Multiple sclerosis imaging

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Multiple sclerosis imaging

  1. 1. Multiple Sclerosis Imaging
  2. 2. Clinical <ul><li>Onset </li></ul><ul><ul><li>20 to 35 year old in female </li></ul></ul><ul><ul><li>35 to 45 year old in male </li></ul></ul><ul><ul><li>rare before 14 or after 60 year old </li></ul></ul><ul><li>70 to 75% of patients are female </li></ul><ul><li>Prevalence </li></ul><ul><ul><li>female:male 2:1 </li></ul></ul><ul><ul><li>more common in white </li></ul></ul><ul><li>Genetic: </li></ul><ul><ul><li>first degree relative 10-20X increased risk </li></ul></ul>
  3. 3. Poser Criteria (1983) <ul><li>  Clinically definite MS </li></ul><ul><ul><li>2 attacks and clinical evidence of 2 separate lesions </li></ul></ul><ul><ul><li>2 attacks, clinical evidence of one and paraclinical evidence of another separate lesion </li></ul></ul><ul><li>Laboratory supported Definite MS </li></ul><ul><ul><li>2 attacks, either clinical or paraclinical evidence of 1 lesion, and CSF immunologic abnormalities </li></ul></ul><ul><ul><li>1 attack, clinical evidence of 2 separate lesions & CSF abnormalities </li></ul></ul><ul><ul><li>1 attack, clinical evidence of 1 and paraclinical evidence of another separate lesion, & CSF abnormalities </li></ul></ul><ul><li>Clinically probable MS </li></ul><ul><ul><li>2 attacks & clinical evidence of 1 lesion </li></ul></ul><ul><ul><li>1 attack & clinical evidence of 2 separate lesions </li></ul></ul><ul><ul><li>1 attack, clinical evidence of 1 lesion, and paraclinical evidence of another separate lesion </li></ul></ul><ul><li>Laboratory supported probable MS </li></ul><ul><ul><li>2 attacks & CSF abnormalities </li></ul></ul>
  4. 4. Clinical Types <ul><li>Asymptomatic </li></ul><ul><li>Symptomatic </li></ul><ul><ul><li>85% start out as relapsing remitting. </li></ul></ul><ul><ul><ul><li>About 10% remains benign at 20 years </li></ul></ul></ul><ul><ul><ul><li>55% RR-MS: Relapsing remitting MS - attacks occurring average once per year </li></ul></ul></ul><ul><ul><ul><li>30% SP-MS: Secondary Progressive MS </li></ul></ul></ul><ul><ul><ul><li>About 50% of RR-MS will become SP-MS. </li></ul></ul></ul><ul><ul><li>10-15% starts as progressive disease. </li></ul></ul><ul><ul><ul><li>10% PP-MS: Primary progressive MS. Most commonly first develop symptom at age 40-60. 5% PR-MS: Progressive relapsing </li></ul></ul></ul>
  5. 5. Prognosis <ul><li>Overall prognosis of untreated MS at fifteen years (Minden et al 1993; Weinshenker 1995). </li></ul><ul><ul><li>70 to 80%: of patients have impaired ability to work </li></ul></ul><ul><ul><li>50% need an assistive device to walk </li></ul></ul><ul><ul><li>30%: are wheelchair bound  </li></ul></ul><ul><li>Better for female, and those with predominantly sensory symptoms </li></ul><ul><li>Kurtzke 5 year rule: absence of significant motor or cerebellar dysfunction at 5 years correlates with limited disability at 15 years. </li></ul><ul><li>MS is active in most patients </li></ul><ul><li>Only a small minority have true benign disease </li></ul><ul><li>Disease abnormalities are widespread and clinically underestimated </li></ul>
  6. 6. MRI in MS <ul><li>MRI findings that strongly suggestive of MS </li></ul><ul><ul><li>4 or more white matter lesions (each > 3mm) </li></ul></ul><ul><ul><li>3 white matter lesions, 1 periventricular Lesions </li></ul></ul><ul><ul><li>6 mm diameter or greater </li></ul></ul><ul><ul><li>Ovoid lesions, oriented perpendicular to ventricles </li></ul></ul><ul><ul><li>Corpus callosum lesions </li></ul></ul><ul><ul><li>Brainstem lesions </li></ul></ul><ul><ul><li>Open ring appearance of gadolinium enhancement </li></ul></ul>
  7. 7. Diagnosis MR <ul><li>Supportive </li></ul><ul><ul><li>3-4 scattered lesion without mass effect throughout white matter </li></ul></ul><ul><li>Specific </li></ul><ul><ul><li>>6mm </li></ul></ul><ul><ul><li>Oval shape in parasagital region </li></ul></ul><ul><ul><li>Infratentorial and spinal </li></ul></ul>
  8. 8. Methods <ul><li>Gadolinium </li></ul><ul><ul><li>BBB breakdown </li></ul></ul><ul><li>PD </li></ul><ul><ul><li>Inflammation </li></ul></ul><ul><li>T2 </li></ul><ul><ul><li>Established lesion </li></ul></ul><ul><li>MRS </li></ul><ul><ul><li>Loss of NAA for DD </li></ul></ul><ul><li>Magnetization transfer imaging </li></ul><ul><ul><li>Lesion in otherwise normal appearing white matter </li></ul></ul>
  9. 9. Prognosis Sensitivity <ul><li>Gad – Twice sensitive than T2 monthly MR (0.1mmol/kg) </li></ul><ul><li>Weekly Gad MR more sensitive </li></ul><ul><li>Spinal imaging </li></ul><ul><li>Triple load Gad (0.3mmol/kg) 70% more sensitive and 50%more new lesions </li></ul><ul><li>Magnetization transfer T1 </li></ul><ul><li>Delayed scanning </li></ul><ul><li>Thinner slices 3mm </li></ul><ul><li>Fast flair 1mm and 3mm 3D increases 30% lesion in sub cortical and cortical lesion. </li></ul>
  10. 10. MRI:Prognostic indicator <ul><li>MRI as a prognostic indicator in clinically isolated syndromes: </li></ul><ul><ul><li>MRI normal at presentation </li></ul></ul><ul><ul><ul><li>5 years follow-up: 6% with clinically definite MS </li></ul></ul></ul><ul><ul><ul><li>10 years follow-up: 10% with clinically definite MS </li></ul></ul></ul><ul><ul><li>MRI with 1.2 cc or greater T2 involvement </li></ul></ul><ul><ul><ul><li>5 years follow-up: 96% with clinically definite MS </li></ul></ul></ul><ul><ul><ul><li>10 years follow-up: 86% with clinically definite MS (some patients in the 5 year cohort not included in 10 year cohort) </li></ul></ul></ul><ul><li>Patients with early, relapsing-remitting MS studied by monthly MRIs over several months </li></ul><ul><ul><li>approximately 70% have at least one enhancing lesion during a 3 month period. </li></ul></ul><ul><ul><li>frequency of contrast enhancing lesion activity fluctuates from month to month. </li></ul></ul>
  11. 11. CSF in MS <ul><li>Cell count: </li></ul><ul><ul><li>RBC usually none. </li></ul></ul><ul><ul><li>WBC: 1/3 has 5 to 50 lymphocytes </li></ul></ul><ul><li>Protein: 1/4 of patients has mild elevation </li></ul><ul><li>Myelin basic protein: </li></ul><ul><ul><li>presence indicates demyelination </li></ul></ul><ul><ul><li>can be found in first 2 weeks after a substantial exacerbation in 50-90% of patients </li></ul></ul><ul><ul><li>can be seen in other neuro disease, such as infarct, infection etc </li></ul></ul><ul><li>Immunoglobulin: IgG synthesis rate </li></ul><ul><ul><li>Indicates activity of Plasma cells </li></ul></ul><ul><ul><li>>3 in 80-90% of MS </li></ul></ul><ul><ul><li>elevated in 12% of normal individual, and 30-50% of CNS infections </li></ul></ul><ul><li>Immunoglobulin: IgG index </li></ul><ul><ul><li>>0.7 in 86-94% of MS first CSF abnormality in early MS </li></ul></ul><ul><li>Oligoclonal bands </li></ul><ul><ul><li>present in over 90% of definite MS </li></ul></ul><ul><ul><li>seen in other inflammatory diseases </li></ul></ul><ul><ul><li>seen in 7% of normal control </li></ul></ul>
