2. VIRAL ENCEPHALITIS GENERAL CONSIDERATION

     Encephalitis may be defined as an inflammatory process of the CNS that results in altered function of various portions of the brain and spinal cord and is usually accompanied by signs of systemic infection.
     Viral encephalitis may be characterized by: 1. A mild abortive infection; 2. A type of illness clinically indistinguishable from aseptic meningitis; and 3. A severe involvement of the CNS. The latter is often characterized by a sudden onset, high fever, meningeal signs, stupor, disorientation, tremors, convulsions, spasticity, coma and death. Case fatality ranges from 1% to 34.9%. The sequelae are more common in infants. A specific diagnosis can be made either by demonstrating a rise in the level of antibody in the serum of the convalescent patient or by isolating a virus from the CNS or CSF.
     In traditional Chinese medicine, the condition is considered to be caused by epidemic Qi, a pathogenic factor of high infectivity. The terms of diagnosis are "acute or fulminating infectious disease in summer," or "summer-heat convulsion," or "acute febrile disease with prolonged onset."

CLINICAL MANIFESTATIONS

     There are many types of viral encephalitides. They vary from benign forms,
resembling aseptic meningitis, lasting a few days and are followed by complete
recovery to fulminating encephalitis with the clinical manifestations of paresis,
sensory changes, convulsions, increased intracranial pressure, coma and death.
     The onset of viral encephalitis may be sudden or gradual and is marked by fever,
headache, dizziness, vomiting, apathy and stiffness of the neck. Ataxia, tremors,
mental confusion, speech difficulties, stupor or hyperexcitability, delirium, convulsions and coma, and death may follow. In some cases there may be a prodromal
period of 1 to 4 days characterized by chills and fever, headache, malaise, sore throat, conjunctivitis, and pains in the extremities and abdomen followed by encephalitic signs just mentioned. Abortive forms with headache and fever only or a syndrome resembling aseptic meningitis may occur.
     The many variations in the clinical patterns of encephalitis depend on the
distribution, location and concentration of neuronal lesions. Ocular palsies and ptosis are uncommon. Cerebellar incoordination is seen. Flaccid paralysis of the extremities resembling that of poliomyelitis is sometimes encountered. Paralysis of the shoulder girdle muscle is described as a singular feature of a tick-bone encephalitis.
     The CSF is clear and manometric readings of pressure vary from normal to markedly elevated. As a rule, pleocytosis of 40 to 400 cells, chiefly mononuclear, is found. The protein and glucose values may be slightly elevated or normal.
DIAGNOSIS
     A diagnosis of acute encephalitis is indicated by the clinical findings. The
circumstances in which the disease occurs are important. The specific type of encephalitis can be determined only by isolation and identification of the virus or by demonstration of the formation of or rise of level of antibody in convalescence.
Arboviruses are rarely detected in the CSF, blood or other materials during life. It is generally fruitless and inappropriate to search for them except in CNS tissue removed with sterile precautions at necropsy. A serologic diagnosis may be reached by means of the complement fixation or hemagglutination-inhibition test. Paired serum specimens are necessary. The first should be drawn as soon after onset as possible and the second, 2 or 3 weeks later.

TREATMENT

I. Treatment in Western medicine.

     Although there has been little to offer in the way of specific treatment for viral encephalitis in the past, recent evidence indicates that antiviral chemotherapy may be worth using in patients with encephalitis caused by herpes simplex virus. It appears that a number of compounds interfere with DNA metabolism and inhibit multiplication of herpes simplex virus. Herpes simplex virus encephalitis carries a high fatality rate of 35%, which may justify the use of potentially toxic drugs. Clinical manifestations of temporal lobe involvement are common and may be supported by electroencephalograms and brain scan. It is recommended that the diagnosis be established by biopsy of the involved temporal lobe for isolation of herpes simplex virus or by identification of herpes virus antigen with fluorescent-antibody methods before treatment is begun. Treatment is most beneficial when given early in the course of the disease before brain damage occurs from infection or increased intracranial pressure.
     The use of antimicrobial agents to prevent infection is contraindicated because
it predisposes to infection by resistant organisms. The use of tetracycline should be avoided especially because it can give rise to intracranial hypertension.
     There is no evidence that steroids are beneficial in the treatment of viral
encephalitis. Systemic and intracranial hypertension and other well-known side
effects should discourage the use of steroids in viral encephalitis.
     The use of mannitol and other hypertonic solutions may effect a temporary drop
in intracranial pressure, but the usual rebound effect diminishes their value.
     Immune serum globulin, whole blood and pooled plasma are of no value in the
treatment of encephalitis. There is no evidence that vaccinia immune globulin alters
the course of postvaccinal encephalitis.
     The usual sedatives are indicated for hyperexcitability and convulsion. Hyperthermia is usually controlled by giving the patient tepid sponge baths or by using an ice blanket. Intravenous infusions may be necessary to maintain proper balance of water and electrolytes. Severe involvement of the medulla, with impairment of swallowing and accumulation of secretions in the throat and paralysis of the vocal cords or respiratory muscles, should be treated in the same way as that of bulbar poliomyelitis. If gentle aspiration fails to keep the airway open,