Optic neuritis is an acute or chronic inflammation of the optic nerve. Often a nerve demyelination (destruction of the protective myelin sheath around the nerve fibers) takes place, similar to multiple sclerosis. Multiple sclerosis, diabetes, poor circulation, trauma, chemical poisoning and other less common eye insults can cause it.  There is often a sudden loss of visual acuity and pain with movement of the eye. The eye doctor can diagnose optic neuritis by examining the back of the eye. There is venous engorgement around the optic nerve head and arterial contraction. There are often small hemorrhages near the swollen optic nerve.

Optic neuropathy is often the first sign of multiple sclerosis (MS). Two follow-up studies showed a greater than 40% development of MS after 8 years. (Ghezzi et al,, 1999, Druschky et al., 1999). There is also a strong nutritional correlation. An epidemic neuropathy broke out in Cuba in 1991, and an analysis of showed that those affected had a broad range of specific dietary deficiencies, including a sugar intake exceeding 15% of total caloric intake, alcohol consumption, low intake of protein, fats and micronutrients (Gay et al., 1995).

As far back as 1976, it was noted that "An enriched feed, specially prepared to affect reproduction of mice, significantly suppressed the onset of disease in subacute myelo-optico-neuropathy virus-infected mice, whereas low-calorie feed enhanced the incidence of disease (Inoue and Nishibe, 1976). One researcher noted that "Since sunlight influences the metabolism of fatty acids in the retina, it may also influence the development of retrobulbar optic neuritis-a common antecedent of multiple sclerosis" (Hutter and Laing, 1996). Ocular toxicity has resulted from many prescription medicines, including isoniazid, thioridazine, steroids, and amiodarone therapy (To and Townsend, 2000). Therefore, it can safely be assumed that a good diet with nutrient enrichment, attention to digestion of fats and avoidance of toxins will be protective.

The goal of herbal therapy at time of onset is to quickly remove blood congestion and restore arterial circulation. Immediately give two grams of concentrated tien chi root three times per day for up to a week, then reducing the dosage to twice a day for several months. This can be done in conjunction with standard Western use of steroid therapies to reduce swelling.  In addition, I use high doses of antioxidants, DHA (an important end-stage fatty acid), lipoic acid (500 mg per day), and blood moving herbs that cool, such as salvia root and red peony root.  In one case Dr. Abel referred a patient from Philadelphia who had lost vision in one eye down to 20/400, and three ophthalmologists told him that there would be no return of vision. Although I saw him six weeks afterwards, we were able to restore vision to 20/80 in a month or so. I think that ideally patients should be given this herbal therapy within one week of onset.

Long Term Treatment

When prevention and emergency treatment fail, there is a role for long term herbal treatment.  Although it is widely believed that neurological regeneration is not possible, this is changing, and there are some encouraging signs in the research field (MacLaren, 1999, Brustle, 1999). The goal of long-term herbal therapy is to reduce residual optic nerve inflammation, improve microcirculation, nourish the optic nerve, and stimulate nerve repair as much as possible. This strategy is also useful for optic neuropathy. Optic atrophy and optic neuritis share many characteristics, but with atrophy the shrinkage of the arteries and resulting pallor are more pronounced (Warner et al., 1997). Although progress is very, very slow, I have seen some mild to moderate improvements in vision.  We use a complex protocol similar to the one described in the section on multiple sclerosis.

Important herbs in addition to the ones mentioned include ginkgo leaf and bala.  I remember one very interesting case in which a Southern lady had completely lost both vision and sense of smell for close to a decade. After about six months on the protocol, she began to report flashes of light. Such subjective observations are difficult to assess, and often attributed to wishful thinking.  However, one day she suddenly regained the ability to smell vanilla, and a few months later coffee.  In a strikingly similar case I treated a person with no sense of smell due to chronic nasal obstruction and life-long sinus infections, and after severa months he too had a sudden retun of the ability to smell his wifes perfume. There was no further improvement in either case over the next six months, so I think that we may have a partial answer, but much more research is obviously needed. It is important to realize how important even tiny improvements can be to a person with visual or neurological impairment.