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.
IN THE UNITED STATES COURT OF FEDERAL CLAIMS OFFICE OF SPECIAL MASTERS
CHILD, a minor,by her Parents and Natural Guardians, Petitioners,
v.
SECRETARY OF HEALTH AND HUMAN SERVICES, Respondent.
RESPONDENT'S RULE 4(c) REPORT
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.
FACTS
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.
ANALYSIS
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,
PETER D. KEISLER
Assistant Attorney General
TIMOTHY P. GARREN
Director
Torts Branch, Civil Division
MARK W. ROGERS
Deputy Director
Torts Branch, Civil Division
VINCENT J. MATANOSKI
Assistant Director
Torts Branch, Civil Division
s/ Linda S. Renzi by s/ Lynn E. Ricciardella
LINDA S. RENZI
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
v.
SECRETARY OF THE DEPARTMENT F HEALTH AND HUMAN SERVICES,
* * * * * * * * * * * * * * *
Michael G. McLaren, Esq., Black & McLaren, Memphis, Tennessee, for Petitioner;
Alexis B. Babcock, Esq., United States Department of Justice, Washington, D.C., for Respondent.
ENTITLEMENT RULING BELL, Special Master:
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....
I. FACTUAL RECORD
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....
~~~~~~~~~~~~~~~~~~~~~
THE TELEGRAPH
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.
by Rebecca Smith, Medical Editor, 29 May 2009
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."
