Thus, it is biologically plausible that injection of an inactivated virus, bacterium, or live attenuated virus might induce in the susceptible host an autoimmune response by deregulation of the immune response, by nonspecific activation of the T cells directed against myelin proteins, or by autoimmunity triggered by sequence similarities of proteins in the vaccine to host proteins such as those of myelin. The latter mechanism might evoke a response to a self-antigen, so-called molecular mimicry (Fujinami and Oldstone, 1989).



Historically, encephalopathy has been a vague term that is difficult to define. Encephalopathy has been used in the literature to characterize a constellation of signs and symptoms reflecting a generalized disturbance in brain function (Institute of Medicine, 1991). Encephalopathy has been defined as ''a diffuse interference with brain function resulting from a generalized or multifocal insult that causes a widespread disorder in the function of neurons'' (Dodson, 1978, p. 416). Fenichel (1982) noted that the terms encephalopathy and encephalitis are used interchangeably to denote a variety of symptoms including alterations in behavior or state of consciousness, convulsions, headache, and focal neurologic deficit. In general, when pleocytosis in cerebrospinal fluid is present, the term encephalitis is used, implying an inflammatory response within the brain. The term encephalopathy is used when an illness clinically appears like an encephalitis but no inflammatory response is evident (Cherry et al., 1988). Encephalitis is a type of encephalopathy. That is, every case of encephalitis is also a case of encephalopathy, but not every case of encephalopathy is due to an inflammatory response, and thus is not a case of encephalitis.

There are both clinical and pathologic definitions of encephalopathy. For a patient to be considered to have a case of encephalopathy, the patient must have clinical signs and there must be reason to assume there is an underlying pathologic, structural, or persistent biochemical abnormality. For example, seizures can result from extremes of temperature or metabolic changes with no underlying pathologic, structural, or persistent biochemical change. Recurrent seizures without any known precipitating event, on the other hand, could imply a pathologic change sufficient to use the term encephalopathy. Alternatively, there may be pathologic changes in the brain without clinically detectable signs. For example, an increase in size or number of astrocytes may be detectable pathologically, but be sufficiently mild to have only a subclinical association.

Recently, in proposed changes to the Aids to Interpretation of the Vac-

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