This case was reported by a lawyer and described the occurrence of nerve injury in a male subject who was vaccinated with Engerix, Dtap, Hib, OPV, MMR II, and Varivax for prophylaxis. The subject was vaccinated with Engerix B on 08 September 1993. He was vaccinated with Recombivax on 11 October 1993 and 03 January 1994. According to the legal complaint, at an unspecified time after vaccination with hepatitis B vaccine, the subject experienced "serious and permanent neurological injuries" which were "alleged to be caused by Thimerosal. "In October 1997, approximately 4 years after vaccination with Engerix B, the subject was diagnosed pervasive developmental disorder, confirmed in January 1998. He also experienced a neurodevelopmental disorder. This case was assessed as medically serious by manufacturer. Follow up information was received on 30 March 2007 via medical records. On an unknown date, progress notes indicated that the subject experienced developmental delay including speech delay. A school evaluation performed in February 1996 indicated that the subject experienced an approximately 25 percent delay in the areas of cognitive and fine motor skills. On 07 May 1996, the subject was evaluated by an otolaryngologist for communication, and a physical examination was within normal limits. Physical examination revealed "possible PREE". In a letter dated 30 May 1996, the subject's pediatrician chronicled the subject's history of "numerous ear infections" and antibiotic therapy, and noted that the subject was referred for consultation due to "persistent concerns regarding speech delay". According to the history provided by the pediatrician, the subject was making "two meaningful vocalizations" at 9 months, and by one year was able to say "mama, dada, and one meaningful word". At 18 months he used four to ten words, and at 24 months was using two word phrases and approximately 70 recognizable words. At the time of the subject's four year old visit, he demonstrated some echolalia and it was noted that "interaction during the exam did not appear to be normal". On 31 November 1997, the subject underwent a neurological consultation for evaluation of developmental delay. The mother described concerns at approximately one and a half years old, when "she felt his language skills were delayed and he was difficult to engage socially." General physical examination was unremarkable. Observations included little eye contact and occasional echolalia. Sensory examination, auditory acuity, and motor examination were essentially normal. The neurologist indicated that the history of apparent regression of language skills, language impairments, and qualitative impairments of social interactions was suggestive of pervasive developmental disorder. On 14 January 1998, a developmental neuropsychological evaluation was conducted. At that time, the subject was receiving speech language and occupational therapy, and it was noted that prior electroencephalogram, genetics, and metabolic work-up results were within normal limits. Overall intelligence was assessed to be "at least borderline to low average". Ability to use language and language comprehension were impaired. It was noted that the subject exhibited "some hyperlexia in the form of very rapid memorization of songs." Assessment indicated language and executive symptoms associated with Pervasive Developmental disorder; however, the evaluation neuropsychologist noted that the subject's social skills are better than generally found in this population". Enrollment in a special education program was recommended. In March 1998, the subject was referred for an audiologic evaluation which revealed no evidence of ear pathology or longstanding otologic disease process with respect to the subject's speech language and global developmental delay. An initial neurologic evaluation was performed on 16 December 1999, and resulted in an assessment of childhood disintegrative disorder. The evaluating neurologist noted that the "late and continued regression in language skills, behavior, and cognitive function" implied a more severe process than usually associated with regression at 18 to 24 months of age in the syndrome of autism, and expressed concern regarding a possible metabolic disorder. An electroencephalogram was performed in February 2000, for an indication of autism. According to a letter dated 16 March 2000, the subject was believed to have high-functioning autism at four years old, followed by significant regression in language and behavior. Notes associated with diagnostic testing dated 17 May 2000 indicated that the subject had been diagnosed with encephalopathy. On 17 May 2000, the subject was seen for neurological follow-up of childhood disintegrative disorder (regressive encephalopathy), with notable lack of language and relative preservation of sociability. At the time of examination, the subject used only high-pitched sustained sounds and had decreased auditory perception. According to a neurologist's letter dated 16 February 2001, the subject carried a diagnosis of "childhood disintegrative disease", characterized by a sudden regression in language, social interaction, and play skills at four years of age. The subject was seen for neurology follow upon 14 June 2001 for repeated episodes of regression constituting childhood disintegrative disorder. It was noted at that time that the subject's "activity level and history suggests a possible bipolar subtype." It was noted that he was not aggressive or self-injurious, but exhibited high levels of activity and movement. A psychological examination on an unknown date in 2001 assessed the subject to be "appropriately coded as autistic", and noted lack of progress in school and possible deterioration of skills and disabilities. According to the Childhood Autism Rating Scale (CARS), the subject fell within the severely autistic range. In March 2002, the subject's problem list included autism spectrum disorder.