AGE OF AUTISM

Conversion Disorder in Leroy NY?

By Teresa Conrick

I have been following all of the news and reports on the teens and now two adults who have developed sudden onset tics and Tourette-like symptoms in upper NY.  It is an unanswered medical phenomenon still and one that is devastating.  One thing that seems certain -- the issue of Conversion Disorder vs Immune Disorder needs a further analysis.  A report titled, "Investigation of Neurologic Symptoms among Le Roy Jr/Sr High School Students, October 2011 – January 2012"  has been made available for viewing and some interesting pieces of information seem worthy of our attention:

All cases were female. Three of the 12 cases were identified as having pre-existing medical conditions associated with tic disorders. Two of the three cases, who were tic free for a period of time, experienced an exacerbation of tic symptoms during this time period. The third case was identified as having a previous diagnosis of Tourette’s disorder and did not have a new onset of tic symptoms, but rather an acceleration of on-going tics during this time period. Onsets of tic symptoms ranged from May 2011 to December 2011 for the nine new onsets.

My good and learned friends here at Age of Autism, Mark Blaxill and Dan Olmsted, have been writing about LeRoy and some of the intriguing (AofA Tics and Toxins A History of Building Woes) and significant environmental factors that may be at play. (AofA Tics and Toxins Playing Fields on FEMA Flood Hazard)  Kevin Barry, an avid Age of Autism reader and researcher,  also included some historical, pertinent pieces as to what could be making some of the teens so ill.  Having my own daughter with similar issues of sudden onset motor and vocal tics, seizures and a history of repeated Strep infections, parasites, and lengthy viral illnesses has made the search for the source of this mystery all the more important to me.

The Name Game

By Teresa Conrick

With tics and Tourette-like illness in the news so much right now due to the increasing number of students at LeRoy HS in NY exhibiting them, it is with irony that P.A.N.D.A.S.,  a possible medical diagnosis for what we are seeing in LeRoy, is again up for scrutiny and denial somewhere else.  Here on Age of Autism, we are keeping up with the dizzying news that is our epicenter of what we are all about here - that many children are suffering with PHYSIOLOGICAL illnesses yet being wrongly diagnosed with PSYCHIATRIC disorders.  What is unraveling in Leroy has been happening for YEARS and for those of us with children stricken by regression after vaccination or immune illnesses, like PANDAS, the question that needs to be asked by many professionals denying what we all have known is - why are there so many sick children with immune and autoimmune diseases?

A few weeks back,a study came out, which wasn't really a study but more of an analysis steering an opinion. The name,  "Moving from PANDAS to CANS,- unavailable for public access -"  was quite a surprise as another name had been decided that would encompass the growing bacterial and viral issues of this increasing, medical misery - PANS," Pediatric Acute-onset Neuropsychiatric Syndrome."  PANS would change the criteia from the sole and hated Streptococcus bacteria to other various bacteria and viral infections, showing that not only Strep could trigger neuropsychiatric symptoms.  Vickie Blavat, a mother of an affected child with PANDAS and a research marvel on the PANDAS website, did a very nice job analyzing, "Moving from PANDAS to CANS" as well as other good information on this page:

In 2010, the NIMH hosted a think tank of various doctors and researchers to discuss PANDAS and its future. At that meeting, it was determined that a name change was in order and we would experience a shift from PANDAS to a new name…PANS. PANS would stand for Pediatric Acute-onset Neuropsychiatric Syndrome. To date, the new name has been verbally used by Drs. Swedo, Cunningham and others at conferences, symposiums and in layperson articles. They explain how various bacteria and infections, not soley strep, can trigger neuropsychiatric symptoms. We still wait for official confirmation and documentation of the change, diagnostic criteria, and treatment plans. One thing is definite, it was voted on and the name is PANS.......Imagine the PANDAS community’s surprise when a new article surfaces from the often referred to “naysayers” of PANDAS. .......They deem it should be called CANS (Childhood Acute-onset Neuropsychiatric Symptoms). Their CANS would be a very big umbrella for any person that has a sudden onset of neuropsychiatric symptoms, even if the cause is not infection triggered. Example, in addition to infection and autoimmune triggered events, if the cause for the sudden onset is drug induced (including illegal drugs like cocaine), psychogenic, metabolic, trauma, abuse, heavy metals, etc. the person can be diagnosed with CANS. The only prerequisite for a CANS diagnosis would be the sudden onset of symptoms. In other words, their CANS is a dump diagnosis.

