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Multiple Sclerosis Phenotypes 2013
- 1. Preceptorship en Esclerosis Múltiple Junio 16-18 2016 Medellín
- 2. Fenotipos en Esclerosis Múltiple Dr. Cesar A Franco Neurólogo Preceptorship en Esclerosis Múltiple Centro de Enfermedades Desmielinizantes Junio 16-18 2016
- 3. Fenotipos 1996 Comité de ensayos clínicos de NMSS. Para estudios poblacionales, ensayos clínicos y terminología entre clínicos y frente a pacientes. Lublin FD, et al. Neurology 1996;46:907–911 Remitente Recurrente EMRR Remitente Recurrente EMRR Primaria Progresiva EMPP Primaria Progresiva EMPP Secundaria Progresiva EMSP Secundaria Progresiva EMSP Progresiva Recurrente EMPR Progresiva Recurrente EMPR Preceptorship CEMED-INDEC
- 4. •Rápida incorporación a práctica clínica y criterios para ensayos clínicos. •Aportan para aprobación de medicamentos. •Consenso de expertos, sin claro soporte biológico. •No correlación con Resonancia y otros marcadores. Fenotipos 1996 Lublin FD, et al. Neurology 1996;46:907–911. Preceptorship CEMED-INDEC
- 5. 2011 tarea de reevaluar fenotipos, por NMSS-ECTRIMS y The MS Phenotype Group. •Definir cursos clínicos más exactos. •Incluir clínica, MRI y otras imágenes, biomarcadores, neurofiisología. •Sugerir campos de investigación, si no hay consenso o ausencia de información. Lublin FD, et al. Neurology 2014;83:1–9. Fenotipos 2013 Preceptorship CEMED-INDEC
- 6. •Se mantienen algunas descripciones originales, con modificaciones y aclaraciones. •Inclusión de Sindrome Clínico Aislado (CIS). •No se incluye Sindrome Radiológico Aislado. •Desaparece categoría de EM Progresiva Recurrente (corresponde a Primaria Progresiva con actividad). Fenotipos 2013 Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC
- 7. Fenotipos 2013 Definiciones Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Definiciones
- 8. Fenotipos 2013 Definiciones Enfermedad Progresiva • Clínica Progresivo aumento de discapacidad o de disfunción neurológica, documentado objetivamente y sin inequívoca recuperación. y/o • Resonancia No hay estandarización aún. No establecido. Aumento de lesiones hipointensas en T1, atrofia, cambios en MTI o DTI Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Definiciones
- 9. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Definiciones
- 10. Progresión o empeoramiento confirmados • Aumento de disfunción neurológica confirmado en un intervalo de tiempo definido. • Progresión confirmada en un intervalo de tiempo de 6 a 12 meses (en vista que en enfermedad recurrente la disfunción puede mejorar) • Evitar el termino “progresión sostenida” de discapacidad Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Definiciones
- 11. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-CIS/EMRR
- 12. EM Primaria ProgresivaEM Primaria Progresiva EM Secundaria ProgresivaEM Secundaria Progresiva Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013- EM progresiva
- 13. •Permite refinar criterios de inclusión/exclusión. •Estratifica mejor subtipos de pacientes •Identifica subtipos específicos que pueden beneficiarse de tratamientos específicos. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013- en Ensayos Clínicos
- 14. •Estudios longitudinales de largo seguimiento para acoplar imagen a clínica, especialmente transiciones entre fenotipos. •Seguimiento estrecho de RIS, correlación imagen-clínica. •Evaluar diferentes momentos para evaluar actividad por imagen y clínica (confirmar o rechazar seguimiento anual). •Estudios con biomarcadores, electrofisiología, RM técnicas especiales,etc. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Investigación a futuro
- 15. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Algoritmos seguimiento
- 16. Evaluar progresiónEvaluar progresión Confirmado empeoramiento o acumulación de discapacidad que persiste 3, 6 o 12 m Confirmado empeoramiento o acumulación de discapacidad que persiste 3, 6 o 12 m Evaluación anual por historia o medidas objetivas (EDSS,MSFC) Evaluación anual por historia o medidas objetivas (EDSS,MSFC) Empeoramiento confirmado en el mismo sistema funcional (definición rigurosa) Empeoramiento confirmado en el mismo sistema funcional (definición rigurosa) Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Algoritmos seguimiento
- 18. Mujer de 24 años, economista. Mayo de 2012 Neuritis Óptica izquierda típica. Resonancia contrastada cerebral normal, excepto por NO izq hiperintenso T2 y T1 Gd+- Descartado diagnóstico diferencial. Bandas Oligoclonales positivas. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 1.
- 19. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso 1. Fenotipo?
- 20. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso 1. Fenotipo
- 21. Abril 2016 Oftalmoplejía internuclear. Resonancia con lesiones, en T2 : yuxtacorticales (2), periventriculares (1), infratentoriales(1). Gd + (3). EDSS: 3.0 (SF Tallo:3.0) Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 1. Evolución
- 22. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 1. 2016. Fenotipo?
- 23. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 1. 2016. Fenotipo
- 24. •Hombre de 47 años •Desde 2012 paraparesia espástica, sin otro compromiso. •Dx. diferencial negativo. •No realizadas BOC. •Dx. de EM (McDonald 2010 para EMPP-DIS cerebral y medular) en 2014 e iniciado IFN B 1 b sc. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 2.
- 25. •2014 EDSS: 4.0 •2015 Ex clínico: paraparesia espástica, Babinski bilateral. EDSS: 5.5. •En 2016 igual, necesidad de bastón.EDSS: 6.0. •Resonancia de neuroeje con lesiones, en T2 : yuxtacorticales (4), periventriculares (7), infratentoriales(3), espinales(6 de uno-dos segmentos). Gd + (0). Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 2.
- 26. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 2. Fenotipo?
- 27. EM Primaria ProgresivaEM Primaria Progresiva EM Secundaria ProgresivaEM Secundaria Progresiva Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 2. Fenotipo
- 28. Mujer de 18 años, sin antecedentes patológicos o neurológicos y consultando por Neuritis óptica derecha típica(subjetiva y objetiva), sin anormalidad al dx diferencial, con Resonancia con NO derecho hiperintenso T2 y T1Gd+, más lesiones cerebrales en T2 : yuxtacorticales (1), periventriculares (2), infratentoriales (0) y lesiones Gd+ (1). Bandas Oligoclonales presentes. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 3.
- 29. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 3. Fenotipo?
- 30. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 3. Fenotipo
- 31. Mujer 46 años, EM desde los 30 años IFN B 1 a sc desde 2003 Desde 2012 episodios anuales de empeoramiento motor Ingresa INDEC en 04/2015 EDSS:4.0 • EDSS:5.5 en 11/ 2015 • 02/2016 episodio paraparesia mayor • 04/2016 EDSS:6.0 • Resonancia 04/2016: • Extenso compromiso • supra e infratetorial, • atrofia, lesión Gd+ T6 Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 4.
- 32. Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 4. Fenotipo ?
- 33. EM Primaria ProgresivaEM Primaria Progresiva EM Secundaria ProgresivaEM Secundaria Progresiva Lublin FD, et al. Neurology 2014;83:1–9. Preceptorship CEMED-INDEC Fenotipos 2013-Caso Clínico 4. Fenotipo
- 34. • Nueva definición de fenotipos de Esclerosis Múltiple, de 2013, reemplazan a los de 1996. • Conserva definiciones base sobre enfermedad recurrente y enfermedad progresiva. • Incluye Síndrome Clínico Aislado en fenotipos de la enfermedad • Exige determinar de actividad (por clínica y RM) y progresión de la enfemedad (en un periodo de tiempo) Preceptorship CEMED-INDEC Fenotipos 2013-Mensajes finales
Notas del editor
- The Committee provided standardized defi- nitions for 4 MS clinical courses: relapsing- remitting (RR), secondary progressive (SP), pri- mary progressive (PP), and progressive relapsing (PR).1 It further recommended that the term relapsing-progressive MS be dropped, as the term was believed to be vague and overlapped with other disease course subtypes. Also recom- mended was that the term chronic progressive be replaced with the more specific terms SP and PP. Definitions were provided for benign MS and malignant MS. These phenotype descrip- tions were believed to represent the spectrum of clinical subtypes of MS but it was recognized that the descriptions might change over time.
