Disorders of the Nervous System and Behavior term “viral meningitis” is used to describe a syndrome characteristic of acute. viral infections of the central nervous system manifested by signs of meningeal irritation, cerebrospinal fluid pleocytosis (predominantly lymphocytic), and a short uncomplicated course. The relative frequency and importance of the many agents that have been implicated vary in different parts of the world. In the United States and in temperate climates generally, the enteroviruses and mumps virus are the most common causes. More than 60 enteroviruses have been identified; not all have yet been associated with meningitis, but in view of the frequent additions from among previously known and newly recognized members of this family of agents, the list can be expected to grow. and herpes zoster.
Viral Etiology of the Aseptic Meningitis Syndrome Enteroviruses Polioviruses (types 1. 2, 3) Coxsackie A (types 1, 2, 4-11, 14; 16-18, 22, 24) Coxsackie B (types 1-6) – Echoviruses (types 1-9, 11-24, 25, 30, 31) Mumps virus Herpes simplex (Herpesvirus hominis) Varicella-zoster (Herpesvirus varicellae) Arthropod-borne encephalitis (arboviruses) Lymphocytic choriomeningitis virus Encephalomyocarditis virus Infectious mononucleosis (presumed viral) Viral hepatitis Adenoviruses no striking seasonal incidence.
Disorders of the Nervous System and Behavior Children are more frequently affected than adults, but in some epidemics, as many as 50 percents of cases occur in persons over 15 years of age. Spread is primarily by contact with an infected person, and the healthy transient carrier is as infectious as the frank case. Dissemination is greatest in areas of poor sanitation with a high density of young preschool children, who are the most frequent carriers. Although one virus tends to be dominant and to account for the bulk of illness at any given time and place, it is not unusual during an epidemic or Mumps meningitis follows the epidemiologic pattern of mumps infections generally, with a peak seasonal incidence in winter and spring.
The infection is endemic in the common house mouse, Mus ‘musculus, and is probably spread to man through dust or food contaminated by mouse excreta. It has no seasonal distribution. However, Stinvasion of the central nervous system. There is evidence that in enteroviral infections in humans, as well as in experimentally infected primates, viremia precedes the onset of illness by several days and has usually disappeared by the time neurologic signs appear. There is experimental evidence that herpes virus is also capable of traveling by neural spread.
In the central nervous system, the lesion of aseptic meningitis is apparently limited to an inflammatory response in the meninges, although in nonparalytic poliovirus infections in monkeys scattered anterior horn cell involvement also occurs. Clinical Manifestations. Whatever the specified viral cause, the symptoms and signs are similar and not readily distinguishable from the pattern of aseptic meningitis from other causes. The onset is commonly abrupt. back and neck, photo-phobia, paresthesias, myalgias, abdominal pain, and chills or chilly sensations. In general, the severity of symptoms increases the age of the patient.
Although sudden onset is characteristic, in some patients there is a prodromal nonspecific “minor illness” followed by several days of well-being before the reappearance of fever and the development of signs of central nervous system involvement. This occurs most commonly with poliovirus infections in young children but may be associated with other enter6viruses and with lymphocytic choriomeningitis. On physical examination, there are few findings. The temperature is elevated (100 to 104° F.), but the patient does not appear as ill as one with bacterial meningitis. Neck and back stiffness is the only neurologic signs in the typical case; Kernig and Brudzinski signs are sometimes positive. Nuchal rigidity may be minimal and apparent only in the last degrees of neck flexion.
The deep tendon reflexes are normal or hyper as. tive. Transient weakness (rarely frank paralysis) has been noted with the Coxsackie B group, Coxsackie A7, and echoviruses 6 and 9. The rash is encountered chiefly in young children. The eruption usually appears with the fever and lasts four to five days, in severe cases eight or nine days. Characteristically it is maculopapular, discrete, erythematous and nonpruritic. The lesions may be confined to the face and neck or may spread over the chest and extremities and sometimes involve the palms and soles.