Manifestation Of Multiple Sclerosis Research Articles

Complete Bilateral Horizontal Gaze Palsy as Initial Manifestation of Multiple Sclerosis: A Case Report

Multiple sclerosis is a chronic inflammatory disease of central nervous system that commonly affects young adults. Although ocular movement disturbances are commonly encountered in multiple sclerosis, bilateral horizontal gaze palsy is quite rare. We present a case of young woman presented with dizziness, intractable vomiting and visual disturbances for one week, on examination found to have complete bilateral horizontal gaze palsy while vertical gaze was intact. Brain MRI showed a small lesion in posterior part of medial pontine tegmentum bilaterally which was responsible for patient`s symptoms. She received five doses of one-gram methylprednisolone, her symptoms gradually improved over one week after treatment.

Resveratrol nanoparticles are neuroprotective in a model of multiple sclerosis

AbstractPurposeOptic neuritis is the most common clinical manifestation of multiple sclerosis. Axonal damage and neuronal loss lead to permanent neurological disability in patients and its animal model, experimental autoimmune encephalomyelitis (EAE). Presently, treatments of this condition aim to reduce inflammation without showing any neuroprotection. Resveratrol is a natural polyphenol found in red wine with neuroprotective effects but poor solubility in water. Thus, a novel nanoparticle formulation of resveratrol was developed and assessed in a mouse model of EAE.MethodsResveratrol nanoparticles (RNs) were formulated using a thin rehydration technique and assessed for stability with spectrophotometric techniques. C57/BL6 mice were immunized with the myelin oligodendroglial glycoprotein peptide. From EAE induction, mice were treated daily for 30 days by oral gavage of RNs (n = 6), vehicle (n = 5) or unconjugated resveratrol (UnRSV); n = 6). Mice were assessed for EAE signs daily and for visual function weekly by optokinetic responses (OKR). Optic nerve and spinal cord inflammation were assessed by hematoxylin and eosin (H&E). Retinal ganglion cells were immunostained with Brn3a.ResultsResveratrol nanoparticles (RNs) containing >10 mg/ml resveratrol were stable over 3 months with an encapsulation efficiency >70%. 16.9 mg/kg RNs reduced the EAE clinical score at day 30 compared to 16.9 mg/kg vehicle (1.4 ± 0.4 versus 3.0 ± 0.4, p < 0.05) whereas up to 100 mg/kg UnRSV did not lead to reduction of EAE scores. OKR, optic nerve inflammation and spinal cord inflammation were not significantly modified by oral administration of RNs. 16.9 mg/kg RNs reduced RGC loss compared to 16.9 mg/kg vehicle (347 ± 12 versus 172 ± 12 cells/standardized field, p < 0.0001). Importantly, to get a similar reduction, at least 100 mg/kg of UnRSV were needed suggesting that RNs increase resveratrol bioavailability.ConclusionsResveratrol nanoparticles (RNs) increase resveratrol solubility and bioavailability. They show neuroprotection by reducing RGC loss. However, as previously reported for resveratrol, these nanoparticles do not have any anti‐inflammatory effect.

Autophagy in Multiple Sclerosis: Two Sides of the Same Coin.

Multiple sclerosis (MS) is a complex auto-immune disorder of the central nervous system (CNS) that involves a range of CNS and immune cells. MS is characterized by chronic neuroinflammation, demyelination, and neuronal loss, but the molecular causes of this disease remain poorly understood. One cellular process that could provide insight into MS pathophysiology and also be a possible therapeutic avenue, is autophagy. Autophagy is an intracellular degradative pathway essential to maintain cellular homeostasis, particularly in neurons as defects in autophagy lead to neurodegeneration. One of the functions of autophagy is to maintain cellular homeostasis by eliminating defective or superfluous proteins, complexes, and organelles, preventing the accumulation of potentially cytotoxic damage. Importantly, there is also an intimate and intricate interplay between autophagy and multiple aspects of both innate and adaptive immunity. Thus, autophagy is implicated in two of the main hallmarks of MS, neurodegeneration, and inflammation, making it especially important to understand how this pathway contributes to MS manifestation and progression. This review summarizes the current knowledge about autophagy in MS, in particular how it contributes to our understanding of MS pathology and its potential as a novel therapeutic target.

CD8+ T Cell-Mediated Mechanisms Contribute to the Progression of Neurocognitive Impairment in Both Multiple Sclerosis and Alzheimer's Disease?

Neurocognitive impairment (NCI) is one of the most relevant clinical manifestations of multiple sclerosis (MS). The profile of NCI and the structural and functional changes in the brain structures relevant for cognition in MS share some similarities to those in Alzheimer's disease (AD), the most common cause of neurocognitive disorders. Additionally, despite clear etiopathological differences between MS and AD, an accumulation of effector/memory CD8+ T cells and CD8+ tissue-resident memory T (Trm) cells in cognitively relevant brain structures of MS/AD patients, and higher frequency of effector/memory CD8+ T cells re-expressing CD45RA (TEMRA) with high capacity to secrete cytotoxic molecules and proinflammatory cytokines in their blood, were found. Thus, an active pathogenetic role of CD8+ T cells in the progression of MS and AD may be assumed. In this mini-review, findings supporting the putative role of CD8+ T cells in the pathogenesis of MS and AD are displayed, and putative mechanisms underlying their pathogenetic action are discussed. A special effort was made to identify the gaps in the current knowledge about the role of CD8+ T cells in the development of NCI to “catalyze” translational research leading to new feasible therapeutic interventions.

Demyelinating or hereditary optic neuropathy? Comparison of selected disease entities

The paper discusses retrobulbar optic neuritis secondary to multiple sclerosis, Leber’s hereditary optic neuropathy, and Leber’s hereditary optic neuropathy with multiple sclerosis-like disease – Harding’s syndrome. Retrobulbar optic neuritis secondary to multiple sclerosis is the most common disease (neuropathy) of the optic nerve in young adults and often the first clinical manifestation of multiple sclerosis. Despite a characteristic triad of symptoms and evident focal demyelination in brain magnetic resonance, misdiagnoses still occur. Leber’s hereditary optic neuropathy (atrophy) is a genetic mitochondrial disease, which manifests as a subacute painless loss of vision, and thus can be mistaken for retrobulbar optic neuritis. The coexistence of hereditary optic neuropathy and Harding’s syndrome is another diagnostic difficulty. All these three conditions, the peak of incidence of which occurs in the second to third decade of life, initially manifest only with visual symptoms due to uni- or bilateral optic neuropathy. Magnetic resonance imaging of the brain may show demyelination, while optical coherence tomography of the fundus may detect thinning of the retinal nerve fibre layers in all these neuropathies. We present clinical differences, as well as variances in retinal optical coherence tomography and magnetic resonance imaging between retrobulbar optic neuritis secondary to multiple sclerosis, Leber’s hereditary optic neuropathy, and Leber’s hereditary optic neuropathy with multiple sclerosis-like disease.

Multiple Sclerosis Walking Scale-12 (MSWS-12) and its Relationship With Fatigue in People With Multiple Sclerosis

Background and Objectives: Walking disorder is one of the most important manifestations of multiple sclerosis (MS), and indicates the progression of the disease. Fatigue and walking are considered as key symptoms affecting the patient’s quality of life. Therefore, this study aimed to investigate the relationship between walking status and fatigue, in people with MS. Methods: A total number of 60 Iranian patients with MS completed the Persian version of the Multiple Sclerosis Walking Scale-12 (MSWS-12), the Modified Fatigue Impact Scale, and the Hospital Anxiety and Depression Scale. Data were analyzed using SPSS V. 20 software. The multivariate correlation and linear regression analyses were conducted to investigate the relationship between fatigue, anxiety, depression, demographic characteristics, and MSWS-12 scores. Results: Gait problems were observed in 46.7% of the study participants. Also, the MSWS-12 scores were significantly associated with fatigue severity (P=0.001), in these patients. Moreover, depression, cognitive status, anxiety, and gait status were the most important factors affecting fatigue. Conclusion: According to the present results, the presence of depression, cognitive problems, anxiety, and gait disorders are the most important factors affecting fatigue, in patients with MS.

