PANS PANDAS are newer diagnoses that your child’s pediatrician or psychiatrist may not be aware of.
They are disorders that are loosely defined as a sudden onset of acute anxiety and mood variability accompanied by OCD (Obsessive Compulsive Disorder) and/or tics.
PANDAS stands for Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections. With PANDAS, the onset of symptoms is typically preceded by streptococcal -A infection (“strep throat”). However, in some cases, children may not have presented with a full-blown, acute strep throat infection.
PANDAS is included in the larger umbrella of PANS, Pediatric Acute-onset Neuropsychiatric Syndrome. PANS includes not only PANDAS, but also diagnoses such as Lyme disease, OCD and ODD.
Recent statistics indicate that roughly one in 200 children in the United States is affected with PANS PANDAS. In the United States, 500,000 children are diagnosed with OCD and 138,000 have Tourette’s Syndrome. In addition, 1.5 million American children are diagnosed with anxiety, phobias, OCD and/or bipolar disorder.
PANS PANDAS Symptoms
Typically, PANS PANDAS are accompanied by an acute onset of extreme behavioral and emotional symptoms, although sometimes there appears to be a slow onset.
Symptoms can include, but are not limited to:
- OCD (Obsessive Compulsive Disorder)
- Excessive anxiety, especially separation anxiety
- ODD (Oppositional Defiant Disorder)
- Tics such as:
- Hair pulling
- Eyelash pulling
- Motor tics
- Repetitive or compulsive coughing or throat-clearing when not sick
- Excessive temper tantrums
- Mood swings
- Behavioral regression
- Developmental regression
- Sensory processing difficulties
- Sleep problems
- Gastrointestinal pain
- Severe food restriction
- Decline in handwriting skills
- Decline in math skills
- Inability to concentrate
- Head banging
- Refusal to go to school
- Increased desire to be left alone
Children diagnosed with PANS PANDAS are typically between one and 13 years of age, with 60% of diagnoses for children between the ages of four and nine.
Please note that there is an overlap of general symptoms between PANS and PANDAS, and that PANS usually results in severely restricted food intake as well as at least two of the symptoms described above. Clinical diagnosis of PANDAS is defined as the presence of significant OCD behavior and/or tics in addition to the above symptoms.
In addition, your child may have a combination of both PANS and PANDAS.
Anti-Dopamine Receptor Antibodies
In PANDAS, the cross-reactive antibodies created in response to strep attack the dopamine receptors in the basal ganglia of the brain because of a blood-brain barrier breach.
However, these antibodies can be also be created in response to microbes other than Streptococcus, as well as to environmental toxins, which is why the umbrella term of PANS more accurately describes these disorders.
The basal ganglia are a group of nuclei located at the base of the brain and are linked to the thalamus.
Basal ganglia have traditionally been associated with movement disorders, such as Huntington’s and Parkinson’s disease.
In addition to voluntary movement control, the basal ganglia are also associated with procedural learning, eye movements, cognitive function and emotional function.
The basal ganglia are also the site of two dopamine receptors.
Dopamine is a neurotransmitter associated with attention, movement and the pleasure/reward centers of the brain.
- The D1 receptor is a direct pathway in the basal ganglia that facilitates movement.
- The D2 receptor is an indirect pathway that inhibits movement.
When the cross-reactive antibodies associated with strep or other antigens attack the dopamine receptors in the basal ganglia of the brain, it causes a fluctuation in dopamine, which results in OCD, tics and other neuropsychiatric symptoms.
Some doctors also refer to this as autoimmune-mediated basal ganglia dysfunction.
Blood-Brain Barrier Breaches
Pathogens can easily make their way inside your child’s brain if there has been a blood-brain barrier breach.
Traumatic Brain Injury
Concussion-related cause and relapse of PANS PANDAS (including Lyme disease) is very common because the blunt-force trauma can breach the blood-brain barrier.
Excessive EMF exposure has been documented to cause a blood-brain barrier breach.
It is important to lower exposure to EMFs from cell phones, ultrasounds, wireless phones, baby monitors, smart meters, large electrical devices and WiFi systems as much as possible.
