Presentation on theme: "Palmetto Health Richland August 2008"— Presentation transcript:
1Palmetto Health Richland August 2008 35 yo AAF presents with confusion, agnosia, apraxia, right-sided lower extremity paresisSymptoms first noticed 2 hours agoCT scan- no bloodMRI- single hyperintense lesion in the left periventricular white matterStarted IV steroids, ran a panel of CSF & blood studies3 days later- Symptoms resolvedDiagnosed with Multiple Sclerosis
2Jessica Floyd, M4The Imaging of Multiple Sclerosis * Utility of MRI * Differential of White Matter Lesions * Future direction of neuroradiology
3What is Multiple Sclerosis? Chronic Inflammatory demyelinating disease of the CNS2nd-3rd decade of life (“belongs to the climax of life”)2:1 Female predominance,000 people with MS in the USCyclical inflammatory reactions followed by remission of symptoms and variable recoveryRelapsing-Remitting- 80%Primary Progressive- 20%; closer incidence M:FSecondary ProgressiveThere is a whole host of interesting topics to discuss with MS but since this is focused mainly on the imaging of MS, we will save that for another time.
4Charcot’s description First described by Charcot in 1835Patient history, physical exam, autopsySalpetriere (1865) to the United StatesBlood vessel at the center of each lesionPreserved axis cyllinderAtrophy of the medullary sheathTypes:CephalicSpinalMixed: cerebrospinal
6Symptoms Fatigue Post Partum worsening of Symptoms ~ 4wk Worse in the afternoonPhysiologic increases in temperaturePost Partum worsening of Symptoms ~ 4wkUhthoff’s symptom- hot shower, hot bathPseudoexacerbations with fever
7Symptoms Highly suggestive of MS: Less common: Paroxysmal pain, paresthesiasTrigeminal neuralgiaEpisodic clumsiness, nysarthriaTonic limb posturingLess common:Prominent cortical signsAphasia, apraxia, recurrent seizures, visual field loss, early dementiaExtrapyramidal phenomenaChorea, rigidity
9Brain Lesions Most sensitive modality is MRI Sensitive to inflammationSensitive to demyelinationCT is a poor tool unless very severe destructionCallosal atrophyWhole brain atrophy
10T2 LesionsInflammation (water) & Demyelination (loss of fat) Hyperintensities on T2 weighted imagesConfirm with FLAIR imagesRound, OvoidVary in size. Few mm Few cmPeriventricular region, corpus callosumPerivascular distribution, penetrating venulesDawson’s fingersJuxtacortical Lesions, U-fibers
11T2 Lesions Temporal Lobe Brainstem- peripherally Deep Gray Matter- BG, Thalamus (LC)CerebellumSpinal CordRecurrent Lesions in Same Area CONFLUENT lesionsMC anterior & posterior to lateral ventricleVasogenic edema = “fuzzy extension” of T2 signalLARGE DIFFERENTIAL FOR T2 HyperintensitiesThese will help with differentiating from vascular pathology
12T2 Lesions- FLAIR Red arrow- involvement of the temporal lobe Green arrow- juxtacortical lesions, touching the cortexBlue arrow- involvement of the corpus callosumPeriventricular lesions- touching the ventricles
14T1 Holes SEVERE Tissue Injury T1 dark signals Rarely seen in the spinal cord or post fossaStronger correlation with demyelination & axonal loss than T2 hyperintensitiesEvolution of enhancing lesions T1 Holes associated with more progressive disease
15T2 lesions & T1 HolesFig 3 = Typical ovoid periventricular lesions of ms in 31 yo man with 10 yr h/o RR neurologic SxA : First echo T2 MR sequence showing several ovoid lesions with T2 prolongation, with long axes perpendicular to ventricular wallsB: T1-weighted MRI shows that T1 is also prolonged within lesions
16Gadolinium-Enhancing Lesions Indicates breakdown of the blood-brain barrierVery active inflammationPattern of enhancementHomogenousRing reactivation of an old lesionHeterogeneousEnhancement duration varies- days, weeks5% pts have >3 months of single lesion enhancement
18Spinal Cord Lesions Round, Ovoid on T2 Limited to 1-2 spinal cord segments80% involve half of cord cross sectional areaDdx- ITM, Devic’s DzTypically unilateralInflammatory edema temporary cord expansionDdx- Tumor (bx)Gadolinum enhancment with active BBBBPost mortem path studies show greater demyelination than assumed with conventional t2 imagingBut can be central or bilateralNot the case with Brain demyelination- not seen outside of T2 lesion
1935 yo female- acute onset Quadriparesis Figure 5 = MS involving upper spinal cord in 35 yo woman with acute onset of quadriparesis.T2 weighted MRI shows a large area of demyelination in upper cervical spinal cord and cervicomedullary junction