So it sounds like the doctors who are listed on this paper,  Singer HS, Gilbert DL, Wolf DS, Mink JW, Kurlan R  are establishing some sort of new criteria that does not make sense moving forward in helping these ill children.  Is it possible that like Autism, there are some folks in the psychiatric world, like in the development of DSM-5, who want to keep fighting the reality of immune illness versus mental illness in our children?  They keep trying to prove that their methods are the only treatments and that kids will get better with them.  Yet their their big hitter medicines are proven ineffective for a big piece of both Autism and P.A.N.D.A.S.--- REPETITIVE behavior:

- A new multi-center study suggests the prescribed antidepressant  citalopram [ Celexa] is no more effective than placebo in altering obsessive features of autism

According to background information in the study, the use of antidepressants in children with autism spectrum disorder took off before there was strong scientific proof about its effectiveness.

In the last decade, its use has grown so that today more than 40 percent of autistic children swallow a daily dose of an antidepressant in an attempt to control spinning, rocking and repetitive behavior.

- These results showed that fluoxetine [PROZAC] was not effective for reducing repetitive behaviors in children and adolescents with Autistic Disorder.

LeRoy NY Girls With Neurological Tics: Science Offers Reasons When Government Officials Won't

By Teresa Conrick

I have a teen daughter very affected with vocal tics, OCD, enuresis, estrogen-related seizures and a significant past history of streptococcus infections as well as numerous viral illnesses.  Her diagnosis in 1995 - AUTISM - and additionally in 2011 - an autoimmune diagnosis - based on two positive results for antinuclear antibodies.  Armed with that knowledge, I was lured to an article this week called, Le Roy Parents Want Answers about Mysterious Illness .  I was shocked to read a horrific account of twelve high school girls, all from the same school, who had each begun to have severe symptoms similar to Tourette's syndrome, with tics and verbal outbursts.  These are familiar symptoms to me and for any parent who has a child who regressed into an immune or autoimmune disease.

I have researched and done much reading about Autism and also P.A.N.D.A.S.  (Pediatric Autoimmune Neuropsychiatic Disorders Associated with Streptococcal Infections)  because both seem to be related  to Megan and to each other, as the immune system seems to be a big, common denominator.  Seeing a story that describes previously healthy teens, teen girls, become so ill with movement and vocal tics, should alarm everyone.  The many articles on this story offer bits and pieces of clues as we all read it is "a mystery:"  Autism and P.A.N.D.A.S. used to be mysteries but over the years, many parents have reported that regression into each often came about due to vaccination or acute illness from bacterial or viral infections.  Streptococcus bacteria also known as "Strep Throat" for many, has been implicated often for P.A.N.D.A.S. but parents are also seeing regression and further exacerbation with other infections, such as Lyme (Borrelia bacterium) and Pneumonia ( Mycoplasma pneumonia). Are we seeing a rise in these immune-mediated diseases over the past years of increased vaccinations?

These are some facts:

1- A mysterious disorder which exhibits symptoms similar to Tourette's Syndrome has affected twelve female students at the same high school in LeRoy, NY.

 
2- Tourette's Syndrome is a neurological disorder defined by involuntary motor and vocal tics.

3- The New York State Department of Health says since September, 12 girls in Le Roy suddenly developed tics. Some are so bad, they had to be pulled out of school and tutored at home.

Autism and The Ghosts of Christmas Past

By Teresa Conrick

Those are my two daughters in 1995.  They were watching a favorite Christmas video, The Snowman,  based on the UK story by Raymond Briggs. Unlike our giddy, holiday Frosty, the Snowman, the UK version is a beautiful, haunting story of love and loss.  The many times I watched it with Meg -- winter, summer, fall,spring -- it didn't matter the season.  Nights she woke up crying from gastrointestinal pain or intense, physical distress, she wanted to watch, The Snowman, but she could never, ever watch when he melted.  She would leave the room.

