Dr. Peter Harvey: In Memoriam
Katie Weisman of Coalition for SafeMinds Informs IACC of Mercury Dangers in Public Comments

Anti-NMDA-Receptor Encephalitis Added to DSM A Medical Causation of Autism

Broken headBy Teresa Conrick

It was last year that I reported on Anti-NMDA-Receptor Encephalitis and a connection to Autism.  My daughter had some prominent symptoms and I was looking into the dynamics of this increasing medical condition.  Meg tested negative and subsequent  labs showed that  her positive antinuclear antibodies [autoimmunity] to be associated with Gad65 [ glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2.]   It is no coincidence that Megan's symptoms seemed to mirror some of those in Anti-NMDA-Receptor Encephalitis as the two, GAD65 and N-methyl-D-aspartate receptor, are connected

Below is a study now showing that Anti-NMDA-Receptor Encephalitis has been added into the current Diagnostic and Statistical Manual of Mental Disorders as a true, medical causation to an Autism diagnosis.  In other words, an antibody causing autoimmunity can cause regression of behaviors and skills, and then appear to present as a primary psychiatric disorder .  Immediate and proper medical care must be given to prevent further damage and permanent disability  -- "Patients with early immunotherapy performed significantly better. The most severe deficits were observed with inefficient or delayed initial treatment. " --

Researchers must not be afraid to admit that vaccinations can cause this increasing and horrific medical phenomenon:

Anti-NMDA receptor encephalitis after TdaP-IPV booster vaccination: cause or coincidence?

Researchers must not deny its connection to other childhood immune disorders with cute names:

"In about 50% of the patients Mycoplasma pneumonia serum IgM is positive. Although the significance of this is unknown, infections may trigger an autoimmune encephalitic process akin to PANDAS (pediatric autoimmune neuropsychiatric illness associated with streptococcal infections) mediated by antistreptococcal-antineuronal antibodies."

Researchers must not avoid the Anti-N-methyl-D-aspartate receptor encephalitis connection to research involved in Autism and autoimmunity:

"NR1 and NR2b glutamate receptor immunoreactivity patterns are abnormal in the hippocampi of thimerosal treated SJL mice."

Tijdschr Psychiaty 2012;54(5):475-9.

[Anti-NMDA-receptor encephalitis: a new axis-III disorder in the differential diagnosis of childhood disintegrative disorder, early onset schizophrenia and late onset autism].

[Article in Dutch]


Psychiatrie & Psychologie, Masstricht.


Childhood disintegrative disorder (CDD), early onset schizophrenia (EOS), and late onset autism (LOA) often follow a similar course: initially, development is normal, then there is a sudden neuropsychiatric deterioration of social interaction and communication skills, which is combined with a decline in intelligence and reduction in daily activities. A 9-year-old boy was admitted to the paediatric ward with acute onset of secondary epileptic seizures. It was not long until the boy's symptoms resembled that of patients with cdd, eos and loa. Intensive tests led to the diagnosis of anti-NMDA-receptor encephalitis. Anti-NMDA-receptor encephalitis should be regarded as a possible organic cause underlying the syndromal presentation of CDD, EOS and LOA.

Teresa Conrick is Contributing Editor for Age of Autism.



Teresa and Benedetta, I've been asking for 15 years why babies who are exclusively breastfed --NO bottles-- have such a drastically reduced risk of autism, and why, when they do have autism, it is nearly always less severe.


Sorry I meant IgGs when I said IVIGs
pasterized Colostrum does damage some of the IgGs.


I am sorry and don't mean to keep on.
But I find myself looking at - like many others - vet medicine.

What happens if you feed newborn calves (dairy are taken from thier mothers) pasterized colostrum - full of IVIGs
Does it matter.
The answer is yes. So they have a problem of giving the new born calves some disease from other mother cows or not giving enough colostrum. Believe me - 30 years of being around them - that is a death sentence for sure in about 3 months or so.

The answer was to give more-- of the pasterized colostrum - like a whole 4 quarts of the pasterized colostrum in the first couple of hours - and then another quart within six hours of birth.

what happnes to calves health if they are given prolonged meals of colostrum.

The answer (well they decided to test to see how well each group of calves was breaking down sugars) Considering Tereasa's last article - maybe they know a lot more than we think!!!

