Toxic and nutritional optic neuropathy is a group of medical disorders defined by visual impairment due to optic nerve damage secondary to a toxic substance and/or nutritional deficiency. The causes of these disorders are various, but they are linked by shared signs and symptoms, which this article will describe. In several of these disorders, both toxic and nutritional factors play a role, acting synergistically. Signs and symptoms
Vision loss in toxic and nutritional optic neuropathy is bilateral, symmetric, painless, gradual, and progressive. Dyschromatopsia, a change in color vision, is often the first symptom. Some patients notice that certain colors, particularly red, are less bright or vivid; others have a general loss of color perception. Loss of visual acuity may start with a blur or haze at the point of fixation, followed by a progressive decline. The degree of vision loss can extend to total blindness, but a loss beyond 20/400 is rare, except in the case of methanol ingestion. Peripheral vision is usually spared since the pattern of loss typically involves a central or cecocentral scotoma, a visual field defect at or surrounding the point of fixation. This pattern can be revealed via visual field testing. Upon examination, the pupils usually demonstrate a normal response to light and near stimulation. In those who are practically blind, the pupils will be dilated with a weak or absent response to light. The optic disc may appear normal, swollen, or hyperemic in early stages. With hyperemia, disc hemorrhages may also be present.
Contributing causes include thin and fragile epithelium leading to incomplete removal, cyst extensions extending into cancellous bone, satellite cysts found in the wall, experience of the surgeon, formation of further new cysts from other remnants of the dental epithelium. With current treatment techniques the recurrence rate is around 2-3% but can be as high as 50%. Recurrence can occur as early as 5 years and as late as 40 years after removal. Recurrence is usually seen within 5 years of treatment. Early findings of recurrence can be easily treated with minor surgery and curretage. Any fragment of the cyst that is left behind has the potential to survive and grow. Therefore, the success of enucleation depends on how well the cyst is removed. Larger cysts have a higher rate of recurrence after enucleation as they are more difficult to remove. Pronto genie keratocysts are well known to recur in the posterior mandible. A substantial amount of odontogenic keratocysts also recur in the tooth-bearing area of the jaws, requiring attention from clinicians.The neoplastic nature of odontogenic keratocysts has been debated. Due to high recurrence rate, late detection when the cyst has grown very large and causation by tumour suppressor gene inactivation, some have classified OKCs as benign neoplasms. The best evidence to suggest that this type of cyst is not a neoplasm is that it responds very well to marsupialisation. See also
Cysts of the jaws

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