OVERVIEW
Epidemic encephalitis A, also known as sleeping encephalitis, is also known as VonEconomo encephalitis, after Dr. Constantine von Eichenheimer described clinical and pathological findings of the disease in April 1917 and proposed a separate disease. Clinical manifestations include sleep disorders (narcolepsy, sleep reversal, or insomnia), lethargy, Parkinson’s syndrome, movement disorders, and neuropsychiatric symptoms.
Etiology.
The pathogenesis of this disease is unknown. Recent studies have found positive cerebrospinal fluid oligoclonal zone bands in some patients and effective steroid hormone therapy, suggesting that the disease may be a post-infectious autoimmune disease of the central nervous system.
Symptoms
The clinical manifestations of epidemic encephalitis A are categorized into three clinical syndromes, i.e., drowsy oculomotor paralysis syndrome, hyperkinetic syndrome, and dystonic dyskinesia syndrome. Clinical symptoms begin with drowsiness manifestations, with some patients showing lethargy at work and at meals, and others showing abnormal behavior. These abnormal behaviors are sometimes misdiagnosed as psychiatric abnormalities.
1. Drowsy eye muscle paralysis syndrome
Fever, dizziness, lethargy, somnolence, trance, coma, convulsions, seizures, paralysis of limbs or cerebral nerves, eye movement disorders caused by bilateral ophthalmoplegia are common. Diplopia, strabismus, eyelid ptosis, dilated or constricted pupils and other symptoms can be seen in other cerebral nerve involvement.
2. Hypermotility syndrome
Facial muscle stiffness, expression indifference, excitement and agitation, clonus or chorea, dystonia, hand and foot movement and other symptoms may appear.
3. Dystonia dyskinesia syndrome
Symptoms such as generalized muscle stiffness, fatigue, tiredness, weakness, tremor, dystonia, ataxia, difficulty in walking, etc. may appear. Most patients die in the acute stage due to serious complications, and only a very few patients survive but are left with sequelae such as severe Parkinson’s syndrome, dysphagia, diplopia, and so on.
Examination
1. Laboratory examination
The peripheral blood leukocyte count is mildly elevated and neutrophils are increased. Cerebrospinal fluid cell count is mildly increased, and the classification is mainly lymphocytes, protein is mildly increased, sugar and chloride quantification is normal, and there may be positive oligoclonal bands.
2. Other auxiliary examinations
In severe cases, electroencephalogram abnormalities can be seen. Inflammatory changes in the deep gray matter can be found in about 40% of the patients on cranial MRI.
Diagnosis
Diagnosis can be made on the basis of clinical manifestations (e.g. lethargy, involuntary movements, motor nerve palsy and Parkinson’s syndrome, etc.), combined with epidemiologic data and laboratory tests. The disease should be differentiated from diseases such as epilepsy and hysteria.
Complications
Cerebral edema and brain herniation may complicate the acute stage of the disease.
Treatment
There is no effective treatment at present. In the early stage of the disease, the main symptomatic treatment, careful care and maintenance of body functions require admission to intensive care treatment. As the condition stabilizes, in addition to the maintenance of physical function, physical therapy, speech disorder correction therapy, and nutritional support therapy are relied upon to improve physical function. The application of glucocorticoids, plasma exchange, or other immunotherapy is effective in some patients. In addition, psychotherapy and emotional therapy are important.
Prognosis
About 30% of patients recover completely; 30% become chronic with sequelae; the mortality rate is 30%.
Prevention
The patient should be isolated and the respiratory tract should be cut off.