Paroxysmal Symptoms in Multiple Sclerosis—A Review of the Literature

Paroxysmal symptoms are well-recognized manifestations of multiple sclerosis (MS). These are characterized by multiple, brief, sudden onset, and stereotyped episodes. They manifest as motor, sensory, visual, brainstem, and autonomic symptoms. When occurring in the setting of an established MS, the diagnosis is relatively straightforward. Conversely, the diagnosis is significantly more challenging when they occur as the initial manifestation of MS. The aim of this review is to summarize the various forms of paroxysmal symptoms reported in MS, with emphasis on the clinical features, radiological findings and treatment options.

Homonymous visual field defects in patients with multiple sclerosis: results of computerised perimetry and optical coherence tomography.

Visual dysfunction is frequent in multiple sclerosis, usually resulting from retrobulbar optic neuritis or papillitis. Less frequently, demyelinating lesions can affect the retrochiasmal pathways. There are few reports of homonymous visual field defects (HVFD) in multiple sclerosis and little is known about their evolution. The purpose of this study was to better define both the clinical profile and the evolution of HVFD in patients with multiple sclerosis. We performed a retrospective study of all multiple sclerosis patients who presented HVFD and were examined by automated static perimetry. A subset of patients benefited from macular assessment with optical coherence tomography (OCT). We also reviewed the worldwide literature on the subject. Twenty patients were retrieved from the neuro-ophthalmology database of the Hôpital Ophtalmique Jules-Gonin. There were 11 women and 9 men, and their average age was 35 ± 11 years. The relapsing-remitting form of multiple sclerosis was most common (18/20; 90%), the primary progressive form (1/20; 5%) and the secondary progressive form (1/20; 5%) were rare. HVFD were the presenting symptom of multiple sclerosis in seven patients (35%). The recovery was complete in 12/20 patients (60%), and the median time to recovery was 10 weeks (2-13 weeks). An incomplete recovery was found in 5/20 subjects (25%) and no recovery occurred in 3/20 subjects (15%). Magnetic resonance imaging disclosed a definite lesion explaining the HVFD in 7/11 patients: five within the optic radiations (71.4%), one within the optic tract (14.3%) and one within the lateral geniculate nucleus (14.3%). Our results were comparable to those compiled from our literature search (29 publications, totalling 70 cases). A recurrent episode of HVFD occurred in three patients (15%). OCT was performed in 10/20 patients. Retinal ganglion cell layer thickness was assessed and revealed a homonymous thinning in three patients, diffuse unilateral or bilateral thinning (resulting from previous episodes of optic neuritis) in six patients, and normal retinal ganglion cell layer thickness in one patient. HVFD in multiple sclerosis are found mostly in young patients with relapsing-remitting multiple sclerosis, which is consistent with the epidemiology of multiple sclerosis. HVFD can be the first manifestation of multiple sclerosis and have a relatively good prognosis. Like optic neuritis, HVFD can recur. The incidence of HVFD in multiple sclerosis is unknown, as it is probably underdiagnosed. Systematic automated static perimetry and OCT could help to determine the true incidence of HVFD in multiple sclerosis. &nbsp.

Headache due to intracranial hypertension at the time of first manifestation of multiple sclerosis.

Headache due to intracranial hypertension at the time of first manifestation of multiple sclerosis.

Cognitive impairment in multiple sclerosis: lessons from cerebrospinal fluid biomarkers.

