Ishikawa M, Endo K, Saito N, Kukiyama Y, Yamamoto T
Department of Neurology, Fukushima Medical College.
Rinsho Shinkeigaku. 1994 May;34(5):479-83.
A 23-year-old woman in her 23rd week of gestation became febrile and then developed cutaneous eruption typical of measles on July 16, 1993. Two weeks prior to this, her 8-month-old daughter has developed measles. The woman became comatose in a few days and was admitted to our hospital where coma, flaccid paralysis of all four limbs and midbrain corectopia were apparent. High titers of anti-measles antibodies were found in the serum and cerebrospinal fluid. She received a 3-day course of pulse-dose intravenous methylprednisolone, however, without effect. Her consciousness gradually improved and after 1 month, subtle volitional movements were observed. However, fetal death was found and the fetus was removed by cesarean section. In MRI T2-weighted images, earlier in her illness, high signal intensity areas were scattered deeply in the cerebral white matter and the posterior limbs of the internal capsule. However, T1-weighted image was unremarkable. Marked, diffuse cerebral atrophy was noticed 3 months later by both CT and MRI, which was accompanied by wide spread high signal intensity areas around the lateral and fourth ventricles. Regarding the pathogenesis, there are two possibilities, i.e., her encephalitis was due to direct measles viral invasion into the CNS, or due to the autoimmune processes triggered by measles infection. Immune dysfunction known to occur during pregnancy might be responsible for the severity of encephalitis the patient suffered from. A recent increase in the number of adult measles infection might be an admonition that pregnant women are not exceptional to measles infection and that the infection could give rise to a severe form of measles encephalitis.
