Articulos libres sobre neuritis óptica,
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1. | Arq Neuropsiquiatr. 2011 Oct;69(5):824-8.Atypical presentations of neuromyelitis optica.Sato D, Fujihara K.SourceTohoku University Graduate School of Medicine, Sendai, Japan. AbstractNeuromyelitis optica (NMO) is an inflammatory disease of central nervous system classically characterized by acute, severe episodes of optic neuritis and longitudinally extensive transverse myelitis, usually with a relapsing course. The identification of an autoantibody exclusively detected in NMO patients against aquaporin-4 (AQP-4) has allowed identification of cases beyond the classical phenotype. Brain lesions, once thought as infrequent, can be observed in NMO patients, but lesions have different characteristics from the ones seen in multiple sclerosis. Additionally, some AQP-4 antibody positive patients may present with a variety of symptoms not being restricted to optic neuritis and acute myelitis during the first attack or in a relapse. Examples are not limited to, but may include patients only with brain and/or brainstem lesions, narcolepsy with hypothalamic lesions or patients with intractable hiccups, nausea and vomiting. The prompt identification of NMO patients with atypical presentations may benefit these patients with institution of early treatment to reduce disability and prevent further attacks. |
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2. | Clin Ophthalmol. 2011;5:1447-50. Epub 2011 Oct 7.Nonglaucomatous optic neuropathies in Port Harcourt.Pedro-Egbe CN, Cookey S, Awoyesuku EA, Ani N.SourceOphthalmology Unit, University of Port Harcourt, Port Harcourt, Nigeria. AbstractAIM:To review the types of nonglaucomatous optic neuropathies seen in Port Harcourt, Nigeria. MATERIALS AND METHODS:Medical case records of all cases of nonglaucomatous optic neuropathy seen in the Eye Clinic of University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria over a 5-year period were reviewed. Relevant data including patient demography, presenting visual acuity and intraocular pressure, and fundus findings were extracted. Other details included central visual field analysis and color vision results. Cases of glaucomatous optic neuropathy were excluded. RESULTS:Ninety-nine cases of optic neuropathy were seen over this time period. There were 52 (52.5%) males and 47 females. The mean age of those with optic neuropathy was 40 ± 18.774 years. Twenty-two patients (22.2%) had bilateral involvement, while the rest were unilateral. About 40% of the patients with optic neuropathies had optic atrophy. Nutritional causes accounted for 31.3% and optic neuritis 27.3%. Over 60% of the patients presented with visual acuities ≤6/60. Most patients (40%) had cecocentral scotoma. CONCLUSION:Nonglaucomatous optic neuropathies resulting in optic atrophy is not uncommon in our environment and several factors may be implicated but the actual cause is difficult to determine because of late presentation of most patients. |
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3. | Medicina (Kaunas). 2011;47(5):263-9.Diagnostic value of conventional visual evoked potentials applied to patients with multiple sclerosis. [Article in English, Lithuanian] Balnytė R, Ulozienė I, Rastenytė D, Vaitkus A, Malcienė L, Laučkaitė K.SourceDepartment of Neurology, Medical Academy, Lithuanian University of Health Sciences, Eivenių 2, Kaunas, Lithuania. rbalnyte@yahoo.com AbstractOBJECTIVE:The aim of this study was to determine the sensitivity and specificity of this classical technique employed at the Hospital of Lithuanian University of Health Sciences for the patients with multiple sclerosis and to assess its possible correlations with affected neurological systems. MATERIAL AND METHODS:Pattern shift visual evoked potentials were recorded in 63 patients with multiple sclerosis, 17 (27%) of whom had a history of optic neuritis, and in 63 control patients with other neurological diseases. The latencies and amplitudes of P100 were measured. In total, 126 patients were referred to the inpatient department of neurology for differential diagnosis of demyelinating disorders between January and December of 2007. RESULTS:Abnormalities of visual evoked potentials were observed by 73% more frequently in patients with multiple sclerosis than in control patients (α=0.05, β<0.01). The combined monocular/interocular test showed a specificity of 90.5% and a sensitivity of 82.5%. The probability of an affection of the pyramidal system was 5 times greater (95% CI, 2.2-11.0; P<0.01) and the probability of the optic pathways involvement was 4.8 times greater (95% CI, 1.9-11.9; P<0.01) in patients with multiple sclerosis than in controls. CONCLUSION:Conventional visual evoked potentials must be reappraised in light of their diagnostic value in multiple sclerosis given their high diagnostic efficiency, relatively easy, short, and cheap implementation, and easy availability in everyday clinical practice. |
