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3: J Med Microbiol. 2005 Oct;54(Pt 10):987-91.
Differences between the gut microflora of children with autistic spectrum
disorders and that of healthy children.
Parracho HM, Bingham MO, Gibson GR, McCartney AL.
Food Microbial Sciences Unit, School of Food Biosciences, The University of
Reading, Whiteknights, PO Box 226, Reading RG6 6AP, UK.
Children with autistic spectrum disorders (ASDs) tend to suffer from severe
gastrointestinal problems. Such symptoms may be due to a disruption of the
indigenous gut flora promoting the overgrowth of potentially pathogenic
micro-organisms. The faecal flora of patients with ASDs was studied and compared
with those of two control groups (healthy siblings and unrelated healthy
children). Faecal bacterial populations were assessed through the use of a
culture-independent technique, fluorescence in situ hybridization, using
oligonucleotide probes targeting predominant components of the gut flora. The
faecal flora of ASD patients contained a higher incidence of the Clostridium
histolyticum group (Clostridium clusters I and II) of bacteria than that of
healthy children. However, the non-autistic sibling group had an intermediate
level of the C. histolyticum group, which was not significantly different from
either of the other subject groups. Members of the C. histolyticum group are
recognized toxin-producers and may contribute towards gut dysfunction, with their
metabolic products also exerting systemic effects. Strategies to reduce
clostridial population levels harboured by ASD patients or to improve their gut
microflora profile through dietary modulation may help to alleviate gut disorders
common in such patients.
Publication Types:
Comparative Study
Research Support, Non-U.S. Gov't
PMID: 16157555 [PubMed - indexed for MEDLINE]
4: Arch Neurol. 1981 Mar;38(3):191-4.
Acquired reversible autistic syndrome in acute encephalopathic illness in
children.
DeLong GR, Bean SC, Brown FR 3rd.
In seeking the neurologic substrate of the autistic syndrome of childhood,
previous studies have implicated the medial temporal lobe or the ring of
mesolimbic cortex located in the mesial frontal and temporal lobes. During an
acute encephalopathic illness, a clinical picture developed in three children
that was consistent with infantile autism. This development was reversible. It
was differentiated from acquired epileptic aphasia, and the language disorder was
differentiated aphasia. One child has rises in serum herpes simplex titers, and a
computerized tomographic (CT) scan revealed an extensive lesion of the temporal
lobes, predominantly on the left. The other two, with similar clinical syndromes,
had normal CT scans, and no etiologic agent was defined. These cases are examples
of an acquired and reversible autistic syndrome in childhood, emphasizing the
clinical similarities to bilateral medial temporal lobe disease as described in
man, including the Klüver-Bucy syndrome seen in postencephalitic as well as
postsurgical states.
Publication Types:
Case Reports
PMID: 6162440 [PubMed - indexed for MEDLINE]
5: J Neurovirol. 2005 Feb;11(1):1-10.
Autistic disorder and viral infections.
Libbey JE, Sweeten TL, McMahon WM, Fujinami RS.
Department of Neurology, University of Utah, Salt Lake City, Utah 84132-2305,
USA.
Autistic disorder (autism) is a behaviorally defined developmental disorder with
a wide range of behaviors. Although the etiology of autism is unknown, data
suggest that autism results from multiple etiologies with both genetic and
environmental contributions, which may explain the spectrum of behaviors seen in
this disorder. One proposed etiology for autism is viral infection very early in
development. The mechanism, by which viral infection may lead to autism, be it
through direct infection of the central nervous system (CNS), through infection
elsewhere in the body acting as a trigger for disease in the CNS, through
alteration of the immune response of the mother or offspring, or through a
combination of these, is not yet known. Animal models in which early viral
infection results in behavioral changes later in life include the influenza virus
model in pregnant mice and the Borna disease virus model in newborn Lewis rats.