Megan, now eighteen, has both an autism diagnosis and an autoimmune diagnosis.  Rare?  Unrelated? I think not.  I believe as we end 2011 and enter into 2012, the upcoming year will bring us more facts and research into the connection between autism and autoimmunity.   With that, let's say goodbye to the autism ghosts of Christmas past which gave little hope for meaningful research on preventing new cases of autism (regression) or research on medical treatments for those currently affected (progression)  Junky genetic studies,  Drosophilia eye-gazing, unknown autism prevalence, and bullshit research has to END.  We know that bacteria, viruses  and metals  can cause autoimmune effects and the research needs to be centered around that.

Going back in time each holiday season, the ghosts of past Christmases can haunt those living with autism and autoimmunity.  In 1995, my daughter's autism diagnosis was never related to her ongoing illnesses with Streptoccocus and other bacterial infections as well as numerous viral infections.  Labs now have shown IgG quantitative titers for each -- Measles-Mumps-Rubella --  to be elevated.  That was the vaccine that dramatically affected my daughter with many days of rash, fever, GI issues, loss of language and then odd visual issues.  Brief definition of IgG:

Antibody testing
Measles and mumps (rubella)  antibodies are virus-specific proteins produced by the immune system  in response to an infection by the measles or mumps ( & rubella) virus, or in response to vaccination. There are two types of antibodies produced, IgM and IgG. The first type to appear in the blood after exposure or vaccination is IgM antibodies. Levels of IgM antibodies increase for several days to a maximum concentration and then begin to taper off over the next few weeks. IgG antibodies take a bit longer to appear, but once they do, they stay in the bloodstream for life, providing protection against re-infection..  

There are very sick children and young adults with an autism diagnosis, and there seems to be mounting evidence  that the MMR (Measles Mumps Rubella) vaccine has quite possibly left its mark in them.  So back to high titers and autism.  If a toddler is vaccinated at 15 months, what is happening to produce very high titers 18 years later?  Why are the Drosophilia scientists not dropping the fruit flies and looking at viral titers -- or Strep in those affected by autism?

Autism and PANDAS

By Teresa Conrick

My daughter, Megan's recent diagnosis of an autoimmune condition coupled with an abnormal EEG are big, red flags that help illustrate why she is so ill.  Finding that out hardly ends my journey for more answers to help improve her health and her life.  The disturbing behaviors and symptoms of vocal tics, dilated pupils, agitation, enuresis, and OCD are a barometer of brain dysfunction.  Add in estrogen-induced seizures that developed at age seventeen in tandem to her autoimmune diagnosis and that may be another clue.  As a result, I have been exploring more of the issues that connect her to those children who have a P.A.N.D.A.S. (Pediatric Autoimmune Neuropsychiatric Diagnosis Associated with Streptococcal Infections) diagnosis as Megan has had numerous bouts of Strep and other infections that exploded into severe movement and vocal tics over the years.  Her original regression into an autism diagnosis slowly happened after vaccinations along with increasing viral and bacterial infections as a toddler, then an acute rash, fever and loss of language after her MMR vaccine.  We now seem to be in the land of chronic waxing and waning of symptoms and the most sobering part --- we are not alone.

More parents are finding each other and connecting via their child's medical issues.  Autism and P.A.N.D.A.S. may be cousins of a similar origin as there is overlap in symptoms, both behavioral and medical.  A good place to learn more about P.A.N.D.A.S. is this informative site.  A warrior mother in the P.A.N.D.A.S. trenches, Diana Pohlman, developed it in 2009 as she decided to bring parents, research and researchers together to investigate why their children were becoming acutely affected by a monster that Streptococcus bacteria seemed to awaken.  Like so many of us, she saw her son regress into an immune illness that severely affected his mood, behaviors, functioning -- his life.  More and more children each year seem to be developing tics, severe anxiety, obsessive compulsions, involuntary movements and psychiatric issues, not randomly, but due to an infection affecting the brain.  It is usually Streptococcus, an evil little bacteria that these mothers despise, because it is stealing their children.  So Autism parents and P.A.N.D.A.S.parents are beginning to link arms to tackle both cause and cure. As it states on Diana's website above, "Parents Helping Parents," is a key for many families to compare medical issues and treatments.

P.A.N.D.A.S. is a medical diagnosis yet many still do not understand it thus, there is confusion on its causation, how to diagnose it and then appropriate treatments.  We in the trenches of Autism are familiar with these issues as we have been dealing with them for too many years.  Our toddler or child becomes ill, either through an infection or after vaccination and there is a regression in skills. Odd, perseverative and debilitating behaviors creep in.  Life forever changes.  Doctors dismiss the cause and labels are given.  Precious time is lost then more medical symptoms, more labels. A stinging reality -- lack of proper medical treatments cause worsening behaviors.  This continues to happen at an alarming rate.

