Childhood Vaccine Controversy

CBS News has found that since 1988, the vaccine court has awarded money judgments, often in the millions of dollars, to thirteen hundred and twenty two families whose children suffered brain damage from vaccines.


One such case:

On Novermber 9, 2007, the US Court (DVIC) determined:

"In sum, DVIC has concluded that the facts of this case meet the statutory criteria for demonstrating that the vaccinations CHILD received on July 19, 2000, significantly aggravated an underlying mitochondrial disorder, which predisposed her to deficits in cellular energy metabolism, and manifested as a regressive encephalopathy with features of autism spectrum disorder. Therefore, respondent recommends that compensation be awarded to petitioners in accordance with 42 U.S.C. § 300aa-11(c)(1)(C)(ii)."

"DVIC has concluded that CHILD’s complex partial seizure disorder, with an onset of almost six years after her July 19, 2000 vaccinations, is not related to a vaccine-injury."

Do vaccines cause autism?

Sugiura & Yamada (Pediatr Infect Dis J, 1991;Vol 10(3):209-13) describe what happened in Japan. Very briefly, when the MMR triple vaccine was shown to cause meningitis in 1 in 2026 recipients, not only did the Japanese health authorities recognise the causal link to this vaccine, they also discontinued its use (and also significantly, no unusually large epidemic of any of these infections followed).  Not surprisingly, the incidence of vaccine-caused (and overall) meningitis plummeted (the minority who were hell-bent on getting the vaccine could still get it). So, there is a precedent of a whole major country abandoning the offending vaccine and of a recognition of the causal link between the offending vaccines and the observed reactions.  Yet despite this, medical "authorities" in other countries, such as Australia, the UK and the US, continue to ignore (or not read?) the research in published, refereed medical journals, and claim that there is only a temporal and coincidental association.  



CHILD, a minor,by her Parents and Natural Guardians, Petitioners,




In accordance with RCFC, Appendix B, Vaccine Rule 4(c), the Secretary of Health and Human Services submits the following response to the petition for compensation filed in this case.


CHILD ("CHILD") was born on December –, 1998, and weighed eight pounds, ten ounces. Petitioners’ Exhibit ("Pet. Ex.") 54 at 13. The pregnancy was complicated by gestational diabetes. Id. at 13. CHILD received her first Hepatitis B immunization on December 27, 1998. Pet. Ex. 31 at 2.

From January 26, 1999 through June 28, 1999, CHILD visited the Pediatric Center, in Catonsville, Maryland, for well-child examinations and minor complaints, including fever and eczema. Pet. Ex. 31 at 5-10, 19. During this time period, she received the following pediatric vaccinations, without incident:

Vaccine Dates Administered

Hep B 12/27/98; 1/26/99

IPV 3/12/99; 4/27/99

Hib 3/12/99; 4/27/99; 6/28/99

DTaP 3/12/99; 4/27/99; 6/28/99

Id. at 2.

At seven months of age, CHILD was diagnosed with bilateral otitis media. Pet. Ex. 31 at 20. In the subsequent months between July 1999 and January 2000, she had frequent bouts of otitis media, which doctors treated with multiple antibiotics. Pet. Ex. 2 at 4. On December 3,1999, CHILD was seen by Karl Diehn, M.D., at Ear, Nose, and Throat Associates of the Greater Baltimore Medical Center ("ENT Associates"). Pet. Ex. 31 at 44. Dr. Diehn recommend that CHILD receive PE tubes for her "recurrent otitis media and serious otitis." Id. CHILD received PE tubes in January 2000. Pet. Ex. 24 at 7. Due to CHILD’s otitis media, her mother did not allow CHILD to receive the standard 12 and 15 month childhood immunizations. Pet. Ex. 2 at 4.

According to the medical records, CHILD consistently met her developmental milestones during the first eighteen months of her life. The record of an October 5, 1999 visit to the Pediatric Center notes that CHILD was mimicking sounds, crawling, and sitting. Pet. Ex. 31 at 9. The record of her 12-month pediatric examination notes that she was using the words "Mom" and "Dad," pulling herself up, and cruising. Id. at 10.

At a July 19, 2000 pediatric visit, the pediatrician observed that CHILD "spoke well" and was "alert and active." Pet. Ex. 31 at 11. CHILD’s mother reported that CHILD had regular bowel movements and slept through the night. Id. At the July 19, 2000 examination, CHILD received five vaccinations – DTaP, Hib, MMR, Varivax, and IPV. Id. at 2, 11.

According to her mother’s affidavit, CHILD developed a fever of 102.3 degrees two days after her immunizations and was lethargic, irritable, and cried for long periods of time. Pet. Ex. 2 at 6. She exhibited intermittent, high-pitched screaming and a decreased response to stimuli. Id. MOM spoke with the pediatrician, who told her that CHILD was having a normal reaction to her immunizations. Id. According to CHILD’s mother, this behavior continued over the next ten days, and CHILD also began to arch her back when she cried. Id.

On July 31, 2000, CHILD presented to the Pediatric Center with a 101-102 degree temperature, a diminished appetite, and small red dots on her chest. Pet. Ex. 31 at 28. The nurse practitioner recorded that CHILD was extremely irritable and inconsolable. Id. She was diagnosed with a post-varicella vaccination rash. Id. at 29.

Two months later, on September 26, 2000, CHILD returned to the Pediatric Center with a temperature of 102 degrees, diarrhea, nasal discharge, a reduced appetite, and pulling at her left ear. Id. at 29. Two days later, on September 28, 2000, CHILD was again seen at the Pediatric Center because her diarrhea continued, she was congested, and her mother reported that CHILD was crying during urination. Id. at 32. On November 1, 2000, CHILD received bilateral PE tubes. Id. at 38. On November 13, 2000, a physician at ENT Associates noted that CHILD was "obviously hearing better" and her audiogram was normal. Id. at 38. On November 27, 2000, CHILD was seen at the Pediatric Center with complaints of diarrhea, vomiting, diminished energy, fever, and a rash on her cheek. Id. at 33. At a follow-up visit, on December 14, 2000, the doctor noted that CHILD had a possible speech delay. Id.

CHILD was evaluated at the Howard County Infants and Toddlers Program, on November 17, 2000, and November 28, 2000, due to concerns about her language development. Pet. Ex. 19 at 2, 7. The assessment team observed deficits in CHILD’s communication and social development. Id. at 6. CHILD’s mother reported that CHILD had become less responsive to verbal direction in the previous four months and had lost some language skills. Id. At 2.

On December 21, 2000, CHILD returned to ENT Associates because of an obstruction in her right ear and fussiness. Pet. Ex. 31 at 39. Dr. Grace Matesic identified a middle ear effusion and recorded that CHILD was having some balance issues and not progressing with her speech. Id. On December 27, 2000, CHILD visited ENT Associates, where Dr. Grace Matesic observed that CHILD’s left PE tube was obstructed with crust. Pet. Ex. 14 at 6. The tube was replaced on January 17, 2001. Id.

Dr. Andrew Zimmerman, a pediatric neurologist, evaluated CHILD at the Kennedy Krieger Children’s Hospital Neurology Clinic ("Krieger Institute"), on February 8, 2001. Pet. Ex. 25 at 1. Dr. Zimmerman reported that after CHILD’s immunizations of July 19, 2000, an "encephalopathy progressed to persistent loss of previously acquired language, eye contact, and relatedness." Id. He noted a disruption in CHILD’s sleep patterns, persistent screaming and arching, the development of pica to foreign objects, and loose stools. Id. Dr. Zimmerman observed that CHILD watched the fluorescent lights repeatedly during the examination and

would not make eye contact. Id. He diagnosed CHILD with "regressive encephalopathy with features consistent with an autistic spectrum disorder, following normal development." Id. At 2. Dr. Zimmerman ordered genetic testing, a magnetic resonance imaging test ("MRI"), and an electroencephalogram ("EEG"). Id.

Dr. Zimmerman referred CHILD to the Krieger Institute’s Occupational Therapy Clinic and the Center for Autism and Related Disorders ("CARDS"). Pet. Ex. 25 at 40. She was evaluated at the Occupational Therapy Clinic by Stacey Merenstein, OTR/L, on February 23, 2001. Id. The evaluation report summarized that CHILD had deficits in "many areas of sensory processing which decrease[d] her ability to interpret sensory input and influence[d] her motor performance as a result." Id. at 45. CHILD was evaluated by Alice Kau and Kelley Duff, on May 16, 2001, at CARDS. Pet. Ex. 25 at 17. The clinicians concluded that CHILD was developmentally delayed and demonstrated features of autistic disorder. Id. at 22.

CHILD returned to Dr. Zimmerman, on May 17, 2001, for a follow-up consultation. Pet. Ex. 25 at 4. An overnight EEG, performed on April 6, 2001, showed no seizure discharges. Id. at 16. An MRI, performed on March 14, 2001, was normal. Pet. Ex. 24 at 16. A G-band test revealed a normal karyotype. Pet. Ex. 25 at 16. Laboratory studies, however, strongly indicated an underlying mitochondrial disorder. Id. at 4.

Dr. Zimmerman referred CHILD for a neurogenetics consultation to evaluate her abnormal metabolic test results. Pet. Ex. 25 at 8. CHILD met with Dr. Richard Kelley, a specialist in neurogenetics, on May 22, 2001, at the Krieger Institute. Id. In his assessment, Dr. Kelley affirmed that CHILD’s history and lab results were consistent with "an etiologically unexplained metabolic disorder that appear[ed] to be a common cause of developmental regression." Id. at 7. He continued to note that children with biochemical profiles similar to CHILD’s develop normally until sometime between the first and second year of life when their metabolic pattern becomes apparent, at which time they developmentally regress. Id. Dr. Kelley described this condition as "mitochondrial PPD." Id.