Many studies over the years have presented evidence both for and against the
association of autism with various viral infections. The best association to date
has been made between congenital rubella and autism; however, members of the
herpes virus family may also have a role in autism. Recently, controversy has
arisen as to the involvement of measles virus and/or the measles, mumps, rubella
(MMR) vaccine in the development of autism. Biological assays lend support to the
association between measles virus or MMR and autism whereas epidemiologic studies
show no association between MMR and autism. Further research is needed to clarify
both the mechanisms whereby viral infection early in development may lead to
autism and the possible involvement of the MMR vaccine in the development of
autism.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 15804954 [PubMed - indexed for MEDLINE]
6: Eur Child Adolesc Psychiatry. 2002 Jun;11(3):142-6.
Autistic symptoms following herpes encephalitis.
Ghaziuddin M, Al-Khouri I, Ghaziuddin N.
Division of Child and Adolescent Psychiatry, University of Michigan Medical
Center, Ann Arbor 48109-0390, USA. mghaziud@umich.edu
Autism is a childhood onset neurodevelopmental disorder characterized by
reciprocal social deficits, communication impairment, and rigid ritualistic
interests, with the onset almost always before three years of age. Although the
etiology of the disorder is strongly influenced by genes, environmental factors
are also important. In this context, several reports have described its
association with known medical conditions, including infections affecting the
central nervous system. In this report, we describe an 11-year-old Asian
youngster who developed the symptoms of autism following an episode of herpes
encephalitis. In contrast to previous similar reports, imaging studies suggested
a predominant involvement of the frontal lobes. At follow-up after three years,
he continued to show the core deficits of autism. This case further supports the
role of environmental factors, such as infections, in the etiology of autism, and
suggests that in a minority of cases, autistic symptoms can develop in later
childhood.
Publication Types:
Case Reports
Research Support, Non-U.S. Gov't
PMID: 12369775 [PubMed - indexed for MEDLINE]
7: J Autism Dev Disord. 1992 Mar;22(1):107-13.
Brief report: autism and herpes simplex encephalitis.
Ghaziuddin M, Tsai LY, Eilers L, Ghaziuddin N.
Department of Child and Adolescent Psychiatry, University of Michigan Hospital,
Ann Arbor 48109-0390.
Publication Types:
Case Reports
PMID: 1592760 [PubMed - indexed for MEDLINE]
8: Dev Med Child Neurol. 1991 Oct;33(10):920-4.
Autistic syndrome with onset at age 31 years: herpes encephalitis as a possible
model for childhood autism.
Gillberg IC.
Department of Pediatrics and Child Psychiatry, University of Göteborg, Sweden.
The author describes a previously healthy man who contracted herpes encephalitis
at the age of 31 years, and over the following months developed all the symptoms
considered diagnostic of autism. This case report casts doubt on the notion of
autism as an exclusively developmental disorder. It is suggested that temporal
lobe damage may cause autism in some cases.
Publication Types:
Case Reports
Research Support, Non-U.S. Gov't
PMID: 1743418 [PubMed - indexed for MEDLINE]
9: Can J Psychiatry. 1991 Nov;36(9):686-92.
Autism: its primary psychological and neurological deficit.
Fotheringham JB.
Department of Psychiatry, Queen's University, Kingston, Ontario.
Autism is a perplexing condition because of its unique presenting signs and high
degree of variability. Evidence is presented that the basic underlying
information processing disorder is a dysfunction of the appreciation of the
emotional significance of incoming stimuli and attaching motivational value to
the stimuli. It is proposed that this dysfunction occurs when the amygdaloid
nucleus and/or its connections are disrupted, resulting in the variability of the
presentation of this syndrome among individuals. Herpes simplex encephalitis
sometimes results in signs of autism. The virus has a predilection to attack
specific areas of the brain, which provides information on the probable
underlying neurological dysfunction in autism.
Publication Types:
Review
PMID: 1773407 [PubMed - indexed for MEDLINE]
10: J Autism Dev Disord. 1986 Sep;16(3):369-75.
Onset at age 14 of a typical autistic syndrome. A case report of a girl with
herpes simplex encephalitis.
Gillberg C.