Exposure to Antibiotics
Antibiotics exposure cause gut-microbe disruptions, which can cause immune dysregulation.
Any kind of stressful event, whether physical, emotional or biomedical, can cause a relapse, which is why it is important to teach your child stress-relieving skills (see below).
Many healthcare practitioners specializing in PANS PANDAS think that blood-brain barrier breaches may also be due to exposure to environmental toxins.
Autism, ADD/ADHD and SPD Comorbidities
Knowledgeable practitioners have found that roughly 30-50% of children with autism, ADD/ADHD and Sensory Processing Disorder (SPD) also have PANS PANDAS.
In addition, it is very common for younger siblings of children diagnosed with autism, ADD/ADHD or Sensory Processing Disorder to be diagnosed themselves with PANS and PANDAS.
If this is the case, consider that your older child may have PANS PANDAS as well.
In many cases, these children have both a PANDAS diagnosis as well as that of Lyme disease.
Another way to think of PANS PANDAS, as well as any neurodevelopmental disorder such as autism, ADD/ADHD, Sensory Processing Disorder and even learning disabilities, is that these disorders may fall under the larger umbrella of autoimmune encephalitis (AE).
Autoimmune encephalitis is a disorder in which the immune system attacks the brain, impairing function.
Encephalitis is inflammation and swelling of the brain, often due to infection, which in many of these cases causes an autoimmune attack on the microglia cells of the brain.
A child with this type of damage may typically never have or may lose motor skills and/or the ability to speak, similar to an adult who has had a stroke.
Encephalitis is a common symptom of this type of damage, and it often shows up as an increase in the child’s head-circumference percentile, especially in the first year of life.
The prestigious science journal Nature pointed this out by stating that “brain volume overgrowth was linked to the emergence and severity of autistic social deficits.”
Anti-NDMA Receptor Encephalitis
The N-methyl-D-aspartate receptor (also known as the NMDA receptor), is a glutamate receptor found in nerve cells.
It is activated when the amino acids glutamate and glycine bind to it.
NMDA receptors have been implicated by a number of studies to be strongly involved with excitotoxicity, the process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters such as glutamate.
Excitoxicity can cause encephalopathy and seizures.
Glutamate and its analogs are found in processed foods not only as MSG (monosodium glutamate), but also in chemical food additives such as:
- Hydrolyzed vegetable protein
- Soy protein isolate
- Yeast extract
- Barley malt
- Natural flavoring
- Artificial flavoring
- Soy sauce
Even natural foods such as tomatoes, bone broth and seaweed may naturally have high levels of glutamate.
Strep also increases glutamate in the brain.
What Your Doctor May Tell You About PANS PANDAS
Most pediatricians and psychiatrists may not be aware of PANS PANDAS.
These diagnoses are clinical diagnoses and are diagnoses of exclusion.
If you suspect that your child has PANS PANDAS, you might be able to work with your child’s doctor to have them perform tests that could lead them to a clinical diagnosis.
If not, you may need to find a practitioner that specializes in PANS PANDAS, many of whom are listed in our practitioner directory.
Testing for PANS PANDAS
To begin with, your child’s doctor may choose to have blood tests performed on your child.
The Cunningham Panel is a series of tests that was developed by Madeleine Cunningham, PhD to help physicians diagnose and treat infection-induced neuropsychiatric disorders.
These tests measure circulating levels of auto-antibodies directed against specific neuronal antigens, including:
- Dopamine D1 receptor (DRD1)
- Dopamine D2L receptor (DRD2L)
- Lysoganglioside GM1
- CaM kinase
If any of these antibodies is elevated, this is an indication of autoimmunity. Also, please note that the Cunningham panel only establishes autoimmunity, not what is causing the autoimmunity. Additional testing is necessary to determine the cause of autoimmunity.
PANDAS Specific Testing
- Serum ASO titer (Anti-Streptolysin O): This is produced between one week to one month after the onset of an infection.
- Serum ASDB titer (Anti-Streptococcal DNase B): This peaks four to six weeks after infection and remains elevated longer than ASO.