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4. | PLoS One. 2011;6(8):e23489. Epub 2011 Aug 18.The use of serum glial fibrillary acidic protein measurements in the diagnosis of neuromyelitis optica spectrum optic neuritis.Storoni M, Petzold A, Plant GT.SourceThe National Hospital for Neurology and Neurosurgery, London, United Kingdom. m.storoni@doctors.net.uk AbstractBACKGROUND:Glial fibrillary acidic protein (GFAP) is a specific intermediate filament of the cytoskeleton of the astrocyte and may be used as a specific marker for astrocytic damage. It is detectable in the cerebrospinal fluid following a relapse caused by Multiple Sclerosis (MS) and Neuromyelitis Optica (NMO) spectrum disease. Higher levels are found following an NMO-related relapse. It is not known if GFAP is also detectable in the serum following such relapses. In particular, it is not known if lesions limited to the optic nerve release GFAP in sufficient quantities to be detectable within the serum. The aim of this study was to ascertain the extent to which serum GFAP levels can distinguish between an episode of optic neuritis (ON) related to NMO spectrum disease and ON from other causes. METHODOLOGY/PRINCIPAL FINDINGS:Out of 150 patients consecutively presenting to our eye hospital over the period March 2009 until July 2010, we were able to collect a serum sample from 12 patients who had presented with MS-related ON and from 10 patients who had presented with NMO spectrum disease-related ON. We also identified 8 patients with recurrent isolated ON and 8 patients with a corticosteroid-dependent optic neuropathy in the absence of any identified aetiology. GFAP was detectable in the serum of all but three patients (two patients with MS-related ON and one with recurrent optic neuritis). The median serum GFAP level in the patient group with NMO spectrum disease was 4.63 pg/mL whereas in all other cases combined together, this was 2.14 pg/mL. The difference was statistically significant (P = 0.01). A similar statistically significant difference was found when cases with pathology limited to the optic nerve were compared (P = 0.03). CONCLUSIONS:Glial pathology in NMO related optic neuritis is reflected in elevated serum GFAP levels independently of whether or not there is extra-optic nerve disease. |
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5. | Korean J Ophthalmol. 2011 Aug;25(4):294-7. Epub 2011 Jul 22.A congruous superior quadrantanopsia following a junctional scotoma induced by asperogillosis.Park IK, Lee SH, Chun YS.SourceDepartment of Ophthalmology, Kyung Hee University School of Medicine, Seoul, Korea. AbstractA 69-year old man presented to us with decreased vision in his right eye and a relative afferent pupillary defect. Under the presumption that he was suffering from retrobulbar optic neuritis or ischemic optic neuropathy, visual field tests were performed, revealing the presence of a junctional scotoma. Imaging studies revealed tumorous lesions extending from the sphenoid sinus at the right superior orbital fissure, with erosion of the right medial orbital wall and optic canal. Right optic nerve decompression was performed via an endoscopic sphenoidectomy, and histopathologic examination confirmed the presence of aspergillosis. The patient did not receive any postoperative antifungal treatment; however, his vision improved to 20 / 40, and his visual field developed a left congruous superior quadrantanopsia 18 months postoperatively. A junctional scotoma can be caused by aspergillosis, demonstrating the importance of examining the asymptomatic eye when a patient is experiencing a loss of vision in one eye. Furthermore, damage to the distal optic nerve adjacent to the proximal optic chiasm can induce unusual congruous superior quadrantanopsia. |
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6. | Front Neurol. 2011;2:50. Epub 2011 Aug 2.Optic neuritis and retinal ganglion cell loss in a chronic murine model of multiple sclerosis.Quinn TA, Dutt M, Shindler KS.SourceF.M. Kirby Center for Molecular Ophthalmology, Department of Ophthalmology, University of Pennsylvania Scheie Eye Institute Philadelphia, PA, USA. AbstractMultiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are neurodegenerative diseases with characteristic inflammatory demyelination in the central nervous system, including the optic nerve. Neuronal and axonal damage is considered to be the main cause of long-term disability in patients with MS. Neuronal loss, including retinal ganglion cell (RGC) apoptosis in eyes with optic neuritis (ON), also occurs in EAE. However, there is significant variability in the clinical course and level of neuronal damage in MS and EAE. The current