FEAT DAILY NEWSLETTER
Sacramento, California http://www.feat.org
November 12, 2001
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RESEARCH (Four New Abstracts)
·
Autism And MMR Vaccination: Controversy Laid To Rest?
·
Autism Linked to Disturbance of the Pontine Tegmentum?
·
Possible Chromosome Deletion Markers for Autism
·
West Syndrome Focal Temporal Region Abnormalities Seen
In Autism
·
Ritalin May Alter Brain, Study Shows
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11700148&dopt=Abstract <-- address ends here.
DeStefano F, Chen RT.
National Center on Birth Defects and Developmental Disabilities,
Atlanta, Georgia, USA.
It has been suggested that vaccination, particularly with measles-mumps-rubella
(MMR) vaccine, may be related to the development of autism. The main evidence
for a possible association is that the prevalence of autism has been increasing
at the same time that infant vaccination coverage has increased, and that in
some cases there is an apparent temporal association in which autistic
characteristics are first noted shortly after vaccination.
Although the prevalence of autism and similar disorders
appears to have increased recently, it is not clear if this is an actual
increase or the result of increased recognition and changes in diagnostic
criteria. The apparent onset of autism in close proximity to vaccination may be
a coincidental temporal association. The clinical evidence in support of an association
derives from a series of 12 patients with inflammatory bowel conditions and
regressive developmental disorders, mostly autism.
The possibility that measles vaccine may cause autism
through a persistent bowel infection has generated much interest, since it
provides a possible biological mechanism. Epidemiological studies, however,
have not found an association between MMR vaccination and autism.
The epidemiological findings are consistent with current
understanding of the pathogenesis of autism, which has a strong genetic
component and in which the neurological defects probably occur early in
embryonic development. It seems unlikely that a vaccination that is given after
birth could cause autism. A minority of cases of autism may have onset after 1 year
of age (regressive autism), but the single epidemiological study that included
such cases did not find an association with MMR vaccination.
Currently, the weight of the available epidemiological and
related evidence does not support a causal association between MMR vaccine, or
any other vaccine or vaccine constituent, and autism.
PMID: 11700148 [PubMed - in process]
* * *
Polysomnographical assessment of the pathophysiology of
West syndrome.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11701248&dopt=Abstract <-- address ends here.
Kohyama J.
Division of Human Ontogeny and Childhood Development, Graduate
School, Tokyo Medical and Dental University, Tokyo, Japan
In this brief review, the sleep studies on patients with
West syndrome (WS) were summarized. In addition to the previously reported
common finding for sleep in WS - reduction of the amount of rapid-eye-movement
(REM) sleep - weakness of phasic suppression of chin muscle activity in WS patients
has recently been found. The degree of this weakness is quantified by the
phasic inhibition index (PII), which has been found to reflect a patient’s
prognosis as to convulsions.
PII is proposed to be a useful parameter for assessing the
prognosis of WS. Since the pontine tegmentum is involved in the production of
the REM-related phasic loss of muscle activity in REM sleep, WS patients are hypothesized
to have a functional instability of the pontine tegmentum.
After adrenocorticotropin (ACTH) treatment, PII decreased significantly
in all WS patients examined. Taken together with the effects of corticosteriods
on PII, and the incidence of phasic chin muscle activity in patients with
congenital adrenal hyperplasia and nephrotic syndrome, ACTH is hypothesized to
suppress the spasms in WS patients not only through corticosteroids, but also
through a direct action on the pontine tegmentum.
Since PII has been reported to be elevated in patients
with an autistic tendency, the appearance of an autistic tendency is also hypothesized
to be involved in the functional disturbance of the pontine tegmentum.
PMID: 11701248 [PubMed - in process]
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* * *
Molecular Genetic Delineation of 2q37.3 Deletion In Autism
and osteodystrophy: report of a case and of new markers for deletion screening by
PCR.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11701947&dopt=Abstract <-- address ends here.
1: Cytogenet Cell Genet 2001;94(1-2):15-22
Smith M, Escamilla JR, Filipek P, Bocian ME, Modahl C,
Flodman P, Spence MA. Department of
Pediatrics, University of California, Irvine CA (USA).
We recently studied a patient who meets criteria for
autistic disorder and has a 2q37 deletion. Molecular cytogenetic studies were
carried out using DNA isolated from 22 different 2q37 mapped BACs to more
precisely define the extent of the chromosome deletion.
