Speciality
Spotlight

 




 


Neurology


 

 




Multiple Sclerosis

    

  • N Scolding, R Franklin, S Stevens, et al 
    (MRC Cambridge Centre for Brain Repair,
    England; Univ of Cambridge, England; Inst of
    Neurology, London; et al)


    Oligodendrocyte
    Progenitors Are Present in the Normal Adult Human
    CNS and in the Lesions of Multiple Sclerosis.



    Brain 
    121: 2221-2228, 1998.


       


    Partial remyelination occurs in many lesions in
    patients with multiple sclerosis (MS) – upto 40%.


         

    The cell responsible for limited spontaneous myelin
    repair has not been precisely identified.  
    In a rodent model, the most efficient
    remyelinating cell is the proliferative
    oligodendrocyte progenitor – this cell has also been
    found in cultures from the normal human brain.


        

    The rabbit polyclonal R7 anti-platelet-derived growth
    factor-a
    receptor antibody is a useful marker of bipolar
    proliferative human oligodendrocyte progenitors in
    vitro.


       

    The adult, mature oligodendrocyte has been thought to
    be an uncertain source of repair.

    The authors have shown that a platelet-derived growth
    factor-a
    expressing oligodendrocyte progenitor is present
    both in the lesions of MS patients and in normal
    human adult white matter.

        

  • A
    Tourbah, A Clapin, O Gout, et al (Universite Paris)


    Systemic
    Autoimmune Features and Multiple Sclerosis: A 5-Year
    Follow-up Study.


    Arch Neurol 55:
    517-521, 1998.
     

        

    This article is a prospective study of 161 patients
    with probable multiple sclerosis where the presence
    of lupus anticoagulant anticardiolipin antibodies (aCls),
    ANAs, (antinuclear antibodies) antiphospholipid
    antibodies (aPLs) and anti double-stranded DNA
    antibodies were assessed.


       

    About half of the patients had abnormalities
    suggestive of other autoimmune disease.

         

  • AD
    Sadovnick, IML Yee, GC Ebers, et al (Univ of
    British Columbia, Vancouver, Canada; Univ of Western
    Ontario, Canada; Stanford Univ, Calif)


    Effect of Age
    at Onset and Parental Disease Status on Sibling
    Risks for MS.


    Neurology 50:
    719-723, 1998.
     

       

    Both age of onset and genetic influences seem to
    affect susceptibility to MS.


       

    Sisters of affected patients were at 2.5 times higher
    risk than were brothers of affected patients. For siblings with a parent who had MS risk was 4 times higher
    than for siblings without an affected parent.


        

    The group at highest risk were siblings of affected
    patients who were aged 20 years or less at the time
    of MS onset.

        

  • JN
    Lycke, J-E Karlsson, O Andersen, et al (Goteborg
    Univ, Sweden)


    Neurofilament
    Protein in Cerebrospinal Fluid: A Potential Marker
    of Activity in Mulitple Sclerosis.


    J Neurol
    Neurosurg Psychiatry 64: 402-404, 1998
     

     
       

    For neuronal degeneration in the animal brain, the
    light subunit of the neurofilament protein (NFL) has
    been used experimentally as a marker.


       

    Increased concentrations of NFL have been reported in
    CSF from patients with Alzheimer’s disease and
    amyotrophic lateral sclerosis. The concentration of NFL in CSF might be
    useful in future clinical trials of MS.

              

  • GC
    Ebers, for the PRISMS (Prevention of Relapses and
    Disability by Interferon b-1a
    Subcutaneously in Multiple Sclerosis Study Group
    (London Health Sciences Centre, Ont, Canada)


    Randomised
    Double-blind Placebo-controlled Study of Interferon
    b-1a in Relapsing/Remitting Multiple Sclerosis.


    Lancet 
    352: 1498-1504, 1998.
     

       

    The effects of subcutaneous interferon b-1a were investigated in 560 patients with
    relapsing/remitting Multiple Sclerosis.


       

    Subcutaneous interferon b-1a
    was well tolerated. It effectively reduced the
    relapse rate, disability and adverse MR outcomes in
    a dose-dependent manner. 
    With further follow-up, long-term benefits
    may become clearer.

           

  • L
    Kappos, for the European Study Group on Interferon b-1b in Secondary Progressive MS (Univ Hosp
    Basel, Switzerland)


    Placebo-controlled
    Multicentre Randomized Trial of Interferon b-1b
    in Treatment of Secondary Progressive Multiple
    Sclerosis.


    Lancet
    352:1491-1497, 1998.
     

       

    This was a 3-year multicenter, randomized,
    placebo-controlled, double-masked trial where 360
    patients received interferon b-1b 8 million IU subcutaneously every
    alternate day and 358 patients received placebo.


       

    It was found that interferon b-1b delays sustained neurologic deterioration
    in patients with secondary progressive multiple
    sclerosis. This
    is the first treatment to offer then a beneficial
    effect.

          

  • KP Johnson, and the Copolymer 1 Multiple Sclerosis
    Study Group (Univ of Maryland, Baltimore; Univ of
    Wisconsin, Madison; Univ of Pennsylvania,
    Philadelphia; et al)


    Extended Use of
    Glatiramer Acetate (Copaxone) is well
    Tolerated and Maintains its Clinical Effect on
    Multiple Sclerosis Relapse Rate and Degree of
    Disability
    .

    Neurology 50:
    701-708, 1998.
     

       

    Glatiramer acetate (copolymer 1), significantly
    reduces the frequency of relapses. A two-year, placebo-controlled trial showed
    significant reductions in relapses, reduced
    neurologic disability and excellent tolerance.


