The diagnosis of optic neuritis due to giant cell arteritis (GCA) may sometimes be difficult due to lack of suspicion or atypical or incomplete clinical manifestations (1). Magnetic resonance imaging (MRI) may be of some help in the management of this condition (2, 3). We report a case of optic neuritis due to GCA where the clinical manifestations and the MRI findings showed evident improvement after corticosteroid treatment.
An 82-year-old woman was sent to our division because of a 24-day history of diminished right visual acuity. Eight days before admission she had been diagnosed with right optic neuritis in another center. At that time, an MRI of the orbit was performed, and showed abnormal hypersignal of right optic nerve (Figure 1). Treatment with 30 mg/day of deflazacort was started. In her medical history, she recalled being diagnosed with a myopic refractive error, which subsequently led to an anisometropic amblyopia in the left eye.
At the time of admission, she reported asthenia, anorexia, headache, and polymyalgia rheumatica symptoms involving the neck, shoulder, and hip girdles; therefore a rheumatology consultation was scheduled. On examination, tenderness to palpation and thickening of the temporal arteries was observed. Also, pain on movement of the neck, shoulders, and hips was found.
Ophthalmologic examination showed a right pallid disc swelling, and splinter hemorrhage suggestive of right anterior ischemic optic neuritis. The patient was able to only see hand motions with her right eye, and anisometropic amblyopia was confirmed in her left eye. Routine laboratory analyses showed a hemoglobin 11.8 gm/dl, an increased erythrocyte sedimentation rate (63 mm/hour, normal <20 mm/hour), and C-reactive protein level (21 mg/dl, normal <5). Other laboratory data, including coagulation test results, anticardiolipin antibodies, and hepatic and renal function parameters were either negative or normal. A plain-film chest radiograph did not show abnormalities.
Because of the suspicion of a diagnosis of GCA, an intravenous pulse of methylprednisolone (1 gm/day) was administered for 3 consecutive days. Afterwards, oral corticosteroid therapy (prednisone 60 mg/day) was continued and antiaggregation treatment with aspirin (100 mg/day) was added.
A biopsy of the right temporal artery performed 24 hours after admission showed interruption of the internal elastic laminae with infiltration of mononuclear and multinucleated giant cells into the media. These pathologic findings were consistent with granulomatous arteritis. Two weeks after admission, the visual acuity in the right eye had improved so that the patient was now able to count fingers at a distance of 2 meters. No visual changes were found in her left eye. The abnormalities previously seen on MRI had disappeared (Figure 2).
GCA can be diagnosed in a straightforward fashion by clinicians who frequently see this condition (4). The original diagnosis of optic neuritis was an unlikely one to begin with, due to the patient's age. This led to the performance of an imaging study to confirm the optic neuritis, and the MRI showed abnormal enhancement of the optic nerve. MRI is helpful in differentiating optic neuritis from GCA. Optic neuritis can be due to a demyelinating disease, an ischemic disease (nonarteritic or arteritic), a compression of the optic nerve (intrinsic or extrinsic), and toxic optic neuropathies. One could speculate that a vasculitis phenomenon may be responsible for the abnormal en hancement of the optic nerve in MRI. However, the usefulness of MRI in diagnosing optic neuritis due to GCA is so far unknown.
In this case, once a diagnosis of GCA was established, pulsed corticosteroid treatment was started, and the visual acuity was partially recovered. Also, the MRI technique was repeated and the abnormalities findings disappeared.
With our case we provide new data on the diagnosis and management of GCA. We recommend that further studies be performed to investigate the precise role of MRI in the diagnosis and prognosis of optic neuritis secondary to GCA.