Optic Neuritis
09/05/11 13:18
The Optic Neuritis Treatment Trial (ONTT) was a carefully performed randomized clinical trial and yielded useful information. Despite the ONTT, the treatment of optic neuritis (ON) remains somewhat controversial.[37, 38] From a vision standpoint, observation without steroid treatment versus intravenous steroid treatment showed no difference in ultimate visual outcome at the 5-year mark.[39]
The ONTT showed strong evidence against the use of oral steroids in isolation in the treatment of ON, because oral steroids alone caused an increased rate of recurrence of ON.[40] Intravenous steroids (methylprednisolone 250 mg qid for 3 d with oral steroid taper) decreased the short-term risk of development of MS in patients with CNS white matter plaques, but had no long-term protective benefit from MS. Intravenous steroids do little to affect the ultimate visual acuity in patients with ON, but they do speed the rate of recovery. Some clinicians advocate intravenous steroids in patients with severe visual loss or bilateral visual loss.
Intravenous steroids are sometimes administered in an outpatient setting or at home. Admission to the hospital is recommended for the duration of high-dose intravenous steroid treatment because of the potential risk of serious adverse effects from this treatment.
Patients with neuromyelitis optica (NMO) often respond to intravenous methylprednisolone. Plasma exchange has been used in patients with no significant improvement with steroids.[41, 42]
In a case series of 20 patients with highly relapsing NMO, Kim et al reported significantly reduced relapse rates and clinical stabilization or improvement with mitoxantrone treatment.[43] Further studies conducted in a prospective and controlled fashion are required to determine whether mitoxantrone is a viable treatment option.
Medication Summary
Pharmacologic therapy in ON is directed at ameliorating the acute symptoms of pain and decreased vision caused by the demyelinating inflammation of the nerve. Varying regimens of corticosteroids have been used for this purpose. A 3-day course of high-dose intravenous methylprednisolone, followed by a rapid oral taper of prednisone has been shown to provide a rapid recovery of symptoms in the acute phase. In addition, this treatment may delay the short-term development of MS after ON. Early reports with a small number of patients found some benefit with plasma exchange in acute, severe ON. Further controlled studies are recommended.
For patients with ON whose brain lesions on MRI indicate a high risk of developing clinically definite MS, treatment with immunomodulators (eg, interferon beta-1a, interferon beta-1b, glatiramer acetate) may be considered.[44]
IV immunoglobulin (IVIG) treatment of acute ON has been shown to have no beneficial effect.
The ONTT showed strong evidence against the use of oral steroids in isolation in the treatment of ON, because oral steroids alone caused an increased rate of recurrence of ON.[40] Intravenous steroids (methylprednisolone 250 mg qid for 3 d with oral steroid taper) decreased the short-term risk of development of MS in patients with CNS white matter plaques, but had no long-term protective benefit from MS. Intravenous steroids do little to affect the ultimate visual acuity in patients with ON, but they do speed the rate of recovery. Some clinicians advocate intravenous steroids in patients with severe visual loss or bilateral visual loss.
Intravenous steroids are sometimes administered in an outpatient setting or at home. Admission to the hospital is recommended for the duration of high-dose intravenous steroid treatment because of the potential risk of serious adverse effects from this treatment.
Patients with neuromyelitis optica (NMO) often respond to intravenous methylprednisolone. Plasma exchange has been used in patients with no significant improvement with steroids.[41, 42]
In a case series of 20 patients with highly relapsing NMO, Kim et al reported significantly reduced relapse rates and clinical stabilization or improvement with mitoxantrone treatment.[43] Further studies conducted in a prospective and controlled fashion are required to determine whether mitoxantrone is a viable treatment option.
Medication Summary
Pharmacologic therapy in ON is directed at ameliorating the acute symptoms of pain and decreased vision caused by the demyelinating inflammation of the nerve. Varying regimens of corticosteroids have been used for this purpose. A 3-day course of high-dose intravenous methylprednisolone, followed by a rapid oral taper of prednisone has been shown to provide a rapid recovery of symptoms in the acute phase. In addition, this treatment may delay the short-term development of MS after ON. Early reports with a small number of patients found some benefit with plasma exchange in acute, severe ON. Further controlled studies are recommended.
For patients with ON whose brain lesions on MRI indicate a high risk of developing clinically definite MS, treatment with immunomodulators (eg, interferon beta-1a, interferon beta-1b, glatiramer acetate) may be considered.[44]
IV immunoglobulin (IVIG) treatment of acute ON has been shown to have no beneficial effect.