the development, a nasal capsule that fails to form, leading to a failure in normal medial orbital migration and also a disturbance in the formation of the cranial base, which can be seen in syndromes like Apert and Crouzon. Treatment
The craniofacial surgery to correct hypertelorism is usually done between five and eight years of age. This aesthetic-focused procedure addresses the psychosocial aspects in the childs early school years. Another reason for a correction age of five years or older is that the surgery should be delayed until the tooth buds have grown out low enough into the maxilla, thus preventing damage to them. Also, before age five the craniofacial bones are thin and fragile, which can make surgical correction difficult. In addition, it is possible that orbital surgery during infancy may inhibit midface growth.For the treatment of hypertelorism there are two main operative options: The box osteotomy and the facial bipartition (also referred to as median fasciotomy). Box osteotomy
This treatment of orbital hypertelorism was first performed by Paul Tessier. The surgery starts off by various osteotomies that separate the entire bony part of the orbit from the skull and surrounding facial bones. One of the osteotomies consists of removing the bone between the orbits. The orbits are then mobilized and brought towards each other.