Multiple Sclerosis
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Multiple Sclerosis

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IS IT INCREASING

IS IT INCREASING

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Multiple Sclerosis Multiple Sclerosis Presentation Transcript

  • MULTIPLE SCLEROSIS  Inflammation  Demyelination  Gliosis(scarring)  Can be relapsing remitting or progressive  Lesions are typically disseminated in time and location
  • anatomy  Lesions size 1-2 mm to several centimeters  Perivenular cuffing with inflammatory mononuclear cells  BBB disrupted at sites of inflammation  Vessel wall is spared unlike in vasculitis  Myelin specific autoantibodies promote demyelination,Astrocytes proliferate(gliosis)  Remyelination by surviving oligodendrocytes leads to shadow plaques
  • physiology  Nerve conduction in myelinated axons occurs in saltatory manner  Conduction block occurs when impulse is unable to traverse demyelinated segment
  • epidemiology  Twice common in women than in men  Age of onset 20-40 yrs  Highest prevalence in orkney islands followed by northern Europe,north america,canada  Low in japan,other Asian countries,equitorial africa,middle east  Indian – prevalence <5 cases per 100,000  Highest prevalence in parsis-26/100,000.  Prevalence increases with increasing distance from equator
  • Genetics  Genetic susceptibility to MS exists  Life time risk to sibling of affected 2%-5%  Concordance rate in monozygotic twins 25%-35%  Concordance rate in dizygotic twins 2%-5%  Inheritance is probably poly genic
  • Immunology&microbiology  Auto antibodies directed against myelin antigens such as myelin oligodendrocyte glycoprotein(MOG)act in concert with a pathogenic auto reactive T lymphocyte response to cause demyelinating lesion  MS risk is high in high SE status(delayed exposure to infectious agents)  High antibody titers against many viruses are seen in csf and serum  Molecular mimicry between viruses and myelin antigen may play role in MS pathogenesis
  • Clinical features of MS  Weakness of limbs(UMN type)  Loss of strength  Fatigue  Gait disturbance  Exercise induced weakness  Spasticity  Hyper reflexia  babinski
  • Optic neuritis  Decreased visual acuity  Decreased color perception in central field  Usually mono ocular may be binocular sometimes  Peri orbital pain precedes visual loss  Optic atrophy usually follows
  • diplopia  Results from inter nuclear ophthalmoplegia(INO)  MLF lesion –impaired adduction on same side,prominent nystagmus in abducting eye  Horizontal gaze palsy  One and a half syndrome(horizontal gaze palsy+INO)  Acquired pendular nystagmus
  • Other symptoms  Sensory-parasthesias,hypesthesia  Ataxia-usually late manifestation  Intention tremor,scanning speech,nystagmus- CHARCOT”S triad  Bladder& bowel dysfunction  Cognitive dysfunction  Depression  Fatigue  Sexual dysfunction
  • Ancillary symptoms  Heat sensitivity  Visual blurring with hot showers(uthoff”s phenomenon)  Lhermitte”s symptoms  Paroxysmal symptoms  Trigeminal neuralgia  Hemi facial spasm  Glosso pharyngeal neuralgia
  • Disease course  Relapsing, remitting MS(RRMS)-85%,acute attacks and complete recovery  Secondary progressive MS(SPMS)-starts as RRMS at some point changes to steady detoriation superimposed on acute attacks  Primary progressive MS(PPMS)-15%-no attacks ,steady decline from disease onset, more even sex distribution, mean age 40 yrs,develops faster  Progressive relapsing MS(PRMS)-steady detoriation from onset,superimposed attacks on progressive course
  • Diagnostic criteria 1.Examination must reveal objective abnormalities of CNS 2.Involvement of predominantly disease of white matter long tract- pyramidal,cerebellar,MLF,optic nerve,post.columns 3.Examination or history must implicate involvement of two or more areas of CNS (a)MRI-MCDONALD’S – criteria- three out of four(1)one Gd enhancing lesion or nine T2 hyper intense lesions(2)at least one infra tentorial lesion(3)at least one juxta cortical lesion((4)at least three peri ventricular lesions (b)evoked response testing may be used to document lesion 4.Clinical pattern(a)two or more episodes of worsening involving different sites of CNS each lasting >24 hrs at least 2 months apart(b)gradual or stepwise progression over 6 months 5.The neurological condition cannot be attributed to another disease
  • Diagnostic categories  Definite MS-all 5 fulfilled  Probable MS-all 5 fulfilled except(a)one objective abnormality despite two symptomatic episodes or(b)one symptomatic episode despite two objective abnormalities  At risk for MS-criteria1,2,3,5 fulfilled; patient has only one symptomatic episode and one objective abnormality
  • Diagnostic tests  MRI-hyper intense T2 lesions oriented perpendicular to ventricular surface(DAWSON’S fingers),irreversible de myelination –hypo intense onT1  EVOKED POTENTIALS-visual, auditory,somato sensory-marked delay in latency suggest demyelination  CSF-mononuclear cell pleocytosis,IgG >12% of total protein,csf IgG index>1.7,two or more oligoclonal bands in csf
  • MRI in MS
  • Differential diagnosis  ADEM,  anti phospholipid antibody syndrome,  bechet’s disease,  CADASIL,  congenital leukodystrophy,  HIV,  MELAS,  SLE,  B12 def.etc
  • Suspect Alternate diagnosis if  Symptoms localized exclusively to post.fossa  Age of onset<15,>60 yrs  Clinical course progressive from onset  Who never experience visual,sensory,bladder symptoms  Atypical lab findings  Rare symptoms like aphasia,chorea, seizures
  • Good prognostic indicators  Optic neuritis,sensory symptoms at onset  Who recovers completely from early attacks  <40 yrs at onset  Women  RRMS  <2 relapses in first year  Minimal impairment after 5 yrs
  • Poor prognostic factors  Childhood onset  Age of onset>40  Truncal ataxia  Action tremor  Pyramidal symptoms  Progressive disease
  • treatment  Acute attacks-gluco corticoids,iv methyl prednisolone 500-1000 mg /day for 5 days;  plasma exchanges ,7 exchanges EOD for 14 days  Disease modifying therapies for relapsing forms-  interferons-beta,  glatiramer acetate,  mitoxantrone,  natalizumab,  Symptomatic treatment