- The 1996 clinical course descriptions were rapidly incorporated into clinical practice and utilized in the eligibility criteria of almost all subsequent MS clinical trials. They were also used to some extent to guide regulatory review and approval of new therapeutics. At times the course descriptions were amalgamated into relapsing (including RR, SP, and PR) and pro- gressive (including PP, SP, and PR) forms with the major distinction being whether the sub- ject’s disease was predominantly relapsing vs predominately progressing, although the dis- tinction was never clearly delineated. When proposed, it was noted that these clini- cal course descriptors were based on subjective views of MS experts and lacked objective biolog- ical support. There was insufficient knowledge to confidently link MS clinical course with MRI findings and biological and other surrogate markers for disease course were lacking. The au- thors suggested that developments in imaging and biological marker research would have a future impact on modifying or complementing the purely clinical course descriptors and that the clinical course subtypes of MS should be re- addressed when such markers became available.
- In 2011, the Committee (now jointly spon- sored by NMSS and The European Commit- tee for Treatment and Research in MS) and other experts (The MS Phenotype Group) re-examined MS phenotypes, exploring clini- cal, imaging, and biomarker advances through working groups and literature searches. In October 2012, we convened to review the 1996 clinical course descriptions and deter- mine if sufficient progress and new insights were available to recommend changes. The specific goals of the meeting were as follows: Re-examine the 1996 phenotype descriptions to determine whether they could be better characteri- zed by including improved clinical descriptive ter- minology, MRI and other imaging techniques, analysis of fluid biomarkers, and other assays including neurophysiology. Produce a summary of our discussions that presents what we know, what we recommend, and what we still need to know. Recommend research strategies to move the field forward where data or consensus are lacking.
- Retaining the basics of the 1996 phenotype descriptions, with clarifications. It was believed that the 1996 phenotype descriptions had become part of standard MS practice and clinical research. The Group recommended that the basic fea- tures of the original descriptions should be maintained, with modifications and clarifications, as discussed below. We noted that the diagnosis of MS should be made on clinical grounds with input from imaging and other paraclinical studies, where needed.2 The clinical phe- notype may be assessed based on current status and historical data, with the understanding that this can be a dynamic process and that the subtype on initial assessment may change over time. For example, an RR subtype may transition into an SP subtype. New disease courses. Clinically isolated syndrome. Clini- cally isolated syndrome (CIS) was not included in the initial MS clinical descriptors. CIS is now recog- nized as the first clinical presentation of a disease that shows characteristics of inflammatory demyelination that could be MS, but has yet to fulfill criteria of dis- semination in time.3 Natural history studies and clin- ical trials of MS disease-modifying therapies have shown that CIS coupled with brain MRI lesions car- ries a high risk for meeting diagnostic criteria for MS.4–7 Clinical trials of MS disease-modifying agents show fewer treated individuals with CIS who develop a second exacerbation (the defining event for “clini- cally definite MS”) and reduced MRI activity.8–11 Regulatory acceptance of agents used in CIS to delay confirmed diagnosis of MS has further established CIS as an element of the MS phenotype spectrum.12 Use of the 2010 revisions to the McDonald MS diag- nostic criteria allows some patients with a single clin- ical episode to be diagnosed with MS based on the single scan criterion for dissemination in time and space,2 reducing the number of patients who will be categorized as CIS.
