This case was reported in a published article. It was ruled in 2001 that the patient who suffered from Aicardi's syndrome, could not be said to have "received" the measles virus vaccine live (Enders-Edmonston) (+) mumps virus vaccine live (Jeryl Lynn) (+) rubella virus vaccine live (Wistar RA 27/3) (HSA) vaccine in utero based on the most restrictive plausible meaning of the word as required at the time by the Vaccine Act's waiver of sovereign immunity. The judge said that he held the case on abeyance in the event that agency addressed the issue, but instead, he said, the petitioners moved for reconsideration based on an intervening court decision. Under decision, the judge said, he may rule for the more persuasive definition, rather than the most limiting. Given that the Vaccine Act was a "remedial" statute under the decision, he said the more persuasive interpretation that the developing fetus receives a vaccine given in the mother even though it had neither ingested not been injected with it as described in the Vaccine Act. It was reported that it was concluded in 2001, that the statutory language was ambiguous in its application to this situation, and that both competing interpretations were at least "plausible" by the judge. Therefore, he concluded, that he was not free to choose the interpretation that he found to be more persuasive. He was bound under the cases, rather, to choose the interpretation that would produce the most narrow and restricted waiver of sovereign immunity. In light on the opinion, however, the judge stated that he was free to weigh relative merits of the two competing interpretations. Further, decision specified that he was free to consider general principles of statutory construction other than the sovereign immunity canon of narrow construction, he could take into account the statutory consideration of liberal construction of remedial statutes. The special master directed the patient's parents to determine whether they could obtain an expert report that the vaccine likely progressed through the patient's mother body into the fetus she was carrying and, if so, whether it caused the patient's seizure disorder, brain malformation and significant developmental delay. The representing parent patient's information was reported. Follow up information has been received from an an article via company representative referring to a female infant of unknown age on 20-MAR-2019. Information about medical history, concurrent condition and concomitant therapy was unknown. On 07-DEC-1995, the mother delivered her first via cesarean section. The patient's older sibling was born full-term, and no congenital abnormalities were noted. The mother became pregnant with last menstrual period (LMP) of 15-FEB-1996 and estimated date of delivery (EDD) of 21-NOV-1996. On 25-MAR-1996 in the first trimester of her pregnancy, the mother was vaccinated with M-M-R II (HSA) (dose, frequency, route, batch/lot number and expiration date were not provided) for prophylaxis. The patient experienced exposure to M-M-R II (transplacentally)(foetal exposure during pregnancy, first trimester)(It was also reported that the patient received the vaccination approximately 2 months into her second pregnancy.). On an unknown date during the pregnancy, confirmatory measurements performed by ultrasound showed the actual delivery date of a full term infant would place this immunization at approximately 26 days after conception. On 19-AUG-1996 approximately 27 weeks into her pregnancy: the mother's first prenatal visit took place. On 28-AUG-1996 and 06-NOV-1996, ultrasounds were performed, and the results were unremarkable. The mother delivered the female patient by repeat cesarean due to cephalopelvic disproportion and ineffectual induced labor. The patient's weight was seven pounds, nine ounces. The patient's scores were 8 and 9. On an unknown date upon discharge from the hospital, the patient was noted to be large for her gestational age and macrocephalic. When the patient was two days old, a neonatal sonogram was performed and showed that the patient had enlarged brain ventricles and possible associated cerebral or mid-brain abnormalities. On that same day, the patient was transferred to another hospital for evaluation of possible hydrocephalus. On an unknown date while in the second hospital, the patient received a hearing screening, a computerized tomography(CT) scan, and a cranial ultrasound. The patient was discharged with a diagnosis of hydrocephalus ex vacuo with insult occurring possibly in utero, and was noted to have had an absent corpus callosum. An eye examination revealed hypoplasia of the optic nerves with retinal hypertrophy, dysgenesis and macular sparing. Serology reports showed a normal complete blood count. The patient had positive IgG titers to rubella at 2.49(k) and herpes type 1 at 3.25(f), and negative titers to toxoplasmosis and Cytomegalovirus (CMV). On 27-NOV-1996, the patient was discharged and was scheduled to follow up with neurosurgery and ophthalmology. On 09-DEC-1996 and 29-JAN-1997, the patient was evaluated by her pediatrician and no abnormalities were noted. On 29-JAN-1997, the patient had a slightly bulging fontanel. In approximately mild March 1997, the patient began having episodes of jerking and colonic movements three times a day, followed by being tired and sleepy. On 10-APR-1997, some spells occurred when the patient turned off to the side for about a second at a time for about 15 times in row, and it was concerned that the patient was having seizures by the pediatrician. The patient had an appointment with a physician in the next week and would probably get an electroencephalogram (EEG). In early May of 1997, the patient began to have episodes of severe and prolonged jerks with eyes shifting back and forth lasting for 5-10 minutes. On 12-MAY-1997, the patient had become more severe and prolonged three to four days prior. The patient was admitted for hydrocephalus and to rule out tumor. On 12-MAY-1997, the patient underwent a magnetic resonance imaging (MRI) without contrast, a CT, and an EEG of her brain, which showed agenesis or partial agenesis of the corpus callosum, at least one interhemispheric cyst, and compensatory dilation of both occipital horns, among other things. There was no evidence of a brain tumor. A retinal exam after dilation showed whate areas around each disc with sharp borders, consistent with the lesion seen in Aicardi syndrome(AS). On 15-MAY-1997 upon discharge from hospital, the patient was diagnosed with infantile spasms, brain malformation, bilateral otitis media, developmental delay, diaper rash, and AS.  