Some significant research continues to evolve with P.A.N.D.A.S., and the names Cunningham, Swedo and Murphy are becoming instrumental in connecting the hated bacteria to the hosts they have kidnapped.  Another interesting development was the apparent acknowledgement from Dr. Tom Insel that P.A.N.D.A.S. was indeed a real, medical illness. For those who do not know him, Dr. Insel is Director of the National Institute of Mental Health (NIMH), the component of the National Institutes of Health "charged with generating the knowledge needed to understand, treat, and prevent mental disorders", per the website,  including Autism and now also, P.A.N.D.A.S.

 
Here is a portion of what he reported a year ago:

Autism, Hospitals and the Belly of the Beast

By Teresa Conrick

My daughter, Megan, diagnosed sixteen years ago with Autism, has had an intense twelve months of.medical symptoms.  I call them "symptoms" but they really are clues as to the true nature of her diagnosis of autism.  It began last Fall with seizures, unusual, hormone-related, monthly ones, that had progressed into episodes of behavioral concern.  An earlier EEG had showed no seizures but instead, a pervasive and ominous diffuse slowing of the brain waves. Excessive estrogen can trigger mania, agitation and seizures in a typical female, so combine that with a diagnosis of autism and you get a full blown detour into an abyss, frighteningly far, far away from normalcy. More testing had shown "estrogen dominance," another "symptom" in Meg's body. Hormone therapy has not yet stopped the behaviors.  Anti-seizure medication has not yet stopped the seizures. An autoimmune diagnosis also has now surfaced, which helped make sense of the increasing irritability, enuresis, plus motor and vocal tics, often screamed out of my lovely daughter's mouth.  Her sister, two years younger, has lived in a path of bewilderment, fear and I am quite sure, shame, as the odd and erratic behaviors of her "older", yet really "younger" sister infiltrated our house. No friends or family have been in our home for so long as we have been living a nightmare. The behaviors were not a choice made by Megan, but instead have been a "symptom" of her immune system kidnapping her.  For me, it has been a painful reminder of how sinister Autism can be, especially when bacterial and viral infections seem to trigger Meg's body into a twilight zone in which I can't reach her.  Was this STILL autism or were we in a new place, like P.A.N.D.A.S. (Pediatric autoimmune neuropsychiatric disorders associated with Streptococci)?  It is like watching her regress again, as she did sixteen years ago. Her recent years have been positive for numerous Strep, candida, clostridia, and other viral infections.

It was decided that Meg needed an MRI and a 24-hour, closed circuit televised, EEG.  Her neurologist, new since Summer for us, saw how my daughter's behaviors were concerning and listened to my description of aggressions, involuntary movements and vocal tics/yells that I am sure the neighbors down the block could hear.  I am thankful that he didn't just see an eighteen year old, severely affected "with autism," and just needing something for the behavioral "symptoms."  Going into a hospital with Meg, overnight and away from the safety of home, took my breath away with fear as I thought about it.  Meg had a 24 hour EEG at age six but the electrodes were fastened to her head at the hospital, yet we were able to go home with a fanny pack monitor. Other EEGs had been just a few hours long.  This EEG was to be video monitored, an important addition as that 24 hour EEG twelve years ago was normal, yet she had just developed generalized tonic clonic seizures at age seventeen.  The video would be able to help us determine if there were subclinical seizures causing these scary behaviors.

There were many departments that we had to pass through in our journey.  Admissions, Ambulatory Services and then MRI, all before noon. Others were to follow later. More than one (in fact 6 people that day) asked if Meg needed, or if I wanted her to get a flu shot. October in a hospital is a continuous infomercial for Flu and Pneumonia vaccines.  I politely declined and wondered if our record had now been flagged, similar to Elaine's from Seinfeld, where it labeled her as a “difficult” patient.  I wasn't trying to be difficult but Meg's decline in health started with mercury-containing vaccines and then the fever and full body rash after her MMR significantly hastened that decline with loss of speech, loss of eye contact and loss of relating to us. 