PANS Specific Testing
Because PANS is the broader umbrella under which PANDAS falls, additional testing may need to be done to check for:
- Lyme disease
- Specific viruses, especially herpetic viruses such as Epstein-Barr virus and herpes simplex viruses
- Pathogenic bacterial infection, such as Staphylococcus aureus
- Mycoplasma pneumoniae infection
- Influenza infection
- Heavy metals and other toxins
Please remember that is quite possible, and often common, for a child to have both PANS and PANDAS, so it is a good idea to test for all of the above triggers before deciding on a course of action.
Conventional Lab Tests Are Not Always Reliable
However, titers are NOT always indicative of an infection.
Titers are often only moderately elevated, or not elevated at all in some children with PANS PANDAS.
According to one study, only 54% of children with strep throat showed an elevated ASO titer and only 45% showed an increase in anti-DNase B.
In addition, throat cultures frequently result in false negatives because of the technique used in obtaining the specimen, mishandling of the specimen and the fact that the strep bacteria may be harbored in other parts of the body than the throat.
Because labs are not always reliable, the diagnosis of PANS PANDAS is a clinical diagnosis.
This means that your healthcare provider will base his or her diagnosis on your child’s history and symptoms.
Typical Western Medicine Treatment of PANS PANDAS
Your child’s doctor will typically address your child’s behavioral and emotional symptoms with psychotropic pharmaceuticals such as anti-depressants.
However, anti-depressants typically have a “black box” warning against these medications by children because they can increase the risk of more aggressive behavior and suicide ideation.
More forward-thinking Western medical doctors now understand that PANS and PANDAS are typically caused by a pathogenic infection and/or acute environmental toxic assault.
To that end, typical treatments include:
Although a 14-day course of beta lactam antibiotics is a typical prescription, antibiotics must often be given over several weeks or months to see improvement.
Many children require multiple rounds of antibiotics, and some stay on antibiotics prophylactically for years.
However, recent research has shown that antibiotics severely alter, often permanently, the microbiome in the gut, which is where most of the body’s immune system is.
In essence, giving antibiotics may “win the battle, but lose the war” because they can alter the body’s immune function and often cause an overgrowth of fungus, such as from Candida albicans.
In addition, antibiotics only work against bacterial infection, so they won’t help in the case of viral, parastic or fungal infection as well as environmental toxic assault.
Steroids and NSAIDs
Both steroids and NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) have been documented to reduce symptoms in children with PANS PANDAS, which is a clue that inflammation is part of what’s behind the child’ symptoms.
However, long-term use of either of these kinds of pharmaceuticals is hard on the body and can cause strain on the liver’s detoxification process as well as lead to nutritional deficiencies, thereby potentially leading to additional symptoms further on down the road.
In addition, steroids can disrupt the microbiome in the gut, which can lead to more symptoms later on.
Intravenous Immunoglobulin (IVIG) treatment is used when a child does not respond well to antibiotics, steroids or NSAIDS because the immune system is severely compromised.
IVIG floods the body with donor antibodies, which helps to overwhelm pre-existing auto-antibodies. IVIG also helps to up-regulate regulatory T cells, thereby improving immune function.
Some children do respond very well to IVIG for relief of their symptoms. IVIG is very expensive, however, and many insurance carriers do not cover it. In addition, one round of treatment may not be enough, especially if the child relapses.
Knowledgeable doctors are saying that IVIG is not addressing the cause, and so the latest Western medicine approach is to treat a child with PANS PANDAS with the biologic IV infusion of Rituxan, which carries its own risks. Rituxan lowers the number of B cells, which is what is was designed to do as an immunosuppressant.
The potential of untested-for contamination in donor immunoglobulins exists as well.
In a plasma apheresis treatment, the child’s blood is collected by a machine, which separates the plasma, red cells and platelets and returns the red cells and/or platelets back to the donor.
Some children do respond well to this treatment, but it is expensive and invasive, so Western medical doctors typically reserve it for treatment of children who are severely affected by PANS PANDAS.
Another Way to Think About PANS PANDAS
Although both PANS and PANDAS are often described in terms of an “acute onset” and/or specific microbial infections, neither of these conditions can be distilled down to a specific causative factor.
