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Neurol Sci 2001 Apr;22(2):151-4 |
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Books
Vaccinations and multiple sclerosis.
Gout O.
Federation of Neurology, Hjpital de la Salpetriere, Paris, France.
Two problems must be considered in regard to the relationship between
vaccinations and MS: Do vaccinations favour the first attack of MS? Do they
increase the short- or long-term risk in patients with known disease? Answers
to these questions are difficult due to the paucity of reported cases, our
ignorance of the precise frequency of neurological adverse events in vaccines
based on prospective studies, and finally by the lack of a well established
pathophysiology. In most instances, the role of the vaccine is based on a
temporal link between the injection and the onset of neurological disease, and
more rarely to a positive reintroduction. Acute disseminated encephalomyelitis
(ADEM), a monophasic and multifocal illness of the white and grey matter, has
been observed following various viral or bacterial infections as well as
vaccine injections for diseases such as pertussis, tetanus and yellow fever.
The similarities between ADEM and experimental allergic encephalitis (EAE) are
suggestive of an immunological process. In addition to the dramatic
presentation of ADEM, more limited white matter involvement, such as optic
neuritis or myelitis, has been reported following vaccine injections, and has
occasionally been counted as the first attack of MS. In France, 25 million
inhabitants, almost half of the population, were vaccinated against hepatitis B
(HB) between 1991 and 1999. Several hundred cases of an acute central
demyelinating event following HB vaccination were reported to the
pharmacovigilance unit, leading to a modification of vaccination policy in the
schools and the initiation of several studies designed to examine the possible
relationship between the vaccine and the central demyelinating events. The
results of these studies failed to establish the causality of the HB vaccine.
Nevertheless, molecular mimicry between HB antigen(s) and one or more myelin
proteins, or a non-specific activation of autoreactive lymphocytes, could
constitute possible pathogenetic mechanisms for these adverse neurological
events.
PMID: 11603617 [PubMed - in process]