Re: Inappropriate laughing/giggling... Yeast or PSEUDOBULBAR AFFECT?

[Guest guest]

WOW...this really caught my attention as my daughter has these same

episodes; however, she has had 2 MRI's in her lifetime and the results were

always negative for lesions. Can this also be a sign of bi-polar?

Tanks,

Inappropriate laughing/giggling... Yeast or PSEUDOBULBAR

AFFECT?

> I found this very, very intriguing so I wanted to post it here to

> see what you all think. A parent that I correspond with on the

> ChildrenwithAutism Group posted something very interesting. She

> said she was talking on the phone with a friend who has MS when her

> autistic child entered the room giggling hysterically. She said to

> her friend, " Can you hear him? " She told her friend with MS that her

> son can go from crying to laughing hysterically for no apparent

> reason. Her friend explained to her that there is a symptom of MS

> called Pseudobulbar that is very dimilar to the behavior exhibited

> by her son. This mother looked up Psuedobulbar and found the

> following:

>

> Affective Release, also called Pseudo-bulbar Affect; a condition in

> which episodes of laughing and/or crying occur with no apparent

> precipitating event. The person's actual mood may be unrelated to

> the emotion being expressed. This condition is thought to be caused

> by lessions in the limbic system, a group of brain structures

> involved in *emotional feeling or expression*.

>

> What do you guys think of this? I really think this is plausable,

> so much so that I asked the Mom if I could spread her story to this

> and other groups to see what everyone thought? It really caught my

> eye b/c I had just read an abstract stating that the Hep. B and

> Influenza vaccines have been implicated as possible triggers for MS

> (a crippling disease in which the body attacks the conductive

> coating of nerve cells in the brain). I've read several posts from

> parents whose children have delayed myelin, so there seem to be

> similarities between Autism and Multiple Sclerosis.

>

>

>

>

>

>

>

>

[Guest guest]

I don't know, but I was wondering if mercury deposits in or near the area of

the brain where the limbic system is located could have the same effect as a

lesion? I'm not a scientist or a doctor, so I don't know if mercury is

selective as to where in the brain it deposits or if mercury is detectable

in an MRI? or other type of brain scan? I just thought for those parents who

have attacked yeast and addressed phenols and still see this behavior, this

might be a legitimate hypothesis why...?

Inappropriate laughing/giggling... Yeast or

PSEUDOBULBAR

> AFFECT?

>

>

> > I found this very, very intriguing so I wanted to post it here to

> > see what you all think. A parent that I correspond with on the

> > ChildrenwithAutism Group posted something very interesting. She

> > said she was talking on the phone with a friend who has MS when her

> > autistic child entered the room giggling hysterically. She said to

> > her friend, " Can you hear him? " She told her friend with MS that her

> > son can go from crying to laughing hysterically for no apparent

> > reason. Her friend explained to her that there is a symptom of MS

> > called Pseudobulbar that is very dimilar to the behavior exhibited

> > by her son. This mother looked up Psuedobulbar and found the

> > following:

> >

> > Affective Release, also called Pseudo-bulbar Affect; a condition in

> > which episodes of laughing and/or crying occur with no apparent

> > precipitating event. The person's actual mood may be unrelated to

> > the emotion being expressed. This condition is thought to be caused

> > by lessions in the limbic system, a group of brain structures

> > involved in *emotional feeling or expression*.

> >

> > What do you guys think of this? I really think this is plausable,

> > so much so that I asked the Mom if I could spread her story to this

> > and other groups to see what everyone thought? It really caught my

> > eye b/c I had just read an abstract stating that the Hep. B and

> > Influenza vaccines have been implicated as possible triggers for MS

> > (a crippling disease in which the body attacks the conductive

> > coating of nerve cells in the brain). I've read several posts from

> > parents whose children have delayed myelin, so there seem to be

> > similarities between Autism and Multiple Sclerosis.

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

> I found this very, very intriguing so I wanted to post it here to

> see what you all think. A parent that I correspond with on the

> ChildrenwithAutism Group posted something very interesting. She

> said she was talking on the phone with a friend who has MS when

her

> autistic child entered the room giggling hysterically. She said to

> her friend, " Can you hear him? " She told her friend with MS that

her

> son can go from crying to laughing hysterically for no apparent

> reason. Her friend explained to her that there is a symptom of MS

> called Pseudobulbar that is very dimilar to the behavior exhibited

> by her son.

Hi,

I haven't seen research on autism that shows the type of damage

found in MS, but immune activation can change how the brain

functions. Below are some of the things I've found that overlap

between the two. Susceptability genes like HLA-DR4, and antibodies

against the milk protein butyrophylin,Chlamydia, HHV-6 & measles.

My son developed OCD in addition to the ASD symptoms. Whenever he

had a flair there was a range of emotions (anger, fear, tears, etc.)

due to basal ganglia dysfunction.

Mult Scler. 2002 Aug;8(4):278-83. Related Articles, Links

Autoreactivity to myelin antigens related to HLA associations with

multiple sclerosis.

Yentur SP, Akman-Demir G, Eraksoy M, Saruhan-Direskeneli G.