Publication Types:
Case Reports
PMID: 3558293 [PubMed - indexed for MEDLINE]
11: Curr Opin Neurol. 2002 Jun;15(3):333-8.
Neurological adverse events associated with vaccination.
Piyasirisilp S, Hemachudha T.
Division of Neurology, Department of Medicine, Chiang Mai University, Chiang Mai
50200, Thailand. spiyasir@mail.med.cmu.ac.th
Public tolerance to adverse reactions is minimal. Several reporting systems have
been established to monitor adverse events following immunization. The present
review summarizes data on neurologic complications following vaccination, and
provides evidence that indicates whether they were directly associated with the
vaccines. These complications include autism (measles vaccine), multiple
sclerosis (hepatitis B vaccine), meningoencephalitis (Japanese encephalitis
vaccine), Guillain-Barré syndrome and giant cell arteritis (influenza vaccine),
and reactions after exposure to animal rabies vaccine. Seizures and
hypotonic/hyporesponsive episodes following pertussis vaccination and potential
risks associated with varicella vaccination, as well as vaccine-associated
paralytic poliomyelitis following oral poliovirus vaccination, are also
described. In addition, claims that complications are caused by adjuvants,
preservatives and contaminants [i.e. macrophagic myofasciitis (aluminium),
neurotoxicity (thimerosal), and new variant Creutzfeldt-Jakob disease
(bovine-derived materials)] are discussed.
Publication Types:
Review
PMID: 12045734 [PubMed - indexed for MEDLINE]
12: J Autism Dev Disord. 2004 Oct;34(5):583-6.
Brief report: autistic disorder in three children with cytomegalovirus infection.
Sweeten TL, Posey DJ, McDougle CJ.
Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN
46202-4800, USA.
Previous research has identified a relationship between autistic disorder
(autism) and specific congenital infections. Three cases of congenital or
perinatal cytomegalovirus (CMV) infection occurring in association with autism
are described. Hypothetical mechanisms relating congenital infection, such as
CMV, to the development of autism are discussed. A better understanding of the
immunologic response to certain congenital infections may provide important
information pertaining to the pathophysiology and etiology of autism in
vulnerable individuals.
Publication Types:
Case Reports
Research Support, Non-U.S. Gov't
PMID: 15628611 [PubMed - indexed for MEDLINE]
13: J Autism Dev Disord. 2003 Aug;33(4):455-9.
Possible association between congenital cytomegalovirus infection and autistic
disorder.
Yamashita Y, Fujimoto C, Nakajima E, Isagai T, Matsuishi T.
Department of Pediatrics and Child Health, Kurume University School of Medicine,
Kurume, 830-0011 Japan. yushiro@med.kurume-u.ac.jp
We encountered seven children with symptomatic congenital cytomegalovirus (CMV)
infection from 1988 to 1995, of whom two (28.6%) developed typical autistic
disorder. Case 1: A boy born at 38 weeks' gestation with a birth weight of 3164 g
showed generalized petechiae, hepatosplenomegaly, and positive serum CMV-specific
IgM antibodies. He was profoundly deaf, mentally retarded, and exhibited a lack
of eye contact, stereotyped repetitive play, and hyperactivity. Case 2: A boy
delivered at 39 weeks gestation with a birthweight of 2912 g showed
non-progressive dilatation of the lateral ventricles observed postnatally.
CMV-specific IgM antibodies were positive and CMV-DNA in the urine was confirmed
by PCR. The boy was mentally retarded but not deaf. He showed no interest in
people and delayed speech development. Subependymal cysts were detected by
cranial ultrasound after birth in both patients. This is the first report
describing subependymal cysts and the later development of AD. Cranial magnetic
resonance imaging revealed an abnormal intensity area in the periventricular
white matter suggestive of disturbed myelination; however, no migration disorders
were found in our patients. These findings suggest that the timing of injury to
the developing brain by CMV may be in the third trimester in some patients with
autistic disorder.