Rather, there are a variety of factors at play:
- Environmental exposures to toxins
- Infectious agents
- Total load
There is no single cause or agent; rather, there are multiple contributing factors that work together in precipitating the disease process.
It is the combination of all of these factors that create a total load syndrome that informs the point of departure and the progression of the disorder.
According to this model, there is never just one causal factor.
There may be the proverbial “straw that broke the camel’s back”, that is, the singular incident after which symptoms began to emerge.
However, the foundation is a complex amalgam of multi-factorial and multi-generational factors.
Bio-Individuality and Total Load
Every person has a unique “tipping point” as well as his or her own unique story.
In some children, infection plays a larger role than environmental exposure to toxins or genes.
In others, genetic predisposition is a larger contributing factor.
Total Load Origins
Scientific research has proven again and again that trans-generational toxins and exposures are passed down from mother to child.
Toxins are passed from a mother to a child in utero.
In addition, the mother’s first-born child is generally the most affected and receives the bulk of the mother’s toxic load, including chemicals, heavy metals and infections such as Lyme disease.
The Role of the Immune System
The immune system is a collection of cells, tissues and organs that work together to protect the body from foreign substances called “antigens”.
Antigens can be both microbes and toxins, such as:
- Heavy metals
- Endocrine disruptors
Lymphocytes are small, white blood cells that do the work of the immune system.
There are two main types of lymphocytes:
B lymphocytes (“B cells”)
B cells mature in the bone and are the equivalent of pedestrians jumping up and down outside a burning building yelling, “FIRE! FIRE!”.
B cells don’t really do anything other than to “draw attention to the burning building”.
T lymphocytes (“T cells”)
T cells mature in the thymus and are the equivalent of the firefighters who organize and put the fire out.
In immune disorders such as PANS and PANDAS, there is an over-proliferation of B cells (the ones yelling “FIRE! FIRE!) and not enough T cells (the ones that stop the screaming or organize how to put out the fire).
In a healthy immune system, lymphocytes are able to recognize the difference between “self” and “non-self” cells.
In autoimmune disorders such as PANS PANDAS, the immune system attacks and destroys its own tissues.
When the immune system is overloaded fending off toxins in the form of daily exposures to chemicals, pesticides and heavy metals, there is little reserve left to ward off infectious agents, which should be the main focus of a healthy immune system.
As a result, the immune response becomes disjointed and overwhelmed.
In a healthy individual, immune cells conjugate at the site of an infection.
Cytokines are immune cells secreted by cells to regulate immune response; they include:
- Growth factors
When the body is overwhelmed by toxicity, however, cytokines are activated in multiple parts of the body, which leads to systemic inflammation.
High cytokine activity and high inflammation are a hallmark of PANS PANDAS, as well as autoimmune disorders, autism, ADD/ADHD and Sensory Processing Disorder.
The Role of Genetics
Defects in certain genes, such as the MTHFR gene, lead to decreased T cell response and production (firefighter cells).
In addition, an MTHFR mutation can lead to reduced or impaired B cell response (bystander cells yelling “FIRE! FIRE!”).
The human gut microbiome is the name given to the colonies of microbes that live in our digestive system.
These gut microbes are vitally important for communication with the brain and the immune system.
It is believed that 70% of our immune system is located in the digestive tract.
Canadian researcher Derrick McFabe PhD has demonstrated how changes in the gut bacteria affect brain functioning and behaviors, thus proving the theory of the gut/brain axis.
He has shown how specific bad gut bacteria can alter the gut/brain connection as demonstrated in children with autism.
Also in our brain are chemical messengers that transmit signals from one neuron to another telling the brain and body what to do.
These messengers are called “neurotransmitters”, and they are also located in our gastrointestinal tract, which allows for communication with the brain.
If the gastrointestinal tract develops a common condition called “leaky gut syndrome”, then this means there has been too much foreign matter that has permeated the gut lining.
As a result, many bad pathogens, bacteria, viruses, yeast, fungus and parasites can populate the gastrointestinal tract and disrupt communication with the neurotransmitters in the brain causing the neurotransmitters to misfire.