Cognitive impairment is a common clinical manifestation of multiple sclerosis, but its pathophysiology is not completely understood. White and grey matter injury together with synaptic dysfunction do play a role. The measurement of biomarkers in the cerebrospinal fluid and the study of their association with cognitive impairment may provide interesting in vivo evidence of the biological mechanisms underlying multiple sclerosis-related cognitive impairment. So far, only a few studies on this topic have been published, giving interesting results that deserve further investigation. Cerebrospinal fluid biomarkers of different pathophysiological mechanisms seem to reflect different neuropsychological patterns of cognitive deficits in multiple sclerosis. The aim of this review is to discuss the studies that have correlated cerebrospinal fluid markers of immune, glial and neuronal pathology with cognitive impairment in multiple sclerosis. Although preliminary, these findings suggest that cerebrospinal fluid biomarkers show some correlation with cognitive performance in multiple sclerosis, thus providing interesting insights into the mechanisms underlying the involvement of specific cognitive domains.

Dabigatran Suppresses PAR-1/SphK/S1P Activation of Astrocytes in Experimental Autoimmune Encephalomyelitis Model.

Multiple sclerosis (MS) is an inflammatory autoimmune disease affecting the central nervous system (CNS) that currently does not have any effective treatment. Experimental autoimmune encephalomyelitis (EAE) is often employed as a model to mimic the clinical manifestations of MS, mainly CNS demyelination. Coagulation is known to participate in crosstalk with inflammation and autoimmunity. We herein explored the correlation between the coagulation cascade and CNS immune diseases in vitro using primary astrocytes isolated from mice and in vivo using a mouse model of EAE. We showed that dabigatran, a clinical oral anti-coagulant drug, suppressed the thrombin-induced activation of astrocytes, and the underlying mechanisms are related to the activity of protease-activated receptor-1 (PAR-1), sphingosine-1-phosphate (S1P), and sphingosine kinases (SphKs). Importantly, dabigatran effectively recovered neurological function, reduced inflammation in the spinal cord, and prevented spinal cord demyelination caused by EAE. We suggest that dabigatran, a specific inhibitor of thrombin, antagonized the effect of thrombin in astrocytes by limiting the activation of PAR-1, in turn downregulating SphK1 and disrupting S1P receptor signaling. These findings reveal critical information about the relationship between coagulation mechanisms and CNS immune diseases and will contribute to the clinical translation and development of therapeutic strategies against MS.

Stress cardiomyopathy associated with the first manifestation of multiple sclerosis: a case report

BackgroundWe present a case with a close temporal association of the first diagnosis of multiple sclerosis and stress cardiomyopathy.Case presentationA 19-year-old man experienced severe dyspnoea. The cardiac biomarkers troponin T and NT-proBNP were elevated, and transthoracic echocardiography showed basal hypokinesia. The man was diagnosed with stress cardiomyopathy after main differential diagnoses such as acute coronary syndrome, myocarditis, and pheochromocytoma were excluded. Furthermore, the patient reported vertigo and paraesthesia. Brain and spinal MRI revealed T2-hyperintense lesions with a prominent acute lesion in the pontomedullary area. Cerebrospinal fluid findings revealed a lymphocytic pleocytosis and intrathecal IgG synthesis. Serum neurofilaments were elevated. The patient was diagnosed with MS, and treatment with intravenous Methylprednisolone was initiated. The brainstem lesion due to multiple sclerosis was assumed to be the cause of stress cardiomyopathy. The patient fully recovered.ConclusionStress cardiomyopathy may be linked with the first manifestation of multiple sclerosis in the presented case since pontomedullary lesions could affect the sympathetic nervous system. This case highlights the importance of neurological history and examination in young patients with unexplained acute cardiac complaints.

Cognitive disturbances in the cuprizone model of multiple sclerosis.