On October 4, 2001, Dr. John Schoffner, at Horizon Molecular Medicine in Norcross, Georgia, examined CHILD to assess whether her clinical manifestations were related to a defect in cellular energetics. Pet. Ex. 16 at 26. After reviewing her history, Dr. Schoffner agreed that the previous metabolic testing was "suggestive of a defect in cellular energetics." Id. Dr. Schoffner recommended a muscle biopsy, genetic testing, metabolic testing, and cell culture based testing. Id. at 36. A CSF organic acids test, on January 8, 2002, displayed an increased lactate to pyruvate ratio of 28,1 which can be seen in disorders of mitochondrial oxidative phosphorylation. Id. at 22. A muscle biopsy test for oxidative phosphorylation disease revealed abnormal results for Type One and Three. Id. at 3. The most prominent findings were scattered atrophic myofibers that were mostly type one oxidative phosphorylation dependent myofibers, mild increase in lipid in selected myofibers, and occasional myofiber with reduced cytochrome c oxidase activity. Id. at 7. After reviewing these laboratory results, Dr. Schoffner diagnosed CHILD with oxidative phosphorylation disease. Id. at 3. In February 2004, a mitochondrial DNA ("mtDNA") point mutation analysis revealed a single nucleotide change in the 16S ribosomal RNA gene (T2387C). Id. at 11.

CHILD returned to the Krieger Institute, on July 7, 2004, for a follow-up evaluation with Dr. Zimmerman. Pet. Ex. 57 at 9. He reported CHILD "had done very well" with treatment for a mitochondrial dysfunction. Dr. Zimmerman concluded that CHILD would continue to require services in speech, occupational, physical, and behavioral therapy. Id.

On April 14, 2006, CHILD was brought by ambulance to Athens Regional Hospital and developed a tonic seizure en route. Pet. Ex. 10 at 38. An EEG showed diffuse slowing. Id. At 40. She was diagnosed with having experienced a prolonged complex partial seizure and transferred to Scottish Rite Hospital. Id. at 39, 44. She experienced no more seizures while at Scottish Rite Hospital and was discharged on the medications Trileptal and Diastal. Id. at 44. A follow-up MRI of the brain, on June 16, 2006, was normal with evidence of a left mastoiditis manifested by distortion of the air cells. Id. at 36. An EEG, performed on August 15, 2006,

showed "rhythmic epileptiform discharges in the right temporal region and then focal slowing during a witnessed clinical seizure." Id. At 37. CHILD continues to suffer from a seizure disorder.


Medical personnel at the Division of Vaccine Injury Compensation, Department of Health and Human Services (DVIC) have reviewed the facts of this case, as presented by the petition, medical records, and affidavits. After a thorough review, DVIC has concluded that compensation is appropriate in this case.

In sum, DVIC has concluded that the facts of this case meet the statutory criteria for demonstrating that the vaccinations CHILD received on July 19, 2000, significantly aggravated an underlying mitochondrial disorder, which predisposed her to deficits in cellular energy metabolism, and manifested as a regressive encephalopathy with features of autism spectrum disorder. Therefore, respondent recommends that compensation be awarded to petitioners in accordance with 42 U.S.C. § 300aa-11(c)(1)(C)(ii).

DVIC has concluded that CHILD’s complex partial seizure disorder, with an onset of almost six years after her July 19, 2000 vaccinations, is not related to a vaccine-injury.

Respectfully submitted,

Assistant Attorney General

Torts Branch, Civil Division

Deputy Director
Torts Branch, Civil Division

Assistant Director
Torts Branch, Civil Division

s/ Linda S. Renzi by s/ Lynn E. Ricciardella
Senior Trial Counsel
Torts Branch, Civil Division
U.S. Department of Justice
P.O. Box 146
Benjamin Franklin Station
Washington, D.C. 20044
(202) 616-4133

DATE: November 9, 2007


In the United States Court of Federal Claims FFICE OF SPECIAL MASTERS

No. 02-0738V

Filed: 20 July 2007

BAILEY BANKS, by his father KENNETH BANKS,Petitioner



* * * * * * * * * * * * * * *
Michael G. McLaren, Esq., Black & McLaren, Memphis, Tennessee, for Petitioner;
Alexis B. Babcock, Esq., United States Department of Justice, Washington, D.C., for Respondent.


