Acute idiopathic maculopathy during the treatment of intracranial tuberculomas masquerading as malignant glioma
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LETTER TO THE EDITOR
Acute idiopathic maculopathy during the treatment of intracranial tuberculomas masquerading as malignant glioma Ayman G. Elnahry1 · Iman R. El Mahgoub2 · Gehad A. Elnahry1 Received: 26 March 2020 / Accepted: 8 June 2020 © Belgian Neurological Society 2020
Introduction Acute idiopathic maculopathy (AIM) was first described as a solitary unilateral retinal pigment epithelial (RPE) lesion with associated neurosensory detachment of the macula that follows a flu-like illness in otherwise healthy young adults. It was thought to result from an inflammatory or infectious process that affects the RPE cells and leads to the breakdown of the outer blood–retinal barrier. Some cases were later associated with Coxsackie virus infection [1, 2]. Clinically, there is a localized retinal detachment with underlying grayish RPE thickening. In some cases, it is eccentric to the foveal center with resultant better visual acuity [2]. Optical coherence tomography (OCT) is useful in diagnosis and shows heterogenous hyperreflectivity with thickening at the level of the RPE [3]. Differential diagnosis includes choroidal neovascularization and central serous chorioretinopathy. We report a patient with biopsy-proven intracranial tuberculomas who developed AIM while being successfully treated with anti-tuberculous therapy. To the best of our knowledge, this is the first report of an association between AIM and tuberculosis.
Case report A 24-year-old female presented with blurring of central vision in her right eye of acute onset and stationary course for 3 days. She had a history of left intracranial tuberculomas, diagnosed 2 months ago, for which she was receiving * Ayman G. Elnahry [email protected] 1
Department of Ophthalmology, Faculty of Medicine, Cairo University, Kasr Alainy street, Cairo 11956, Egypt
Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt
2
isoniazid, rifampicin, ethambutol, and pyrazinamide. The intracranial tuberculomas were diagnosed by a brain biopsy which revealed chronic granulomatous inflammation with massive caseation, fibrosis, epithelioid and giant cells. Magnetic resonance imaging (MRI) done at presentation (Fig. 1a, c, d) and following 2 months of anti-tuberculous treatment (Fig. 1b) showed decrease in the size of the tuberculomas in response to treatment. She was originally misdiagnosed as having a malignant glioma which was excluded by the biopsy. She had right visual field affection at presentation together with headache and confusion. She did not have any other systemic complaints. She had no past ocular or medical history. Examination revealed a corrected-distance visual acuity of 20/60 in the right eye and 20/40 in the left eye. External and anterior segment examination was unremarkable. Posterior segment examination of the right eye revealed a grayish juxta-foveal area of thickened RPE surrounded by an area of neurosensory detachment superior to the foveal center. There were no vitreous cells. The left eye was normal. OCT done t
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