studies examine the mechanisms and kinetics of RGC loss in C57/BL6 mice immunized with myelin oligodendrocyte glycoprotein to induce a chronic EAE disease. Clinical progression of EAE was scored daily and vision was assessed by optokinetic responses. At various time points, RGCs were counted and optic nerves were examined for inflammatory cell infiltration. Almost all EAE mice develop ON by day 15 post-immunization; however, RGC loss is delayed in these mice. No RGC loss is detected 25 days post-immunization, whereas RGC numbers in EAE mice significantly and progressively decrease compared to controls from 35 to 50 days post-immunization. The delayed time course of RGC loss is in stark contrast to that reported in relapsing EAE, as well as in rats with chronic EAE. Results suggest that different clinical disease courses of optic nerve inflammation may trigger distinct mechanisms of neuronal damage, or RGCs in different rodent strains may have variable resistance to neuronal degeneration. |
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7. | Intern Med. 2011;50(15):1605-9. Epub 2011 Aug 1.Influenza-associated monophasic neuromyelitis optica.Nakamura Y, Ikeda K, Yoshii Y, Ito H, Hirayama T, Kawabe K, Kano O, Iwasaki Y.SourceDepartment of Neurology, Toho University Omori Medical Centre, Japan. AbstractNeuromyelitis optica (NMO) is an inflammatory demyelinating disorder characterized by optic neuritis and acute myelitis. A parainfectious pathogenesis may play a partial role in the development of this disorder. Several viral infections are known to cause NMO. Here we report the case of a 15-year-old girl diagnosed with postinfluenza monophasic NMO. The patient developed sudden fever and chills, and the rapid diagnostic test for influenza was positive. She was diagnosed as influenza A and was treated with zanamivir hydrate (10 mg/day, inhalation). Three days later, she complained of dysuria and dysesthesia in the lower extremities. After nine days, she experienced blurred vision bilaterally. Neurological examination revealed visual disturbance, dysuria, dysesthesia and hyperreflexia in the lower extremities. Her visual acuity was counting fingers in OD and 2/100 in OS. Pupillary size was 4.0 mm and light reflexes were sluggish on both sides. Ophthalmoscopy showed marked edema of the optic discs. Serum influenza immunoglobulin M antibodies were elevated and serum anti-aquaporin 4 (AQP4) antibodies were undetectable. Spinal cord magnetic resonance imaging (MRI) displayed longitudinally extensive lesions in the thoracic cord. Brain MRI disclosed three subcortical lesions. The patient fulfilled the revised diagnostic criteria for NMO (2006). After methylprednisolone pulse therapy followed by oral administration of prednisolone, visual dysfunction, dysuria, limb dysesthesia and hyperreflexia were improved. Subsequently, she experienced no attacks for 3 years. This is the first case report of influenza A-associated NMO with such features of postinfectious NMO as a pediatric onset, monophasic course and anti-AQP4 antibody-seronegative status. |
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8. | AJNR Am J Neuroradiol. 2011 Oct;32(9):1662-8. Epub 2011 Jul 28.Diffusion tensor imaging of the optic nerve in multiple sclerosis: association with retinal damage and visual disability.Smith SA, Williams ZR, Ratchford JN, Newsome SD, Farrell SK, Farrell JA, Gifford A, Miller NR, van Zijl PC, Calabresi PA, Reich DS.SourceDepartment of Radiology and Radiological Sciences. AbstractBACKGROUND AND PURPOSE:There is a well-known relationship between MS and damage to the optic nerve, but advanced, quantitative MR imaging methods have not been applied to large cohorts. Our objective was to determine whether a short imaging protocol (<10 minutes), implemented with standard hardware, could detect abnormal water diffusion in the optic nerves of patients with MS. MATERIALS AND METHODS:We examined water diffusion in human optic nerves via DTI in the largest MS cohort reported to date (104 individuals, including 38 optic nerves previously affected by optic neuritis). We also assessed whether such abnormalities are associated with loss of visual acuity (both high and low contrast) and damage to the retinal nerve fiber layer (assessed via optical coherence tomography). RESULTS:The most abnormal diffusion was found in the optic nerves of patients with SPMS, especially in optic nerves previously affected by optic neuritis (19% drop in FA). DTI abnormalities correlated with both retinal nerve fiber layer thinning (correlation coefficient, 0.41) and loss of visual acuity, particularly at high contrast and in nerves previously affected by optic neuritis (correlation coefficient, 0.54). However, diffusion abnormalities were overall less pronounced than retinal nerve fiber layer thinning. CONCLUSIONS:DTI is sensitive to optic nerve damage in patients with MS, but a short imaging sequence added to standard clinical protocols may not be the most reliable indicator of optic nerve damage. |
