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Schafer Autism Report - November 5 & 6, 2003 (Double Issue)
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SCHAFER AUTISM REPORT "Healing Autism: No Finer a Cause
on the Planet"
________________________________________________________________ Wed, Nov 5 & NOTE: Update November Calendar of Events
is now out Over 30 New Events Listed Since
Last Week! http://home.doitnow.com/~events RESEARCH * Screening of Nine Candidate Genes For Autism on Chromosome 2q Reveals Rare Nonsynonymous
Variants In The Camp-Gefii
Gene * Postnatal Neurodevelopmental
Disorders: Meeting At The Synapse? * Schizophrenia Risk Again Shown to Rise With Paternal Age TREATMENT * ADVOCACY / EDUCATION * Legislation to Foster More Teachers
Trained for Autism * Northern CARE * Scandal of UK Asylums that Lock up the
Sane, Aspergers * Homes for Disabled Hit Hard In
Shades of Things to Come
in Rest of US? MEDIA ALERT * "Autism and Informed
Inoculation" COMMENTARY * Increase in Autism Demands That We Act Now RESEARCH Screening of Nine Candidate
Genes For Autism on Chromosome 2q Reveals Rare Nonsynonymous Variants In The Camp-Gefii
Gene http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui ds=14593429&dopt=Abstract Bacchelli E, Blasi
F, Biondolillo M, Lamb JA, Bonora
E, Barnby G, Parr J, Beyer KS, Klauck
SM, Poustka A, Bailey AJ, Monaco AP, Maestrini E. 1Dipartimento di Biologia Evoluzionistica Sperimentale, University of Bologna, Bologna, Italy. The results from several genome scans
indicate that chromosome 2q21-q33 is likely to contain an autism susceptibility
locus. We studied the potential contribution of nine positional and functional
candidate genes: TBR-1; GAD1; DLX1; DLX2; cAMP-GEFII;
CHN1; ATF2; HOXD1 and NEUROD1. Screening these genes for DNA variants and
association analysis using intragenic single
nucleotide polymorphisms did not provide evidence for a major role in the aetiology of autism. Four rare nonsynonymous
variants were identified, however, in the cAMP-GEFII
gene. These variants were present in five families, where they segregate with
the autistic phenotype, and were not observed in control individuals. The
significance of these variants is unclear, as their low frequency in IMGSAC
families does not account for the relatively strong linkage signal at the 2q
locus. Further studies are needed to clarify the contribution of cAMP-GEFII gene variants to autism susceptibility.Molecular
Psychiatry (2003) 8, 916-924. doi:10.1038/sj.mp.4001340 PMID: 14593429 [PubMed
- in process] * * * Postnatal Neurodevelopmental Disorders: Meeting At
The Synapse? http://www.sciencemag.org/cgi/content/full/302/5646/826?maxtoshow=&HITS=10&h its=10&RESULTFORMAT=&fulltext=autism&searchid=1067863825964_3470&stored_sear ch=&FIRSTINDEX=0&fdate= Departments of Pediatrics,
Neurology, and Molecular and Human Genetics, Division of Neuroscience, and
Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030,
USA. We often think of neurodevelopmental
disorders as beginning before birth, and many certainly do. A
handful, however, strike many months after birth, following a period of
apparently normal growth and development. Autism and Rett
syndrome are two such disorders, and here I consider some of their similarities
at the phenotypic and pathogenic levels. I propose that both disorders result
from disruption of postnatal or experience-dependent synaptic plasticity. ---------------------------------------------------------------------------- ---- Falling silent.
After a child is born, parents watch with anticipation the normal developmental
program that ensues. The baby smiles and follows faces at 6 weeks, acquires
sufficient motor control to sit and transfer toys by 6 months, and typically
walks and says a couple of words by 12 to 15 months. Language and thought
continue to develop as children begin to understand make-believe play, to use
verbs to describe a mental state, and to imitate complex actions. Ashley
delighted her parents as she progressed through early developmental milestones.