On 26 June 2002, the Petitioner filed a petition for compensation under the National Childhood Vaccine Injury Act of 1986 (Vaccine Act or Act)2 alleging that, as a result of the MMR vaccination received on 14 March 2000, his child, Bailey, suffered a seizure and Acute Disseminated Encephalomyelitis (“ADEM”),3 which led to Pervasive Developmental Delay (“PDD”),4 a condition from which he continues to suffer (the "Petition"). By the terms of the Petition itself, Petitioner brought this action under an actual causation theory of recovery, as the seizure was alleged to have occurred on 30 March 2000, sixteen days after the vaccination date, and outside of the time periods set on the Table. Petition at 2.

This petition was reassigned to my chambers on 22 December 2004. Eventually, a telephonic evidentiary hearing on the ultimate issue of entitlement for compensation was held on 1 June 2006 Hearing Transcript ("Tr.") at 1. Whereupon, the Court heard from medical expert witnesses for both parties: Dr. Ivan Lopez for the Petitioner and Dr. John MacDonald for the Respondent. Subsequent to that hearing, the parties filed closing briefs with the Court, and the case is now ripe for a ruling….


Despite their accord on certain factual predicates contained in Bailey’s medical records, there is, unsurprisingly, a pronounced conflict between the parties as to the following issues: whether a biologically plausible link exists between ADEM and pervasive developmental delay (PDD) in a direct chain of causation, whether Bailey did in fact suffer from ADEM, and ultimately whether the administration of the MMR vaccine to Bailey actually caused ADEM which would then cause PDD that currently besets Bailey today….




One in every 64 children could have autism, Cambridge researchers find

Hundreds of thousands of children with autism have not been diagnosed, Cambridge University scientists have found.

A study of schoolchildren in Cambridge has found that for every three children who have been diagnosed with autism spectrum disorder there are around two who have the condition but have not been given a formal diagnosis.

It is estimated that around one in 100 children between five-years-old and nine-years-old have autism, meaning there are around 500,000 in the UK. But when researchers carried out more detailed assessments of 11,700 children, they found the true prevalence could be as high as one in 64.

This would mean that there are an additional 300,000 children in Britain with autism spectrum disorder but who have not yet been identified.

The study was led by Professor Simon Baron-Cohen at the Autism Research Centre and is published in the British Journal of Psychiatry.

Autism is a spectrum disorder with cases ranging from relatively mild problems with social interaction to more severe difficulties in behaviour such as not speaking, copying, rigid routines and social isolation.

Prof Baron-Cohen said: "We shouldn’t assume that what we are currently diagnosing is the full picture, there is no room for complacency. But equally we shouldn’t be alarmist and say we should be going out and actively looking for these cases. We should wait until those people want help. It is always better if the patient or their family is looking for help rather than it being thrust upon them."

He said the undiagnosed cases are likely to be at the mild end of the spectrum, are coping well with their families and may not need a diagnosis.

Prof Baron-Cohen said that for some families the autism label may ‘raise anxieties’ and be intrusive, rather than helpful.

The researchers used the Special Educational Needs (SEN) registers in schools, covering 8,824 children attending 79 schools and found 83 cases of autism-spectrum conditions giving a prevalence of one in 106 children.

Then they sent a diagnosis survey to the parents of 11,700 children in Cambridgeshire. From the 3,373 completed surveys, 41 cases were reported corresponding to a prevalence of one in 101.

Finally, the team sent the Childhood Autism Screening Test (CAST) to parents of the same 11,700 children to help identify any undiagnosed cases of autism-spectrum conditions.

All children who scored highly, along with a selection of medium and low scorers, were called in for further assessment.

Excluding the 41 cases already known about, the team found an additional 11 children who met research diagnostic criteria for an autism spectrum condition but had not yet been diagnosed.

The research said this could mean that for every three cases of autism spectrum that are diagnosed, there may be another two that are undiagnosed, giving a ratio of known to unknown cases of 3:2.

Prof Baron-Cohen said: "The two independent sources of information – the SEN register and diagnosis survey – provide converging evidence on the prevalence of autism spectrum conditions as being around one per cent of primary school-age children. This is about 12 times higher than 30 years ago; including the previously undiagnosed cases, this means that one in 64 children may at some point in their lives require support and services."

The increase in the prevalence of autism is probably due to better recognition of the condition by both parents and doctors, wider diagnostic criteria and more diagnostic services.

Prof Tony Charman, chairman in Autism Education, Institute of Education, London, said: "This study confirms findings from other recent work, including our own, that around on per cent of school age children have an autism spectrum disorder. The study also shows that in a significant proportion of cases children meeting research criteria for an autism spectrum disorder were unrecognised by schools and local health services. Accurate figures for the prevalence of autism spectrum disorders are important for planning health, social and education services."

Mark Lever, Chief Executive of the National Autistic Society, said: "This is important research, which for the first time gives us an estimate of the number of people who don’t have an autism diagnosis but may be in need of support. Getting the right support at the right time is vitally important and access to appropriate diagnostic services is crucial."