Etiology Papillitis

❖ Inflammatory processes: These include infectious diseases such as Lyme disease, malaria, and syphilis, and manifestations in the optic nerve of inflammation of the orbit, paranasal sinuses, or base of the skull.

❖ Autoimmune disorders: These include lupus erythematosus, polychondritis, regional enteritis (Crohn's disease), ulcerative colitis, nodular panarteritis, and Wegener's granulomatosis.

❖ Toxic damage due to agents such as methanol, lead, Myambutol (ethambu-tol hydrochloride), and chloramphenicol. In 70% of these cases, the cause is not determined.

Retrobulbar optic neuritis. The primary causes of this disorder are demyeli-nating diseases of the central nervous system such as diffuse encephalitis. In 20% of all cases, retrobulbar optic neuritis is an isolated early symptom of diffuse encephalitis. However, a differential diagnosis should always also consider the other causes of papillitis mentioned above.

Symptoms: The cardinal symptom is sudden loss of vision, which may occasionally be accompanied by fever (Uhthoff symptom). The field of vision is typically impaired by a central scotoma (Fig. 13.11 b), paracentral scotomas, a centrocecal scotoma involving the macula and blind spot, and wedge-shaped visual field defects up to and including complete blindness.

Other symptoms include pain that increases in extreme positions of gaze and when pressure is applied to the globe, and reduced perception of color intensity.

Diagnostic considerations: Ophthalmoscopic findings in papillitis (Fig. 13.11 a) include edema and hyperemia of the head of the optic nerve. This flattens the optic cup and obscures the margin of the optic disk. Bleeding at the margin of the optic disk may or may not be present. The elevation of the optic disk is considerably less than in papilledema.

The optic disk will appear normal in retrobulbar optic neuritis.

In retrobulbar optic neuritis, the patient sees nothing (due to a central scotoma), and the physician sees nothing (the fundus appears normal).

Other findings upon examination include an afferent pupillary defect (this is regularly encountered; see Chapter 9), red-green color vision defect, and delayed latency in the visual evoked potential.

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