She learned to crawl, babble, walk, and sing nursery rhymes, all at the
expected ages. At 18 months, however, her progress ceased. No more songs or
words, only a vacant stare. Ashley's ability-or inclination-to use her hands
was overwhelmed by incessant handwringing; tremors,
rocking, and loss of balance robbed her of normal motor control; apnea and
hyperventilation indicated autonomic control was going haywire, too. Her head
growth slowed, and her social interactions became almost nonexistent. Alex, born to a different family at a different
time, has a similar story. He was a healthy boy who smiled and followed faces
by 6 weeks, made eye contact, and enjoyed interactive games. At 10 months of
age he showed an unusually intense interest in wheels, but he continued to
interact socially and was saying several words and walking by 13 months. Some
time between 15 and 18 months, however, Alex, like Ashley, fell silent. He
stopped trying to communicate through gestures or words. He lost interest in
social interactions and became utterly absorbed with lines on a tile or wheels
on a toy. He seemed less sensitive to pain but hypersensitive to heat. He
flapped his hands constantly and picked at his skin. Similar histories, different diagnoses:
Ashley has Rett syndrome and Alex is autistic. Both
disorders become manifest after a period of apparently normal development. Both
disrupt social and language development and are accompanied by unusual stereotypies. Despite the intellectual regression that
marks the majority of Rett patients and 30% of
autistic patients (1, 2), neither disease is
neurodegenerative in nature. Many children can improve somewhat as they get
older. Although neither Ashley nor Alex have any language skills, they do have
better eye contact now and seem to recognize family and friends at their
respective ages of 23 and 11 years. The onset of both disorders after neurogenesis, neuronal migration, and maturation have
occurred suggests that these disorders might affect synaptic maturation,
connectivity, or stabilization. Rett Syndrome: One Gene, Many
Phenotypes Rett syndrome
was first described by the Austrian pediatrician Andreas Rett
(3), but skeptical clinicians doubted its identity as a distinct syndrome until
1983, when Hagberg and colleagues reported on 35 patients
with an undeniably unique postnatal developmental disorder (4). One difficulty
in diagnosis was (and is) that clinical and laboratory tests are nonspecific.
The electroencephalogram (EEG) is typically normal the first 2 to 3 years of
life (5, 6), after which the background activity gradually slows, and
repetitive high-amplitude spike and wave discharges appear in 60 to 70% of
these patients. Imaging studies reveal changes in blood flow reminiscent of
patterns seen in young infants, suggesting some arrest in development (7, 8).
Pathological studies show other changes, also nonspecific. Neurons are
abnormally small and densely packed, and have markedly shortened and simplified
dendritic arbors, although migration seems to be
normal (9-11). A degenerative process is unlikely, because brains of Rett syndrome children weigh about 30% less than normal at
any given age (12, 13). Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene
cause the majority of Rett syndrome cases (1, 14).
Both mutation type and, in females, patterns of X chromosome inactivation (XCI)
create a surprisingly wide range of phenotypes. Females with favorably skewed
XCI can be asymptomatic or have mild learning disability, autism, or mild,
later-onset versions of Rett (15-20). In males, the
range is even wider: mutations that would cause classic Rett
in females produce severe neonatal encephalopathy, motor abnormalities,
respiratory dysfunction, and death by the second year. Mutations that cause
little or no phenotype in female carriers cause male children to develop
X-linked mental retardation with seizures, tremors, spasticity,
macrocephaly, or bipolar disease (21-25). One boy
with a receptive language disorder developed childhood-onset schizophrenia
(26). This phenotypic diversity (Table 1) raises questions about the
differential effects of the mutations, regional or neuronal vulnerability to
MeCP2 dysfunction, effects of genetic modifiers, and the nature of MeCP2's role
in the brain. ---------------------------------------------------------------------------- ---- Table 1. Postnatal neurodevelopmental phenotypes associated with mutations in
genes for MECP2 and NLGN-3 and -4, and 15q duplications. Gene Females Males MECP2 Rett syndrome including more severe congenital
Fatal encephalopathy Rett if form or milder preserved
47, XXY, or speech variant
somatic mosaicism Angelman syndrome phenotype Mental retardation, tremors,
and seizures Autism Mental retardation Mental retardation, Mild learning
disability spasticity, and psychosis NLGN-3 Asymptomatic NLGN-4 Asymptomatic Autism
or Asperger Autism or Asperger Duplications of 15q11-q13 Autistic spectrum disorder
or (especially
maternally inherited)
autism plus one or more of the
following: Mental retardation,
hypotonia, seizures,
short
stature, and abnormal epicanthal
folds ---------------------------------------------------------------------------- ---- MeCP2 was first identified as a member of
the methyl-CpG-binding domain (MBD) protein family
(27) and has been thought to serve as a methylation-dependent
repressor (28, 29). MeCP2 dysfunction could thus disrupt the normal
developmental program of gene silencing, but how this might result in a
predominantly neurological phenotype has been a pressing question. It is
interesting that MeCP2 is more abundant in brain tissue than most peripheral
tissues (30, 31), is expressed in neurons but not in glia,
and is localized to cell nuclei (30-32). Even more interesting, MeCP2 levels
increase in cortical neurons throughout development (31-34) (Fig. 1). In
addition to providing one possible explanation to the postnatal onset of
symptoms, this expression pattern suggests that MeCP2 might help maintain or
modulate neuronal maturity and plasticity. ---------------------------------------------------------------------------- ---- http://www.sciencemag.org/cgi/content/full/302/5646/826/FIG1 Fig. 1. Spatial
and temporal distribution of MeCP2 during human development. MeCP2 is
abundant in mature neurons and has an expression pattern that correlates with
the ontogeny of the CNS-spinal cord first, cerebral cortex last. Cajal-Retzius (C-R) neurons are the first cortical neurons
to mature and express MeCP2, followed by midbrain, thalamus, cerebellum, and
deep cortical neurons. Expression in basal ganglia, hypothalamus, hippocampus,
and superficial cortical layers appears later, and the number of MeCP2-positive
neurons in the cerebral cortex continues to increase until 10 years of age. Wg, weeks of
gestation. ---------------------------------------------------------------------------- ---- Evidence from animal models and humans
supporting transcriptional alteration of neuronal genes is somewhat mixed.