Publication Types:
Case Reports
PMID: 12959425 [PubMed - indexed for MEDLINE]
14: Neuropediatrics. 1990 May;21(2):102-3.
Autism as one of several disabilities in two children with congenital
cytomegalovirus infection.
Ivarsson SA, Bjerre I, Vegfors P, Ahlfors K.
Department of Pediatric, University of Lund, Malmö General Hospital, Sweden.
Two children with congenital cytomegalovirus (CMV)-infection, severely disabled
where autism was one of the disabilities are described. The characterization of
the maternal infection have been possible and the connection between congenital
CMV-infection and autism is discussed.
Publication Types:
Case Reports
PMID: 2163029 [PubMed - indexed for MEDLINE]
15: J Autism Dev Disord. 1984 Jun;14(2):183-9.
Autism and congenital cytomegalovirus.
Stubbs EG, Ash E, Williams CP.
Two cases of congenital cytomegalovirus infection associated with autism are
reported. The viral hypothesis of autism is discussed along with a brief review
of the literature. Suggestions are made for future research.
Publication Types:
Case Reports
PMID: 6086566 [PubMed - indexed for MEDLINE]
16: J Autism Dev Disord. 1983 Sep;13(3):249-53.
Autism in a child with congenital cytomegalovirus infection.
Markowitz PI.
A case is reported of early infantile autism associated with a congenital
cytomegalovirus infection. The diagnosis of autism is based on the child's
failure to develop good interpersonal relationships, poor eye contact, delayed
and deviant use of language, and her rote and nonthematic use of objects and
playthings. Resistance to change and self-stimulatory behavior were also present.
Onset was before 2 years of age. Congenital cytomegalovirus infection was
suggested by the presence of an antibody response to the virus, culture of the
virus from the urine, sensorineural hearing loss, and inflammatory damage to the
retina of the eye. Although over time improvement was noted, at last examination
at the age of 5 years her behavior is still markedly deviant. This and other
reported cases suggest that congenital viral infection may be an important cause
of infantile autism. It is hypothesized that an ability of the agent to establish
chronic infection may predispose to behavioral aberration.
Publication Types:
Case Reports
PMID: 6315673 [PubMed - indexed for MEDLINE]
17: J Autism Dev Disord. 1980 Dec;10(4):451-8.
Transfer factor immunotherapy of an autistic child with congenital
cytomegalovirus.
Stubbs EG, Budden SS, Burger DR, Vandenbark AA.
Publication Types:
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
PMID: 6100889 [PubMed - indexed for MEDLINE]
18: J Autism Child Schizophr. 1978 Mar;8(1):37-43.
Autistic symptoms in a child with congenital cytomegalovirus infection.
Stubbs EG.
A case of intrauterine cytomegalovirus infection with onset of autistic symptoms
apparently after 6 months of age is reported. Physicians who find autistic
symptoms in very young children might include cytomegalovirus in their
differential to document the presence or absence of a correlation.
Publication Types:
Case Reports
PMID: 205531 [PubMed - indexed for MEDLINE]
19: Med Hypotheses. 2008;70(5):967-74. Epub 2007 Nov 5.
The association between tick-borne infections, Lyme borreliosis and autism
spectrum disorders.
Bransfield RC, Wulfman JS, Harvey WT, Usman AI.
Department of Psychiatry, Riverview Medical Center, 225 State Route 35, Red Bank,
NJ, United States.
Chronic infectious diseases, including tick-borne infections such as Borrelia
burgdorferi may have direct effects, promote other infections and create a
weakened, sensitized and immunologically vulnerable state during fetal
development and infancy leading to increased vulnerability for developing autism
spectrum disorders. A dysfunctional synergism with other predisposing and
contributing factors may contribute to autism spectrum disorders by provoking
innate and adaptive immune reactions to cause and perpetuate effects in
susceptible individuals that result in inflammation, molecular mimicry,
kynurenine pathway changes, increased quinolinic acid and decreased serotonin,
oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the
development of the amygdala and other neural structures and neural networks
resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in
autism spectrum disorders and/or exacerbating autism spectrum disorders from
other causes throughout life. Support for this hypothesis includes multiple cases
of mothers with Lyme disease and children with autism spectrum disorders; fetal
neurological abnormalities associated with tick-borne diseases; similarities
between tick-borne diseases and autism spectrum disorder regarding symptoms,
pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging
data; positive reactivity in several studies with autistic spectrum disorder
patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma;
similar geographic distribution and improvement in autistic symptoms from
antibiotic treatment. It is imperative to research these and all possible causes
of autism spectrum disorders in order to prevent every preventable case and treat
every treatable case until this disease has been eliminated from humanity.
PMID: 17980971 [PubMed - in process]
20: J Neuroimmunol. 2002 Aug;129(1-2):168-77.
Erratum in:
J Neuroimmunol 2002 Sep;130(1-2):248.
Antibodies to neuron-specific antigens in children with autism: possible
cross-reaction with encephalitogenic proteins from milk, Chlamydia pneumoniae and
Streptococcus group A.
Vojdani A, Campbell AW, Anyanwu E, Kashanian A, Bock K, Vojdani E.
Section of Neuroimmunology, Immunosciences Laboratory, Inc., 8693 Wilshire
Boulevard, Suite 200, Beverly Hills, CA 90211, USA. immunsci@ix.netcom.com
We measured autoantibodies against nine different neuron-specific antigens and
three cross-reactive peptides in the sera of autistic subjects and healthy
controls by means of enzyme-linked immunosorbent assay (ELISA) testing. The
antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG),
ganglioside (GM1), sulfatide (SULF), chondroitin sulfate (CONSO4), myelin
oligodendrocyte glycoprotein (MOG), alpha,beta-crystallin (alpha,beta-CRYS),
neurofilament proteins (NAFP), tubulin and three cross-reactive peptides,
Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin
(BTN). Autistic children showed the highest levels of IgG, IgM and IgA antibodies
against all neurologic antigens as well as the three cross-reactive peptides.
These antibodies are specific because immune absorption demonstrated that only
neuron-specific antigens or their cross-reactive epitopes could significantly
reduce antibody levels. These antibodies may have been synthesized as a result of
an alteration in the blood-brain barrier. This barrier promotes access of
preexisting T-cells and central nervous system antigens to immunocompetent cells,
which may start a vicious cycle. These results suggest a mechanism by which
bacterial infections and milk antigens may modulate autoimmune responses in
autism.
PMID: 12161033 [PubMed - indexed for MEDLINE]
21: Behav Brain Res. 2007 Jan 10;176(1):141-8. Epub 2006 Jul 21.
Abnormal social behaviors in young and adult rats neonatally infected with Borna
disease virus.
Lancaster K, Dietz DM, Moran TH, Pletnikov MV.
Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns
Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Autism spectrum disorders (ASD) have been the focus of a great deal of research
and clinical speculation. This intense interest relates to both the perplexing
pathogenesis and devastating consequences of these disorders. One of the
obstacles to understanding the pathogenesis of autism and to developing efficient
treatment has been the paucity of animal models that could be used for
hypotheses-driven mechanistic studies of abnormal brain and behavior development
and for the pre-clinical testing novel pharmacological treatments. In this
report, we briefly review our animal model of ASD based on neonatal Borna disease
virus (BDV) infection and present new data about abnormal social interaction in
adult BDV-infected rats. We found that neonatal BDV infection profoundly affected
social behaviors in adult rats. Compared to the control rats, both 90- and
180-day-old infected rats spent less time in active social interaction and more
time in following their partners. In the intruder-resident test, the BDV-infected
resident rats exhibited less aggression towards the intruders and showed more the
following-the-intruder behavior. The following-the-partner behavior may be an
example of "stereotypic" activity due to BDV-induced abnormal social
communication between rats. The previously published results and present findings
indicate that neonatal BDV infection significantly altered the normal pattern of
social interaction in rats. Co-localization of activated microglia and dying
Purkinje cells in BDV-infected rats suggests that the BDV model could be used to
study a pathogenic link of Purkinje cell dropout and neuroinflammation to
abnormal social behaviors.