But the calves that had prolonged meals of Colostrum did much better at breaking down sugars than the other two groups of calves - one group received no colostrum at all the other group - what a typical newborn calf would receive - colostrum in the first six hours of life.

Soooo, now - what is in that camel milk?
Too high, couldn't afford it.
What about that powdered colostrum they have down at the feed store? Not for humans but it is pasterized- but still not for human comsumption.

Well what about the ketogenic diet or the Atkins diet that is being so successful in treating epilepsy - it has a lot of cream in it.
What about powdered Whey?
But then we have some kids that are allergric to milk???
I pray each night for each day to give us answers.


anti-NMDA antibodies are seen in lupus patients with neurological symptoms as well.

Ann Rheum Dis. 2005 Aug;64(8):1210-3. Epub 2005 Feb 11.
Autoantibodies to a NR2A peptide of the glutamate/NMDA receptor in sera of patients with systemic lupus erythematosus.
Husebye ES, Sthoeger ZM, Dayan M, Zinger H, Elbirt D, Levite M, Mozes E.
Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.


{oral immunoglobin}; is for celiacs disease, and Irritable bowel syndrome and for new born babies of low birth rate and it is suppoe to stop the destructive inflammation of the intestine -necrotizing enterocolitis.

{Intervenous immunoglobin}

bone marrow transplant
Chronic lymphocytic leukemia
Common variable immunodeficiency (CVID) a group of approximately 150 primary immunodeficiencies (PIDs), which have a common set of features (including hypogammaglobulinemia) but which have different underlying causes
Idiopathic thrombocytopenic purpura
Pediatric HIV
Primary immunodeficiencies
Kawasaki disease
Chronic inflammatory demyelinating polyneuropathy (CIDP). Only the "Gamunex" brand manufactured by Talecris is approved for CIDP (in 2008), under the U.S. Orphan Drug law provisions
Kidney transplant with a high antibody recipient or with an ABO incompatible donor
[testing in the US (as of December 2008)Alzheimer's Disease
Early experimental results in 2012 from a small clinical trial in humans have shown hints that it may protect against the progression of Alzheimer's Disease.

According to experts at the Alzheimer's Association International Conference 2012 in Vancouver, the immune therapy called IVIG/Gammagard is first long-term treatment shown to halt the progression of Alzheimer's disease

More off label uses are:
Capillary leak syndrome
Chronic fatigue syndrome
Clostridium difficile colitis
Dermatomyositis and polymyositis
Graves' ophthalmopathy
Guillain-Barré syndrome
Muscular Dystrophy
Inclusion body myositis
Lambert-Eaton syndrome
Lupus erythematosus
Multifocal motor neuropathy
Multiple sclerosis
Myasthenia gravis
Neonatal alloimmune thrombocytopenia
Parvovirus B19
Post-transfusion purpura
Renal transplant rejection
Spontaneous Abortion/Miscarriage
Sjogren's Syndrome
Stiff person syndrome
Opsoclonus Myoclonus
Severe sepsis and septic shock in critically ill adults[12]
Toxic epidermal necrolysis
In chronic lymphocytic leukemia and multiple myeloma, as well as various rare deficiencies of immunoglobulin synthesis (e.g. X-linked agammaglobulinemia, hypogammaglobulinemia), IVIG is administered to maintain adequate immunoglobulin levels to prevent infections.
[edit] Complications and side effectsAlthough routine use of IVIG is common practice, sometimes for long term treatments, and is considered safe, complications of IVIG therapy are known and include:

dermatitis - usually peeling of the skin of the palms and soles.
infection (such as HIV or viral hepatitis) by contaminated blood product; there is also an as of yet unknown risk of contracting variant CJD (vCJD) however the process whereby the product is extracted shows that the contaminants are usually not present in the product.
pulmonary edema from fluid overload, due to the high colloid oncotic pressure of IVIG
allergic/anaphylactic reactions; for example, anaphylactic shock, especially in IgA deficient patients, who by definition can still produce IgG antibodies (IgA deficient patients are more likely to produce IgG against the IVIG administration than normal patients).
damage such as hepatitis caused directly by antibodies contained in the pooled IVIG.
acute renal failure[13]
venous thrombosis
aseptic meningitis

Oh and it is only taken from 1000 blood donors not the 10,000. It is now in very short supply because of so many needing it.

Carolyn M


There is preservative-free immunoglobulin. It is also possible to take it orally; an antacid has to be taken 1.5 hours before the gamma globulin. The person taking it would also have to refrain from eating for 1 - 1.5 hours afterward as well.

