Brain, Vol 120, Issue 3 451-464, Copyright © 1997 by Oxford University Press
H Maier, M Schmidbauer, B Pfausler, E Schmutzhard and H Budka
Thirteen autopsy cases of patients with clinical criteria of the
Guillain-Barre syndrome were investigated for pathological changes and
cellular composition of inflammatory infiltrates in the CNS and PNS. The
survival times from the onset of neurological symptoms until death ranged
from 1 day to 12 months. In the CNS, degeneration of spinal posterior
tracts was seen in three cases. Mononuclear infiltrates consisted of evenly
proportioned lymphocytes and macrophages in cases with survival of 1 and 2
days, whereas macrophages predominated in cases with survival of 5 days and
longer. Infiltrates presented as nodular clusters around blood vessels and
neurons, or were scattered diffusely. They were found within the spinal
cord in eight out of 13 cases, within the medulla oblongata in eight out of
12 cases, within the pons in five out of nine cases, and in one out of four
midbrains. Activation of microglia, either focal or diffuse, was found in
various degrees in 11 out of 13 cases, involving the spinal cord (six out
of 13 cases), the medulla oblongata (10 out of 12 cases), the pons (five
out of nine cases) or as subependymal rims along the walls of the
ventricular system and the central canal of the spinal cord (seven out of
13 cases). In the PNS, myelin loss (12 out of 13 cases), axonal
degeneration (six out of 13 cases) and mononuclear cell infiltrates (13 out
of 13 cases) were seen in segmental and cranial nerves, spinal ganglia and
spinal roots in varying distribution and severity. Mononuclear cell
infiltrates were composed of macrophages and T lymphocytes, with even
distribution in cases with short survival (1 and 2 days), and predominance
of macrophages in cases with protracted clinical course. T lymphocytes were
equally composed of OPD4+ and CD8+ cells without obvious differences
between cases of short and long duration, or between PNS and CNS
infiltrates in 11 out of 12 cases, whilst two cases had a dominant OPD4+
subset. We conclude that CNS pathology is frequent in patients with
Guillain-Barre syndrome. It involves axons with secondary myelin
impairment, microglial activation and inflammatory infiltration. In this
series, primary demyelination is not found in the CNS. Changes such as
degeneration of spinal posterior tracts are secondary to pathology in the
PNS. Inflammatory cell reactions in the CNS are similar to those in the PNS
and to CNS pathology in experimental allergic neuritis. This inflammation
might reflect CNS immune activation in the absence of the relevant antigen,
in addition to cellular reactions accompanying secondary CNS changes. The
presence of distinct pathology in the CNS is in contrast with other recent
studies on the pathology of Guillain-Barre syndrome which, unlike this
study, may have been influenced by recently introduced treatments.
ARTICLES
Central nervous system pathology in patients with the Guillain-Barre syndrome
Institute of Neurology, University of Vienna, Austria.
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