We also analyzed 2q37 mapped polymorphic markers. In
addition DNA sequences of BACs in the deletion region were scanned to identify microsatellite
repeats. We describe four new polymorphic microsatellite repeat markers in the
2q37.3 region.
These markers enabled us to determine the parental origin
of the deletion in our patient. DNA from 8-13 unrelated individuals was used to
determine heterozygosity estimates for these markers. We review four genes deleted
in our patient - genes whose known functions and sites of expression in the
brain and/or bone make them candidates for involvement in autism and/or the
osteodystrophy observed in patients with 2q37.3 deletions.
PMID: 11701947 [PubMed - in process]
* * *
West Syndrome Focal Temporal Region Abnormalities Seen In
Autism Long-term Outcome Of Patients With West Syndrome.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11701277&dopt=Abstract <-- address ends here.
Riikonen R.
Department of Child Neurology, Kuopio University Hospital, P.O.
Box 1777, 70211, Kuopio, Finland
The long-term outcome of Finnish children with West
syndrome was evaluated. Two hundred and fourteen patients were followed up for
20-35 years or until death. A third of the patients died before the age of 3 years.
The most common cause of death was infection.
Autopsy revealed brain anomalies in 25 of 38 (66%)
autopsied patients. Intellectual
outcome was normal or slightly impaired in a quarter of the patients. All of
them completed their education at a normal school or in a school for the
educationally impaired children. Another fourth were taught in special training
schools.
Specific cognitive deficits were seen in some patients
with normal intelligence. Nine attended secondary schools and seven of them had
a professional occupation. Ten were married and five had children. One third of
the patients were seizure-free, another third had seizures daily or monthly,
and the remaining patients had seizures less frequently.
Factors associated with a good prognosis were cryptogenic
etiology, normal development before the onset of the spasms, a short treatment
lag, and a good response to adrenocorticotropic hormone; this was seen in both the
symptomatic and the cryptogenic group, and there were no relapses.
In this study, the late appearance of focal abnormalities
in electroencephalography was not associated with an unfavorable outcome. Focal
abnormalities in temporal region were often seen in patients with autism. The location of an abnormality may be of
importance for the prognosis.
In this study, all the patients (100%) could be followed,
which may be due to the special circumstances characteristic of Finland. The
outcome in children with West syndrome seems to be better than is generally
believed.
PMID: 11701277 [PubMed - in process]
* * *
Ritalin May Alter Brain, Study Shows
Changes appear similar to those caused by amphetamine
[From Reuters.]
http://www.msnbc.com/news/655981.asp?0si=-
The stimulant Ritalin, a drug used to help children with
attention deficit hyperactivity disorder, may cause long-term changes in the
brain, researchers reported on Sunday.
‘Children have been given Ritalin daily for many years ...
but it’s not quite as simple as a short-acting drug.’ says Joan Baizer, ritalin
researcher.
The changes look similar to those seen with other
stimulants such as amphetamine and cocaine, at least in rats, the team at the
University of Buffalo found.
“Clinicians consider Ritalin to be short-acting,” Joan
Baizer, a professor of physiology and biophysics who led the study said in a statement.
“When the active dose has worked its way through the
system, they consider it ‘all gone.’ Our research with gene expression in an
animal model suggests that it has the potential for causing long-lasting
changes in brain cell structure and function.”
But Baizer said that Ritalin, known generically as
methylphenidate, probably is not addictive in the way drugs of abuse are if it
is used properly.
“Children have been given Ritalin daily for many years,
and it is extremely effective and beneficial, but it’s not quite as simple as a
short-acting drug,” she said. “We need to look at it more closely.”
High doses of amphetamine and cocaine have been found to
switch on genes known as “immediate early genes” in brain cells. One of the
genes, called c-fos, has been linked with addiction when it is activated in
certain parts of the brain.
The researchers gave rat pups sweetened milk carrying
methylphenidate in comparable doses and at similar times to what a child would
get.
C-fos genes were activated in their brains in a pattern
similar to that seen in cocaine and amphetamine use, the researchers told a
meeting of the Society for Neuroscience in San Diego.
“These data do suggest that there are effects of Ritalin
on cell function that outlast the short term and we should sort that out,”
Baizer said.
She said perhaps a gene chip — a microarray - could be
used to see just which genes are turned on and off by methylphenidate.
Lenny Schafer, Editor Catherine Johnson PhD
Ron Sleith Kay Stammers
Editor@feat.org Edward Decelie CALENDAR: Michelle Guppy events@feat.org
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