Also, please note that if an antacid is taken regularly over a long period of time, there is a possibility of xenobiotic overgrowth.

Teresa Conrick

Hi Lisa B

There are labs that do this. This is the one I am familiar with -

NMDA Receptor (NR1) Antibody Test

Best ...

Lisa B

Is there a general or basic way to test for this?


Seems promising !!!


I hope my post goes through.
But I wanted to add.
That I am so sorry that you have suffered so.
I hope your shingles are at least under control.

I alos read that the hypothalmus is suppose to regulate the pitiutary into making IgGs and like a horomone the IgGs are then suppose to control the amount of T cells produced in the thylmus.

Did this happen before you had your kids?


Do you know why they gave it to you?
Imunoglobin is not a vaccine?

And to come to think of it it is not a shot though - it is given as and IV and takes a long time--- like a whole day to be given.

It has been standard treatment for the last decade for Kawasakis.

Also my sister-in-law after getting pneumonia again and again - her immune system is terrible -Was hooked up to an IV and they gave it to her once a month. She would take a blanket and a book - but she was too tired and always fell asleep - they also had televsions for her to watch.

IT is taken from 10,000 blood donors and spun down or what ever - It is IgGs.

There is a good possiblity that the patient will get meningitis from it - it is not viral or bacteria - just an immune reaction and if that happens there is nothing they can do but wait it out.

There can also be other severe reactions to it. The thought is - if the patient has gone into a later phase (this may not be right) but their body has a lot of IgMs - then it is more of a chance to have a reaction to the IVIGs.

Wether they put mercury or alumiunium or sorbate or MSGs - or dye -- baking soda in it - - I would like to know for sure maybe we can track it down somewhere and find out.

But it does work - most of the time if they use it in time for Kawasakis. And it worked for my sister-in-law - she stopped getting bacteria pneumonia and almost dying -
Of course she just got over viral pneumonia just last week.
She now has acquired mythenis gravis.

How do you acquire something like that?

The immune system is actually attacking ATP - you know AT --- and then the P as it comes off makes energy.
At least that is what they use to think.


@Benedetta: isn't immunoglobulin give as a thimerosal-preserved shot?

I was given thimerosal-preserved gamma globulin, along with MMR, thimerosal-preserved DPT, thimerosal-preserved hepB (because they were out of the recommended hepA), all for a work trip to mainland China in the late '80's.

Within a month, i started symptoms of what was later diagnosed as Hashimoto's,, I started having symptoms of gluten intolerance, and I had the worst case of shingles the doctor had ever seen (active phase lasted 6 weeks). All autoimmune stuff.


Thank you for a very interesting article. I don't fully understand all the science but I do "get" that new scientific discoveries are being ignored by those you mandate vaccines as well as pediatricians who don't bother to consider biological causes for cognitive problems. Here is a treatable condition that can improve a child's chances for a normal life that as far as I can tell is being ignored. No doubt some big pharm workshop will eventually come along and promote some quick fix drug so that doctors can say that they have a treatment. Recently with Obamacare more people are coming into the system and the outcry is that there aren't enough doctors, but if doctors don't treat illnesses I'm not sure it makes much difference whether there are more or less. And maybe less might be better; at least less can do less harm.


Holy Toledo, look what happens when people study sick kids clinically instead of with epidemiology! They suddenly get (almost) as smart as Teresa!

Teresa Conrick

Hi Benedetta- So sorry the link appears bad but here is a better one to that Hornig et al paper-


Your questions are exactly what is needed -- and we need research specific to these issues.


So, GAD enzyme is it being attacked by antibodies - do they know - anything about what kind of antibodies - T cells? This IgM -- I remember off the top of my head is that IgG is given in immunoglobin at the early stages of Kawasakis - but won't work if given later because IgG have given the job over to IgMs.
colostrum - first milk has IgGs
but later milk has IgMs.

Where is the GAD enzyme being produced at or where in the body does it all begin to be signaled for?

is it a receptor hooked on to each and every cell in the ---- Brain that the antibodies is attacking?

Sorry to be so clueless.


This link you had in your article is not working; or at least for me - it says page not found;
Researchers must not avoid the Anti-N-methyl-D-aspartate receptor encephalitis connection to research involved in Autism and autoimmunity:

My son became catitonic after his reaction to the DPT shot.