The Vicious Truth: Vaccines, Autism, P.A.N.D.A.S. and Autoimmunity

My daughter, Megan, diagnosed sixteen years ago this month with autism, has now been diagnosed as having an autoimmune disorder, or -- is it -- an autoimmune disease?  Disease sounds profound but with all of her very serious symptoms for years, now worsening, it makes sense in my head, but in my heart  --- it is devastating.  We have tested twice now, using the antinuclear antibodies test, and both times it came out "positive," showing her body was indeed, fighting itself.  Although Lupus has been ruled out, we don't know yet what type of antigen is causing the autoimmune response so for now, it is a nameless monster. We do know that estrogen seems to trigger these episodes for Megan.

Because Meg has had numerous symptoms of other disorders and diseases, such as motor and vocal tics, loss of speech, choreiform movements, agitation, rigid OCD (obsessive-compulsive disorder), enuresis, transient psychotic features, aggression, and then a culminating seizure, I have needed to read, research and try to understand the overlap so we could hopefully find both cause and cure.  The key, it appears, is a 10.0, richter scale magnitude quote that Dr. Madeleine Cunningham used in her Autism One presentation recently   in Chicago.  Dr. Cunningham is a brilliant mind who, according to her website, is focused on, "the study of autoimmunity and behavior which is manifest in diseases such as Sydenham's chorea following group A streptococcal infection.  Our study identified antibody mediated neuronal cell signaling as the basis for the choreic movement disorder. Other related movement and psychiatric disorders such as obsessive compulsive disorder, Tourette's Syndrome and Tics are under investigation for subsets that may be related to streptococcal infection and/or to autoantibodies which signal in the brain."  She has been on the hunt since 1985 for Streptococcus and its many haunting manifestations.  Many families of P.A.N.D.A.S. (Pediatric autoimmune neuropsychiatric disorders associated with Streptococci) children have reported a family history of Strep, Sydenham's Chorea, Rheumatic Fever and other autoimmune diseases. Here is that quote from Dr. Cunningham:

“If autoantibodies are proven to affect behaviors, it will change the way we think about and treat mental disorders forever.”

To me, that significant sentence sums up so much of what I see in Meg, read in the research and believe in my heart.  There are other researchers also looking into autoimmunity, behavioral symptoms, and illness.  Here was a two part series, long but worth the read.  I have taken excerpts that relate to autism, Megan and her autoimmine issues: Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1

Ancestry of Pink Disease (Infantile Acrodynia) Identified as Risk factor for Autism

By Teresa Conrick

Yet another study has come out to add to the growing list of research showing that autism can be connected with exposure to mercury.  This study took the idea of heritability and paired it with a known exposure to mercury, Pink Disease.   Also known as Infantile Acrodynia,  Pink Disease was a mysterious ailment that affected 1: 500 children.  Its origin was teething powders and also worm medicines that contained mercury, given to babies and children, but it took YEARS for that truth to be accepted. Here is a description and opinion from,  A REVIEW OF INFANTILE ACRODYNIA ('PINK DISEASE'), NOVEMBER 30, 1949, of the painful and sometimes deadly symptoms seen: NIH Acrodynia

CARDIOVASCULAR: Tachycardia, hypertension; occasionally epistaxis, melaena, gangrene.

EMOTIONAL.: Depression, apathy, fretfulness, perversion of appetite, loss of interest, insomnia.

NERVOUS SYSTEM.:Myasthenia, hypotonia, photophobia; sweating, incontinence; head-banging, rocking and salaaming; paraesthesia, possibly 'thalamic' pain; disturbed temperature regulation; occasionally tremor, convulsions.

SKIN AND MUSCOAE:. Erythema, swelling of hands and feet; ulceration of mouth, loosening of teeth; dystrophy of nails and hair.

METABOLIC:. Hyperglycaemia, glycosuria; loss of weight: increased basal metabolic rate; enlargement of liver.

ENDOCRINE: Cessation of growth; diuresis.

DIGESTIVE: Vomiting, diarrhoea; occasional prolapse of rectum; occasional intestinal spasm, rarely progressing to intussusception.

BLOOD. Neutrophil leucocytosis.

And like Autism, Pink Disease was a "mystery", with many different opinions on causation yet the clues seem so clear now:

"The concept of diet deficiency, for example, has been abandoned, attractive as it seemed at one time, partly because the disease, whether in symptoms or pathology, resembles no known deficiency disease in man, and partly because it is found very frequently in conditions which seem to preclude malnutrition. The limits of age within which authentic cases have been reported are from the third week (Wyllie and Stern, 1931) to the fourth year;.....above this age there are probably a few cases......very rare cases reported in adults...indeed it is unlikely that a disease which appears not to have its origins in prenatal life or birth itself should be confined to the first four years....a lively baby becomes increasingly apathetic, loses interest in its surroundings, ceases to play, sleeps little, cries a lot. Older children cease to stand or walk or talk, and do not resume their progress in activity until the illness is past. No smile can be provoked, and the child resents being lifted or handled unless to be nursed very quietly."

And like Autism, when hard science pokes its way in, that reality may provoke feelings of denial:

Late Onset Autism and Anti-NMDA Receptor Encephalitis Part 2

By Teresa Conrick

In Part 1 of our examination of Anti-NMDA Receptor Encephalitis, I presented a late-onset case of autism.  Similar cases have been shown to be caused by antibodies against NR1–NR2 heteromers of the NMDA receptor. There was really very little about the precipitating event that explained why the 9 year-old boy became a victim of such an extreme medical and behavioral illness.  Because of its acute psychiatric manifestation, Anti-NMDA Receptor Encephalitis is often misdiagnosed as a psychiatric issue rather than a neurological-medical disease.  Its apparent increase in cases has been debated as -- a true increase or just better diagnosing?  I have to say it -- we, in the autism community, really dislike that phrase as it has become a mantra of ignorance in the face of truth.

Some further investigating brought me to another case of Anti-NMDA Receptor Encephalitis that presents with some more tangible facts.  Here is the Pubmed excerpt:

J.Neurol 2011 Mar;258(3):500-1. Epub 2010 Sep 30.  Anti-NMDA receptor encephalitis after TdaP-IPV booster vaccination: cause or coincidence?  Hofmann C, Baur MO, Schroten H.

And that's it.  There was no abstract but after some searching, I did find a link:

Anti-NMDA receptor encephalitis after TdaP–IPV booster vaccination .

LETTER TO THE EDITORS

Anti-NMDA receptor encephalitis after TdaP–IPV booster vaccination: cause or coincidence?
Caroline Hofmann • Marc-Oliver Baur • Horst Schroten
Received: 5 September 2010 / Accepted: 13 September 2010 / Published online: 30 September 2010

Springer-Verlag 2010

Dear Sirs,

Anti-NMDA receptor encephalitis is a recently described autoimmune disorder mediated by antibodies to the NR1 subunit of the N-methyl-D-aspartate receptor. It was first
recognized as a paraneoplastic syndrome in young women with ovarian teratoma [1]. Further studies have shown that about 40% of the patients with anti-NMDA receptor
encephalitis do not have a clinically detectable tumor, and men and children are also affected [2]. The mechanisms triggering the disorder, especially in patients without an
associated neoplasm are unknown. The high incidence of prodromal viral-like symptoms suggests a possible infection triggering the autoimmune response [3]. We report about a 15-year-old female patient who was diagnosed with anti-NMDA receptor encephalitis after receiving a booster vaccination against tetanus/diphtheria/pertussis and polio (TdaP-IPV). Within the first 24 h after the injection she developed a low-grade fever and general fatigue. During the following weeks, her family observed an unusual need for sleep. Psychiatric symptoms became apparent 5 weeks after the immunization and included disorganized thinking and hallucinations. Within a few days she became increasingly agitated with orofacial dyskinesia, opistotonic posturing, and choreic movements of the upper extremity. She grew unresponsive to verbal commands and required intensive care treatment due to autonomic instability. The unique pattern of clinical symptoms led to the consideration of anti-NMDA receptor encephalitis, which was confirmed by the detection of anti-NMDAR antibodies in plasma and cerebrospinal fluid. Other possible causes of encephalopathy including intoxication,infectious and metabolic diseases were ruled out; repetitive brain scans showed no abnormalities. After confirming the diagnosis, an extensive tumor search was performed without any proof of malignancy; biopsy of a prominent ovarian cyst revealed no teratoma. The onset of prodromal symptoms shortly after the immunization is intriguing and suggests the vaccination as a possible trigger of anti-NMDA receptor encephalitis. Neurological adverse events including autoimmune disorders have been discussed in literature for many years; a definite causal association between vaccination and disease was seldom established. For example, the 1976 swine influenza vaccine was associated with an increased frequency of Guillain-Barre Syndrome (GBS) [4]. A recent study about the safety of TdaP vaccination in adolescents revealed no increased risk of neurological adverse events [5], even though rare cases of GBS have been reported. To our knowledge, this is the first possible case of vaccination associated anti-NMDA receptor encephalitis. Therefore, not only infectious agents and tumor antigens but also vaccines should be considered as a possible trigger of immune response in this recently described disorder.
Conflict of interest None.

