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 man, complained about a 3-day history of bilateral blurred vision. He had a past medical history of kidney transplantation 5 years ago and was receiving systemic immunosuppressive therapy. The patient was hospitalized for chickenpox and was treated with systemic antivirals 3 weeks prior to ocular symptoms onset. On ophthalmic examination, the patient’s best corrected visual acuity (BCVA) was 20/200 in the right eye (RE) and 20/25 in the left eye (LE). Slit-lamp examination showed stromal keratitis and few fine keratic precipitates in the RE (Fig. ) and 1+ anterior chamber cells in both eyes. Intraocular pressure was 22 mmHg in the RE and 20 mmHg in the LE. There were no vitreous cells, and results of dilated fundus examination were unremarkable in both eyes. The patient was diagnosed with keratouveitis in the RE and acute anterior uveitis in the LE secondary to chickenpox. He was treated with topical acyclovir five times a day, dexamethasone six times a day, beta blockers, and atropine 1% twice daily. He was lost to follow-up. One year later, he presented with a 1-week history of blurry vision bilaterally. On ophthalmic examination, BCVA was 20/200 in the RE and 20/30 in the LE. Slit-lamp examination showed “mutton-fat” pigmented keratic precipitates (Fig. ), 1+ anterior chamber cells, corneal scars, patchy iris atrophy with circumscribed depigmented spots of the iris, and distorted pupil (Fig. ) in both eyes. Intraocular pressure was 27 mmHg in the RE and 24 mmHg in the LE. Assessment of posterior segments revealed no abnormalities in both eyes. A diagnosis of recurrent granulomatous anterior uveitis was made. The patient was treated with topical dexamethasone six times a day, topical acyclovir five times a day, beta blockers, and atropine 1% twice daily. Intraocular inflammation gradually resolved, and visual acuity improved. Topical steroids and acyclovir were slowly tapered. Visual acuity improved to 20/25 in both eyes one month after presentation. No recurrence of intraocular inflammation was observed over a follow-up period of 24 months.