20Spinal Lesions- Gad-enhancement Sagittal (A) T2 weighted and (B) post-gad T1 weightedimages froma pt with MS showing a discrete enhancing T2 lesion; and a nonenhancing lesion seen in the medulla (arrow)
21Brain Atrophy Significant Clinical Implications Correlates with clinical disabilityPredictive of later progressive disabilityMany standard therapies slow progression of atrophy over time
22Callosal AtrophyFigure 4 = Callosal involvement with MS in 48 yo woman with clinically definite MS for 20 years.A: T1 weighted midline sagittal MRI shows diffuse callosal atrophyB: Inner Callosal hyperintensity, and multiple confluent periventricular lesions, are shown on first echo of T2-weighted series
23DiagnosisEnsuring MS is of high suspicion, consider prevalence and a priori probability
25How suspicious are you?Imaging is only one part of the story, clinical pictureIncidental Finding versus Manifesting ClinicallyNormal Aging or Virchow Robin SpacesVascular diseaseInfarctionMulti-infarct DementiaHypertensive encephalopathySarcoidosis- ACE level, pulmonary Sx, CXRSLE- discoid/malar rash, other organ involvmentLyme Disease- CN7 palsy, rash, influenza-like illnessHIV- test, immunocompromisedProgressive Multifocal Leukoencephalopathy- immunocompromisedLargest differential concerns Vascular versus MS
26Normal Aging & Fazeka’s Can have caps and bands around the ventriclesI: small punctate lesions in the deep white matter- considered normal in agingII: larger WMLs that are beginning to become confluent- abnormal in pts <75 yoIII: abnormal in any age group; probably due to microangiopathy and seen more frequently in patients with vascular risk factors.
27Virchow Robin SpacesCSF spaces around penetrating leptomeningeal vesselsTypically located in the BG, anterior commissure and in the middle of the brainstem; they follow the signal intensity of CSF; enlarge with age and HTN secondary to atrophy of surrounding structures
29Vascular disease vs Multiple Sclerosis 66 yo MaleT2 HyperintensitiesNone being OvoidFew Periventricular LesionsNo Juxtacortical lesionsFigure 6 = Multiple Ischemic WM Lesions in 66 yo man with Sx of cerebellar infarction. First echo of T2 weighted MR sequence shows hyperintensities similar to those of demyelinating dz, but none are ovoid and few periventricular lesions are present
30Vascular vs. Multiple Sclerosis Juxtacortical lesions- specific for MSThis is not subcortical.In Small vessel dz, these juxtacortical U-fibers are not involved, there will be a dark band between the WML and the cortex which is also bright
31Criteria for Diagnosis of MS Since MRI revolutionized the diagnosis of MS, needed specific criteriaCrux of the Dx is demonstrating attacks of neurologic dysfunction are separated in space and timeClinical criteria* pt hx, PE findings,Laboratory Criteria* oligoclonal bands, IgG indexMRI * 2001 McDonald Criteria, 2005 revised
34Diagnostic CriteriaFig 1 = typical cerebral lesions of MS in 64 yo woman with sudden onset of diplopia & ataxia; Multiple periventricular lesions of MS, with lumpy-bumpy contour, on first echo of T2 weighted MR sequenceFig 2 = MS lesions in brainstem of 38 yo man with bilateral weakness & sensory Sx in LE. T2 weighted MRI shows lesion of MS in R cerebral peduncle
35Dissemination in TIME- 3 months Re-examined 3 months after the first clinical attack.Multiple Enhancing lesions, many touch the cortex & must be located in the U-fibersThese enhanced lesions are all new lesions, since Gad enhancement is only visible for about 1 month, so this finding is proof of dissemination in time
36One episode, treat or not to treat? Cannot diagnose MS on MRI alone- need the clinical exam & historyHowever, MRI can now show us what even a vigorous clinical exam cannotRevolutionizing treatment treat earlierMild cognitive deficits discovered earlier
3742 yo woman with MS, no SxFigure 7 = Multiple sclerosis in 42 yo woman with clinically definite MS but no acute SxA: T1 weighted MRI after administration of gadolinum shows several enhancing ovoid lesions in cerebral white matter bilaterally. Contrast enhancement defines areas of acute inflammation; indicating areas of BBB breakdownB: First echo of T2 weighted series at same level as A shows many more white matter lesions; primarily periventricular in distribution.