PMID: 16860408 [PubMed - indexed for MEDLINE]
22: Front Biosci. 2002 Mar 1;7:d593-607.
Borna disease virus infection of the neonatal rat: developmental brain injury
model of autism spectrum disorders.
Pletnikov MV, Moran TH, Carbone KM.
Department of Psychiatry, The Johns Hopkins University School of Medicine, Ross
618, 720 Rutland Avenue, Baltimore, MD 21205, USA.
pletnikov@cbs5055530.cber.FDA.gov
Autism spectrum disorders (ASD) have been the focus of a great deal of research
and clinical speculation. This intense interest relates to both the perplexing
pathogenesis and devastating consequences of these disorders. One of the
obstacles to understanding the pathogenesis of autism and its efficient treatment
has been the paucity of animal models that could be used for hypotheses-driven
mechanistic studies of abnormal brain and behavior development and for the
pre-clinical testing novel pharmacological treatments. The present review
provides a detailed analysis of a new animal model of ASD. This model utilizes
neonatal Borna disease virus (BDV) infection of the rat brain as a unique
experimental teratogen to study the pathogenesis of neurodevelopmental damage.
For more than a decade, studies of the BDV animal model have yielded much insight
into the pathogenic processes of abnormal brain development and resulting
autistic-like behavioral abnormalities in rats. The most recent experiments
demonstrate the utility of the BDV model for studying the pathophysiological
mechanisms of the gene-environment interaction that determines differential
disease outcomes and variability in responses to treatments.
Publication Types:
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 11861216 [PubMed - indexed for MEDLINE]
23: Ann N Y Acad Sci. 2001 Jun;939:318-9.
Rat model of autism spectrum disorders. Genetic background effects on Borna
disease virus-induced developmental brain damage.
Pletnikov MV, Jones ML, Rubin SA, Moran TH, Carbone KM.
Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore,
Maryland, USA.
PMID: 11462786 [PubMed - indexed for MEDLINE]
24: Curr Top Microbiol Immunol. 2001;253:157-77.
Borna disease virus infection of adult and neonatal rats: models for
neuropsychiatric disease.
Hornig M, Solbrig M, Horscroft N, Weissenböck H, Lipkin WI.
Laboratory for the Study of Emerging Diseases, 3101 Gillespie Neuroscience
Research Facility, University of California, Irvine, CA 92697-4292, USA.
Animal models provide unique opportunities to explore interactions between host
and environment. Two models have been established based on Borna disease virus
infection that provide new insights into mechanisms by which neurotropic agents
and/or immune factors may impact developing or mature CNS circuitry to effect
complex disturbances in movement and behavior. Note in press: Since this chapter
was submitted, several manuscripts have been published that extend findings
reported here and support the relevance of BDV infections of neonatal Lewis rats
as models for investigating mechanisms of neurodevelopmental damage in autism.
Behavioral abnormalities, including disturbed play behavior and chronic emotional
overactivity, have been described by Pletnikov et al. (1999); inhibition of
responses to novel stimuli were described by Hornig et al. (1999); loss of
Purkinje cells following neonatal BDV infection has been demonstrated by Eisenman
et al. (1999), Hornig et al. (1999), and Weissenböck et al. (2000); and
alterations in cytokine gene expression have been reported by Hornig et al.
(1999), Plata-Salaman et al. (1999) and Sauder et al. (1999).
PMID: 11417134 [PubMed - indexed for MEDLINE]
25: J Autism Dev Disord. 2006 Nov;36(8):1039-51.
Etiologies of autism in a case-series from Tanzania.
Mankoski RE, Collins M, Ndosi NK, Mgalla EH, Sarwatt VV, Folstein SE.
Tufts University School of Medicine and Sackler School of Graduate Biomedical
Sciences, Boston, MA, USA.
