cussed the possibility of asking for a review, at a later time, of the question of newborn and infant death following vaccination.

The committee also is not assessing the possible role of hepatitis B vaccine in relation to undefined conditions with a neurological component, given the lack of information on which to base a causality assessment. The committee is aware of the case reports of disabling health effects experienced by some recipients of hepatitis B vaccine, but those reports do not offer adequate information for a meaningful review of either the health outcomes or the mechanisms by which the vaccine might produce those outcomes. The committee does not dismiss or undervalue the disability experienced by these people. Their suffering is real and information on the pathophysiology of these cases is needed. A detailed review of these individual cases would be required to begin gaining a meaningful understanding of the putative link between receipt of the hepatitis B vaccine and the subsequent onset of neurological dysfunction. The Immunization Safety Review Committee, however, is neither equipped nor charged to conduct such a review.

The adverse events considered in this report are all diseases involving demyelination of nerve cell axons in either the central or peripheral nervous systems. Myelin, a principal component of what is referred to as the white matter of the nervous system, normally surrounds the axons of many nerve cells, providing protection and contributing to the transmission of signals through the nervous system. In the CNS (the brain, spinal cord, and optic nerves), myelin is synthesized by oligodendrocytes; in the PNS, it is synthesized by Schwann cells. Oligodendrocytes typically ensheath several axonal processes, and the expression of myelin genes by the oligodendrocytes appears to depend on the presence of astrocytes. In contrast, the external cell membrane of each Schwann cell surrounds a single axon, and the expression of myelin genes is regulated by contact between the axon and the myelinating Schwann cell.

Demyelination occurs when the sheaths around nerve cell axons are damaged by inflammatory or other injurious processes. The focus of this report is on autoimmune mechanisms of demyelination. This exposes the axon to the risk of injury and interferes with the transmission of nerve impulses. Remyelination can occur and is more effective in the PNS than in the CNS. This is probably related to the respective tissue environments, with peripheral nerves exposed to growth factors and other mediators that are not present in or are less accessible to the CNS (Waubant and Stuve, 2002).