- The Committee provided standardized defi- nitions for 4 MS clinical courses: relapsing- remitting (RR), secondary progressive (SP), pri- mary progressive (PP), and progressive relapsing (PR).1 It further recommended that the term relapsing-progressive MS be dropped, as the term was believed to be vague and overlapped with other disease course subtypes. Also recom- mended was that the term chronic progressive be replaced with the more specific terms SP and PP. Definitions were provided for benign MS and malignant MS. These phenotype descrip- tions were believed to represent the spectrum of clinical subtypes of MS but it was recognized that the descriptions might change over time.
- MS = multiple sclerosis; DIS = dissemination in space; DIT = dissemination in time; PPMS = primary progressive multiple sclerosis.a Reprinted with permission from Polman CH, et al, Ann Neurol.4 B 2011 American Neurological Association. onlinelibrary.wiley.com/ b doi/10.1002/ana.22366/full. If the Criteria are fulfilled and there is no better explanation for the clinical presentation, the diagnosis is ‘‘MS’’; if suspicious, but the Criteria are not completely met, the diagnosis is ‘‘possible MS’’; if another diagnosis arises during the evaluation that better explains c the clinical presentation, then the diagnosis is ‘‘not MS.’’ An attack (relapse; exacerbation) is defined as patient-reported or objectively observed events typical of an acute inflammatory demyelinating event in the CNS, current or historical, with duration of at least 24 hours, in the absence of fever or infection. It should be documented by contemporaneous neurologic examination, but some historical events with symptoms and evolution characteristic for MS, but for which no objective neurologic findings are documented, can provide reasonable evidence of a prior demyelinating event. Reports of paroxysmal symptoms (historical or current) should, however, consist of multiple episodes occurring over not less than 24 hours. Before a definite diagnosis of MS can be made, at least 1 attack must be corroborated by findings on neurologic examination, visual evoked potential response in patients reporting prior d visual disturbance, or MRI consistent with demyelination in the area of the CNS implicated in the historical report of neurologic symptoms. Clinical diagnosis based on objective clinical findings for 2 attacks is most secure. Reasonable historical evidence for 1 past attack, in the absence of documented objective neurologic findings, can include historical events with symptoms and evolution characteristics for a e prior inflammatory demyelinating event; at least one attack, however, must be supported by objective findings.No additional tests are required. However, it is desirable that any diagnosis of MS be made with access to imaging based on these criteria. If imaging or other tests (for instance, CSF) are undertaken and the results are negative, extreme caution needs to be taken before making a diagnosis of MS, and alternative diagnoses must be considered. There must be no better explanation for the clinical f presentation, and objective evidence must be present to support a diagnosis of MS.Gadolinium-enhancing lesions are not required; symptomatic lesions are excluded from consideration in subjects with brainstem or spinal cord syndromes.
- Diagnosis and Differential Diagnosis of Multiple Sclerosis Katz Sand, Ilana B. MD; Lublin, Fred D. MD, FAAN, FANA. Continuum (Minneap Minn). August 2013; 19(4 Multiple Sclerosis): 922Y943. Abstract Purpose of Review: When a patient presents with symptoms or imaging suggestive of multiple sclerosis (MS), making the correct diagnosis may at times be straightforward but in many cases is quite challenging. Symptoms may be difficult for patients to characterize and for clinicians to interpret; findings on examination may be subtle; imaging is not always specific; and the differential diagnosis of possible demyelinating disease is quite broad. Making a correct diagnosis of MS early in the disease course is likely to become even more important over time as new disease-modifying therapies, particularly those with potential neuroprotective benefits, are introduced. This article reviews the current diagnostic criteria for MS and illustrates their application as well as reviews the differential diagnosis for patients presenting with symptoms or imaging suggestive