Age: 0.5
Sex: M
Vaccine: DT, HEP, HIBV, IPV
Symptoms: Listless, Muscle twitching, Nervous system disorder, Neurodevelopmental disorder, Psychomotor hyperactivity
Clinical narrative: This case was reported by a lawyer and described the occurrence of neurological damage in a male subject who was vaccinated with hepatitis B vaccine and or unidentified hepatitis B vaccine for prophylaxis. On an unspecified date the subject received unspecified dose of hepatitis B vaccine. According to the legal complaint, at an unspecified time after vaccination with hepatitis B vaccine, the subject experienced neurological damage which was attributed to cumulative mercury toxicity. The following information was received via medical record: The subject received hepatitis B vaccination on 3/11/94, and hepatitis B vaccinations on 4/8/94 and 9/7/94. The subject was also vaccinated with tetanus and diphtheria toxoids absorbed, live attenuated oral poliomyelitis vaccine, Haemophilus influenzae type B vaccine, live attenuated MMR (strain not specified) combination diphtheria and tetanus toxoids and pertussis absorbed and Haemophilus influenzae type B conjugate vaccine for prophylaxis. It was noted that the subject experienced an abnormal reaction after his first DPT dose (Tetramune) described as a seizure-like reaction, with symptoms including listlessness and hyporesponsiveness followed by periods of being startled and twitching his tongue. Thereafter, the subject received only DT vaccinations. On 9/7/94, at the time of the third hepatitis B vaccination, the patient was rolling over both ways, trying to sit up, and saying "da da". A progress note dated 2/28/95 indicated that the subject experienced hyperactivity attributed to antihistamine use. At 18 months of age, the subject experienced social regression and decreased eye contact, with abnormal interactions. He was diagnosed with autism on an unspecified date. In 1997, at three years of age, the subject was evaluated for severe speech and language delays that were assessed to be consistent with pervasive developmental delay. An evaluation performed on 3/27/97 at 36 months oaf age revealed personal and social skills at a six month old range, adaptive skills at 19 to 20 months, gross motor skills at 21 to 24 months, fine motor skills at 23 to 25 months, receptive language at 23 to 25 months, expressive language at 11 to 15 months, and cognitive skills at 17 to 19 months. On 1/12/98, it was noted that the subject had no obvious genetic syndrome, and that prior testing revealed normal karyotype and negative factor X. On 5/11/98, marked dyspraxia was observed, with deficits in communication, social interaction, and ply behaviors consistent with a diagnosis of pervasive developmental delay. Upon examination 5/21/98, the subject was noted to avoid eye contact and was difficult to examine. The subject was admitted to the hospital on 7/16/98 for a primary diagnosis of active infantile autism/autistic encephalopathy. Admission noted indicated that the subject used two-word phrases prior to two years of age, and subsequently regressed to the use of no words at three years and three months. He was discharged in good condition on 7/17/98 after undergoing an electroencephalogram that showed no abnormalities. When treated in the emergency room on 11/12/98 for fever and vomiting, the subject held his head hunched over, which was described by his parents as normal posturing. At that time, medications included Luvox for sleep and staring. A progress note dated 3/12/99 indicated that the subject was enrolled in an autistic preschool. On follow up examination, on 11/10/99, the subject exhibited improvement, in receptive and expressive language skills, eye contact, and social skills. Toilet training was ongoing, and he exhibited obsessive thought processes and poor interactive play. The subject would rub his fingers or wring his fingers until the skin was worn off, which was noted to increase with excitement or anxiety. Physical and neurological examination revealed stable findings. Treatment included melatonin for poor sleep. By 7/14/00, the subject was using language to communicate and his vocabulary was significantly increased. Self-stimulating behaviors and sleep disruption persisted. Luvox therapy was initiated with some improvement of spontaneous language and eye contact.