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A 37-year-old woman was admitted to the hospital on October 4, 1991 because of fever, headache, and abnormal behavior. Although she was treated with aciclovir, she developed encephalitis, which slowly manifested itself over the next month as meningeal irritation, loss of consciousness, partial seizure, and quadriparesis. Her cerebrospinal fluid showed mild lymphocytic pleocytosis without protein elevation. Serum IgG antibody titer to rubella virus was elevated, but the rubella virus could not be detected in the cerebrospinal fluid by PCR amplification. Her consciousness level improved slowly, and by the end of November she suffered only dystonic posture of her right arm and hand. By the middle of December, there were no abnormal neurological findings except some extrapyramidal tract signs and symptoms, such as tremor and rigidity. The serum rubella virus IgG titer had fallen back into the normal range. Her illness was diagnosed as subacute panencephalitis, and she recovered completely about 5 months after the onset of the disease. The lack of rubella virus in the cerebrospinal fluid suggests that panencephalitis may not be dependent on virus replication within the central nervous system. Specific T cells sensitized to proteolipid protein synthetic peptides (PLP158-166) identified with rubella virus were detected in this case during the active stage. These observations imply that subacute panencephalitis may be dependent on an immune-mediated mechanism and that PLP-specific T cells may play an important role in pathogenesis of the disease.

We reported a case of a 29-year-old man who had been in good health until contracting brain stem encephalitis due to a rubella virus 5 years previously, at which time the ECG revealed complete right bundle branch block and right axis deviation. An ECG obtained 6 months earlier had been within normal limits. Since yearly health checkups continued to show the same abnormalities, the patient was admitted for closer examination. At the time of admission, physical findings and blood tests revealed no abnormalities. No cardiomegaly nor pulmonary congestion was observed on chest X-rays either at the time of the original illness or at this time. An endomyocardial biopsy specimen obtained from the right ventricle revealed size variation of cardiac myocytes, moderate disarrangement, and mild myocardial interstitial fibrosis, indicative of post-myocarditic changes. The above findings suggest that bifascicular block (right bundle branch and posterior fascicle) appeared at the time of the rubella virus infection, in the pathogenesis of which the involvement of myocarditis was strongly suspected. Some patients developing myocarditis do not manifest cardiac symptoms such as heart failure. In these cases, conduction disturbances are the sole sequelae. To differentiate pathogenesis in such cases, endomyocardial biopsy was thought to be of value.