of demyelinating disease. Recent Findings:The diagnostic criteria for MS were revised by the International Panel on Diagnosis of Multiple Sclerosis in 2010. Summary: The diagnostic criteria for MS have been revised several times over the years, most recently giving rise to the McDonald 2010 criteria. The diagnosis of MS begins with a patient who presents with symptoms typical for the disease, termed the ‘‘clinically isolated syndrome,’’ which most commonly affects the optic nerves, brainstem, or spinal cord. If the patient’s symptoms and imaging are typical for MS, the clinician can then apply the appropriate diagnostic criteria. If atypical clinical or imaging findings are present, alternative etiologies must be pursued as appropriate. Key Points & All recent formulations of the diagnostic criteria begin with an initial clinical presentation that includes symptoms typical for a multiple sclerosis attack (also called a relapse or exacerbation). Typical presentations usually involve the optic nerves (optic neuritis), brainstem (for example, internuclear ophthalmoplegia), or spinal cord (for example, partial transverse myelitis). & Once multiple sclerosis has been established as the most likely etiology of the symptoms, the clinician must evaluate for evidence of dissemination in space, which requires involvement of multiple areas of the CNS, and for dissemination in time, which requires ongoing disease activity over time. * 2013, American Academy of Neurology.Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. & Dissemination-in-space MRI criteria now require at minimum only two lesions: at least one T2 lesion in at least two of the four sites typically affected by multiple sclerosis (periventricular, juxtacortical, infratentorial, or spinal cord). & Dissemination in time can be demonstrated with a single MRI if simultaneous asymptomatic gadolinium-enhancing and nonenhancing lesions are present. & Primary progressive multiple sclerosis is characterized by the insidious onset of symptoms followed by gradual deterioration over time. Clinical disease in these patients typically presents as a progressive myelopathy, and less frequently as a brainstem or cerebellar syndrome. & Secondary progressive multiple sclerosis is diagnosed when, after an initial relapsing-remitting course, a patient demonstrates disease progression independent of relapses for at least 6 months. & Radiologically isolated syndrome is diagnosed when a patient is incidentally found to have imaging findings suggestive of multiple sclerosis, which are not better explained by another medical condition, in the absence of clinical symptoms. & For patients who present with symptoms that are typical for multiple sclerosis, have typical imaging findings, and meet relapsing-remitting multiple sclerosis criteria, often no further diagnostic evaluation is necessary. However, if any element of the clinical history, examination, or imaging is atypical, additional testing to exclude other etiologies is warranted. & Patients with optic neuritis related to underlying multiple sclerosis typically present with painful, subacute, unilateral visual loss that manifests as visual blurring or a scotoma. & The presence of any features that are not typical for optic neuritis associated with underlying multiple sclerosis merits consideration of alternative diagnoses and may require additional evaluation, dependent on the remainder of the clinical picture. & A classic presentation of a brainstem syndrome suggestive of clinically isolated syndrome is diplopia due to internuclear ophthalmoplegia, which is often bilateral. & Patients with a spinal cord syndrome suggestive of clinically isolated syndrome characteristically present with a partial transverse myelitis, which is usually dominated by sensory symptoms. & On MRI, spinal cord lesions due to multiple sclerosis are typically peripheral, with the dorsolateral cord being the most common plaque location. Multiple sclerosis lesions are usually less than two vertebral segments in length and occupy less than half of the cross-sectional cord area. & Common areas for multiple sclerosis lesions include periventricular, juxtacortical, and infratentorial regions, as well as the spinal cord. & Involvement of the paracentral corpus callosum, particularly at the callosal-septal interface (but not the midline corpus callosum), is common in multiple sclerosis.
