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 35 yo AAF presents with confusion, agnosia, apraxia, right-sided lower extremity paresis  Symptoms first noticed 2 hours ago  CT scan- no blood  MRI-

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Presentation on theme: " 35 yo AAF presents with confusion, agnosia, apraxia, right-sided lower extremity paresis  Symptoms first noticed 2 hours ago  CT scan- no blood  MRI-"— Presentation transcript:

1  35 yo AAF presents with confusion, agnosia, apraxia, right-sided lower extremity paresis  Symptoms first noticed 2 hours ago  CT scan- no blood  MRI- single hyperintense lesion in the left periventricular white matter  Started IV steroids, ran a panel of CSF & blood studies  3 days later- Symptoms resolved  Diagnosed with Multiple Sclerosis

2 Jessica Floyd, M4

3  Chronic Inflammatory demyelinating disease of the CNS  2 nd -3 rd decade of life (“belongs to the climax of life”)  2:1 Female predominance  ,000 people with MS in the US  Cyclical inflammatory reactions followed by remission of symptoms and variable recovery  Relapsing-Remitting- 80%  Primary Progressive- 20%; closer incidence M:F  Secondary Progressive

4  First described by Charcot in 1835  Patient history, physical exam, autopsy  Salpetriere (1865)  to the United States  Blood vessel at the center of each lesion  Preserved axis cyllinder  Atrophy of the medullary sheath  Types:  Cephalic  Spinal  Mixed: cerebrospinal

5  Sensory disturbances  Unilateral optic neuritis  Diplopia- Internuclear opthalmoplegia  Nystagmus  Lhermitte’s sign  Limb weakness  Clumsiness  Gait ataxia  Neurogenic bladder  Bowel symptoms

6  Fatigue  Worse in the afternoon  Physiologic increases in temperature  Post Partum worsening of Symptoms ~ 4wk  Uhthoff’s symptom- hot shower, hot bath  Pseudoexacerbations with fever

7  Highly suggestive of MS:  Paroxysmal pain, paresthesias  Trigeminal neuralgia  Episodic clumsiness, nysarthria  Tonic limb posturing  Less common:  Prominent cortical signs ▪ Aphasia, apraxia, recurrent seizures, visual field loss, early dementia  Extrapyramidal phenomena ▪ Chorea, rigidity

8 WHAT DOES IT LOOK LIKE?

9  Most sensitive modality is MRI  Sensitive to inflammation  Sensitive to demyelination  CT is a poor tool unless very severe destruction  Callosal atrophy  Whole brain atrophy

10  Inflammation (water) & Demyelination (loss of fat)  Hyperintensities on T2 weighted images  Confirm with FLAIR images  Round, Ovoid  Vary in size. Few mm  Few cm  Periventricular region, corpus callosum  Perivascular distribution, penetrating venules  Dawson’s fingers  Juxtacortical Lesions, U-fibers

11  Temporal Lobe  Brainstem- peripherally  Deep Gray Matter- BG, Thalamus (LC)  Cerebellum  Spinal Cord  Recurrent Lesions in Same Area  CONFLUENT lesions  MC anterior & posterior to lateral ventricle  Vasogenic edema = “fuzzy extension” of T2 signal  LARGE DIFFERENTIAL FOR T2 Hyperintensities

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14  SEVERE Tissue Injury  T1 dark signals  Rarely seen in the spinal cord or post fossa  Stronger correlation with demyelination & axonal loss than T2 hyperintensities  Evolution of enhancing lesions  T1 Holes associated with more progressive disease

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16  Indicates breakdown of the blood-brain barrier  Very active inflammation  Pattern of enhancement  Homogenous  Ring  reactivation of an old lesion  Heterogeneous  Enhancement duration varies- days, weeks  5% pts have >3 months of single lesion enhancement

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18  Round, Ovoid on T2  Limited to 1-2 spinal cord segments  80% involve half of cord cross sectional area  Ddx- ITM, Devic’s Dz  Typically unilateral  Inflammatory edema  temporary cord expansion  Ddx- Tumor (bx)  Gadolinum enhancment with active BBBB  Post mortem path studies show greater demyelination than assumed with conventional t2 imaging

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21  Significant Clinical Implications  Correlates with clinical disability  Predictive of later progressive disability  Many standard therapies slow progression of atrophy over time

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23  Ensuring MS is of high suspicion, consider prevalence and a priori probability

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25  Imaging is only one part of the story, clinical picture  Incidental Finding versus Manifesting Clinically  Normal Aging or Virchow Robin Spaces  Vascular disease ▪ Infarction ▪ Multi-infarct Dementia ▪ Hypertensive encephalopathy  Sarcoidosis- ACE level, pulmonary Sx, CXR  SLE- discoid/malar rash, other organ involvment  Lyme Disease- CN7 palsy, rash, influenza-like illness  HIV- test, immunocompromised  Progressive Multifocal Leukoencephalopathy- immunocompromised  Largest differential concerns Vascular versus MS

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29 66 yo Male T2 Hyperintensities None being Ovoid Few Periventricular Lesions No Juxtacortical lesions

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31  Since MRI revolutionized the diagnosis of MS, needed specific criteria  Crux of the Dx is demonstrating attacks of neurologic dysfunction are separated in space and time  Clinical criteria* pt hx, PE findings,  Laboratory Criteria* oligoclonal bands, IgG index  MRI * 2001 McDonald Criteria, 2005 revised

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36  Cannot diagnose MS on MRI alone- need the clinical exam & history  However, MRI can now show us what even a vigorous clinical exam cannot  Revolutionizing treatment  treat earlier  Mild cognitive deficits discovered earlier

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38  MR Spectroscopy- N-acetyl aspartate, Lactate  Diffusion Tensor Imaging  Able to pick up on lesions not yet detectable on MRI  Ability to give you information on precisely how damaged the lesion is compared to other lesions

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40 o 3-D water diffusion o Mean Diffusivity- overall diffusion o Fractional anisotropy- amount of elongatedness of diffusion o Colorized primary eigenvector maps- illustrate different directions of the primary fiber tract o RED = L-R o GREEN = Up-Down o BLUE = In-Out of page

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