MS Since the late 1300s, individuals with a progressive illness suggestive of MS have - PowerPoint Presentation

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MS

Since the late 1300s, individuals with a progressive illness suggestive of MS have been observed. It wasn’t until 1868 that the famous neurologist, 

Jean-Martin Charcot, lectured on the features of MS and gave it a name 'la sclérose en plaques‘. The word sclerosis comes from the Greek word "skleros,"  meaning hard = "plaques"

A glimpse Into History

What is multiple sclerosis?

Multiple sclerosis (MS) is a chronic disease characterized by inflammation and demyelination of the central nervous system (CNS) associated with variable degrees of axonal and neuronal damage.

It usually presents with recurrent, subacute, focal neurologic symptoms and signs that improve (at least to some extent) over several weeks or months. The disease may initially present with (less often) or evolve into (more common) a relentless progressive decline of neurologic functioning, commonly affecting locomotion, bladder function, and cognition.

MS phases

High Risk

RR

PP

Pathogenesis

B/T lymphocytes

Meningeal lymphoid follicle like aggregate

Axonal injury

Demyelinated plaques

MS

T and B lymphocyte–mediated disease, affect both grey and white matter

Autoreactive lymphocytes that gain access to the CNS start a pathogenic cascade that culminates in demyelination,

neuroaxonal

degeneration, synaptic loss, dying-back

oligodendrogliopathy

, and, eventually, tissue loss and astrogliosis.Demyelinated plaques : pathologic markers of MS , loss of oligodendrocytes, loss of myelin sheaths, and astrocytic scars.Axonal injury is present, even from the earliest stages of MS, contributes disability.

Meningeal lymphoid follicle–like aggregates : ongoing sequestered intrathecal inflammation might be a factor contributing to progression.

Schumacher Criteria

McDonald Criteria

2010

Revised McDonald

Criteria

2017

Diagnostic Criteria

Schumacher

Criteria

The identification of a syndrome “typical” of MS-related demyelination

Objective evidence of central nervous system (CNS) involvement

Demonstration of dissemination in space

Demonstration of dissemination in time

“No better explanation” other than MS

The identification of a syndrome “typical” of MS-related demyelination

Transverse myelitis

Cerebellar syndromes

Brainstem syndromes Optic neuritis

Objective evidence of central nervous system (CNS) involvement

ClinicalRadiographic

Para-clinical

Dissemination

in SpaceFulfillment of dissemination in space requires detection of lesions in more than one distinct anatomic location within the CNS (periventricular, cortical or juxtacortical, infratentorial brain regions and the spinal cord)

Dissemination

in TimeFulfillment of dissemination in time requires confirmation of new CNS lesions over time.

“No Better Explanation”: the Differential Diagnosis of Relapsing-Remitting Multiple Sclerosis

As no single biomarker for MS exists, each revision of MS diagnostic criteria has also specified that there must be a determination of “no better explanation for the clinical presentation under consideration.The authors of the 2017 McDonald criteria also recommend application with caution in diverse populations (nonwhite) and patients younger than 11ys or older than 50ys , in whom the 2017 McDonald criteria have not been evaluated.

Better Explanation for Typical Syndromes

Clinical, laboratory, or radiographic findings atypical for MS and suggestive of an alternative diagnosis that may offer a better explanation than MS for the clinical presentation.NMO/neurosarcoidosis more commen in non-white than MS.Longitudinally extensive transverse myelitis may suggest NMOSD, neurosarcoidosis

, anti-MOG–associated myelitis, systemic rheumatologic disease, or a paraneoplastic disorderSevere or bilateral optic neuritis may suggest NMOSD

Transverse myelitis associated with prodromal symptoms or MRI T2 signal abnormality confined to spinal cord gray matter may suggest anti-MOG–associated myelitis

Multiple cranial nerve involvement might suggest neurosarcoidosis.Transverse myelitis or optic neuritis accompanied by high CSF pleocytosis should also prompt investigation into infectious or inflammatory disorders other than MSSystemic symptoms such as joint pain, skin changes, and weight loss might suggest either rheumatologic or paraneoplastic disease

Expanding the Differential Diagnosis and Red Flags to

Noninflammatory DisordersLets play a game

Avoid Misdiagnosis

Don’t count cortical/subcortical lesions , >3mm , >6mm.CSF oligoclonal band –ve < repeat later.On atypical presentation, dig deeper , investigate more. Juxatcotrical/periventricular lesions should abut the cortex/ventricles.Age 11-50 , white.Callosospetal lesion favor MS.

Always re-evaluate preexisting MS diagnosis.16

McDonald Criteria

Radiological cases

https://radiopaedia.org/cases/optic-neuritis-multiple-sclerosis?lang=ushttps://radiopaedia.org/cases/multiple-sclerosis-teaching?lang=ushttps://radiopaedia.org/cases/neuromyelitis-optica-4?lang=us

https://radiopaedia.org/cases/multiple-sclerosis-42?lang=gbhttps://radiopaedia.org/cases/tumefactive-multiple-sclerosis-1?lang=gb

PPMS

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