Human brain tissues show alterations in gene expression (35), but the role of
these changes in pathogenesis is difficult to ascertain because of the
confounding effects of chronic disease. Male Mecp2-null mice are small,
hypoactive, clasp their hind limbs, have breathing abnormalities, and die by 3
months of age; female mice develop similar features but a bit later than males
(36, 37). Conditional deletion of Mecp2 in postmitotic
neurons recapitulates these fea tures,
albeit more slowly (36). Yet transcriptional profiling of brain tissue from
Mecp2-null mice has revealed no dramatic changes in gene expression (38).
Elevated levels of acetylated histone H3, however, were
found in brains of mice bearing a truncating mutation similar to one found in
classic Rett patients (Mecp2308). These mice develop
a progressive neurological phenotype reminiscent of Rett
syndrome, and that supports the hypothesis that transcriptional misregulation could account for at least some aspects of
the phenotype (39). In Xenopus,
absence of xMeCP2 function disrupts normal neuronal differentiation mediated by
the Notch-Delta signaling pathway. Normally, xMeCP2 interacts with the SMRT
(silencing mediator for retinoid and thyroidhormone
receptors) corepressor complex and silences xHairy2a
by binding a methylated CpG
site in its promoter. Expression of MeCP2 lacking a transcriptional repression
domain causes an increase in the number of differentiated neurons due to
abnormal regulation of xHairy2a expression (40). Whether
similar specific neuronal targets will be identified in mice and human remains
to be seen. Loss of MeCP2 in mammals does not alter neurogenesis,
probably because the timing of its expression in the CNS is different from that
of its Xenopus homolog, but it is conceivable that misregulation of HES1 (the mammalian homolog of Hairy2a)
contributes to neuronal dysfunction. The future of Rett
research clearly depends on identifying MeCP2 targets in the CNS and
understanding the cascade of events that follows their dysregulation. Autism: Many Genes, One
Family of Phenotypes Like Rett
syndrome, autism covers a range of phenotypes. Infantile autism, described in
1943 by Leo Kanner as an inability of affected
children to develop social reciprocity (41), is the more severe form. Hans Asperger used the term autistic psychopathy
to describe similar patients in 1944; Asperger
syndrome patients typically do not have significant delay in language or
cognitive development-indeed, they can function at quite a high level- but suffer social deficits
and various stereotypies. Unlike Rett
children, autistic individuals tend to have larger head size than expected for
a given age (42-44). Autistic brains are larger; the white matter is more
prominent, although the cerebral cortex, hippocampus, and amygdala
are smaller than normal (44, 45). It is interesting that, at birth, the brains
of autistic children tend to be smaller than those of healthy infants, but
between 6 and 14 months of age they undergo abnormally accelerated growth (46).
