Optic nerve
The optic nerve contains axons of nerve cells that emerge from the retina, leave the eye at the optic disc, and go to the visual cortex where input from the eye is processed into vision. There are 1.2 million optic nerve fibers that derive from the retinal ganglion cells of the inner retina. Treatments
While optic neuropathy cannot be outright cured, there are surgical options to alleviate pain and symptoms associated with such diseases. The Endoscopic Endonasal Approach method (EEA) is a preferred method of relieving pressure associated with tumors formed in the brain that press upon the optic nerve. It is a minimally invasive surgery. However, due to the genetic and developmental nature of most causes of optic neuropathy, no other surgeries have been proven to cure these diseases. See also
Optic neuritis
Ophthalmoplegia
Glaucoma

References
External links

NCBI Genetic Testing Registry
Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. Signs of puberty can develop as early as an age of 1 year.The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an autosomal dominant condition with a mutation of the luteinizing hormone (LH) receptor. As FMPP is a gonadotropin-independent form of precocious puberty, gonadotropin-releasing hormone agonists (GnRH agonists) are ineffective. Treatment is with drugs that suppress or block the effects of gonadal steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone. Alternatively, the combination of the androgen receptor antagonist bicalutamide and the aromatase inhibitor anastrozole may be used.Robert King Stone, personal physician to American president Abraham Lincoln, described the first case of FMPP in 1852. See also
Follicle-stimulating hormone insensitivity
Gonadotropin-releasing hormone insensitivity
Hypergonadism, hyperandrogenism, and precocious puberty
Inborn errors of steroid metabolism
Leydig cell hypoplasia (or LH insensitivity)

References
External links
Testotoxicosis at NIHs Office of Rare Diseases