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9. | Pediatr Rep. 2011 Jun 16;3(2):e11.Unilateral optic neuritis as a presentation of neurobrucellosis.Marques R, Martins C, Machado I, Monteiro JP, Campos N, Calhau P.SourcePediatric Department, Hospital Garcia da Orta, Almada, Portugal; AbstractNeurobrucellosis manifesting as optic neuritis is a rare disease in childhood. We report a case of neurobrucellosis in a 11 year old girl leading to visual impairment and headache. Physical examination revealed mild oedema of right tibiotarsic joint and optic neuritis. Investigations showed CSF pleocytosis and a Brucella serum agglutination titer of 1/640. Complete reversal of the symptoms was observed after appropriate antibiotic treatment. To our knowledge only four cases of neurobrucellosis manifesting with visual impairment in childhood are previously reported in literature. |
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10. | J Med Case Reports. 2011 Jul 19;5:319.Bilateral optic neuritis in a 26-year-old man with common variable immunodeficiency: a case report.Sempere AP, Tahoces M, Palao-Duarte S, Garcia-Perez A.SourceNeurology Department, Hospital General Universitario de Alicante, Alicante, Spain. aperezs@mac.com. AbstractABSTRACT: INTRODUCTION:Common variable immunodeficiency encompasses a group of heterogeneous conditions linked by a lack of immunoglobulin production and primary antibody failure. Although primary immunodeficiencies are typically characterized by recurrent infections, autoimmune manifestations have increasingly been recognized. Neurological complications are extremely rare and to the best of our knowledge optic neuritis has not been described previously. We report the case of a patient with common variable immunodeficiency who developed loss of vision secondary to bilateral optic neuritis. CASE PRESENTATION:A 26-year-old Caucasian man with a diagnosis of common variable immunodeficiency presented to our facility with loss of vision secondary to bilateral optic neuritis. Results of a thorough study for infectious, neoplastic and autoimmune diseases were negative. Our patient was treated with intravenous methylprednisolone with almost complete improvement and he remained asymptomatic at a 12-month follow-up. CONCLUSIONS:Bilateral optic neuritis should be added to the list of autoimmune disorders related to common variable immunodeficiency. If a patient with common variable immunodeficiency experiences loss of vision, the possibility of bilateral optic neuritis should be considered as rapid initiation of high-dose corticosteroids may improve visual recovery. |
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11. | Middle East Afr J Ophthalmol. 2011 Apr;18(2):178-82.Herpes zoster ophthalmicus: disease spectrum in young adults.Gupta N, Sachdev R, Sinha R, Titiyal JS, Tandon R.SourceCornea and Refractive Surgery Services, Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India. AbstractPURPOSE:To establish the clinical profile of herpes zoster ophthalmicus (HZO) in adults younger than 40 years and correlate the clinical manifestation with their immune status. MATERIALS AND METHODS:A retrospective chart review was performed of patients younger than 40 years who presented with HZO. Data were collected on demographics, medical history, clinical presentation, results of serological investigations, and visual outcome. RESULTS:The study cohort comprised 18 subjects with a mean age of 29.7 ± 6.2 years. Ophthalmic features included lid edema, ptosis, cicatricial lid deformities, sclerokeratitis, peripheral ulcerative keratitis, neuroparalytic keratitis, keratouveitis with concomitant glaucoma, secondary bacterial keratitis and superficial punctate keratitis with dry eye, optic neuritis, and trochlear nerve palsy. Eight of 18 (44.4%) subjects were found to be positive for Human Immunodeficiency Virus (HIV). Disseminated herpetic lesions were seen present in 5 (63%) of these 8 subjects. Postherpetic neuralgia was noted in 6 (75%) of 8 HIV-positive subjects and in 1 HIV-negative patient. Final visual acuity was 20/40 or better in 90% of the immunocompetent subjects and 20/200 or worse in 100% of the HIV-positive subjects. CONCLUSIONS:Immunocompetent young adults do present with features of HZO. However, the disease spectrum in HIV-negative patients is localized, less severe, and more amenable to therapy as compared with young adults with HIV. |
