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 28-year-old caucasian woman presented to the emergency room with a history of a pressure-type frontal headache during the previous week; there was no exacerbation when lying down nor with Valsalva maneuvers and no accompanying features, namely, visual symptoms. Medical history was unremarkable except for venous thrombosis on her left leg 5 years before. She was not taking any drugs other than oral contraceptives. She had a son who was diagnosed with chickenpox two weeks before. She was febrile (temperature of 38°C), and there was a rash suggestive of chickenpox. Uncorrected visual acuity was 20/20 in both eyes, and the optic discs were swollen and hyperemic, with ophthalmological and neurological examinations otherwise normal. Two days later, she complained of ocular pain on eye movement and bilateral blurred vision. By that time, examination revealed reduced visual acuity of 20/32 in her right eye (OD) and 20/60 in her left eye (OS) and relative afferent pupillary defect on her left eye. She reported a difference in brightness of the red color, with less saturation in the left eye.\nRoutine blood testing and immunological workup (ANA, ANCA, anticardiolipin antibodies, and complement levels) were normal. HIV serology was negative as well as VDRL, Toxoplasma, Bartonella, and Borrelia antibodies.\nCerebral computed tomography (CT) scan and magnetic resonance imaging (MRI) were normal.\nCerebrospinal fluid (CSF) examination was unremarkable: clear fluid with a normal opening pressure of 130–140 mm H2O with no block when pressing the jugular vein, normal protein and glucose levels, less than 5 leukocytes, and no oligoclonal bands. Antibodies for the following microorganisms were negative in the CSF: Cytomegalovirus, Epstein Barr virus, Parvovirus, Herpes simplex virus, Varicella zoster virus, Mycoplasma pneumoniae, Borrelia burgdorferi, and Leptospira species. VDRL was also negative in the CSF.\nGoldmann perimetry showed an enlarged blind spot and constriction of the nasal field, especially in her left eye (). Farnsworth Munsell 100 color vision test was abnormal in both eyes (in the red axis), with more pronounced defect in her left eye.\nShe was started on acyclovir 4 g/day per os, as is indicated to treat adult chickenpox.\nTwo days after the initial visual symptoms, visual acuity began to increase, and one week later, the optic disc edema had almost resolved (). Visual acuity continued to improve, and two months later, she had a visual acuity of 20/20 bilaterally. Retinal fluorescein angiography one month after presentation was normal. She has been free of further attacks of optic neuritis for three years after the admission.