Most autism has a genetic cause although post-encephalitis cases are reported. In
a case-series (N = 20) from Tanzania, 14 met research criteria for autism. Three
(M:F = 1:2) had normal development to age 22, 35, and 42 months, with onset of
autism upon recovery from severe malaria, attended by prolonged high fever,
convulsions, and in one case prolonged loss of consciousness. In four other cases
(M:F = 3:1), the temporal relationship between onset of autism and severe
infection was close, but possibly spurious since malaria is common in Tanzania
and there were indications of abnormal development in the child or a family
member. In seven cases, (M:F = 6:1) autism onset was unrelated to malaria. The
excess of non-verbal cases (N = 10) is related local diagnostic practice.
Publication Types:
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
PMID: 16897390 [PubMed - indexed for MEDLINE]
26: Lakartidningen. 1992 Jan 29;89(5):279-80.
[Information-based adjustment of sex education clinics for adolescents]
[Article in Swedish]
Ruusuvaara L.
Ungdomshälsan, kvinnokliniken, Akademiska sjukhuset, Uppsala.
PMID: 1738248 [PubMed - indexed for MEDLINE]
27: J Autism Child Schizophr. 1977 Mar;7(1):49-55.
Depressed lymphocyte responsiveness in autistic children.
Stubbs EG, Crawford ML.
Although there are associations linking autism with prenatal rubella,
cytomegalovirus, syphilis, and varicella, the etiology of the autistic state
remains obscure. Host defense against the etiologic agents postulated to be
responsible for the autism-associated syndromes is believed to be primarily of
the cell-mediated type. In this preliminary study, cellular immune function was
assessed in vitro by phytohemagglutinin (PHA) stimulation of lymphocyte cultures.
Twelve autistic children and 13 control subjects were compared. The autistic
group exhibited a depressed lymphocyte transformation response to PHA when
compared to the control subjects (p less than .01).
Publication Types:
Comparative Study
In Vitro
Research Support, U.S. Gov't, Non-P.H.S.
PMID: 139400 [PubMed - indexed for MEDLINE]
28: Curr Psychiatr Ther. 1982;21:225-39.
Psychiatric aspects of infectious diseases.
Schwab JJ.
Publication Types:
Case Reports
Review
PMID: 6761074 [PubMed - indexed for MEDLINE]
29: Med Hypotheses. 1984 Apr;13(4):399-405.
Reptilian behavioural patterns in childhood autism.
Thong YH.
Childhood autism may be caused by damage to three phylogenetically distinct
regions of the brain, or their major pathways and connections. Injury to the
neocortex results in loss of language and cognitive function, while injury to the
limbic cortex results in autistic withdrawal and abolition of play behaviour.
Injury to the more primitive striatal complex, mammalian counterpart of the brain
of reptiles, results in a bizarre and truncated form of stereotyped and
ritualistic behaviour. The causes of brain injury in childhood autism could be
those common in the perinatal period including cerebral anoxia, haemorrhage,
phenylketonuria, neurolipidoses , meningitis, toxoplasmosis, and congenital
rubella. All these conditions have previously been shown to be associated with
childhood autism.
PMID: 6727722 [PubMed - indexed for MEDLINE]
30: Curr Neurovasc Res. 2006 May;3(2):149-57.
Autoantibodies associated with psychiatric disorders.
Margutti P, Delunardo F, Ortona E.
Dipartimento di Malattie Infettive, Parassitarie e Immunomediate, Istituto
Superiore di Sanità, Rome, Italy. ortona@iss.it.
Growing evidence suggests that autoantibodies to neuronal or endothelial targets
in psychiatric disorders exist and may be pathogenic. This review describes and
discusses the possible role of autoantibodies related to the psychiatric
manifestations in autoimmune diseases, autoantibodies related to the psychiatric
disorders present in post-streptococcal diseases, celiac disease, chronic fatigue
syndrome and substance abuse, and autoantibodies related to schizophrenia and
autism, disorders now considered of autoimmune origin.
Publication Types:
Review
PMID: 16719797 [PubMed - indexed for MEDLINE]
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