The patient was started on phenobarbital and adrenocorticotropic hormone injection treatment, which ultimately decreased the frequency and severity of the seizures. On 01-JUL-1997, the patient had been no seizures since discharge on 05-DEC-1997. It was noted that although the anterior segment of each eye was normal, but the funduscopic examination did show characteristic fundus lesions of Aicardi's syndrome. On 07-OCT-1997, it was noted that the patient had AS and that she continued to have about 10 sets of spasm-like episodes per day. On 03-DEC-1997, the patient had responded somewhat to Adrenocorticotropic hormone (ACTH), although she still had as many as ten mild clusters a day until recently. On 06-OCT-1998, when the patient was almost two years old, the infant had a history of AICARDI syndrome and infantile spasms. The infant was cruising but was not walking independently. The infant's verbal development was a little more advanced than her gross motor skills, with perhaps 10 words, a good listening vocabulary, good social interaction, and a sense of humor". On 11-DEC-1998, the patient was re-admitted to hospital for placement of a ventriculoperitoneal shunt, in order to relieve intraventricular pressure. The patient was noted to be more alert and more verbal. On 12-JAN-1999 and 24-AUG-1999, the patient was again noted to have been doing well. On 10-JAN-2001, the patient was seen for a fever. The patient was recently seen at the Emergency Room(ER) for a breakthrough seizure. The patient was acute viral syndrome and AS with seizure disorder. On 15-AUG-2002, the patient was taken to hospital because she was having seizures. the patient's was prescribed an increase in phenobarbital. On 22-APR-2004, the patient had been fairly stable since her last visit. The patient was had been taking 120 mg of phenobarbital a day and 500 mg of lamotrigine (LAMICTAL) twice a day. The patient's condition further stabilized, and at a follow-up appointment on 29-JUL- 2004, the patient was having only two or three brief seizures a week. The patient was recommended decreasing her phenobarbital to 105mg a day in divided dosages. The patient returned 03-FEB-2005. The mother complained that the patient had periods of behavioral outbursts and questioned whether her shunt was working properly. During the exam, the patient was uncooperative and had poor eye contact. A CT scan was recommended, and the patient's prescribed phenobarbital dosage was decreased due to infrequent seizures (occurring only once every two weeks). The CT scan results from 07-MAR-2005 showed hydrocephalus (more pronounced on the left side) and indicated that the shunt tube may not be working. The patient was seen at a Neurology Center on 06-APR-2006. The patient's EEG results from January 2006 were described as profoundly abnormal and the patient was noted to be symptomatic of secondary generalized epilepsy syndrome. Other medical impressions were AS, West's Syndrome, Mental Retardation, Cerebral Palsy, and possible Lennox-Gastaut Syndrome. The patient's seizures were poorly controlled and the patient was resistant to medication. On 28-AUG-2007, the patient was prescribed an increase in her Lamictal to 200mg twice a day. On 30-APR-2008, the patient was noted to be stable and her medication was tolerated well. The working impression of the patient's condition was Lennox-Gastaut Syndrome with a history of pharmacoresistant epilepsy. The patient returned to the Neurology Center on 30-SEP-2008, the patient was indicated that had a remarkable reduction in the frequency of breakthrough seizures on the medication topamax. On 15-FEB-2010, an EEG resulted in findings consistent with a diffuse underlying disturbance of neuronal function with superimposed interictal features of a secondary generalized epilepsy such as that can be seen in Lennox-Gastaut syndrome. On 21-JUN-2012, the patient's diagnoses included AS and chronic seizure disorder (now only on one medication). The physician also noted that the patient was having an increasing amount of interaction with family members and more difficulty with discipline. At her follow-up visit on 16-AUG-2012, the patient was still having seizures, as well as daily partial spells. The patient was also having grand mal seizures during her menstrual period. An increase in her anticonvulsant medication, banzel, to three a day, appeared to decrease the number of generalized seizures. On 13-MAY-2013, the patient was noted to have mental retardation, AS and frequent seizures. The patient's medications included medroxyprogesterone acetate (DEPO-PROVERA) and rufinamide (BANZEL).  The outcome of foetal exposure during pregnancy, first trimester was recovered. The outcome of other events was unknown. The causality assessments between all the events and ineffectual induced labor and M-M-R II were considered as related. Upon internal review, aicardi's syndrome, Lennox-Gastaut syndrome and seizure were determined to be medically significant. Literature report: Judge in favor of petitioner. Mother case was captured into US-009507513-1903USA011163.; Sender's Comments:  US-009507513-1903USA011163: