ENCEPHALITIS. — In the strictest sense, the term should refer exclusively to morbid processes of an inflammatory nature that affect the substance of the brain, whether in the gray matter (polioencephalitis) or in the white matter (leucoencephalitis or demyelinating encephalitis). In practice, however, the term is used generically to denote forms in which the causal element may not be infectious and the anatomopathological lesions are not strictly those of classical inflammation; in these cases, toxic factors operate, or the action of a virus is only presumed and not demonstrable; for these, the more accurate expression would be "pseudoencephalitis" or "encephalosis."
Such uncertainty and impropriety of terminology reflect the frequent difficulty in identifying the causal element and the fact that encephalitis sometimes appears as a secondary manifestation in the course of various infectious morbid processes (direct action of the virus and its toxins), exogenous intoxications (alcohol, lead, medications, etc.), or endogenous intoxications due to altered metabolism (diabetes, nephritis, gravidic toxicoses, avitaminoses, endocrine disorders, etc.). Encephalitis may present in an acute form, so severe as to cause death within 1–2 days (epidemic encephalitis), or in a chronic form with progressive symptomatology.
Given the high anatomical and functional dignity of the tissue affected, encephalitis is always accompanied, to a greater or lesser extent, by nervous symptomatology (anesthesia and paralysis corresponding to the topography of the foci), particularly in circumscribed purulent forms of cerebral abscesses, or by psychic symptomatology involving a decrease or complete loss of consciousness (v. COMA), or partial impairment of the various elementary activities that constitute it and of which they are the manifestation (interest, attention, perception, memory, intelligence, will, affectivity), or of moral character. Particular damage is inflicted, in addition to nervous functionality, upon the psychic personality of the individual if the encephalitis, especially when associated with meningitis, occurs during the fetal or infantile period of life; in such cases, the developing brain suffers damage and developmental arrest, sometimes so slight as to be barely demonstrable from an anatomopathological standpoint, yet always sufficient to produce true psychoses (v. MENTAL DEFICIENCY). Such "psychically handicapped" individuals deserve the greatest consideration, not only from a medical standpoint but also from educational, legal, and moral perspectives, as they require care, partial recovery, and social integration, albeit on a lower plane of values. In adults, whose brain development is complete and whose ideational patrimony is acquired, mental damage may range from more or less severe to complete dementia (v.), as, for example, in progressive paralytic dementia (v.).
Of particular practical importance (from the familial, social, and pastoral perspectives) is the knowledge of the neuropsychiatric picture that develops as a sequel to a specific form: epidemic or lethargic encephalitis (Economo’s disease), which, in its chronic phase, assumes the form of so-called "post-encephalitic parkinsonism." In this condition, alongside ocular and extrapyramidal phenomena (strabismus, spasms, hypertonicity of muscles with jerky and halting movements), neurovegetative disturbances (altered metabolism and endocrine balance) are accompanied by a particular neurasthenic to hysteroid psychic picture, exaggerated emotionality, and marked slowness, difficulty in comprehension, and at times an appearance of incomprehension that may lead to a mistaken diagnosis of catatonia or dementia. On the contrary, in the majority of such patients, intelligence is not substantially altered, memory and perception are nearly normal, as are ideation and discriminative powers, even though these activities are carried out with characteristic slowness (bradypsychism), similar to the slowness and fatigue observed in bodily movements. All authors agree in admitting that, however pronounced the cerebral torpor and delayed the psychic reaction and the capacity to fix new perceptions, and however grave the impediment to the expression of volitional powers and affective manifestations, in post-encephalitic parkinsonism there is no true mental defect, and therefore no true post-encephalitic dementia exists (G. Moglie, op. cit., p. 660).
GIUSEPPE DE NINO