38Coming in the future… MR Spectroscopy- N-acetyl aspartate, Lactate Diffusion Tensor ImagingAble to pick up on lesions not yet detectable on MRIAbility to give you information on precisely how damaged the lesion is compared to other lesions
39Diffusion Tensor Imaging Artist’s depiction of water diffusion. (A) w/in fiber tracts where axons and myelin orient diffusion longitudinally, water diffusion oriented along the fiber tract.(B) In areas of demyelination and axonal injury, water diffusion is greater in overall amount (increased mean diffusivity), and also less ELONGATED (decreased fractional anisotropy). This indicates the diff vectors.
41Gad- enhancement T1 & T2 Dawson Fingers: Ovoid lesions perpendicular to the ventriclesEnhancing lesion on T1 with Gad- indicating active breakdown of BBBMultiple lesions adjacent to the ventriclesResult of inflammation around penetrating venulesEnhancement is present for about one month after the occurrence of a lesion; simultaneous demonstration of enhancing and non-enhancing lesions in MS is the radiological explanation for clinical dissemination in time and space; The edema will regress and finally only the center will remain as a hyperintense lesion on T2
42Dawson’s fingers – T1 & T2Sagittal FLAIR image provide best appreciation of Dawson’s fingers in which lesions extend radially from the ventricular surface into the surrounding white matter (fluid-attentuated inversion recovery)T1 weighted image from typical MS patient/ periventricular lesions dark on T1 but not all are darkAxial T2 and Flair
43FLAIR & T-1 black holeAxial A FLAIR and B T1 weighted images showing a T1 black hole which is mixed hypo-hyperintense on FLAIR
44Confluent Lesions & Atrophy SEMINARSFigure 3 Axial FLAIR images from a 52-year-old patient with multiple sclerosis. The formerly discrete T2 lesions have nowbecome confluent (arrows). Also, significant atrophy can be appreciated through loss of brain parenchyma as well asenlargement of the lateral ventricles, peripheral sulci, and third ventricle (arrowhead). FLAIR, fluid-attenuated inversion recovery.
45Progressive Multifocal Leukoencephalopathy MRI of the brain from a patient with PMLAxial T2 weighted (left and middle) and post-contrast T1 weighted (right) images show two lesions in the left hemisphere without mass effect and contrast enhancement. The outer border of the lesion follows exactly the cortical lesion.
46Sarcoidosis MRI of a patient with sarcoidosis. Post-contrast T1-weighted coronal image of the brain (left) and axial image of the cord (right) show simultaneous enhancement of multiple white-matter lesions, Virchow-Robin spaces (left), and leptomeninges.
47Acute Disseminated Encephalomyelitis Axial FLAIR (left column) and post gad T1 (right) images from pt with ADEM. Most lesions demonstrate gad enhancement suggesting similar age to ongoing inflammatory process