Optic Neuritis In Diabetes

Demyelination

Nothing unusual

Reveals mass

Therapy

High-dose corticosteroids or no therapy

Reduce risk factors

Surgical decompression, radiation, or no intervention

Prognosis, usual course

Substantial recovery

Little or no change

Benign tumors, visual recovery possible

PION posterior optic neuropathy

PION posterior optic neuropathy

Neuritis Cat Scratch Disease

Fig. 8.15. At the acute onset of optic neuritis the optic disc can appear completely normal (left) or swollen

| Pearl

Pain on eye movement is very characteristic of optic neuritis and is reported by more than 90% of affected patients.

Fig. 8.15. At the acute onset of optic neuritis the optic disc can appear completely normal (left) or swollen

3. Age: in a majority of cases, 18 to 45 years

4. Pain on eye movement

5. Central scotomas or nerve fiber bundle patterns of visual field defects

6. Optic disc appearance normal or with mild edema

7. Tendency to begin recovery as soon as 2 weeks after peak visual loss at onset.

8. No evidence of systemic disease (other than MS)

This list is not meant to imply that cases of optic neuritis do not occur outside of these conditions, but these features are thought to be typical. Simultaneous, bilateral onset of optic neuritis is uncommon and suggests that some process other than demyelinating disease might be at work. In addition, in patients known to have MS, optic neuritis can occasionally appear as a slow, chronic process of visual deterioration. Such cases can also have an insidious onset, but are distinctly unusual in comparison to the above criteria.

Children are seldom struck by optic neuritis. When it does occur, a bilateral onset with bilateral optic disc edema is more typical in this age group. The bilateral pattern of onset is more frequent among children than it is among adults, but in absolute terms it is uncommon, hence, atypical. In addition, among children and older adults, optic neuritis can be the first manifestation of MS. Pain or dysesthesias are more likely to be associated with demyelinating disease than it is with other forms of optic neuritis. An uncommon, atypical form of neuritis is neuroretinitis in the absence of any history, signs, or other symptoms of demy-elinating disease. This syndrome is most commonly the presentation of cat-scratch disease, for which the causative agent is usually Bartonella henselae. The presence of neuro-retinitis almost completely excludes demyelinating disease as a causative factor.

Optic Neuritis Mri Findings
Fig. 8.16. The visual field in optic neuritis. In many cases, one finds a poorly defined central scotoma, in this instance affecting a left eye the defect extends inferiorly into the peripheral visual field

If the patient gives no spontaneous history of pain on eye movement, it is helpful to have the patient move through the cardinal positions of gaze, and then to ask whether this might have elicited discomfort.

The visual field loss at the time of presentation of optic neuritis has classically been described as a central scotoma (■ Fig. 8.16). While this is a common presentation, statistical analysis of visual fields gathered from large numbers of patients during the optic neuritis treatment trial (ONTT -a multicenter study on 455 patients) found that there is no typical visual field defect, and that any form of visual field loss could be found, including hemianopic, quadrantic, arcuate and para- or pericentral scotomas, as well as nonspecific, diffuse depression of sensitivity. When hemianopic defects that respect the vertical meridian are encountered, suspicion will fall on a possible tumor near the chiasm. The correct diagnosis is usually not a problem, however, since MRI scanning is commonly used during the study of both compressive and demyelinating forms of optic neuropathy.

The prognosis for vision in acute optic neuritis is largely favorable. The ONTT found that 1 year after the onset of an initial episode of acute optic neuritis, visual acuity of 20/20 was recovered in 70% of cases, and less than 10% of affected eyes had visual acuities of less than 20/40. Most patients recover nearly all of the lost acuity within about 5 weeks, and there is an additional period of up to a year after onset, during which small additional increments of recovery can be found.

Whether the optic disc is acutely edematous or not has no influence on the subsequent clinical course. Nevertheless, if atrophy is seen, the prognosis for visual recovery is not good.

Optic atrophy suggests that the neuritis is more chronic than acute. Either this presentation is a recurrence of an initially subclinical bout of neuritis or the onset of the problem was not noticed by the patient. In the latter case, the physician should be concerned about the possibility of a compressive optic neuropathy.