  12. 12. Evoked potential 70 40 30 BAEP 80 70 50 SSEP 85 60 40 VEP definite MS probable MS possible MS % prolonged in
  13. 13. Clinical correlation <ul><li>Kurtzke Expanded disability status scale (KDSS) </li></ul><ul><ul><li>Subjective </li></ul></ul><ul><ul><li>Poor reproducibility </li></ul></ul><ul><ul><li>Lack of representation of all facets of functional impairment </li></ul></ul><ul><ul><li>Insensitive to change </li></ul></ul><ul><ul><li>No correlation with MR </li></ul></ul><ul><li>Locomotor disability scale reflects spinal cord involvement </li></ul><ul><li>Neuropsychological scale better correlation </li></ul>
  14. 14. Lesion extent <ul><li>Poor correlation between lesion load and EDSS </li></ul><ul><li>Total extent of brain lesion correlate only moderately with locomotor disability </li></ul><ul><li>Clinically isolated syndrome on Brain stem better correlation </li></ul><ul><li>No of brain lesion in MR predicts progress to definite MS in next 1-5years, Poor correlation in next 5years (5-10) </li></ul>
  15. 15. Lesion site <ul><li>Locomotor disability correlate with spinal and post fossa lesion </li></ul><ul><li>T2 lesion load in post fossa and spinal cord do not correlate with EDSS </li></ul><ul><li>Asymptomatic cord lesion with isolated optic neuritis in 40% cases </li></ul><ul><li>Extensive lesion in clinically eloquent pathway without functional consequence </li></ul>
  16. 16. Pathologic nature <ul><li>Acute lesion </li></ul><ul><ul><li>inflammation (perivascular lymphocytes, macrophage, infiltrate edema, active myelin breakdown and axonal damage) </li></ul></ul><ul><li>Subacute lesion </li></ul><ul><ul><li>Variable remyelination </li></ul></ul><ul><li>Chronic lesion </li></ul><ul><ul><li>Complete demyelination with marked astrocytic gliosis, and axonal loss </li></ul></ul><ul><ul><li>Inflammation at the edege </li></ul></ul>
  17. 17. Acute lesion <ul><li>Correlates with Gad enhancement in RR and SP MS for 2-6weeks </li></ul><ul><li>More common during relapse than remission </li></ul><ul><li>Most of them are asymptomatic </li></ul><ul><li>Cord lesion are symptomatic </li></ul><ul><li>Optic nerve lesion correlates with visual loss </li></ul>
  18. 18. Subacute lesions <ul><li>Magnetizing transfer imaging </li></ul><ul><li>T1 hypointense lesion </li></ul><ul><li>MR spectroscopy </li></ul><ul><li>Measurement of atrophy </li></ul><ul><li>Diffusion tensor imaging </li></ul><ul><li>Myelin imaging by T2 decay analysis </li></ul>
  19. 19. Normal appearing White matter with microscopic changes <ul><li>T1, T2 MT ratio and NAA </li></ul><ul><li>Clinical importance not clear </li></ul>
  20. 20. Cortical pathology and synaptic adaptation <ul><li>Synaptic adaptation by functional MR </li></ul><ul><li>Cortical plaque not yet studied </li></ul>

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