This process begins the development of an autoimmune disorder, and, if this happens, your child may experience many problems such as:
- Developmental delays
- Muscle tone issues
- Mood swings
- Sensory overload
- Sympathetic dominance of the nervous system (fight or flight)
- High-anxiety issues
- Inappropriate behaviors
- Self-injurious behaviors
- Inability to cope
- Inability to focus
- Inability to concentrate
Therefore, no matter what autoimmune disorder your child may have, begin with healing the microbiome.
A PANS PANDAS Checklist to Start
Make dietary changes:
- Eat whole foods
- Buy organic foods
- Remove all GMO foods
- Remove all fast and processed foods
- Remove all foods with:
- Artificial colors
- Artificial ingredients
- Remove potentially inflammatory foods such as:
- Strictly limit:
- Refined salt
- Refined carbohydrates
- Join the Feingold Association www.Feingold.org to learn more.
Include plenty of good quality fats, such as:
- Coconut oil
- Olive oil
- Wild salmon
- Organic chicken
- Organic turkey
- Grass-fed ghee
- Pasture-raised eggs
- Grass-fed beef
- Essential fatty acids from:
- Cod liver oil
- Hemp seeds
- Flax seeds
- Evening primrose oil
- Borage oil
- Walnut oil
Remove vegetable oils such as:
Include plenty of high-quality proteins with every meal, such as:
- Pasture-raised eggs and chicken
- Grass-fed beef
- Wild-caught fish
Heal the gut with special diets such as:
- GAPS (Gut And Psychology Syndrome) diet
- Paleo diet
- GF/CF (gluten-free/casein-free) diet
- Body Ecology Diet
- Modified Atkins Diet (replaces the Ketogenic diet)
Learn more about healing diets and foods.
Use digestive aids with your practitioner’s guidance:
- Betaine hydrochloric acid
- Digestive enzymes with DPP-IV for gluten and casein intolerances
- Proteolytic enzymes
Clean up your environment:
Have you identified and removed possible environmental triggers, such as mold, dust, pet dander, and electromagnetic fields (EMFs)?
Have you identified and removed possible toxic exposures in the home from purchased products, such as detergents, soaps, lotions, and other cleaning and personal care products?
- Remove animals (both live and stuffed!)
- Remove carpets
- Use non-toxic cleaners
- Use non-toxic building materials
- Green your home
Avoid exposing your child to chlorine, fluoride, and bromine because all three are in the same family as iodine and can displace iodine in the thyroid gland.
Ask your pediatrician to run some laboratory tests for:
- The Cunningham Panel for circulating levels of auto-antibodies directed against dopamine and other potential antigens
- Possible food sensitivities and allergies
- Enzyme-Linked Immunosorbent Assay (ELISA) IgG, IgA, IgE and IgM
- Nutritional deficiencies in vitamins and minerals. The NutrEval by Genova Diagnostics Labs covers the following areas:
- Cellular energy
- Mitochondrial metabolism
- Neurotransmitter metabolism
- Vitamin deficiencies
- Toxin exposure
- Detoxification need
- Bacterial and yeast overgrowth
- Gluten and casein sensitivities
- Organic acids: The organic acid test by Great Plains Laboratory for:
- Yeast overgrowth (Candida)
- Other microbial infections
- Comprehensive Stool Analysis by Genova Diagnostic Labs to identify:
- Altered gastrointestinal function
- Bacterial/fungal overgrowth
- Chronic dysbiosis
- Neurotransmitters: Neurorelief (Neurosciences Laboratory) is a specialty lab that tests neurotransmitters to determine chemical imbalances in the brain
Use homeopathy specific for:
- Homeopathic drainage: In order to detoxify efficiently, the liver, kidneys and intestines must be open and draining.
- Series therapy for:
- Epstein-Barr virus
- Other viruses or bacteria as determined by your practitioner
Add fermented foods and probiotics daily:
These will keep the gastrointestinal system and microbiome healthy and strong which in turn will keep the immune system strong.
