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Approach to “Visual Loss”
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Aastha Takkar Kapila, Monika Singla, Vivek Lal
Vascular episodes involving posterior circulation may be recurrent. Bilateral optic neuritis also has recurrences, especially in patients of neuromyelitis optica. STEP 4: Is the visual loss progressive?
Rabies and other lyssaviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Thiravat Hemachudha, Jiraporn Laothamatas, Henry Wilde
One patient presented with paresthesia and weakness of the right upper extremity which progressed to involve contralateral arm and subsequently developed ataxia and brain stem signs. MRI revealed T2 signal abnormalities involved C3–C6 levels. Neuromyelitis optica or Devic’s disease was an initial diagnosis [151].
Intense Immunosuppression Followed by Autologous Stem Cell Transplantation in Severe Multiple Sclerosis Cases
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
G.L. Mancardi, R. Saccardi, A. Murialdo, F. Pagliai, F. Gualandi, A. Marmont, M. Inglese, P. Bruzzi, M.P. Sormani, M.G. Marrosu, G. Meucci, L. Massacesi, A. Bertolotto, A. Lugaresi, E. Merelli, M. Filippi
Case 3 is a 40 year old female who reported numbness in the lower limbs followed by visual loss in the right eye occurring three years earlier. Visual evoked potentials (VEPs) were delayed on both sides and MRI of the brain was normal. After a few months, she experienced loss of leg strength. Again MRI was negative, but cerebro-spinal fluid (CSF) examination showed oligoclonal bands in the CSF and serum, with additional bands in the CSF. The patient improved and remained in almost normal condition for 2 years, at which time she experienced a severe tetraparesis. MRI of the brain and spinal cord showed multiple T2 lesions areas, some of which enhanced after a single dose of Gd. After 1 month, paraparesis worsened and visual disturbances recurred. A diagnosis of neuromyelitis optica was established. The patient was treated with CY (1.5 grams IV) and then with plasma exchange, without any significant improvement. At that time, EDSS was 6.5. After 4 months, her neurological condition rapidly worsened, reaching an almost complete paraplegia. When the patient’s EDSS was 8 it was decided to treat her with intense immunosuppression and ASCT, similarly to the other previously reported cases. The patient signed an informed consent. This patient was not included in the frequent MRI study because EDSS was higher than the upper limit established in the protocol.
Neuropsychiatric manifestations in primary Sjogren syndrome
Published in Expert Review of Clinical Immunology, 2022
Simone Appenzeller, Samuel de Oliveira Andrade, Mariana Freschi Bombini, Samara Rosa Sepresse, Fabiano Reis, Marcondes C. França
Definitions for neuropsychiatric manifestations, including a minimal set of investigation and attribution criteria, are the first step toward a standardization. Positive experience has been made in other autoimmune diseases, such as systemic lupus erythematosus. Therefore, we consider that an international, multidisciplinary study could significantly contribute and make an important step toward diagnostic and/or classification criteria for neuropsychiatric manifestations in pSS. So far, these have been classified as PNS, CNS (Diffuse, focal, and spinal cord involvement), and ANS. Some manifestations, such as demyelinating disease, have to be differentiated from multiple sclerosis and neuromyelitis optica. Definition criteria and attribution could significantly impact future studies allowing comparisons of different cohorts and validation of biomarkers.
Pallid Disc Oedema in a Young Patient: Clinical and Diagnostic Challenge
Published in Neuro-Ophthalmology, 2022
Liana Dedina, Mark M. Hassall, Shilpanjali Jesudason, Sumu Simon
This patient with with end-stage kidney disease and past extensive immunosuppression exposure had presented with painless and rapidly progressing vision loss. He was investigated for infective, inflammatory, infiltrative and vasculitic aetiologies. Of note, an immunological work up had been performed earlier in the year for non-specific joint symptoms, and did not identify any significant abnormalities. A blood work-up showed a normocytic anaemia with a haemoglobin level of 86 g/L and a mild neutrophilia. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were elevated at 72 mm/hr and 14.9 mg/L, respectively (note the caveat, ESR is less relevant in a dialysed patient with renal anaemia on erythropoietin). Anti-neuromyelitis optica antibodies were not detected. Rheumatoid factor, anti-cyclic citrullinated peptide (anti-CCP), extractable nuclear antigen (ENA) antibody test, syphilis and tuberculosis screening were negative. A lumbar puncture did not detect cryptococcus, Toxoplasma gondii, herpes simplex viruses, parechovirus, Varicella zoster, Neis-seria meningitidis or Strepto- coccus pneumoniae in the cerebrospinal fluid. A chest radiograph was unremarkable. Non-contrast magnetic resonance imaging (MRI) of the head and orbits did not show any optic nerve compression or infiltration, nor evidence of demyelination. Intravenous methylprednisolone therapy at 1 g/day was given for three days.
A case of neuromyelitis optica spectrum disorder with coexisting systemic lupus erythematosus
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Vikram Sangani, Mytri Pokal, Mamtha Balla, Ganesh Prasad Merugu, Sreedhar Adapa, Srikanth Naramala, Venu Madhav Konala
Neuromyelitis optica is a rare relapsing, inflammatory demyelinating disease of the central nervous system primarily affecting optic nerves and spinal cord. The Aquaporin-4 (AQP4) antibody and complement pathway play an important role in the pathogenesis of NMOSD. NMO-IgG selectively binds to the aquaporin-4 water channel located in astrocyte foot processes at the blood-brain barrier [7] and leads to direct injury to the central nervous system as a result of astrocyte injury by antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) [8,9]. As per International consensus, diagnosis can be made based on the presence of one core clinical characteristics as in Table 5, NMO IgG antibodies with the exclusion of alternative diagnosis [10]. In the absence of NMO IgG antibodies, two core clinical criteria along with exclusion of alternate diagnosis or additional MRI findings will suffice.