Whether the increase in brain size is due to the formation of too many
connections or poor elimination of inappropriate connections is not known. A
study aimed at understanding the neuroanatomical
basis of spatial working deficits in autism found decreased activation in the dorsolateral prefrontal cortex and posterior cingulate cortex with the use of functional magnetic
resonance imaging (MRI) (47). Functional imaging studies during tasks that
invoke mentalizing show that Asperger
patients have less activation in the critical medial prefrontal region,
superior temporal sulcus, and peri-amygdaloid
cortex (48). Neuropathological studies show fewer
Purkinje cells than normal, small neuronal size, and increased packing density
in several nuclei of the amygdala (49); small neurons
with decreased dendritic branches have occasionally
been observed in CA1 and CA4 (50). Twin studies provide the most compelling
evidence for a genetic origin of autism (51). The concordance rate in
monozygotic (MZ) twins is 70 to 90% and for dizygotic
(DZ) twins is 0 to 10% (52-55). The high concordance rate in MZ twins suggests
either de novo sporadic mutations in a single gene for a particular autism
locus or a multilocus model involving two or more
interacting loci (56). Although these models are not mutually exclusive, the
data thus far support the existence of several autism loci with mutations in a
single gene underlying the etiology for a specific locus. A variety of chromosomal rearrangements
have been reported in autistic children, with extra copies of 15q11-q13 being
the most frequently reported (57-68). Nullisomy, disomy, trisomy, and tetrasomy of 15q11-q13 have all been associated with
classic autism or other developmental disabilities, which suggests that dosage
of one or more genes in 15q11-q13 is critical for neuronal function. Because
many of the duplications causing an autism phenotype are of maternal origin,
one cannot help but consider the UBE3A gene, mutated in Angelman
syndrome, a prime candidate for mediating some of the phenotypic features.
ATP10C is another gene that is maternally expressed in some tissues and may
contribute to the phenotype (69). Single gene mutations can also produce an
autistic phenotype. A recent study identified MECP2 mutations in 2 out of 68
females with an autistic disorder (20). These two females had mutations that
typically cause classic Rett syndrome, so it is
likely that modifier genes and/or regional-specific differences in XCI patterns
are responsible for their autism phenotype. Mutations in neuroligin-3 (NLGN-3)
and NLGN-4, mapping to Xp22.3 and Xq13, respectively, can cause autism or Asperger syndrome (70). A screen of 140 male and 18 female
siblings and twins identified a frameshifting
mutation in NLGN-4 and missense mutations in an
evolutionarily conserved residue in NLGN-3. That both mutations were found in
asymptomatic mothers could be explained by XCI, but it is possible that the missense mutation is a benign variant. The case of the
truncating mutation in NLGN-4 is more convincing, given that its de novo nature
has been established. These data show that mutations in a single gene can
indeed reproduce all the classic features of autism and, for some cases,
provide a genetic mechanism for the high male-to-female (4:1) ratio in autism.
They also provide neurobiologists with two excellent molecules with which to
begin studying pathophysiologic mechanisms in autism.
It is tempting to speculate that additional autism genes might be soon
identified by following the pattern of Rett research,
i.e., by focusing on cases with a strictly defined phenotype (e.g., classic
autism with or without regression) to decrease the effects of genetic
heterogeneity. As causative genes are found, they can be tested in patients
with variant phenotypes. Do Rett
and Autism Meet at the Synapse? + Article continues at
(subscription required): http://www.sciencemag.org/cgi/content/full/302/5646/826?maxtoshow=&HITS=10&h its=10&RESULTFORMAT=&fulltext=autism&searchid=1067863825964_3470&stored_sear ch=&FIRSTINDEX=0&fdate= -- > DO SOMETHING ABOUT
AUTISM NOW < -- SUBSCRIBE.
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then Forward the Schafer Autism Report. (Delivered Fresh Daily to Your Emailbox) To Subscribe
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_______________________________________________________ * * * Schizophrenia Risk Again
Shown to Rise With Paternal Age [By Richard Woodman.]