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12. | Can Vet J. 2011 Apr;52(4):398-402.Optic neuritis caused by canine distemper virus in a Jack Russell terrier.Richards TR, Whelan NC, Pinard CL, Alcala FC, Wolfe KC.SourceDepartment of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada. tricha01@uoguelph.ca AbstractAn atypical case of canine distemper (CD) was diagnosed in a vaccinated healthy adult dog. The patient was presented circling, seizuring, and blind. Postmortem examination resulted in a diagnosis of CD. Optic neuritis was diagnosed, a finding not previously described in the context of CD virus infection presenting solely with neurological signs. |
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13. | Ther Adv Neurol Disord. 2011 Mar;4(2):123-34.Clinical approach to optic neuritis: pitfalls, red flags and differential diagnosis.Voss E, Raab P, Trebst C, Stangel M.SourceHannover Medical School, Hannover, Germany. AbstractDemyelinating optic neuritis (ON) is the most common cause of optic neuropathy typically presenting with a subacute painful visual loss. In 20% of patients with multiple sclerosis (MS), ON is the presenting symptom and half of the patients with isolated ON develop MS within 15 years. The diagnosis of ON plays an important role in neurological practice. A correct and early diagnosis is necessary to ensure optimal further investigations and treatment. Other causes of optic neuropathies such as connective tissue disorders, infectious diseases, tumours or ischaemic neuropathies are less frequent but clinical and therapeutic management can differ dramatically. We present five patients admitted to our hospital with suspected demyelinating ON, but the clinical work up revealed different causes of optic neuropathy. We discuss the differential diagnosis of ON and clinical red flags that require careful diagnostic assessment of other diseases. A workflow for the diagnosis of optic neuropathies is presented. |
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14. | Ther Adv Neurol Disord. 2011 Mar;4(2):111-21.Current and future treatment approaches for neuromyelitis optica.Collongues N, de Seze J.SourceCentre d'investigation Clinique, INSERM 002, Nouvel hopital civil, 1 place de l'hopital, BP 426, 67091 Strasbourg cedex, France; Department of Neurology, University Hospitals of Strasbourg, Strasbourg, France. AbstractNeuromyelitis optica (NMO) is an inflammatory disease of the central nervous system (CNS) characterized by severe attacks of optic neuritis and myelitis, and which, unlike multiple sclerosis (MS), commonly spares the brain in the early stages. NMO used to be considered as a special form of MS. During the past 10 years, however, the two diseases have been shown to be clearly different. NMO is a B-cell-mediated disease associated with anti-aquaporin-4 antibodies in many cases and its pathophysiology seems to be near the acute lesion of necrotizing vasculitis. Assessment of prevalence shows that NMO is far less frequent than MS, which explains the absence of randomized clinical trials and NMO treatment strategies validated by evidence-based medicine. Recently, many data have been published that suggest that the therapeutic option in NMO should be immunosuppressive rather than immunomodulatory drugs. In the present study, after a brief overview of NMO, we review therapeutic studies and propose new therapeutic strategies in the relapse and disease-modifying fields. |
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15. | Case Rep Neurol. 2011 May;3(2):109-12. Epub 2011 May 13.Combined Striatum, Brain Stem, and Optic Nerve Involvement due to Mycoplasma pneumoniae in an Ambulatory Child.Bae JW, Kim HJ, Chang GY, Kim EJ.SourceDepartment of Neurology, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Busan, Korea. AbstractIn children, Mycoplasma pneumoniae encephalitis has been characterized by acute onset of an encephalopathy associated with extrapyramidal symptoms and symmetric basal ganglia with or without brain stem involvement on magnetic resonance imaging. Our case, showing unilateral optic neuritis, ophthalmoplegia, no extrapyramidal symptoms, and typical striatal involvement on magnetic resonance imaging, broadens the spectrum of varying clinical manifestations of childhood M. pneumoniae-associated encephalopathy. |
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16. | Case Report Med. 2011;2011:405837. Epub 2011 May 11.Relapse of neuromyelitis optica spectrum disorder associated with intravenous lidocaine.Uzawa A, Mori M, Masuda S, Aoe K, Kuwabara S.SourceDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan. AbstractLidocaine unmasks silent symptoms and eases neuropathic pain in multiple sclerosis patients; however, the effects of lidocaine in neuromyelitis optica have never been reported. We describe the case of a 59-year-old Japanese woman with neuromyelitis optica spectrum disorder who developed optic neuritis 1 day after intravenous lidocaine injection for treating allodynia. Her symptom seemed to result from a relapse of neuromyelitis optica induced by lidocaine administration, and not because of the transient effects of intravenous lidocaine administration. The possibility that lidocaine administration results in relapse of neuromyelitis optica due to its immunomodulating effects cannot be ruled out. |