Optic disc edema is evident in about one third of patients with acute optic neuritis. It merely suggests that the site of damage is located in the anterior portions of the optic nerve. In the ONTT cases, however, it was found that some of the cases with disc edema were surprisingly associated with MRI evidence of inflammation located as far back as the intracanalicular portion of the nerve. The differentiation between papillitis and retrobulbar neuritis is purely descriptive, as far as the optic disc findings are concerned, and has no further meaning or consequence with respect to treatment or prognosis for recovery.

Additional Diagnostic Testing for Patients with Atypical Optic Neuritis

Definition

If the optic neuritis departs from one or more of the features described above, the episode should be recognized as atypical optic neuritis.

In cases with atypical features, the risk of a misdiagnosis is higher, and other systemic diseases are significantly more likely to be involved than in typical cases of optic neuritis. The history taken in such cases should include specific clarification of the following: fever, skin rash, arthritis, symptoms of pulmonary, renal, and/or cardiac disease. Significant clues include a prior diagnosis of rheumatoid disease (particularly systemic lupus erythematosus), sarcoid-osis, borreliosis, and luetic disease. The last two entities are quite uncommon but will respond to antibiotic therapy, which makes their detection particularly important.

In all cases of atypical optic neuritis, an MRI scan is necessary. Aside from imaging of the nerve itself, the study should be done as it is in cases of typical demyelinating neuritis, looking for signs of disease in the deep white matter of the cerebral hemispheres (■ Fig. 8.17).

Additional Diagnostic Testing for Patients with Typical Optic Neuritis

No serological testing is needed when the case presentation is typical for acute optic neuritis. If the patient specifically wants to know the about the chances for future development of a more widespread demyelination, or when the discussion turns to consideration of the optimal treatment for early MS, an MRI scan is necessary.

Fig. 8.17. MRI image of a patient with optic neuritis in the setting of known multiple sclerosis (MS): The typical, white foci of increased signal intensity in T2-weighted images mark the presence of large plaques of demyelination

If the MRI shows at least one locus of probable demye-linating plaques, the risk of future development of clinically definite MS within the next 5 years amounts to about 50%. If the scan shows no such lesions, the risk is significantly lower at about 16%.

CSF studies can help to strengthen the validity of the diagnosis, but as a rule, serologic testing does not provide additional information that is any more useful than the information obtained by MRI imaging. When the diagnosis is uncertain, other tests, such as the visually evoked potential (VEP) or the flicker test of Aulhorn, can help to define a more focused differential diagnosis. In typical cases, however, they provide little in the way of useful information. It should be stressed that although the VEP is virtually always affected by demyelinating events (including prolonged latency and reduced amplitude of responses), it neither confirms nor rules out the diagnosis of optic neuritis. The diagnosis must always be defined by the clinical features that are found in each case.

Treatment of Atypical Optic Neuritis

The approach to clinical management of atypical optic neuritis depends on the probable cause of the neuritis. It is important to consider uncommon infectious disorders, such as borreliosis or luetic disease, since these require immediate treatment with antibiotics. Likewise uncommon, varicella zoster virus can present as an optic neuropathy or retinopathy, and such cases require early institution of intravenous acyclovir therapy. If an autoimmune disorder is the source of the problem, it should also be treated intensively with high doses of corticosteroids. It is commonly impossible to differentiate between idiopathic demyelinat-ing optic neuritis and autoimmune vasculitis of the optic nerve, but both should be treated as early on as possible to protect vision. In cases of uncertain cause, it is often helpful to enlist the participation of a rheumatologist.

Treatment of Typical Optic Neuritis

The treatment of optic neuritis benefited substantially from the findings of the ONTT. The study's initial findings were first published in 1992, and subsequent long-term follow up has added additional, evidence-based improvements to our understanding of the disorder and its optimal management. Treatment is not indicated for the restoration of vision per se, since the prognosis for recovery of vision is favorable, whether with or without intervention. However, therapy does accelerate the rate of recovery and should always be considered in cases where the acute visual impairment is seriously disabling. If MRI scanning reveals one or more foci of demyelination, high-dose intravenous corticosteroid therapy can significantly delay the further development of signs and symptoms of MS in the subsequent 2-year period. Such treatment should always be considered in cases of optic neuritis that have no prior history of demyelination. The regimen consists of 3 days of intravenous methyl prednisone, 250 mg every 6 h for a total of 12 infusions, followed by 10 days of oral prednisone at 1 mg/kg of body weight per day. Alternatively 1000 mg of methyl prednisone are given in a single dose for 3 days.

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  • anke
    Is optic neuritis associated with diabetes?
    26 days ago

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