A healthy 18-year-old man presented with a 2-week history of chickenpox, and was treated with oral acyclovir for 5 days. Ten days after onset of the cutaneous vesicular eruptions, he experienced blurring of vision in his right eye that descended to the level of hand motion (HM) in 6 hours. At presentation, 4 days after blurred vision, visual acuity in his right eye was hand movement. Examination of the anterior segments was unremarkable except for an obvious relative afferent pupillary defect. His extraocular muscle examination was normal. Fundus examinations revealed an edematous disc, retinal whitening and edema along the posterior pole, and the presence of a cherry red spot; no retinal infiltration or vitreous opacity was observed (). His left eye was normal with 20/20 vision. Optical coherence tomography showed increased thickness and hyperreflectivity in the inner retina layer, consistent with inner retina infarction. The early phase of fundus fluorescein angiography demonstrated delayed filling of the optic disc with minimal leakage from the small retinal arteriole, which was more prominent in the macular and optic disc regions. Minimal capillary dropout in the macular area was also noted. Staining of small vessels was observed in the late phase of the angiogram (–). A multifocal electroretinogram (ERG) showed diminished waveform in the entire macular area (). A full field ERG showed decreased b-wave amplitude of both rod and cone response and oscillatory potential wave. Electronegative ERG pattern was evidenced in maximal combined ERG that represented a generalized ischemic process, which involved mainly the inner retina layer (). The patient demonstrated decreased amplitude and increased latency in flash visual evoked potential (VEP), which is consistent with generalized involvement of the entire retina, not limited only to the posterior pole ().\nMinimal increased signal in T2-weighted magnetic resonance imaging and enhancing with contrast limited to the anterior part of the optic nerve could represent an inflammatory response to the ischemic process of the optic nerve head (). Serologic tests were positive for both immunoglobulin (Ig)M and IgG anti-VZV antibodies, confirming recent primary VZV infection. The diagnosis of ischemic vasculitis of the small retinal vessels associated with chickenpox was made. Since this process could either be caused by infection or an immunological response to VZV infection, and there is no consensus on the optimal treatment regimen for this VZV-associated vasculopathy, either treated with antiviral alone or combined with corticosteroid, we decided to treat the patient with antiviral agent according to the acute retinal necrosis treatment guideline published by the American Uveitis Society, ie, with intravenous Acyclovir 10 mg/kg every 8 hours for 2 weeks in conjunction with intravenous methylprednisolone 1 g daily for 3 days, then with oral prednisolone tapering over 1 month and oral Acyclovir 800 mg 5 times daily for 1 month. Despite the treatment, a pale optic disc and attenuated retinal artery resulted. His final best-corrected visual acuity was counting fingers at 1 foot at 6 months’ follow-up.
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.