Department of Immunology, Istanbul University DETAE, Capa-Istanbul,

Turkey.

Multiple sclerosis (MS) is considered as an immune process

influenced by genetic and environmental factors. HLA-DR2 and -DR4

have been documented to be associated with MS. The HLA-dependent

differences of immune response to myelin and other antigens might

point out some relevant mechanisms in MS development The responses

to myelin antigens and to PPD have been compared in 21 MS patients

and 25 healthy controls (HCs) by primary proliferation and by short-

term T-cell lines. There was a significantly higher response to MBP

in DR2+ HCs compared to MS patients (SI: 5.9 versus 1.5, p = 0.02).

In short-term T-cell lines, we observed a higher response to PLP30-

49 in both DR4+ HCs and MS patients This response was significantly

more frequent in DR4+ MS patients (34.6%) than both DR2+ MS patients

(0%, p = 0.0001) and DR4+ HCs (7.7%, p = 0.001). The comparison

between DR2+ and DR4+ MS patients has revealed that the response to

MBP was also increased in DR4+ (p = 0.02). Among DR4+ groups, an

increased PPD response was detected in HCs compared to MS (65.2%

versus 33.3%, p = 0.01). These results may indicate that HLA-related

differences to specific and recall antigens are detectable in MS and

these differences may have implications in the disease pathogenesis.

PMID: 12166496 [PubMed - indexed for MEDLINE]

4: Forsthuber TG, Shive CL, Wienhold W, de Graaf K, Spack EG,

Sublett R, Melms A, Kort J, Racke MK, Weissert R. Related Articles,

Links

T cell epitopes of human myelin oligodendrocyte glycoprotein

identified in HLA-DR4 (DRB1*0401) transgenic mice are

encephalitogenic and are presented by human B cells.

J Immunol. 2001 Dec 15;167(12):7119-25.

PMID: 11739534 [PubMed - indexed for MEDLINE]

AR, Maciulis A, Stubbs EG, Cutler A, Odell D. Related

Articles, Links

The transmission disequilibrium test suggests that HLA-DR4 and DR13

are linked to autism spectrum disorder.

Hum Immunol. 2002 Apr;63(4):311-6.

PMID: 12039413 [PubMed - indexed for MEDLINE]

Mol Chem Neuropathol. 1996 May-Aug;28(1-3):77-81. Related Articles,

Links

Immunogenetic studies in autism and related disorders.

Warren RP, Singh VK, Averett RE, Odell JD, Maciulis A, Burger RA,

s WW, Warren WL.

Utah State University, Logan 84322, USA.

The major histocompatibility complex comprises a number of genes

that control the function and regulation of the immune system. One

of these genes, the C4B gene, encodes a product that is involved in

eliminating pathogens such as viruses and bacteria from the body. We

previously reported that a deficient form of the C4B gene, termed

the C4B null allele (no C4B protein produced) had an increased

frequently in autism. In this study we attempted to confirm the

increased incidence of the C4B null allele in autism and

investigated the presence of a C4B null allele in two other

childhood disorders, attention-deficit hyperactivity disorder and

dyslexia (reading disability). In addition, we explored the

relationship of autism to the DR beta 1 gene, a gene located close

to the C4B in autism. We confirmed the finding of an increased

frequency of the C4B null allele in autism and found that the

related disorders also had an increased frequency of this null

allele. In addition, two alleles of the DR beta 1 gene also had

significantly increased representation in the autistic subjects.

Publication Types:

Review

Review, Tutorial

PMID: 8871944 [PubMed - indexed for MEDLINE]

-------------------------------------------------------------------

J Neuroimmunol. 2003 Feb;135(1-2):117-25. Related Articles, Links

Anti-myelin oligodendrocyte glycoprotein B-cell responses in

multiple sclerosis.

Kennel De March A, De Bouwerie M, Kolopp-Sarda MN, Faure GC, Bene

MC, Bernard CC.

Laboratoire d'Immunologie du CHU, Faculte de Medecine, BP 184, 54500

Vandoeuvre les, 54000, , France.

Humoral auto-immunity to the myelin oligodendrocyte glycoprotein

(MOG) is likely involved in the pathogenesis of multiple sclerosis

(MS). In 44 MS patients and 30 controls, Ig-producing B cells were

identified by their isotype and as MOG-specific spot-forming cells

(SFC). Peripheral anti-MOG antibodies were assayed in ELISA as well

as anti-butyrophilin antibodies to investigate for molecular

mimicry. MS patients had significantly higher levels of IgA- and MOG-

SFC than controls, as well as significantly higher antibody

responses to MOG and butyrophilin. These data provide added support

for the implication of anti-MOG humoral immunity in the

pathophysiology of MS, and suggest a balance of systemic (anti-self)

and mucosal (environment-modulated) immune reactions in an attempt

at regulating the pathogenic specific immune response.

PMID: 12576231 [PubMed - indexed for MEDLINE]

Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9446-51. Epub 2003 Jul

21. Related Articles, Links

Structural insights into the antigenicity of myelin oligodendrocyte

glycoprotein.

