OCCURRENCE OF OLIGOCLONAL GAMMAGLOBULIN IN THE CSF OF CHILDREN WITH PROLONGED and CHRONIC CNS‐INFECTIONS

Abstract

CSF-proteins of 1770 children and adolescents with different neurological diseases and of 75 controls were examined by zone electrophoresis in agarose gel electrophoresis and by immunofixation electrophoresis. The quantitative evaluation of the phoretograms by an analog computer revealed oligoclonal changes of the gamma-globulin profile in 53 patients with subacute or chronic CNS-infections and in 5 children with a medulloblastoma. Seventeen of 37 children with congenital infections had 1--5 oligoclonal gamma-fractions consisting of IgG. Five to seven oligoclonal IgG fractions were detected in each of 16 children with SSPE. All 6 adolescents with multiple sclerosis had 2--5 oligoclonal IgG fractions. One to five oligoclonal gamma-bands occurred transiently in the CSF of 4 children with prolonged meningoencephalitis caused by different viruses, in 3 children with a prolonged non-bacterial meningitis of probable viral origin, in 2 infants with prolonged bacterial meningitis after corticosteroid therapy, and in 1 child with prolonged bacterial meningitis during cytostatic therapy. Four to six oligoclonal gamma-subfractions were found at different times during progressive viral encephalitis that developed during maintenance therapy of acute lymphoblastic leukaemia, and in 2 patients with chronic meningoencephalitis of unknown origin. Since oligoclonal gamma-globulin was detected almost invariably in the CSF of patients with prolonged or chronic neurologic infections, this finding implies persistence of antigens in the CNS and pathologic invasion of lymphocytes with selective proliferation of antigen-stimulated clones.

Cerebrospinal fluid IgG in childhood: The establishment of reference values

“…Studies reporting CSF IgG but no marker for blood-brain barrier (total CSF protein or Alb) 14, 6, 10, 12, 15, 161 are difficult to interpret. Those reporting the ratio of CSF IgG to CSF Alb 12, 11, 141 employ a more appropriate bloodbrain barrier marker than those reporting the ratio of CSF IgG to total CSF protein C3, 7, 8 We suspect that the skewing of CSF IgG/Alb ratio to the upper limits of normal prior to 4 months of age reflects enhanced CNS access for maternally derived serum IgG [2}, whereas the low CSF IgG/Alb ratio during the interval 4 to 15 months of age results from the physiological decline in serum IgG concentration. This CSF IgG nadir has been noted in prior studies C2, 4, 5, 7, 12, 161.…”