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MS or Lyme or neither?

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MS or Lyme or neither?

MS or Lyme or neither?

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    MS or Lyme or neither? MS or Lyme or neither? Presentation Transcript

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