Sex: M
Vaccine: HEP, OPV
Symptoms: DNA test for fragile X, Deafness neurosensory, Developmental delay, Disturbance in social behaviour, Electroencephalogram normal
Clinical narrative: This case was reported by a lawyer and described the occurrence of nerve injury in a male subject who was vaccinated with Engerix B, Dtpa, OPV, Hib, MMR II for prophylaxis. The subject was vaccinated with Engerix B on 05 March 1998, 02 April 1998, and 30 November 1998. According to the legal complaint, at an unspecified time after vaccination with Engerix B, the subject experienced "serious and permanent neurological injuries" which were "alleged to be caused by Thimerosal." On 18 September 2000, the subject was diagnosed with autism, which was confirmed on 01 November 2000. The subject also experienced a neurodevelopmental disorder. The following information was received on 30 March 2007 via medical records. On unknown date (s), the subject was diagnosed with autism and preservative developmental disorder. On 06 October 1999, otolaryngologist's notes indicated that the subject "appears to have a high frequency hearing loss may contribute to his delayed speech development." A report of collaborative assessments performed by the subject's school system was completed on 18 September 2000. Behavioral observations included poor eye contact and attention that was "internally focused". Psychological testing using the Bayley Scales of Infant Development showed cognitive skills developing at a "delayed rate", with problem solving, language, and fine-motor skills evenly developed. Gross motor skills appeared to be more highly developed. Self-help/ adaptive skills were assessed to be mildly deficient according to the Vineland Adaptive Behavior Scales. Intensive early intervention services were recommended at that time. A developmental pediatric evaluation was performed on 18 September 2000 and 21 September 2000. Concerns included lack of speech development, loss of language skills, lack of social interaction, lack of awareness of what is happening around him, poor eye contact, and regressions in behavior and development. The subject reportedly had normal language development until one year old; between 12 and 18 months he exhibited "slight loss" of language and vocabulary skills, which became more noticeable at 27 months. Following examination, diagnostic impressions included autism of unclear etiology. Potential risk factors identified by the evaluating physician included Fragile X-syndrome, altered intestinal permeability associated with recurrent antibiotic use for recurrent otitis media, possible food sensitivities or intolerances, and possible vitamin A and/or a probable essential fatty acid deficiency. By 25 October 2000, the subject had experienced an improvement in symptoms, with some hyperactivity, which the evaluating physician stated "appears related to TMG (trimegestone)". Dietary modifications (gluten-free casein free diet) including vitamin and mineral supplements were initiated. On 01 November 2000, the subject presented for evaluation for speech delay and possible autism. Neurological examination revealed normal muscle mass and strangth and grossly normal tone. Diagnoses included encephalopathy, autistic disorder, and cognition in the borderline to mildly impaired range. On 22 November 2000, the subject presented for cognitive evaluation. According to the Bayley Scales of Infant Development, the subject's cognitive functioning was significantly delayed. In May 2001, follow up examination revealed "significant"improvement in language and behavior and decreased sensory sensitivities and sterotypies. On 08 August 2001, the subject underwent a neurological evaluation. Observations included impairment of communication and language development, impaired social interactions, and some "very subtle" stereotypic movements. He was diagnosed with macrosomia, in addition to encephalopathy and autism. The evaluating neurologist stated "I think it is relatively unlikely that he is going to demonstrate any cerebral abnormalities to explain his condition, but given the large head it may be worth pursuing this investigation."On 16 November 2001, magnetic resonance imaging (MRI) of brain without contrast showed a posterior fossa cyst noted to be a probable arachnoid cyst. A follow up examination on 02 February 2002 revealed no complaints of symptoms that might be associated with the cyst. Neurological examination revealed difficulties with language and social interactions, but without any apparent focal neurological deficits. The evaluating physician indicated that it was unlikely that the arachnoid cyst was related to the subject's autistic features. According to a letter written by the subject's developmental pediatrician on 03 June 2002, the subject had been diagnosed with a central nervous system disorder and hypotonia, in addition to autism. The pediatrician stated that the subject "had been making significant progress with the institution of intensive therapy", including occupational therapy for fine motor skills and rehabilitation for an "acquired neurologic disorder". On 22 July 1999, the subject was diagnosed with ankyloglossia secondary to a short lingual frenulum, and a frenulectomy was subsequently performed. Additional reported events included elevated opiates, bacterial dysbiosis, and yeast overgrowth. These were considered to be incidental findings upon medical record review.