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MS or Lyme or neither?

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MS or Lyme or neither?

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MS or Lyme or neither?

  1. 1. <ul><li>40 year old lady married + 4 children, born in Israel, with presumptive diagnosis of MS presenting with blurred vision of the right eye </li></ul><ul><li>2002 </li></ul><ul><ul><li>Admitted with right leg weakness </li></ul></ul><ul><ul><li>Myelopathic signs on examination </li></ul></ul><ul><ul><li>MRI revealed inflammatory lesion T7-8 </li></ul></ul><ul><ul><li>LP: TP 501, no cells, OCB negative </li></ul></ul><ul><ul><li>Treated with steroids with marked improvement </li></ul></ul><ul><ul><li>No neurological symptoms until current presentation </li></ul></ul><ul><ul><li>At presentation mild sensory symptoms only </li></ul></ul>
  2. 2. Current admission <ul><li>3 days prior to admission, after slight bump to head, noticed blurred vision of R eye </li></ul><ul><li>Vision deteriorated over following 3 days with pain on eye movement </li></ul>
  3. 3. Past history <ul><li>No other neurological problems </li></ul><ul><li>No other clinical features referable to auto-immune disease ( e.g. SLE, Bechets) </li></ul><ul><li>No history of miscarriage </li></ul><ul><li>Serological abnormalities ( to be discussed) </li></ul><ul><li>Had traveled to New England but no history of tick bite </li></ul>
  4. 4. Examination <ul><li>General examination unremarkable </li></ul><ul><li>RAPD on the right </li></ul><ul><li>Fundoscopy normal </li></ul><ul><li>Remainder of examination normal with no evidence of myelopathy </li></ul><ul><li>Steroids started for presumptive “ MS exacerbation” </li></ul>
  5. 5. Laboratory investigation prior to admission <ul><li>Immunology </li></ul><ul><ul><li>ATG 87, 87 ( <100) 3.2003, 1.2004 </li></ul></ul><ul><ul><li>ATPO 793, 538 ( <75)!! (TSH 3.56 - normal) </li></ul></ul><ul><ul><li>ANA +2 / 4 (2002) –ve x2 (2003,2004) </li></ul></ul><ul><ul><li>ENA +ve x1 (2002) –ve x2 </li></ul></ul><ul><ul><li>ANCA –ve x2 </li></ul></ul>
  6. 6. Laboratory investigation prior to admission <ul><li>Serology </li></ul><ul><ul><li>CMV past infection </li></ul></ul><ul><ul><li>EBV past infection </li></ul></ul><ul><ul><li>VZV past infection </li></ul></ul><ul><ul><li>Toxoplasma neg </li></ul></ul><ul><ul><li>Brucella neg </li></ul></ul><ul><ul><li>VDRL neg </li></ul></ul><ul><ul><li>Brucella neg </li></ul></ul><ul><ul><li>Lyme +ve x2 ( 10.2003, 1.2004) </li></ul></ul>
  7. 7. Brain MRI
  8. 8. Laboratory investigation during current admission <ul><li>FBC, Bioch normal </li></ul><ul><li>ESR 18 </li></ul><ul><li>LP: - Pressure 12 cm H 2 O </li></ul><ul><li>- TP 488, no cells, OCB negative </li></ul><ul><li>Anticardiolipin Ab’s negative </li></ul><ul><li>pANCA cANCA negative </li></ul><ul><li>ANA negative </li></ul><ul><li>TSH normal </li></ul><ul><li>Anti TPO 397 ( 0-35) </li></ul><ul><li>Anti TG normal </li></ul><ul><li>Homocysteine Pending </li></ul>
  9. 9. Course <ul><li>Received high dose steroids </li></ul><ul><li>Day 4: Ceftriaxone added, steroids tapered </li></ul><ul><li>Day 5: improvement noted in vision </li></ul><ul><li>Day 6 am : - mild left hemiparesis noted, steroid dose incresed </li></ul><ul><li>Day 6 pm: witnessed tonic-clonic seizure. On examination, severe L hemiparesis </li></ul><ul><li>Brain CT unremarkable </li></ul>
  10. 10. Course cont. <ul><li>Further seizures: Unresponsive to benzodiazepines phenytoin, phenobarbital (RSE) </li></ul><ul><li>Intubation, propofol IV </li></ul><ul><li>MRI: Right MCA infarct </li></ul><ul><li>Anticoagulant treatment commenced </li></ul>
  11. 11. Brain MRI after Seizure
  12. 12. Further Investigation <ul><li>Angiograpghy - decreased perfusion in R MCA territory </li></ul><ul><li>TEE - no clot detected </li></ul>
  13. 13. Course cont. <ul><li>Weaned from propofol and BZD’s </li></ul><ul><li>Extubated </li></ul><ul><li>Marked improvement of hemiparesis </li></ul>
  14. 19. Neurological features of chronic Lyme disease
  15. 20. CSF in Chronic Lyme <ul><li>In early cases of neuroborreliosis, spinal fluid findings may still be negative. </li></ul><ul><li>In cases of chronic disease, only mild elevations of protein may persist. </li></ul><ul><li>In these circumstances, detection of B. burgdorferi DNA by PCR may be important to establish the diagnosis. </li></ul>
  16. 22. Serology <ul><li>Both IgG and IgM responses can persist for over 10 years, even after successful antibiotic treatment </li></ul><ul><li>False positive ELISA results can be caused by other bacteria (e.g. Treponema denticulata ) or by a polyclonal B cell stimulation. </li></ul><ul><li>Positive serology alone is not sufficient to make the diagnosis </li></ul><ul><li>Cross-reactivities with syphilis tests do occur </li></ul><ul><li>Direct detection methods (PCR) diagnostic </li></ul>
  17. 23. Value of Serology
  18. 27. Proposed diagnostic criteria <ul><li>clouding of consciousness with reduced wakefulness, attention, or cognitive function </li></ul><ul><li>no CSF evidence of bacterial or viral infection </li></ul><ul><li>high serum concentration (or titer) of antithyroid microsomal, antithyroid peroxidase, or antithyroglobulin antibodies </li></ul>
  19. 28. Thyroid function
  20. 31. MRI in Hashimoto Encephalopathy
  21. 32. Summary of Neurological Features <ul><li>Stroke-like signs in 23 patients (27%) </li></ul><ul><li>seizures in 56 patients (66%) </li></ul><ul><li>status epilepticus (10 patients [12%]) </li></ul><ul><li>course relapsing and remitting in 51 patients (60%). </li></ul>
  22. 33. CSF in Hashimoto Encephalopathy <ul><li>65 patients (76%), the CSF contained 0 to 3 nucleated cells/mm3 </li></ul><ul><li>In 3 patients (4%), it contained more than 100 cells/mm3 </li></ul><ul><li>CSF protein concentration was high in 66 patients (78%), exceeding 0.01 g/dL in 18 patients (21%). </li></ul>
  23. 34. Imaging <ul><li>11 had cerebral atrophy </li></ul><ul><li>13 had nonspecific subcortical focal white matter abnormality </li></ul><ul><li>8 had diffuse subcortical abnormality, </li></ul><ul><li>7 had focal cortical abnormality </li></ul><ul><li>1 had transient bilateral narrowing of a middle cerebral artery </li></ul>
  24. 35. Antiphospholipid syndrome <ul><li>Can simulate MS </li></ul><ul><ul><li>especially in patients with myelitis and optic neuritis </li></ul></ul><ul><ul><li>Especially in those without OCB’s </li></ul></ul><ul><ul><li>( Karussis et al, Annals of Neurology 1998 ) </li></ul></ul><ul><li>Associated with stroke in the young </li></ul><ul><li>However: </li></ul><ul><ul><li>Anticardiolpin negative during current hospitalisation (steroids should not cause disappearance) </li></ul></ul><ul><ul><li>Lupus anticoagulant not checked prior to heparin treatment </li></ul></ul>
  25. 36. MS <ul><li>Clinical and MRI features fit </li></ul><ul><li>Against </li></ul><ul><ul><li>OCB –ve twice </li></ul></ul><ul><ul><li>Stroke </li></ul></ul><ul><ul><li>( therefore other conditions must be excluded) </li></ul></ul>
  26. 41. Out of 31 MS patients 5 (16%) had Anti TPO Ab’s Normal values: TPO-Ab 0–10 IU/mL;
  27. 44. CNS Vasculitis - GANS - PAN ( but no systemic features) GANS CSF and angiography normal MRI probably “ too severe” given mild clinical features prior to stroke No headache Clinical course typical of MS Stroke Optic nerve and spinal cord involvement rare Can simulate relapsing – remitting course of MS Against For
  28. 45. Is MS associated with alteration of platelet function? “ platelet aggregation and MS” Neu et al 1982 Acta neurologica Scand.
  29. 46. <ul><li>Measured in vitro platelet aggregation in 30 “ definite MS” patients and compared to 15 healthy subjects </li></ul><ul><li>Both spontaneous and “ agonist-induced” aggregation was measured </li></ul>Agg % P < 0.01
  30. 47. Summary <ul><li>MS with stroke is diagnosis of exclusion </li></ul><ul><li>Lyme disease unlikely but should be excluded via PCR because of the stroke </li></ul><ul><li>Hashimoto Encephalopathy attractive diagnosis however no encephalopathy clinically or electrophysiologically. </li></ul><ul><li>APLAS clinically fits..but no lab evidence ( Lupus Anticoagulant not checked) </li></ul><ul><li>Granulomatous angiitis unlikely but cannot be ruled- out 100% without brain biopsy </li></ul><ul><li>HIV should be tested for completeness </li></ul>

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