        

    Glatiramer acetate is regarded as frontline therapy
    for relapse prevention in patients with relapsing
    remitting multiple sclerosis AND as replacement
    therapy for patients not responding or intolerant to
    b-interferons.

       

 



 

 

Speciality Spotlight

 

 
Neurology
 

 

Multiple Sclerosis
    

  • N Scolding, R Franklin, S Stevens, et al  (MRC Cambridge Centre for Brain Repair, England; Univ of Cambridge, England; Inst of Neurology, London; et al)
    Oligodendrocyte Progenitors Are Present in the Normal Adult Human CNS and in the Lesions of Multiple Sclerosis.
    Brain  121: 2221-2228, 1998.
       
    Partial remyelination occurs in many lesions in patients with multiple sclerosis (MS) – upto 40%.
         
    The cell responsible for limited spontaneous myelin repair has not been precisely identified.   In a rodent model, the most efficient remyelinating cell is the proliferative oligodendrocyte progenitor – this cell has also been found in cultures from the normal human brain.
        
    The rabbit polyclonal R7 anti-platelet-derived growth factor-a receptor antibody is a useful marker of bipolar proliferative human oligodendrocyte progenitors in vitro.
       
    The adult, mature oligodendrocyte has been thought to be an uncertain source of repair.
    The authors have shown that a platelet-derived growth factor-a expressing oligodendrocyte progenitor is present both in the lesions of MS patients and in normal human adult white matter.
        

  • A Tourbah, A Clapin, O Gout, et al (Universite Paris)
    Systemic Autoimmune Features and Multiple Sclerosis: A 5-Year Follow-up Study.
    Arch Neurol 55: 517-521, 1998.  
        
    This article is a prospective study of 161 patients with probable multiple sclerosis where the presence of lupus anticoagulant anticardiolipin antibodies (aCls), ANAs, (antinuclear antibodies) antiphospholipid antibodies (aPLs) and anti double-stranded DNA antibodies were assessed.
       
    About half of the patients had abnormalities suggestive of other autoimmune disease.
         

  • AD Sadovnick, IML Yee, GC Ebers, et al (Univ of British Columbia, Vancouver, Canada; Univ of Western Ontario, Canada; Stanford Univ, Calif)
    Effect of Age at Onset and Parental Disease Status on Sibling Risks for MS.
    Neurology 50: 719-723, 1998.  
       
    Both age of onset and genetic influences seem to affect susceptibility to MS.
       
    Sisters of affected patients were at 2.5 times higher risk than were brothers of affected patients. For siblings with a parent who had MS risk was 4 times higher than for siblings without an affected parent.
        
    The group at highest risk were siblings of affected patients who were aged 20 years or less at the time of MS onset.
        

  • JN Lycke, J-E Karlsson, O Andersen, et al (Goteborg Univ, Sweden)
    Neurofilament Protein in Cerebrospinal Fluid: A Potential Marker of Activity in Mulitple Sclerosis.
    J Neurol Neurosurg Psychiatry 64: 402-404, 1998  
     
       
    For neuronal degeneration in the animal brain, the light subunit of the neurofilament protein (NFL) has been used experimentally as a marker.
       
    Increased concentrations of NFL have been reported in CSF from patients with Alzheimer’s disease and amyotrophic lateral sclerosis. The concentration of NFL in CSF might be useful in future clinical trials of MS.
              

  • GC Ebers, for the PRISMS (Prevention of Relapses and Disability by Interferon b-1a Subcutaneously in Multiple Sclerosis Study Group (London Health Sciences Centre, Ont, Canada)
    Randomised Double-blind Placebo-controlled Study of Interferon b-1a in Relapsing/Remitting Multiple Sclerosis.
    Lancet  352: 1498-1504, 1998.  
       
    The effects of subcutaneous interferon b-1a were investigated in 560 patients with relapsing/remitting Multiple Sclerosis.
       
    Subcutaneous interferon b-1a was well tolerated. It effectively reduced the relapse rate, disability and adverse MR outcomes in a dose-dependent manner.  With further follow-up, long-term benefits may become clearer.
           

  • L Kappos, for the European Study Group on Interferon b-1b in Secondary Progressive MS (Univ Hosp Basel, Switzerland)
    Placebo-controlled Multicentre Randomized Trial of Interferon b-1b in Treatment of Secondary Progressive Multiple Sclerosis.
    Lancet 352:1491-1497, 1998.  
       
    This was a 3-year multicenter, randomized, placebo-controlled, double-masked trial where 360 patients received interferon b-1b 8 million IU subcutaneously every alternate day and 358 patients received placebo.
       
    It was found that interferon b-1b delays sustained neurologic deterioration in patients with secondary progressive multiple sclerosis. This is the first treatment to offer then a beneficial effect.
          

  • KP Johnson, and the Copolymer 1 Multiple Sclerosis Study Group (Univ of Maryland, Baltimore; Univ of Wisconsin, Madison; Univ of Pennsylvania, Philadelphia; et al)
    Extended Use of Glatiramer Acetate (Copaxone) is well Tolerated and Maintains its Clinical Effect on Multiple Sclerosis Relapse Rate and Degree of Disability.
    Neurology 50: 701-708, 1998.  
       
    Glatiramer acetate (copolymer 1), significantly reduces the frequency of relapses. A two-year, placebo-controlled trial showed significant reductions in relapses, reduced neurologic disability and excellent tolerance.
        
    Glatiramer acetate is regarded as frontline therapy for relapse prevention in patients with relapsing remitting multiple sclerosis AND as replacement therapy for patients not responding or intolerant to b-interferons.
       

 

 

By |2022-07-20T16:44:16+00:00July 20, 2022|Uncategorized|Comments Off on Multiple Sclerosis

About the Author: