Multiple SclerosisMultiple Sclerosis

Jaimie Lynn Maines, MS-IV

SYB #3

5 March 2008

Jaimie Lynn Maines, MS-IV

SYB #3

5 March 2008

What is Multiple Sclerosis?What is Multiple Sclerosis? Chronic, inflammatory,

demyelinating disease that affects the CNS Onset usually in young

adulthood Women > men

Affects neurons in white matter of brain and spinal cord Destroys

oligodendrocytes loss of myelin sheath

Chronic, inflammatory, demyelinating disease that affects the CNS Onset usually in young

adulthood Women > men

Affects neurons in white matter of brain and spinal cord Destroys

oligodendrocytes loss of myelin sheath

Signs and SymptomsSigns and Symptoms Changes in sensation

(hypoesthesia) Muscle weakness Abnormal muscle

spasms Difficulty with

movement Ataxia Dysarthria Dysphagia

Changes in sensation (hypoesthesia)

Muscle weakness Abnormal muscle

spasms Difficulty with

movement Ataxia Dysarthria Dysphagia

Nystagmus, optic neuritis, diplopia

Fatigue and acute or chronic pain syndromes

Bladder and bowel difficulties

Cognitive impairment, depression

Lhermitte’s Sign Classic finding in MS

Nystagmus, optic neuritis, diplopia

Fatigue and acute or chronic pain syndromes

Bladder and bowel difficulties

Cognitive impairment, depression

Lhermitte’s Sign Classic finding in MS

Disease Course and Clinical SubtypesDisease Course and Clinical Subtypes Relapsing Form - new

symptoms occur in discrete attacks

Progressive Form - new symptoms slowly accumulate over time

Relapse-Remitting Form - between attacks, symptoms resolve completely, but permanent neurological problems persist May develop Secondary

Progressive MS

Relapsing Form - new symptoms occur in discrete attacks

Progressive Form - new symptoms slowly accumulate over time

Relapse-Remitting Form - between attacks, symptoms resolve completely, but permanent neurological problems persist May develop Secondary

Progressive MS

DiagnosisDiagnosisDifficult to diagnose in early stages

Definitive diagnosis cannot be made until other possible causes for symptoms have been ruled out

In Relapsing-Remitting: there must be evidence of at least 2 anatomically separate demyelinating events separated by at least 30 days

In Primary Progressive: there must be slow progression of si/sx over at least 6 months

Difficult to diagnose in early stagesDefinitive diagnosis cannot be made until

other possible causes for symptoms have been ruled out

In Relapsing-Remitting: there must be evidence of at least 2 anatomically separate demyelinating events separated by at least 30 days

In Primary Progressive: there must be slow progression of si/sx over at least 6 months

McDonald CriteriaMcDonald CriteriaClinical data alone - 2 separate episodes of

neurologic symptoms characteristic of MS, consistent PE

MRI - areas of demyelination appear as bright spots (active plaques enhance with Gad)

CSF - evidence of chronic inflammationOligoclonal bands combined with MRI and PE can

make definitive diagnosisVisual or Somatosensory Evoked Potentials -

brain with MS responds less actively to stimulation

Clinical data alone - 2 separate episodes of neurologic symptoms characteristic of MS, consistent PE

MRI - areas of demyelination appear as bright spots (active plaques enhance with Gad)

CSF - evidence of chronic inflammationOligoclonal bands combined with MRI and PE can

make definitive diagnosisVisual or Somatosensory Evoked Potentials -

brain with MS responds less actively to stimulation

Imaging StudiesImaging StudiesMRI

Test of choice to support clinical diagnosisCharactertistic lesion - cerebral or spinal plaque;

periventricular region, corpus callosum, centrum semiovale, deep white matter structures, basal ganglia

Typically ovoid in appearance, arranged at right angles to corpus callosum

Hyperintense on T2 MRI, hypointense on T1 Diffusion imaging may identify plaques better Gad-enhancing plaques active lesions

Discrete region of demyelination

MRITest of choice to support clinical diagnosisCharactertistic lesion - cerebral or spinal plaque;

periventricular region, corpus callosum, centrum semiovale, deep white matter structures, basal ganglia

Typically ovoid in appearance, arranged at right angles to corpus callosum

Hyperintense on T2 MRI, hypointense on T1 Diffusion imaging may identify plaques better Gad-enhancing plaques active lesions

Discrete region of demyelination

Differential DiagnosisDifferential DiagnosisNeuromyelitis Optica

Autoimmune disease - attack of optic nerves and spinal cord

StrokeAcute Disseminated Encephalomyelitis

Immune mediated disease of brain following viral infection or vaccination; multiple inflammatory cell deposits found in white matter

Lyme DiseaseTumorsLupus

Neuromyelitis OpticaAutoimmune disease - attack of optic nerves and

spinal cordStrokeAcute Disseminated Encephalomyelitis

Immune mediated disease of brain following viral infection or vaccination; multiple inflammatory cell deposits found in white matter

Lyme DiseaseTumorsLupus

Medical TreatmentMedical TreatmentThere is NO cureTreatments aimed at returning function

following an attack, preventing new attacks, and preventing disability IV steroids for acute attacksInterferon - disease modifying treatmentNeurorehabilitation to ease burden of

progressive impairment

There is NO cureTreatments aimed at returning function

following an attack, preventing new attacks, and preventing disability IV steroids for acute attacksInterferon - disease modifying treatmentNeurorehabilitation to ease burden of

progressive impairment