Late Onset Autism and Anti-NMDA-Receptor Encephalitis: Part 1

By Teresa Conrick

My daughter, Megan, continues to be severely affected by both the medical and behavioral symptoms of autism. As a result, I continue to read studies and research that correlate with the symptoms that she has.  Some of the factors, if we were to list them like they do in a journal, would be -- seizures, autism, nmda/glutamate dysfunction, cancer signalling, encephalopathy, agitation.  Surprisingly, there was a current, case study just out that had many of these key words:

Late onset autism and anti-NMDA-receptor encephalitis    The Lancet, Vol 378. Issue 9785, Page 98, 2 July 2011

Caroline Creten, MD, Sanne van der Zwaan BSc, Roos J Blankenspoor BSc, Arien Maatkamp, PhD, Prof Jim van Os PhD, Dr Jan NM Schieveld PhD

In December, 2009, a 9-year-old boy was admitted to our hospital with an acute onset of secondary generalised seizures. He had no medical or psychiatric history and functioned very well socially and academically. He presented with speech and swallowing difficulties, which after 10 days developed into a severely agitated catatonic state with opisthotonic posturing, tonic posturing of limbs, insomnia, and dyskinesia. Initially the electroencephalogram showed a normal background pattern with epileptic discharges, and oligoclonal bands were present in cerebrospinal fluid (CSF). Brain MRI and extensive blood tests were normal. The neurological diagnosis was atypical childhood epilepsy with centrotemporal spikes, for which oral corticosteroids and anti-epileptic drugs were prescribed. His catatonia was treated with benzodiazepines. In January, 2010, our patient presented in a robotic state with complete mutism and negativism, and he did not respond to any form of contact. We provisionally diagnosed acute late onset autism with a differential diagnosis of childhood disintegrative disorder or early onset schizophrenia.

Childhood disintegrative disorder, early onset schizophrenia, and late onset autism often share a final common pathway: previous normal development, followed by sudden neuropsychiatric regression of social interaction and communication skills, and a decline in intelligence and daily activities. 1 The disorders are sometimes misrecognised and collectively called as autistic disorder. Although judged to be functional psychiatric diagnoses, the marked deterioration and poor prognosis suggest an organic cause, especially in children with catatonia, a normal development up to at least 5 years of age, or both1,2. In our patient, late onset autism was considered because: it is associated with neurological disorders; 2  it is a known end stage of acquired brain injury; progression of symptoms was fast and severe, unlike in early onset schizophrenia; the absence of positive symptoms made schizophrenia less plausible; the age of onset and rare prevalence made chronic disintegrative disorder unlikely; 1 and accompanying catatonic features were present. 3 After extensive diagnostic assessments, our patient was finally diagnosed with anti-NMDA-receptor encephalitis on the basis of slightly raised anti-NMDA-receptor antibody titres in serum and highly raised titres in CSF. 4 Clinical characteristics of this condition are acute major neuropsychiatric symptoms including anxiety, aggression, agitation, behavioural changes and catatonia, delusional thoughts, progressive speech deterioration, and hallucinations. Neurological symptoms such as dyskinesia, abnormal seizure-like movements, and diffuse and profound autonomic instability have also been reported.4.5 Anti-NMDA-receptor encephalitis can occur in the context of malignant disease; 4 however for our patient extensive oncological investigations were negative. Electroconvulsive therapy was given for the severe catatonic state, and monoclonal antibody treatment (rituximab) was started because of the unsatisfactory response to the initial treatment with benzodiazepines. The acquired autism gradually subsided, he spoke fluently and was able to draw a happy picture (figure). In June, 2011, he only had some mild cognitive dysfunction.