Cognitive problems frequently accompany neurological manifestations of multiple sclerosis (MS). However, during screening of preclinical candidates, assessments of behaviour in mouse models of MS typically focus on locomotor activity. In the present study, we analysed cognitive behaviour of 9 to 10-week-old female C57Bl/6J mice orally administered with the toxin cuprizone that induces demyelination, a characteristic feature of MS. Animals received 400 mg/kg cuprizone daily for 2 or 4 weeks, and their performance was compared with that of vehicle-treated mice. Cuprizone-treated animals showed multiple deficits in short touchscreen-based operant tasks: they responded more slowly to visual stimuli, rewards and made more errors in a simple rule-learning task. In contextual/cued fear conditioning experiments, cuprizone-treated mice showed significantly lower levels of contextual freezing than vehicle-treated mice. Diffusion tensor imaging showed treatment-dependent changes in fractional anisotropy as well as in axial and mean diffusivities in different white matter areas. Lower values of fractional anisotropy and axial diffusivity in cuprizone-treated mice indicated developing demyelination and/or axonal damage. Several diffusion tensor imaging measurements correlated with learning parameters. Our results show that translational touchscreen operant tests and fear conditioning paradigms can reliably detect cognitive consequences of cuprizone treatment. The suggested experimental approach enables screening novel MS drug candidates in longitudinal experiments for their ability to improve pathological changes in brain structure and reverse cognitive deficits.

Changes in oxygen saturation and the retinal nerve fibre layer in patients with optic neuritis associated with multiple sclerosis in a 6-month follow-up.

PurposeOptic neuritis (ON) is an inflammatory demyelinating disorder of the optic nerve, which can be the first manifestation of multiple sclerosis (MS). The main goal was to assess changes in the retinal nerve fibre layer (RNFL) and in retinal oxygen saturation [arterial (AS), venous (VS) and arterio‐venous (A‐V) difference] in the affected and unaffected eye.MethodsFifty patients with ON due to MS within 3 months of onset of symptoms were enrolled (17 males, mean age 35.3). All patients were examined at baseline (V1) and after 6 months (V2) using optical coherence tomography (OCT) to get RNFL values; automatic retinal oximetry to obtain saturation values; and ultrasound to exclude arterial stenosis, and orbital colour Doppler imaging was performed in the ophthalmic artery.ResultsAt V1, AS was significantly increased in affected eye compared to unaffected eye (99.5% versus 98.0%, p = 0.03). Significant decrease in A‐V difference from baseline was detected in both eyes for ON eye: 32.0% versus 29.0%, p = 0.004; for fellow eye: 31.4% versus 30.0%, p = 0.04. We did not observe any changes in retinal vessel diameter. There were no changes observed in blood flow in ophthalmic artery. At V1, there were no significant differences in RNFL, and significant loss of RNFL was confirmed in the affected eye at V2 (95 μm versus 86 μm, p = 0.0002) and in comparison with the fellow eye (86 μm versus 94 μm, p = 0.0002). There were no correlations between RNFL and saturation values at V1, although at V2, there was a negative correlation between the RNFL and AS (Spearman's rho = −0.480, p = 0.003) and between the RNFL and VS (rho = −0.620, p = 0.00007).ConclusionRetinal oximetry is altered in both eyes in MS patients with unilateral ON. During the course of the disease, the retinal oxygen consumption decreases to a different degree in each eye and this change is not completely followed by changes in the RNFL thickness, suggesting either sub‐clinical ON or systemic effects in the clinically unaffected eye. Since this is the first and initial longitudinal evaluation of the saturation changes in MS patients, the clinical value of these findings needs to be deeper evaluated in the future studies.

Treatment and management of cognitive dysfunction in patients with multiple sclerosis.

Cognitive impairment is a common and devastating manifestation of multiple sclerosis (MS). Although disease-modifying therapies have been efficacious for reducing relapse rates in MS, such treatments are ineffective for treating cognitive dysfunction. Alternative treatment approaches for mitigating cognitive problems are greatly needed in this population. To date, cognitive rehabilitation and exercise training have been identified as possible candidates for treating MS-related cognitive impairment; however, cognitive dysfunction is still often considered to be poorly managed in patients with MS. This Review provides a comprehensive overview of recent developments in the treatment and management of cognitive impairment in people with MS. We describe the theoretical rationales, current states of the science, field-wide challenges and recent advances in cognitive rehabilitation and exercise training for treating MS-related cognitive impairment. We also discuss future directions for research into the treatment of cognitive impairment in MS that should set the stage for the inclusion of cognitive rehabilitation and exercise training into clinical practice within the next decade.