Here's one more study;


Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis.

Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R.
SourceDepartment of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. [email protected]


Since its discovery in 2007, the encephalitis associated with antibodies against the N-methyl-D-aspartate receptor (NMDAR) has entered the mainstream of neurology and other disciplines. Most patients with anti-NMDAR encephalitis develop a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration into a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability. The disorder predominantly affects children and young adults, occurs with or without tumour association, and responds to treatment but can relapse. The presence of a tumour (usually an ovarian teratoma) is dependent on age, sex, and ethnicity, being more frequent in women older than 18 years, and slightly more predominant in black women than it is in white women. Patients treated with tumour resection and immunotherapy (corticosteroids, intravenous immunoglobulin, or plasma exchange) respond faster to treatment and less frequently need second-line immunotherapy (cyclophosphamide or rituximab, or both) than do patients without a tumour who receive similar initial immunotherapy. More than 75% of all patients have substantial recovery that occurs in inverse order of symptom development and is associated with a decline of antibody titres. Patients' antibodies cause a titre-dependent, reversible decrease of synaptic NMDAR by a mechanism of crosslinking and internalisation. On the basis of models of pharmacological or genetic disruption of NMDAR, these antibody effects reveal a probable pathogenic relation between the depletion of receptors and the clinical features of anti-NMDAR encephalitis.



Thank you Theresa. This is very interesting. I wonder what percentage of our kids have this condition but were never properly screened for it. I did a search on line to find out in what kind of interventions are recommended to treat NDMA receptor encephalitis and found these two studies below. The second study says NDMA receptor encephalitis is often under-recognized.


Successful treatment of anti-N-methyl-D-aspartate receptor encephalitis presenting with catatonia.
Schimmel M, Bien CG, Vincent A, Schenk W, Penzien J.
SourceDepartment of Paediatrics, Klinikum Augsburg, Stenglinstrasse 2, Augsburg, Germany.


The case of a 12-year-old girl with the typical clinical symptoms of the recently described anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is reported. Within 6 weeks the full clinical spectrum of this condition presented with seizures, agitation, stupor, autonomic instability, dysphagia and hypoventilation leading to a diagnosis of pernicious catatonia. MRI and CSF glucose, protein and lactate were repeatedly normal. EEG revealed rhythmical slowing. No teratoma was detected. Recognition of the unique pattern of the clinical symptoms led to early consideration of this disease which was confirmed by detection of anti-NMDAR antibodies. After high dose prednisolone without clinical improvement, plasmapheresis was followed by a rapid reduction in antibodies and recovery within a few weeks. To our knowledge this is the youngest patient with anti-NMDAR encephalitis to have been described to date. We speculate that NMDAR antibodies may be directly involved in the pathogenesis of this disease.



Update on anti-N-methyl-D-aspartate receptor encephalitis in children and adolescents.

Florance-Ryan N, Dalmau J.
SourceDivision of Neurology, Department of Pediatrics, Children's Hospital of Philadelphia, and Division of Neuro-Oncology, Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.


PURPOSE OF REVIEW: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a recently identified disorder that is increasingly recognized in children and adolescents. Prompt diagnosis and treatment are important to obtain full recovery. We review here the main clinical features and differential diagnosis and provide algorithms of the clinical correlates of antibody-mediated decrease of NMDAR and a suggested treatment approach.

RECENT FINDINGS: The sharp increase of patients identified with anti-NMDAR encephalitis reveals a multistage disorder that usually presents with psychiatric manifestations progressing to a decrease of verbal output, catatonia, seizures, dyskinesias, and frequent autonomic instability and hypoventilation. In adults, the disorder often occurs in association with a tumor that expresses NMDAR (usually ovarian teratoma), but in male patients and children the presence of a tumor is rare. Given that patients' antibodies have pathogenic effects on the NMDAR, immunotherapy and tumor resection, when appropriate, are often effective. The outcome is usually good, but the recovery is slow with frequent protracted symptoms of frontal lobe dysfunction.

SUMMARY: Anti-NMDAR encephalitis is a severe but treatable disorder that frequently affects children and adolescents and is likely under-recognized. The syndrome is highly predictable, recognizable on clinical grounds and can be confirmed with the demonstration of NMDAR antibodies.



That is quite an admission. Hopefully it translates to better understanding of vaccine side effects, better treatment for children and more justice in vaccine court!

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