Kristin Wall
Oct 31, 2011

15 minutes could save you from going blind

  Of the five senses (or six, if you’re a little boy in an M. Night Shyamalan movie) most people would agree that vision is their most valuable sense. As people age, this most prized faculty deteriorates, and for some may disappear altogether. Glaucoma is a leading cause of blindness, second only to cataracts, affecting a more modest one in two hundred people under the age of fifty, but escalating to a staggering one in ten people over eighty.   Glaucoma is an eye disorder wherein the optic nerve is damaged, resulting in impaired vision that may progress to complete blindness. The damage involves loss of retinal ganglion cells as a result of increased intraocular pressure. This increased pressure is historically believed to be caused by an increase in production of humor, the watery fluid that fills the front of the eye.   Current treatments for glaucoma include medication, typically administered in the form of eye drops; and surgical procedures, including canaloplasty (a non-penetrating procedure using microcatheter technology), laser surgery, trabeculectomy (surgical removal of part of the trabecular network), glaucoma drainage implants, and laser-assisted non-penetrating deep sclerectomy. Neither the medication nor the surgical procedures are permanent cures, and both include negative side effects. Selective laser trabeculoplasty, the newest and most popular laser treatment, effects a secondary physiological response that leads to a highly undesirable increase in fluid outflow after the procedure is performed.   In a recently issued patent for a method of glaucoma treatment, an inventor rebuts the popular belief that glaucoma is caused by excess humor production, and instead suggests the novel idea that blockage in the trabecular network near Schlemm’s canal (the channel that collects humor and delivers it into the bloodstream) prevents fluid from leaving the eye, thus causing the intraocular pressure. The trabecular meshwork is typically blocked by anatomical changes, pigment, extracellular matrix debris, or pseudoexfoliative material. The inventor also notes that the modern procedure for treating cataracts, the leading cause of blindness, decreases intraocular pressure as an unintended positive side effect. Using this observation, the inventor appropriated and altered the phacoemulsification cataract technology for use in treating glaucoma.   The invention describes a method of applying low intensity ultrasonic energy to the patient’s eye to dislodge built up material in the trabecular meshwork and initiate biochemical processes to reduce and remove extracellular debris, thereby decreasing the intraocular pressure causing the vision impairment. By decreasing the intensity of the ultrasonic energy and targeting the energy at a distance from the tissue rather than engaging it directly, the disclosed method avoids inflicting tissue damage.   The method claimed involves holding an ultrasonic device at a location external to the trabecular meshwork and transmitting the ultrasonic energy at a set frequency for a predetermined time, triggering a presumed integrin response by elevating the temperature within the treatment area to a level below that which creates tissue necrosis and pain, but which initiates biochemical changes in the eye, releasing cytokines that trigger enzymes and macrophage activity. The enzymes break down the extracellular debris clogging the trabecular meshwork, while the macrophages clear the broken-down debris, thus dislodging material built up in the trabecular meshwork and releasing the intraocular pressure.   The use of ultrasonic devices for treating glaucoma is not novel, however the method in which it is used in the present invention is. Other ultrasonic treatments target the cilliary body (the part of the eye that produces humor) in order to decrease fluid production in the eye. The present invention side-steps humor production, instead providing a treatment for the underlying cause of the intraocular pressure by clearing fluid blockages in the trabecular network.