Breithaupt C, Schubart A, Zander H, Skerra A, Huber R, Linington C,

U.

Abteilung Strukturforschung, Max-Planck-Institut fur Biochemie, Am

Klopferspitz 18a, 82152 sried, Germany. breitha@...

Multiple sclerosis is a chronic disease of the central nervous

system (CNS) characterized by inflammation, demyelination, and

axonal loss. The immunopathogenesis of demyelination in multiple

sclerosis involves an autoantibody response to myelin

oligodendrocyte glycoprotein (MOG), a type I transmembrane protein

located at the surface of CNS myelin. Here we present the crystal

structures of the extracellular domain of MOG (MOGIgd) at 1.45-A

resolution and the complex of MOGIgd with the antigen-binding

fragment (Fab) of the MOG-specific demyelinating monoclonal antibody

8-18C5 at 3.0-A resolution. MOGIgd adopts an IgV like fold with the

A'GFCC'C " sheet harboring a cavity similar to the one used by the

costimulatory molecule B7-2 to bind its ligand CTLA4. The antibody 8-

18C5 binds to three loops located at the membrane-distal side of MOG

with a surprisingly dominant contribution made by MOG residues 101-

108 containing a strained loop that forms the upper edge of the

putative ligand binding site. The sequence R101DHSYQEE108 is unique

for MOG, whereas large parts of the remaining sequence are conserved

in potentially tolerogenic MOG homologues expressed outside the

immuno-privileged environment of the CNS. Strikingly, the only

sequence identical to DHSYQEE was found in a Chlamydia trachomatis

protein of unknown function, raising the possibility that Chlamydia

infections may play a role in the MOG-specific autoimmune response

in man. Our data provide the structural basis for the development of

diagnostic and therapeutic strategies targeting the pathogenic

autoantibody response to MOG.

PMID: 12874380 [PubMed - in process]

J Neuroimmunol. 2002 Aug;129(1-2):168-77. Related Articles, Links

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, 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@...

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]

Ann Neurol. 2003 Feb;53(2):189-97. Related Articles, Links

Cross-reactivity with myelin basic protein and human herpesvirus-6

in multiple sclerosis.

Tejada-Simon MV, Zang YC, Hong J, VM, Zhang JZ.

Multiple Sclerosis Research Unit, Department of Neurology and Baylor

Multiple Sclerosis Center, Baylor College of Medicine, Houston, TX

77030, USA.

Viral infections are though to play an important role in the

pathogenesis of multiple sclerosis (MS) potentially through

molecular mimicry. An identical sequence was found in both myelin

basic protein (MBP, residues 96-102), a candidate autoantigen for

MS, and human herpesvirus-6 (HHV-6 U24, residues 4-10) that is a

suspected viral agent associated with MS. In this study, we showed

that greater than 50% of T cells recognizing MBP(93-105) cross-

reacted with and could be activated by a synthetic peptide

corresponding to residues 1 to 13 of HHV-6 U24 in MS patients. The

estimated precursor frequency of these cross-reactive T cells

recognizing both peptides, MBP(93-105) and HHV-6 (U24)(1-13), was

significantly elevated in MS patients compared with that in healthy

controls. These cross-reactive CD4+ T cells represented the same Th1

phenotype as that of monospecific T cells recognizing MBP(93-105).

There were increased antibody titers for both peptide HHV-6 (U24)(1-

13) and peptide MBP(93-105) in the same patients with MS compared

with those in healthy controls, suggesting B-cell sensitization to

the antigens in MS patients. The study provides important evidence

in the understanding of the potential role of HHV-6

infection/reactivation in the activation of autoimmune reactivity to

MBP and its implication in the pathogenesis of MS.

PMID: 12557285 [PubMed - indexed for MEDLINE]

Clin Immunol Immunopathol. 1998 Oct;89(1):105-8. Related Articles,

Links

Serological association of measles virus and human herpesvirus-6

with brain autoantibodies in autism.

Singh VK, Lin SX, Yang VC.

College of Pharmacy, University of Michigan, Ann Arbor, Michigan,

48109-1065, USA.

Considering an autoimmunity and autism connection, brain

autoantibodies to myelin basic protein (anti-MBP) and neuron-axon

filament protein (anti-NAFP) have been found in autistic children.

In this current study, we examined associations between virus

serology and autoantibody by simultaneous analysis of measles virus

antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG),

anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG

titers were moderately higher in autistic children but they did not

significantly differ from normal controls. Moreover, we found that a

vast majority of virus serology-positive autistic sera was also

positive for brain autoantibody: (i) 90% of measles-IgG-positive

autistic sera was also positive for anti-MBP; (ii) 73% of measles-

IgG-positive autistic sera was also positive for anti-NAFP; (iii)

84% of HHV-6-IgG-positive autistic sera was also positive for anti-

MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also

positive for anti-NAFP. This study is the first to report an

association between virus serology and brain autoantibody in autism;

it supports the hypothesis that a virus-induced autoimmune response

may play a causal role in autism. Copyright 1998 Academic Press.

PMID: 9756729 [PubMed - indexed for MEDLINE]