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17. | J Neuroimmunol. 2011 Jul;236(1-2):65-71. Epub 2011 May 28.Identification of peptide targets in neuromyelitis optica.Yu X, Green M, Gilden D, Lam C, Bautista K, Bennett JL.SourceDepartment of Neurology, University of Colorado School of Medicine, 12700 E. 19th Avenue, Box B182, Aurora, CO 80045, United States. xiaoli.yu@ucdenver.edu AbstractNeuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and spinal cord. Recombinant antibodies (rAbs) generated from clonally expanded plasma cells in an NMO patient are specific to AQP4 and pathogenic. We screened phage-displayed peptide libraries with these rAbs, and identified 14 high affinity linear and conformational peptides. The linear peptides shared sequence homologies with NMO autoantigen AQP4 on the extracellular surface. Competitive inhibition ELISA and immunocytochemistry demonstrated that these peptides represent epitopes of NMO autoantigen AQP4. Peptide epitopes/mimotopes may have potential uses for disease prognosis, monitoring, and therapy. Copyright © 2011 Elsevier B.V. All rights reserved. |
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18. | PLoS One. 2011;6(5):e19843. Epub 2011 May 17.High resolution spectral domain optical coherence tomography (SD-OCT) in multiple sclerosis: the first follow up study over two years.Serbecic N, Aboul-Enein F, Beutelspacher SC, Vass C, Kristoferitsch W, Lassmann H, Reitner A, Schmidt-Erfurth U.SourceDepartment of Ophthalmology, Medical University of Vienna, Vienna, Austria. AbstractBACKGROUND:"Non-invasive, faster and less expensive than MRI" and "the eye is a window to the brain" are recent slogans promoting optical coherence tomography (OCT) as a new surrogate marker in multiple sclerosis (MS). Indeed, OCT allows for the first time a non-invasive visualization of axons of the central nervous system (CNS). Reduction of retina nerve fibre layer (RNFL) thickness was suggested to correlate with disease activity and duration. However, several issues are unclear: Do a few million axons, which build up both optic nerves, really resemble billions of CNS neurons? Does global CNS damage really result in global RNFL reduction? And if so, does global RNFL reduction really exist in all MS patients, and follow a slowly but steadily ongoing pattern? How can these (hypothesized) subtle global RNFL changes be reliably measured and separated from the rather gross RNFL changes caused by optic neuritis? Before generally being accepted, this interpretation needs further critical and objective validation. METHODOLOGY:We prospectively studied 37 MS patients with relapsing remitting (n = 27) and secondary progressive (n = 10) course on two occasions with a median interval of 22.4±0.5 months [range 19-27]. We used the high resolution spectral domain (SD-)OCT with the Spectralis 3.5 mm circle scan protocol with locked reference images and eye tracking mode. Patients with an attack of optic neuritis within 12 months prior to the onset of the study were excluded. PRINCIPAL FINDINGS:Although the disease was highly active over the observation period in more than half of the included relapsing remitting MS patients (19 patients/32 relapses) and the initial RNFL pattern showed a broad range, from normal to markedly reduced thickness, no significant changes between baseline and follow-up examinations could be detected. CONCLUSIONS:These results show that caution is required when using OCT for monitoring disease activity and global axonal injury in MS. |
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19. | Isr Med Assoc J. 2011 Mar;13(3):182-4.Pathogenic role of aquaporin antibodies in the development of neuromyelitis optica in a woman with celiac disease.Matijaca M, Pavelin S, Kaliterna DM, Bojić L, Matijaca A.SourceDepartment of Neurology, University Medical Center Split, Split, Croatia. meri.matijaca@st.htnet.hr |
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20. | Indian J Pharmacol. 2011 Apr;43(2):212-3.Paradoxical response to anti-tubercular treatment.Zaki SA, Shenoy P.SourceDepartment of Pediatrics, Lokmanya Tilak Municipal General Hospital and Medical College, Sion, Mumbai 400022, India. AbstractWe report a 5-year-old boy who developed optic neuritis as a paradoxical reaction to anti-tuberculous therapy. Steroids were re-started in the patient with gradual recovery of his vision. The case emphasizes the importance of recognizing paradoxical reactions in patients on anti-tuberculous therapy. Prompt recognition and treatment of such reactions will reduce the associated morbidity. |
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