A 47-year-old caucasian man presented with a new visual field defect. He had been diagnosed with pulmonary sarcoidosis 15 years previously on the basis of mediastinal lymph node biopsy and chest imaging consistent with stage three disease. Other than an eruption of cutaneous sarcoidosis 5 years after initial diagnosis, his disease had been quiescent on maintenance medication of prednisolone 15 mg per day and hydroxychloroquine 200 mg per day. Several attempts to wean his steroids were unsuccessful. He had a documented long-standing T-cell lymphopenia, and at the time of presentation, his lymphocyte count was 488 × 106/l (T-cells 394 × 106/l, CD4 cells 131 × 106/l). The patient was a hotel manager, had no other significant medical conditions and was a life-long non-smoker with moderate alcohol consumption. On routine annual ophthalmologic follow-up, perimetry demonstrated a new partial left superior quadrantanopia. On further questioning, the patient admitted to recent visual field problems, particularly during playing golf when he had a tendency to ‘lose’ the ball out to the left. Pre- and post-contrast magnetic resonance imaging (MRI) of brain at this time demonstrated numerous high signal foci throughout both cerebral hemispheres including a lesion of the right geniculate-striate pathway as well as the right midbrain and upper pons. There was one isolated focus of enhancement in the left cerebellar peduncle. There was no meningeal thickening or enhancement (Figure 1). Analysis of cerebrospinal fluid including oligoclonal bands was within normal limits. Visual evoked responses were also normal. Figure 1. ( a ) Axial FLAIR sequence at the level of the ventricles demonstrated punctate high signal in the deep white matter lesions of the left parietal lobe. ( b ) Axial FLAIR sequence at a higher level demonstrated further punctate high signal lesions in the right fronto-parietal deep white matter. The consensus opinion from ophthalmology, pulmonology, neurology and radiology specialities was that …