Sex: F
Vaccine: MMR
Symptoms: Ultrasound antenatal screen normal
Clinical narrative: This literature marketed report has been received from a consumer via company representative referring to a female patient of unknown age.  The patient delivered her first baby via cesarean section. The child was born full-term, and no congenital abnormalities were noted. Information about concurrent condition or concomitant therapy was unknown. The patient 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 patient was vaccinated with M-M-R II (HSA) (dose, frequency, route, batch/lot number and expiration date were not provided) for prophylaxis (Vaccine exposure during pregnancy). On an unknown date during the pregnancy, confirmatory measurements performed by ultrasound showed the actual delivery date of a fullterm infant would place this immunization at approximately 26 days after conception. It was also reported that the patient received the vaccination approximately 2 months into her second pregnancy. On 19-AUG-1996 approximately 27 weeks into her pregnancy: the patient's first prenatal visit took place. On 28-AUG-1996 and 06-NOV-1996, ultrasounds were performed, and the results were unremarkable. On 21-NOV-1996, the patient delivered a female infant by repeat cesarean due to cephalopelvic disproportion and ineffectual induced labor. The infant's weight was seven pounds, nine ounces. The infant's scores were 8 and 9. The outcome of cesarean due to cephalopelvic disproportion and ineffectual induced labor  was unknown. The causality assessment between repeat cesarean due to cephalopelvic disproportion and ineffectual induced labor and M-M-R II were considered as related. On an unknown date upon discharge from the hospital, the infant was noted to be large for her gestational age and macrocephalic. On 23-NOV-1996 when the infant was two days old, a neonatal sonogram was performed and showed that the infant had enlarged brain ventricles and possible associated cerebral or mid-brain abnormalities. On that same day, the infant was transferred to another hospital for evaluation of possible hydrocephalus. On an unknown date while in the second hospital, the infant received a hearing screening, a computerized tomography(CT) scan, and a cranial ultrasound. The infant 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 infant 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 infant was discharged and was scheduled to follow up with neurosurgery and ophthalmology. On 09-DEC-1996 and 29-JAN-1997, the infant was evaluated by her pediatrician and no abnormalities were noted. On 29-JAN-1997, the infant had a slightly bulging fontanel. In approximately mild March 1997, the infant 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 infant turned off to the side for about a second at a time for about 15 times in row, and it was concerned that the infant was having seizures by the pediatrician. The infant had an appointment with a physician in the next week and would probably get an electroencephalogram (EEG). In early May of 1997, the infant 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 infant had become more severe and prolonged three to four days prior. The infant was admitted for hydrocephalus and to rule out tumor. On 12-MAY-1997, the infant 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 infant was diagnosed with infantile spasms, brain malformation, bilateral otitis media, developmental delay, diaper rash, and AS. The infant was started on Phenobarbital and Adrenocorticotropic hormone injection treatment, which ultimately decreased the frequency and severity of the seizures. On 01-JUL-1997, the infant 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 infant had AS and that she continued to have about 10 sets of spasm-like episodes per day. On 03-DEC-1997, the infant 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 infant was almost two years old, the infant had a history of AICARDI syndrome and infantile spasms. The infant is cruising but is 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 infant was re-admitted to hospital for placement of a ventriculoperitoneal shunt, in order to relieve intraventricular pressure. The infant was noted to be more alert and more verbal. On 12-JAN-1999 and 24-AUG-1999, the infant was again noted to have been doing well. On 10-JAN-2001, the infant was seen for a fever. The infant was recently seen at the Emergency Room(ER) for a breakthrough seizure. The infant was acute viral syndrome and AS with seizure disorder. On 15-AUG-2002, the infant was taken to Hospita because she was having seizures. the The infant's was prescribed an increase in Phenobarbital. On 22-APR-2004, the infant had been fairly stable since her last visit. The infant was had been taking 120 mg of phenobarbital a day and 500 mg of Lamictal twice a day. The infant's condition further stabilized, and at a follow-up appointment on 29-JUL- 2004, the infant was having only two or three brief seizures a week. The infant was recommended decreasing her phenobarbital to 105mg a day in divided dosages. The infant returned 03-FEB-2005. The patient complained that the infant had periods of behavioral outbursts and questioned whether her shunt was working properly. During the exam, the infant was uncooperative and had poor eye contact. A CT scan was recommended, and the infant'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 infant was seen at a Neurology Center on 06-APR-2006. The infant's EEG results from January 2006 were described as profoundly abnormal and the infant 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 infant's seizures were poorly controlled and the infant was resistant to medication. On 28-AUG-2007, the infant was prescribed an increase in her Lamictal to 200mg twice a day. On 30-APR-2008, the infant was noted to be stable and her medication was tolerated well. The working impression of the infant's condition was "Lennox-Gastaut Syndrome with a history of pharmacoresistant epilepsy. The infant returned to the Children's Neurology Center o 30-SEP-2008, the infant 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 infant's diagnoses included AS and chronic seizure disorder (now only on one medication). The physician also noted that the infant 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 infant was still having seizures, as well as daily partial spells. The infant 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 infant was noted to have mental retardation, AS, and frequent seizures. The infant's medications included medroxyprogesterone acetate (DEPO-PROVERA) and rufinamide (BANZEL). Upon internal review, repeat cesarean due to cephalopelvic disproportion and ineffectual induced labor were determined to be medically significant. Literature report. Baby case was captured into US-009507513-1007USA02495.; Sender's Comments: US-009507513-1007USA02495: