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IntroductionOptic neuritis (ON) results in acute loss of vision with pain on eye movement. It may be the first manifestation of multiple sclerosis (MS) and usually follows a resolving course. Here we describe five patients with MS who developed severe unilateral ON resulting in persistent visual loss without significant resolution.MethodsA retrospective clinical review of five cases identified from a database of 550 patients with MS.ResultsAll patients were female and the mean age was 30 years at onset (range 25–40). All patients had no light perception at diagnosis, and received treatment with high dose intravenous methylprednisolone. Two patients also had plasma exchange. All of the patients were subsequently treated with immunomodulatory therapy. The patients were followed for a mean period of 13.3 years (range 2 months to 31 years). None of the patients had significant improvement in their visual acuity, with most achieving vision of 6/60. The mean retinal nerve fibre layer thickness was 66.33 microns (range 46–98 microns) in the affected eye, compared to 86.7 microns (69–105 microns) in the unaffected eye. All patients were aquaporin-4 antibody negative and oligoclonal band positive, with the MRI brain and spine being diagnostic for MS. Interestingly, none of the patients developed significant symptoms in the contralateral eye with vision of 6/5. All patients had an EDSS score of 4.0 predominantly due to visual impairment.ConclusionSevere unilateral ON is rarely seen in MS. This case series highlights a phenotypically distinct group of female MS patients with severe unilateral ON, and no improvement in visual acuity after prolonged follow-up and despite treatment with steroids and potent immune therapies. In such patients, where the diagnosis of MS is confirmed by MRI and CSF analysis, the patient might be reassured that visual loss in the fellow eye is unlikely.References. Wilhelm H, Schabet M. The diagnosis and treatment of optic neuritis. Deutsches Arzteblatt International2015;112(37):616–626.. Dachsel RM, et al. Optic neuropathy after retrobulbar neuritis in multiple sclerosis: Are optical coherence tomography and magnetic resonance imaging useful and necessary follow-up parameters?Der Nervenarzt2015;86(2):187–96.

umol/L (reference range <0.32 umol/L). Intrinsic factor and gastric parietal cell antibodies were detected. Conclusion Our patient had a clinical presentation consistent with B12 deficiency with an erroneously high active B12 level. Functional assays confirmed B12 deficiency, and a serological diagnosis of pernicious anaemia was made. This case illustrates the importance of not relying on any single test to exclude B12 deficiency.

Background Autoimmune encephalitis is an increasingly recognised disease that presents with seizures, neuropsychiatric symptoms, dystonic movements, and autonomic dysfunction 1 . As the mainstay of treatment immunosuppressive therapies are most effective when subject to early initiation and timely escalation, both of which are recognised to affect outcomes 2 . Nevertheless approximately half of patients with NMDA-R antibody encephalitis do not respond adequately to first-line therapy, and a significant proportion (12-30%) relapse 2 . Cases A 19 year old lady presented with new-onset seizures and psychosis. EEG showed focal spike-and-wave discharges and MRI brain a focal area of restricted diffusion consistent with recent seizure activity. NMDA-R antibodies were present in both CSF and serum. Following early treatment with corticosteroid, plasma exchange, IVIG and rituximab the patient recovered, returning to college after 6 months.A 50 year old gentleman presented with a two day history of myalgias and confusion. EEG showed spike-and-wave discharges and MRI brain increased T2 signal in the mesial temporal lobes. NMDA-R antibodies were present in both CSF and serum. He was treated with corticosteroid, plasma exchange, IVIG and rituximab, and continued on oral prednisone and mycophenolate. Response to treatment was poor with persistent ongoing physical and cognitive impairment at 6 months. Serial MRI showed substantial (~30%) loss of parenchymal brain volume. Discussion These cases illustrate that timely and aggressive management of NMDA-R antibody encephalitis with favourable prognostic markers is no guarantee of recovery. Several novel clinical and immunological predictors of response to therapy have been postulated, and currently await broader validation. 3

IntroductionNeuromyelitis optica spectrum disorders (NMOSDs) are immune-mediated demyelinating disorders affecting the brain and spinal cord. There are case-series of post-traumatic multiple sclerosis, but only one case-report previously of post-traumatic neuromyelitis optica.CaseA 57 year old man presented to hospital following a fall down two flights of stairs while intoxicated, and was found on CT to have small bi-frontal subdural haematomas, traumatic subarachnoid haemorrhage, bilateral occipital contusions, and non-displaced fractures through the right parietal bone and bilateral petrous temporal bones. While agitated, he developed subacute onset of visual loss and paraplegia at day 22. An MRI spine at day 12 showed only degenerative changes. However a repeat MRI brain and spine at day 26 revealed enhancing longitudinally extensive optic nerve lesions, indicative of optic neuritis and an extensive segment of intramedullary enhancement within the mid to lower thoracic cord, consistent with longitudinally extensive transverse myelitis. A CSF sample revealed raised protein (9.81 g/L), elevated lactate (3.54 mmol/L), 1 red cell, 41 monocytes. CSF oligoclonal bands, aquaporin 4 antibodies, MOG antibodies, anti-neuronal antibodies and ACE were negative. Serum anti-neuronal antibodies, HTLV-1 and 2 serology, ANA, ENA, ACE, MOG and aquaporin 4 antibodies were also negative. Treatment with iv methylprednisolone, plasma exchange and mycophenolate led to recovery of gait at 2 months and ability to drive by 1 year. Patient remains stable at 2 year follow-up.ConclusionWe report a case of bilateral optic neuritis and longitudinally extensive thoracic transverse myelitis following a traumatic brain injury. The presentation was consistent with an NMOSD and the patient responded to immunomodulatory therapy. The hypothesis is that the traumatic brain injury led to a defect in the blood brain barrier, allowing autoantibodies to enter the CNS and incite inflammation.

umol/L (reference range <0.32 umol/L). Intrinsic factor and gastric parietal cell antibodies were detected. Conclusion Our patient had a clinical presentation consistent with B12 deficiency with an erroneously high active B12 level. Functional assays confirmed B12 deficiency, and a serological diagnosis of pernicious anaemia was made. This case illustrates the importance of not relying on any single test to exclude B12 deficiency.