Anisocoria as initial manifestation of multiple sclerosis. Use of 3 tesla magnetic resonance imaging

Abstract A 21-year-old woman seen in this clinic with non-reactive mydriasis in the right eye that contracted with 1% pilocarpine. Cranial angio-CT and 1.5 T magnetic resonance imaging (MRI) did not detect any disease. Given a subsequent limitation of adduction, supraduction, and infarction of the right eye, a 3 T MRI was requested. This showed a lesion of the midbrain at the exit of the 3rd cranial nerve. After improvement, no new episodes were observed until 18 months later, when the patient presented with probable optic neuritis and systemic symptoms. At this time the 1.5 T MRI detected infratentorial and supratentorial demyelinating plaques. A subsequent lumbar puncture and clinic outcome confirmed the diagnosis of relapsing-remitting multiple sclerosis.

Fingolimod after a first unilateral episode of acute optic neuritis (MOVING) \u2013 preliminary results from a randomized, rater-blind, active-controlled, phase 2 trial

BackgroundNeuroprotection and promotion of remyelination represent important therapeutic gaps in multiple sclerosis (MS). Acute optic neuritis (ON) is a frequent MS manifestation. Based on the presence and properties of sphingosine-1-phosphate receptors (S1PR) on astrocytes and oligodendrocytes, we hypothesized that remyelination can be enhanced by treatment with fingolimod, a S1PR modulator currently licensed for relapsing-remitting MS.MethodsMOVING was an investigator-driven, rater-blind, randomized clinical trial. Patients with acute unilateral ON, occurring as a clinically isolated syndrome or MS relapse, were randomized to 6 months of treatment with 0.5 mg oral fingolimod or subcutaneous IFN-β 1b 250 μg every other day. The change in multifocal visual evoked potential (mfVEP) latency of the qualifying eye was examined as the primary (month 6 vs. baseline) and secondary (months 3, 6 and 12 vs. baseline) outcome. In addition, full field visual evoked potentials, visual acuity, optical coherence tomography as well as clinical relapses and measures of disability, cerebral MRI, and self-reported visual quality of life were obtained for follow-up. The study was halted due to insufficient recruitment (n = 15), and available results are reported.ResultsPer protocol analysis of the primary endpoint revealed a significantly larger reduction of mfVEP latency at 6 months compared to baseline with fingolimod treatment (n = 5; median decrease, 15.7 ms) than with IFN-β 1b treatment (n = 4; median increase, 8.15 ms) (p < 0.001 for interaction). Statistical significance was maintained in the secondary endpoint analysis. Descriptive results are reported for other endpoints.ConclusionPreliminary results of the MOVING trial argue in support of a beneficial effect of fingolimod on optic nerve remyelination when compared to IFN-β treatment. Interpretation is limited by the small number of complete observations, an unexpected deterioration of the control group and a difference in baseline mfVEP latencies. The findings need to be confirmed in larger studies.Trial registrationThe trial was registered as EUDRA-CT 2011–004787-30 on October 26, 2012 and as NCT01647880 on July 24, 2012.

Prevalence of Ophthalmological Manifestations of MS

Abstract Objective The aim of this study is to highlight the neuro-ophthalmic manifestations and their correlation with visual dysfunction in patients of multiple sclerosis (MS). Patients and Methods One hundred patients diagnosed with MS according to the Revised McDonald’s Criteria of 2010 from the MS Unit at Ain Shams University Hospitals were included in the study from May to September 2017. A detailed medical history was taken and full ophthalmic examination was done to all patients including best corrected visual acuity (BCVA), pupillary reflexes, ocular motility, confrontation test, contrast sensitivity (CS) test, color test, slit-lamp biomicroscopy and dilated fundus examination. Results Acute ON was the first manifestation of the disease in 36% of patients and in 44% it occurred during the course of the disease. Although most patients’ visual acuity recovered to baseline after an episode of optic neuritis (ON), residual deficits in CS are common. Acute ocular motor manifestations were reported in 6 patients (6%) as a presenting symptom of MS. During the course of the disease 31 patients (31%) had at least one attack of acute abnormal eye movement. One patient (1%) among the studied group had anterior uveitis. There is a statistically significant correlation between CS in patients with no ON relapses and patients with at least 1 relapse (P value= 0.005). There is a statistically significant correlation between relative afferent pupillary defect (RAPD) in patients with no ON attacks and patients with at least 1 relapse (P value= 0.032). Also there is a statistically significant correlation between disc pallor in patients with no ON relapses and patients with at least 1 relapse (P value= 0.007). There is a statistically significant correlation between number of relapses of ocular motor symptoms and visual function impairment; BCVA (P = 0.025), CS (P = 0.027) and color vision (P = 0.039). Conclusion Our study emphasizes the high prevalence of ophthalmic manifestations among MS patients and that optic neuropathy is the most common manifestation. Detection of these symptoms and signs during ophthalmologic evaluation may lead to early diagnosis and treatment of MS that offer better outcome for those patients.

