A 48-year-old male presented with complaints of severe headache of two-week duration. The headache was in the right parietal region accompanied by nausea and vomiting. There was neither any history of fever, photophobia, blurring of vision or diplopia, nor any significant past medical history. He was previously seen in another hospital; the brain Computed Tomography (CT) scan was reported to be normal.\nOn physical examination, the vital signs were within normal limits, and the patient was afebrile. Mental status examination did not reveal any abnormality. On clinical examination of the motor system, the tone and power in all the four limbs were normal with exaggerated (3+) reflexes. There was no neck stiffness, and Kernig’s sign was negative. Gait and coordination were normal. The sensory system and the cranial nerves were normal. Fundoscopy did not reveal any abnormality. No significant finding was revealed in other systemic examinations.\nRoutine full blood count and biochemistry did not show any abnormality. However, enzyme-linked immunosorbent assay (ELISA) of the patient’s serum was positive for anti- herpes simplex virus (HSV) IgM antibody. Lumbar puncture was not carried out since the patient refused it. The electroencephalogram (EEG) did not reveal any abnormality. The Magnetic Resonance Imaging (MRI) brain revealed bright T2/FLAIR cortical images at right parietal and temporal region ().\nA presumptive diagnosis of herpes simplex encephalitis (HSE) was made on the basis of serological and MRI findings; empirical treatment with intravenous acyclovir 750 mg eight hourly was initiated. He also received hydrocortisone 8 mg intravenous followed by oral prednisolone 40 mg daily. The headache was relieved, and the patient had no complaint while in the ward. A repeat brain MRI, which was done one week later, showed that the cortical enhancement has markedly reduced indicating response to treatment (). On discharge the patient was advised to repeat MRI and EEG after one week.\nThree weeks after the initial admission, the patient presented again with complaints of right retro-orbital pain of two days duration. The pain was accentuated with eye movements. The patient also noticed that he could not see clearly with the affected eye. Clinical examination revealed red colour desaturation and reduced visual acuity. Ophthalmoscopic examination showed a swollen right optic disc. Visual evoked potential (VEP) revealed small amplitude and delay in the right P100 latency (right: 122.40 ms, left: 113.10 ms). Right optic neuritis was diagnosed, which was treated with intravenous methylprednisolone 250 mg six hourly. The right eye pain was relieved, and the vision gradually improved. A diagnosis of post encephalitic right optic neuritis was made.
A 39-year-old woman with rheumatoid arthritis, sleep apnea and a body mass index of 55 presented with nausea, vomiting and floaters in the right eye for two days. Two weeks prior, she developed positional headaches, blurry vision and transient visual obscurations. On presentation, her best corrected visual acuity was 20/25 in each eye, there was no relative afferent pupillary defect and the examination of external structures and anterior segment was unremarkable.\nFunduscopic examination revealed Frisen grade 4 papilledema in the right eye with vitreous, subretinal and intraretinal hemorrhages, and grade 3 in the left eye with flame-shaped hemorrhages (A, ).\nHead CT with contrast appeared normal, an MRI was not possible due to body habitus and weight restrictions. Lumbar puncture under fluoroscopic guidance revealed opening pressure of 310 mm CSF with normal composition. Humphrey visual field 24-2 SITA Fast was reliable with an enlarged blind spot and a few central changes in the right eye (mean deviation −4.00 dB) and was essentially full with mild central depression in the left eye (mean deviation −3.55 dB).\nShe was started on acetazolamide 500 mg twice daily, which was titrated up to 1500 mg twice daily with gradual resolution of symptoms over a month. At two month follow up, the vitreous hemorrhage had resolved and there was marked improvement in the papilledema bilaterally ( C, D).