- Diagnosis and Differential Diagnosis of Multiple Sclerosis Katz Sand, Ilana B. MD; Lublin, Fred D. MD, FAAN, FANA. Continuum (Minneap Minn). August 2013; 19(4 Multiple Sclerosis): 922Y943. Abstract Purpose of Review: When a patient presents with symptoms or imaging suggestive of multiple sclerosis (MS), making the correct diagnosis may at times be straightforward but in many cases is quite challenging. Symptoms may be difficult for patients to characterize and for clinicians to interpret; findings on examination may be subtle; imaging is not always specific; and the differential diagnosis of possible demyelinating disease is quite broad. Making a correct diagnosis of MS early in the disease course is likely to become even more important over time as new disease-modifying therapies, particularly those with potential neuroprotective benefits, are introduced. This article reviews the current diagnostic criteria for MS and illustrates their application as well as reviews the differential diagnosis for patients presenting with symptoms or imaging suggestive of demyelinating disease. Recent Findings:The diagnostic criteria for MS were revised by the International Panel on Diagnosis of Multiple Sclerosis in 2010. Summary: The diagnostic criteria for MS have been revised several times over the years, most recently giving rise to the McDonald 2010 criteria. The diagnosis of MS begins with a patient who presents with symptoms typical for the disease, termed the ‘‘clinically isolated syndrome,’’ which most commonly affects the optic nerves, brainstem, or spinal cord. If the patient’s symptoms and imaging are typical for MS, the clinician can then apply the appropriate diagnostic criteria. If atypical clinical or imaging findings are present, alternative etiologies must be pursued as appropriate. Key Points & All recent formulations of the diagnostic criteria begin with an initial clinical presentation that includes symptoms typical for a multiple sclerosis attack (also called a relapse or exacerbation). Typical presentations usually involve the optic nerves (optic neuritis), brainstem (for example, internuclear ophthalmoplegia), or spinal cord (for example, partial transverse myelitis). & Once multiple sclerosis has been established as the most likely etiology of the symptoms, the clinician must evaluate for evidence of dissemination in space, which requires involvement of multiple areas of the CNS, and for dissemination in time, which requires ongoing disease activity over time. * 2013, American Academy of Neurology.Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. & Dissemination-in-space MRI criteria now require at minimum only two lesions: at least one T2 lesion in at least two of the four sites typically affected by multiple sclerosis (periventricular, juxtacortical, infratentorial, or spinal cord). & Dissemination in time can be demonstrated with a single MRI if simultaneous asymptomatic gadolinium-enhancing and nonenhancing lesions are present. & Primary progressive multiple sclerosis is characterized by the insidious onset of symptoms followed by gradual deterioration over time. Clinical disease in these patients typically presents as a progressive myelopathy, and less frequently as a brainstem or cerebellar syndrome. & Secondary progressive multiple sclerosis is diagnosed when, after an initial relapsing-remitting course, a patient demonstrates disease progression independent of relapses for at least 6 months. & Radiologically isolated syndrome is diagnosed when a patient is incidentally found to have imaging findings suggestive of multiple sclerosis, which are not better explained by another medical condition, in the absence of clinical symptoms. & For patients who present with symptoms that are typical for multiple sclerosis, have typical imaging findings, and meet relapsing-remitting multiple sclerosis criteria, often no further diagnostic evaluation is necessary. However, if any element of the clinical history, examination, or imaging is atypical, additional testing to exclude other etiologies is warranted. & Patients with optic neuritis related to underlying multiple sclerosis typically present with painful, subacute, unilateral visual loss that manifests as visual blurring or a scotoma. & The presence of any features that are not typical for optic neuritis associated with underlying multiple sclerosis merits consideration of alternative diagnoses and may require additional evaluation, dependent on the remainder of the clinical picture. & A classic presentation of a brainstem syndrome suggestive of clinically isolated syndrome is diplopia due to internuclear ophthalmoplegia, which is often bilateral. & Patients with a spinal cord syndrome suggestive of clinically isolated syndrome characteristically present with a partial transverse myelitis, which is usually dominated by sensory symptoms. & On MRI, spinal cord lesions due to multiple sclerosis are typically peripheral, with the dorsolateral cord being the most common plaque location. Multiple sclerosis lesions are usually less than two vertebral segments in length and occupy less than half of the cross-sectional cord area. & Common areas for multiple sclerosis lesions include periventricular, juxtacortical, and infratentorial regions, as well as the spinal cord. & Involvement of the paracentral corpus callosum, particularly at the callosal-septal interface (but not the midline corpus callosum), is common in multiple sclerosis.