Optimization of spectral domain optical coherence tomography and visual evoked potentials to identify unilateral optic neuritis

BackgroundOptic neuritis is a common manifestation of multiple sclerosis and frequently the presenting sign. The diagnosis of MS is heavily based on MRI findings but the latter is relatively insensitive in detecting optic nerve lesions. Identification of optic nerve lesion using ancillary tools such spectral-domain optical coherence tomography (SDOCT) by measuring the retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GCIPL), and visual-evoked potentials latencies (VEP) may facilitate early diagnosis and treatment of multiple sclerosis. ObjectiveTo determine the optimal of SDOCT measures in RFNL and GCIPL and the VEP latency value for the identification of a prior symptomatic optic nerve lesion. MethodsThirty patients with diagnosed clinically with optic neuritis and fifty healthy control subjects were tested with SDOCT and VEP and the sensitivity, specificity, negative and positive predictive values of optimal values from healthy controls and optic neuritis patients were determined of for the identification unilateral optic nerve lesion. ResultsThe inter-eye GCIPL difference of 3.5 µm is highly sensitive (100%) and specific (98%) in identifying unilateral optic nerve lesion, while lowest 5th percentile normal GCIPL threshold values of 71 µm was highly sensitive (100%) but less specific (83.3%). The inter-eye RNFL difference of 5.5 µm had a sensitivity of 70% and specificity of 90% in identifying optic nerve lesion while the lower 5th percentile normal RNFL value of 92.3 µm was poorly sensitive (40%). Finally, the 95th percentile normal VEP latency of 104.50 milliseconds had sensitivity of 80% and specificity of 76% in identifying optic nerve lesion. ConclusionsThe inter-eye GCIPL difference is a powerful index for identifying unilateral optic nerve lesion, while the inter-eye RNFL difference and 95th percentile normal VEP latency had very good sensitivity and specificity. These measures can be useful in the evaluation of the first demyelinating event of MS and therefor can facilitate early diagnosis and therapy.

Atypical presentation of optic neuritis with unilateral inferior altitudinal visual field defect in multiple sclerosis

Background: The purpose of this paper was to report a case of retrobulbar optic neuritis as the first manifestation of multiple sclerosis, with atypical presentations which include a sudden painless reduction in vision, without optic disc swelling and presence of unilateral inferior altitudinal visual field defect. Case report: A 17-year-old girl presented to our clinic with right eye sudden painless drop in visual acuity to counting finger associated with headache. Her right eye optic nerve function tests were positive, but her optic disc was not swollen. Bjerrum’s visual field chart noted right eye unilateral inferior altitudinal visual field defect with foveal involvement. Her blood investigations were normal, and magnetic resonance imaging (MRI) of brain and orbit was suggestive of multiple sclerosis. She was commenced on three days of high dose intravenous steroi, and was referred to neuromedical team for further management. At 3-month follow up, her right eye visual acuity improved to 6/6 with the restoration of normal colour vision. Conclusions: In presence of atypical presentation of optic neuritis, multiple sclerosis must be thought of especially in young patients. Hence early co-management with neuromedical discipline is important to reduce the frequency and severity of attacks in the future.