http://www.medscape.com/viewarticle/463766?mpid=20487 Reuters Health - Children of older men
are at increased risk of schizophrenia in later life, possibly because of
mutations in their father's DNA, according to a new study from A link between advancing paternal age and
schizophrenia has been reported before, but it has been unclear whether this is
due to increasing mutations in the male germ line with advancing age, or the
result of inherited personality traits. To investigate, Dr. Stanley Zammit and colleagues at the University of Wales College of
Medicine and The findings, reported in British Journal
of Psychiatry, show that 362 of the former soldiers had been diagnosed with
schizophrenia by 1996. Their fathers' ages varied between 19 and 65, while for
a control group of men without schizophrenia the fathers' ages ranged from 15
to 75. The study found that the odds of
developing schizophrenia increased by 30% for each 10-year increase in paternal
age. Adjusting for poor social integration had only a minimal effect on the
findings, suggesting personality traits were not a major factor. “This supports the hypothesis that
accumulating germ cell mutations may lead to an increase in genetic liability
to schizophrenia in the offspring,” the investigators conclude. Br J Psychiatry 2003. * * * TREATMENT
[From the home page. Thanks to Sheila D.] http://rsaffran.tripod.com/aba.html Richard Saffran
is the father of a school-age child who has autism. He has put together “a
collection of Internet and other resources which parents of children with PDD,
PDD-NOS, autism, Asperger's Syndrome, hyperlexia, or Rett Syndrome may
find useful” as he explains on the home page of his web site. http://rsaffran.tripod.com/aba.html “All the information concerns teaching
methods that are a branch of applied behavior analysis ( This is a partial index of the
comprehensive provided: * Frequently asked questions about
* What is * Autism ("one Dad's view") * *
Special education attorneys and advocates * Private schools claiming to use
* Data-Based Research in Support of
Intensive Early Intervention is an extensive list of references, including
several WWW links, courtesy of Dr. Eric Larsson * A failure of special education (the
Brookline/Newton early childhood program) is a story that will be
familiar to some, cautionary to others * Who is qualified to oversee intensive,
comprehensive behavioral programming for young children with autism/PDD? (contributed in part by Dr. Gina Green) * The Sumlin
program notes, from parents Jim and Megan Sumlin
(pseudonyms), detailed records of a very successful * Parents' stories and letters to me and
to Usenet news groups (most recent), and more parents' stories and letters and
even more parents' stories and letters * Parental stress - * * * * ADVOCACY / EDUCATION Legislation to Foster More
Teachers Trained for Autism [From Laura Nelson.] The TEACH bill being proposed in Congress
would authorize the US Department of Education to invest in programs, grants,
and scholarships to train teachers to teach students with autism spectrum
disorders. It would also provide a loan forgiveness program of up to $20,000
for educators who teach autistic children for three years after graduating. I am sending everyone a template letter,
below that you can send to legislatures regarding the TEACH Bill. Please modify it in any way you want, or send
it as is. They don't care if all of the
letters are they same, they just need to see plenty mail to let them know how
many of us are out there! Re: H.R. 1700 Dear [Congressperson’s title
and name], It is extremely important that my
[child/grandchild] receive an education that prepares [her/him] to live life as
independently as possible. My name is [name] and my [child/grandchild] has
autism. Currently, there are not enough funds
available for schools to train teaching professionals to teach children with
autism effectively. Without properly trained staff, our schools are not
equipped to prepare my son to become a contributing member of society. According to the U.S. Department of
Education, Autism has increased 1300% in the past 8 years. This disorder has become an epidemic that
lawmakers must address. Families are
worried, physicians are overwhelmed, and school districts are scrambling to
find qualified personnel to teach these children. If this is not addressed, we will soon have
an enormous number of children who will grow up to become financially dependent
on our state. There is hope, though. I am aware of legislation introduced by the
Autism Caucus Co-chairs, Representatives Smith and Doyle, H.R. 1700, titled the
"Teacher Education for Autistic Children Act of 2003.". Please become a cosponsor of H.R. 1700. H.R. 1700 would authorize the Department of
Education to invest in programs, grants, and scholarships to train teachers who
teach students with autism spectrum disorders. It would also provide a loan
forgiveness program of up to $20,000 for educators who teach autistic children
for three years after graduating. I am extremely grateful for your time and
attention to this matter and I (and all of my family and friends) hope that you
will become a cosponsor of this important legislation. Sincerely, [Your Name] [Address] [Phone Number] You can locate the Senators and
Representatives for your state and district at: http://thomas.loc.gov/ * * * Parents for Autistic Children’s Education
(PACE), a non-profit parents group, has been working with senior Fairfax County
Public Schools (FCPS) staff to develop a proposal for the first charter school
in For more information contact Randy Nicklas at 703-391-2251 or PACECharterSchool@comcast.net * * * CARE Scandal of UK Asylums that
Lock up the Sane, Aspergers [By Daniel Foggo for the Sunday Sheet=/news/2003/11/02/ixhome.html Up to 60 people are being held in
hospital prisons for the criminally insane despite a
recognition that they have been misdiagnosed and are not mentally ill.
The patients, who were declared to be schizophrenic, are now accepted to have Asperger's syndrome, a mild form of autism which is not an
illness and which is unresponsive to drugs.
Despite that, they remain incarcerated in the special hospitals of Broadmoor, Rampton and Ashworth. The Sunday Telegraph has obtained details
of one such patient at Broadmoor. Piers Bolduc was
earmarked for transfer to a non-secure unit more than two years ago, yet is
still waiting to obtain his freedom. The single act of violence for which he
was committed was carried out while on heavy doses of prescription drugs for
schizophrenia, a condition he did not have. Since being sent to Broadmoor eight years ago, Bolduc, 27, has told his parents
that he has been sexually abused by other patients. Tomorrow David Lidington,
the Shadow Environment Secretary and the Bolducs'
family MP, will call for a Government inquiry to find out how many residents of
special hospitals have Asperger's syndrome. He said: "There needs to be a review to
see how many there are in this situation." Psychiatrists say many people suffering
with Asperger's syndrome were wrongly diagnosed as
schizophrenics up to the mid-1990s. Richard Mills, the Director of Research
for the National Autistic Society, said: "At the top end, you are looking
at 60 to 70 individuals out of a population of 1,400 in these hospitals. "Most of them have been subject to
misdiagnosis and they also tend to stay in the special hospitals longer than
average because people cannot find a way of treating them. Yet in psychological
terms you can't treat them because they are not sick." He said that people with Asperger's syndrome were not intrinsically violent.
"Most clinicians believe that they are more likely to be victims of crime
rather than perpetrators because they tend to be generally socially naive which
means they tend to get bullied and exploited." Many of those misdiagnosed have been
forcibly, and wrongly, given powerful drugs to combat non-existent
schizophrenia. Mr
Mills said: "Antipsychotic drugs given to people who are not psychotic are
very harmful. Some of the effects can be irreversible." A spokesman for the Department of Health
said that it was unable to provide figures for people with Asperger's being kept at
special hospitals. “Piers is not a
Criminal and he’s not Insane: so why is he in Broadmoor?” The Sunday Telegraph, ( Piers Bolduc suffers from Asperger’s syndrome, a mild form of autism. Daniel Foggo discovers the terrible sequence of events that has
led to him being held in Although he turns 28 this week, all the
photographs of Piers Bolduc in his parents’ home show him as no older than
18. There is a reason for this: for the
past 10 years Piers has been incarcerated in secure psychiatric
institutions. His family
have not seen him since 1999. For the past 8 years he has been in Broadmoor, the special hospital for the criminally
insane. Piers, however, is not a
criminal, nor is he insane. The doctors there acknowledged this more
than 7 years ago when they realised that he had been
misdiagnosed with schizophrenia. In
fact, Piers has Asperger’s syndrome, a mild form of
autism which is a condition rather than an illness and therefore unresponsive
to medication. With some support, he
should be able to live quite happily in the outside world. It is a fact now accepted by the
authorities. For almost 3 years, Piers
has been awaiting release to The Hayes, a charity-run, non-secure unit in
It has only 12 beds and Piers has not yet
reached the top of the waiting list. In
the meantime, he languishes in Broadmoor, a place for
criminal psychopaths and the pathologically homicidal, where he says that he
has been sexually abused by other inmates. Piers is not
alone in his suffering. Although last week the authorities were unable to
release exact figures, campaigners believe that there are up to 60 others with Asperger’s syndrome in Broadmoor
and the other two special hospitals, Ashworth and Rampton. Many of them, like Piers, were sent there
after being misdiagnosed with an illness such as schizophrenia. There they remain under conditions of maximum
security while the authorities await the availability of places at The Hayes
Unit and for the relevant local authorities to supply funding. Piers’s story
is a tragic one. He was born on In his formative years, he seemed a
normal child who was considered by teachers at the private school he attended
in In the words of his mother, Cris, 58, “the volcano erupted” when he was 16 and studying
for his GCSEs.
“He was revising and “Piers, who could trot out formulae by
heart, had suddenly forgotten how to work out four times four.” His parents, who had moved to
Buckinghamshire, took him to see a doctor who “didn’t have a clue” what caused
his problem. “Eventually they mentioned obsessive
compulsive disorder and he saw a child psychiatrist when he was 17,” she
said. “He was put on neuroleptic
drugs, which were quite strong and became stronger as the doses increased.” Neuroleptics,
such as tranquillisers, are used to treat people
suffering from delusions, hallucinations and various psychoses. They can cause severe side-effects, including
heart problems, seizures and even death. Piers attended the
children’s ward at Many people with the condition, who are
often of above-average intelligence, are able to lead largely normal lives with
therapeutic support. In the early 1990s,
however, cases such as Piers were often labelled as
schizophrenia. “He was so frightened and
scared. He found it all so confusing,”
said Mrs. Bolduc. “At one point, he was
missing for 3 days and the police had helicopters and dogs looking for
him. When he turned up, I calmly asked
him if he realised the distress he had caused. He looked at me with utter amazement. He just did not have that kind of empathy.” + Article continues: http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2003/11/02/nasp02.xml&s Sheet=/news/2003/11/02/ixhome.html
< - - address ends here.
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In [By Kelly Virella for the Through the program, however, he learned
coping skills that have allowed him to go to work as a recycler at Goodwill
Industries on “He has a purpose in life now,” said his
mother, Sherryl Mantell of
Mauk has bought
furniture for his bedroom with his earnings and donates some to the poor at
Christmas. But his family fears that his 18 years of progress could be in
jeopardy. Suncoast
Residential Center and other providers of services to the developmentally
disabled learned Oct. 24 that the state plans to pay them, on average, 14
percent less for taking care of their clients than what they believed in July
they would be getting. As a result of that change, which is
scheduled to go into effect Saturday, Suncoast is
projecting a $126,000 deficit this year in its $700,000 budget, said Jean-Marie
Moore, the director of human services and operations for Goodwill Suncoast. “We don't know what we're going to do,”
she said. “We just found out about this six days ago.” One thing they've decided to do is take
their cause public. Goodwill was one of 20 service providers that orchestrated
a rally Thursday on the front lawn of Indiana Street Group Home, a six-bed Speaker after speaker harangued the
nearly 200 people gathered, demanding that But it's not going to happen, said Shelly
Brantley, director of the state's Developmental Disabilities Program. The cuts
are necessary to avoid a $27.5-million budget deficit in the program this
fiscal year, she said. “It's the law and we are following the
legislative provisions,” she said. Here's what happened: In July, the state
published a new set of reimbursement rates for providers of services to the
developmentally disabled. The new rate schedule eliminated decades-old
variations in repayment rates, lifting some providers to the new standard. Under the old reimbursement schedule, Suncoast was a loser and last year ran a $160,000 deficit,
which Goodwill Industries Suncoast covered. Under the
new schedule, Suncoast expected to become a
beneficiary that would get just enough in reimbursements to cover its $700,000
in projected expenses. The state set aside $25-million more than
it spent last year to cover the new reimbursements. The state also made another key change.
Instead of capping reimbursements at 240 days per client per year, it decided
to allow all providers to get reimbursed for 365 days of service for the first
time. In the past two months, however,
providers have sought reimbursement for many more days per client than the
state expected. That has created such a run on the additional money the state
allocated that the program's budget would be depleted without budget
adjustments, Brantley said. Since July, the average provider has been
requesting rehabilitation at a rate of 350 days per year, which represents a 38
percent increase in the average number of days reimbursed last year, she said. The state expected to raise the average
provider's reimbursement rate by only 5 percent this fiscal year, and that is
still going to happen, Brantley said. For example, she said, the average
provider is getting an extra $150 per month per client for residential
habilitation and an extra $50 per month for adult day training. If the state spends anything more, it
won't be able to help the thousands of people who are waiting to enter such
programs, she said. “We have 12,600 people currently
waiting,” she said. “Our priority is to make sure that any new dollars
appropriated by the Legislature go to them.” “What am I supposed to do with the people
who are in my group home now?” she said. “You don't get the people off the
waiting list by throwing the people here into the street.” The
sudden budget adjustments have thrown many Suncoast
region providers into disarray. Brantley said she has been meeting and
discussing the problems with two statewide provider associations for weeks. But Curt Thomas, president and chief
executive of PARC, a “We haven't even had time to figure a
solution out,” he said. * * * MEDIA ALERT "Autism and Informed
Inoculation" [Announcement from Lyn Redwood, President
of SafeMinds.] If you get a chance please go to http://www.detnow.com and watch the segment
about "Autism and Informed Inoculation." Investigative reporter Steve Wilson spent 3
months on this issue and has put together an excellent 2 part report which will
air tonight and tomorrow night at If you are not in the You can also contact the reporter, Steve
Wilson, directly at WILSON@DETNOW.COM to let him know about how you feel this
report was done. I think is very important also to contact him between the two
segments to let him know what you think because he does do live feed from the
studio, along with the recorded segments of his stories and may add additional
info to the second broadcast. * * * COMMENTARY Increase in Autism Demands
That We Act Now [By Dawn Koplos.] http://www.sunspot.net/news/opinion/oped/bal-op.autism04nov04,0,6818330.stor y?coll=bal-oped-headlines In 1993, there were 260 students in
In 2002, there were 3,488. It's a staggering increase. Similar increases have been reported
across the country and internationally. In July, U.S. Health and Human Services
Secretary Tommy G. Thompson said: “The number of people diagnosed with autism
is on the rise. The impact on families as well as autism's profound effect on
the nation's educational and health care systems points to the need for a
better understanding of this troubling condition.” My son scores years ahead of his age on
cognitive tests. Yet emotionally and socially, he is behind his peers. He has
issues with sensory integration. When he gets over-stimulated - too much noise
or too many people - he has tantrums lasting an hour or more. He flaps his
hands when excited and he doesn't seem to notice (or care) when people get
angry. My son is autistic, just like thousands
of children who will be diagnosed with an autistic spectrum disorder this year. The federal Individuals with Disabilities
Education Act guarantees a free and appropriate public education with peers, to
the maximum extent appropriate, to all eligible children with disabilities
(ages 3 to 21) who need special education and related services in order to
learn in school. Because of this, parents of autistic kids frequently turn to
their local schools for accommodations and services. A few Linda Carter-Ferrier, president of the
Anne Arundel County Chapter of the Autism Society of America, says, “I think
our schools are working as rapidly as they can to learn as much as they can
about how to most appropriately work with students on the autism spectrum. “Combine that with the demands of a
rapidly rising caseload, due to the significant increase in the number of
children diagnosed with an autism spectrum disorder, and you have a real
problem finding and retaining enough school personnel [special education and
general education teachers, as well as therapists and aides/assistants] who
have received adequate training in working with this population of students.” Studies show the sooner you begin early
intervention, and the more intensive the services, the better the outcomes.
Family doctors and pediatricians can help by increasing their knowledge of the
early signs of autism, learning more about early intervention therapies and
programs and steering families in the right direction when a delay is
discovered or suspected. In Autism is found in every country and
region of the world, and in families of all racial, ethnic, religious and
economic backgrounds. The National Institutes of Health estimates the costs of
health and educational services for children and adults at $3 billion and says
that autism is the fastest-growing disability in Parents can advocate for their children,
but we need a collective public outcry to put autism at the top of the list of
public policy priorities to ensure the funding to provide comprehensive
services, care and support for these kids and their families. We also need to demand funding of
research to identify the reasons for the increase in the numbers of children
being diagnosed, find out what causes autism and what helps - which
interventions work and, ultimately, how best to help children and adults living
with autism. On my son's “good days,” I wonder whether
I've been overly concerned about his prospects for school or worried too much
about his behavioral problems. But then, as we turn down a new street to go
home - resulting in a 40-minute meltdown - I pray that our schools will be
prepared. [The opinions expressed in COMMENTARIES
are those of the writer and do not necessarily reflect the views of the Schafer
Autism Report.]
_______________________________________________________ PROMOTE YOUR MEETINGS, CHAPTER OR
CONFERENCE No Cost to List In the Largest, Widest Read "The Autism
Calendar"tm http://home.sprynet.com/~schafer/frm/calendar-form.htm NOTE CALENDAR DEADLINE NOV 25 FOR
DECEMBER UPDATE
_______________________________________________________ _________________________________________________________________ Lenny Schafer, Editor mailto:edit@doitnow.com Edward Decelie
Debbie Hosseini Richard Miles Ron Sleith
Kay Stammers _______________________________________________ SAReport mailing list SAReport@envirolink.org You can change your options
at: http://lists.envirolink.org/mailman/listinfo/sareport Return to Vaccination News Home Page (for best results, right click to "open in new window") DISCLAIMER: All information, data, and material contained, presented, or provided here is for general information purposes only and is not to be construed as reflecting the knowledge or opinions of the publisher, and is not to be construed or intended as providing medical or legal advice. The decision whether or not to vaccinate is an important and complex issue and should be made by you, and you alone, in consultation with your health care provider.
DISCLAIMER: All information, data, and material contained, presented, or provided here is for general information purposes only and is not to be construed as reflecting the knowledge or opinions of the publisher, and is not to be construed or intended as providing medical or legal advice. The decision whether or not to vaccinate is an important and complex issue and should be made by you, and you alone, in consultation with your health care provider.
Copyright 2012 by Vaccination News, A Non-Profit Corporation. All Rights Reserved. This content may not be copied unless permission in writing from Sandy Gottstein has been obtained. 
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 "A foolish faith in authority is the worst enemy of truth." -- Albert Einstein, letter to a friend, 1901 "I know of no safe depository of the ultimate powers of the society but the people themselves, and if we think them not enlightened enough to exercise control with a wholesome discretion, the remedy is not to take it from them, but to inform their discretion by education." -- Thomas Jefferson, letter to William C. Jarvis, September 28, 1820 "What's the point of vaccination if it doesn't protect you from the unvaccinated?" -- Sandy Gottstein "Who gets to decide what the greater good is and how many will be sacrificed to it?" -- Sandy Gottstein |
