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Optic neuropathy: case reportA 45-year-old man developed optic neuropathy during treatment with ethambutol for tuberculous spondylodiscitis [route not stated].The man, who had tuberculous spondylodiscitis, started receiving antitubercular therapy (ATT). The therapy consisted of ethambutol 15 mg/kg along with isoniazid, rifampicin and pyrazinamide for initial 2 months. It was followed by maintenance therapy with ethambutol, isoniazid and rifampicin. Four months following initiation of ATT, he presented with complaints of visual blurring in both the eyes. Examination showed visual acuity (VA) of 20/40 in the right eye and 20/100 in the left eye. Colour vision was normal in both eyes. Perimetry revealed bitemporal visual field defects as well as bilateral central scotomas. Visual evoked potential (VEP) showed prolonged latencies in N75 and P100 waveforms in both the eyes. Despite being treated with a lower dose of ethambutol and preserved colour vision, symptoms led to suspicion of ethambutol induced optic neuropathy. Subsequently, neuroimaging with dedicated optic pathway imaging was performed which demonstrated abnormal FLAIR and DIR hyperintense signal intesnity involving the optic chiasma and both the optic tracts with sparing of bilateral optic nerves. The findings confirmed the diagnosis of ethambutol-induced optic neuropathy.The man's treatment with ethambutol was discontinued. Following discontinuation, his vision improved gradually over the next eight weeks. VA was to 20/20 on both eyes. Visual field defects were also reversed. Clinically, he improved and repeat neuroimaging was not performed. He showed complete resolution of symptoms with normalisation of the VA and reversal of the visual field defect on perimetry.
Optic neuropathy: case reportA 45-year-old man developed optic neuropathy during treatment with ethambutol for tuberculous spondylodiscitis [route not stated].The man, who had tuberculous spondylodiscitis, started receiving antitubercular therapy (ATT). The therapy consisted of ethambutol 15 mg/kg along with isoniazid, rifampicin and pyrazinamide for initial 2 months. It was followed by maintenance therapy with ethambutol, isoniazid and rifampicin. Four months following initiation of ATT, he presented with complaints of visual blurring in both the eyes. Examination showed visual acuity (VA) of 20/40 in the right eye and 20/100 in the left eye. Colour vision was normal in both eyes. Perimetry revealed bitemporal visual field defects as well as bilateral central scotomas. Visual evoked potential (VEP) showed prolonged latencies in N75 and P100 waveforms in both the eyes. Despite being treated with a lower dose of ethambutol and preserved colour vision, symptoms led to suspicion of ethambutol induced optic neuropathy. Subsequently, neuroimaging with dedicated optic pathway imaging was performed which demonstrated abnormal FLAIR and DIR hyperintense signal intesnity involving the optic chiasma and both the optic tracts with sparing of bilateral optic nerves. The findings confirmed the diagnosis of ethambutol-induced optic neuropathy.The man's treatment with ethambutol was discontinued. Following discontinuation, his vision improved gradually over the next eight weeks. VA was to 20/20 on both eyes. Visual field defects were also reversed. Clinically, he improved and repeat neuroimaging was not performed. He showed complete resolution of symptoms with normalisation of the VA and reversal of the visual field defect on perimetry.
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