- Eat kefir yogurts
- Eat fermented vegetables
- Eat umeboshi plums (very alkalizing)
- Eat miso soup, if soy is tolerated
Some good probiotics are:
- Gut Pro
- Dr. Ohirra’s Live Cultured Probiotics
- Garden of Life
- Klaire Labs
Use herbs, essential oils and natural supplements with your practitioner’s guidance:
- GABA, especially PharmaGABA
- Lithium orotate
- Vitamin D
- Vitamin K
- B vitamins, especially niacin if strep is concerned
- Vitamin C, especially liposomal vitamin C
- Cod liver oil
- Trace minerals
- Methylcobalamin B12
- Folinic acid or 5MTHF if your child has methylation issues
- Colostrum and/or transfer factor for those who do not have severe allergic reactions to dairy
- Mushroom blends such as Core Mycelia
- Turmeric or curcumin
- Antimicrobial herbs and supplements
- Olive leaf
- Oil of oregano
- Grapefruit seed extract
- Samento (cat’s claw)
- Arentyn or Smart Silver colloidal silver
- Apple cider vinegar for gargling
- Manuka honey
- Thieves’ oil
- N-acetylcysteine (NAC): helps with detoxification process and healing of the gastrointestinal tract
- MSM transdermal cream
- Epsom salts bath
- Low-dose naltrexone
Help your child detoxify:
- Ionic foot baths can help detox unwanted pathogens and are easy to do with children
- Infared saunas can detox heavy metals through the skin by sweating.
Lower stress levels:
Viruses, bacteria and other pathogens become more active when the body is in a state of stress.
By teaching your child ways to self-regulate with practices such as prayer, reiki, meditation, yoga, qi gong, tai chi and the Emotional Freedom Technique (tapping), they can become good advocates for themselves and become active participants in the recovery process.
See a neurofeedback practitioner:
Neurofeedback is approved as a level-one intervention by the American Academy of Pediatrics for ADD and ADHD, both of which feature anxiety as a component.
Even if your child doesn’t have ADD or ADHD, they may still benefit from neurofeedback because it can help lower anxiety levels.
Find a practitioner that can perform a QEEG (quantitative electroencephalograph) brain map first so you can understand how your child’s brain works.
See a sensory-integration occupational therapist:
These OTs address a variety of sensory issues with a child using hands-on equipment. This type of therapy calms down the nervous system to help integrate the senses and retained reflexes.
See a chiropractor:
A chiropractor can perform spinal cord adjustments, which can improve communication in the nervous system.
See a craniosacral practitioner:
Craniosacral therapy can reestablish central nervous system functioning.
See a homeopath or naturopath:
These practitioners can diagnose and treat underlying pathogenic infections while supporting the immune system’s function.
Still Looking for Answers?
Aldad, T.S., et al. Fetal Radiofrequency Radiation Exposure From 800-1900 Mhz-Rated Cellular Telephones Affects Neurodevelopment and Behavior in Mice. Sci Rep. 2012;2:312.
Allen, A.J., et al. Case study: a new infection-triggered, autoimmune subtype of pediatric OCD and Tourette’s syndrome. J Am Acad Child Adolesc Psychiatry. 1995 Mar;34(3):307-11.
Banks, W.A., et al. Aluminum-induced neurotoxicity: alterations in membrane function at the blood-brain barrier. Neurosci Biobehav Rev. 1989 Spring;13(1):47-53.
Baytunca, M.B. [Evaluation of a Neuropsychiatric Disorder: From PANDAS to PANS and CANS]. Turk Psikiyatri Derg. 2016 Summer;27(2):0.
Bjarnason, I., et al. Mechanisms of Damage to the Gastrointestinal Tract From Nonsteroidal Anti-Inflammatory Drugs. Gastroenterology. 2018 Feb;154(3):500-514.
Boileau, B. A review of obsessive-compulsive disorder in children and adolescents. Dialogues Clin Neurosci. 2011;13(4):401-11.
Bora, S.A., et al. Regulation of vitamin D metabolism following disruption of the microbiota using broad spectrum antibiotics. J Nutr Biochem. 2018 Jun;56:65-73.
Braniste, V., et al. The gut microbiota influences blood-brain barrier permeability in mice. Sci Transl Med. 2014 Nov 19;6(263):263ra158.
Bravo, J.A., et al. Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16050-5.
Brown, K., et al. Pediatric Acute-Onset Neuropsychiatric Syndrome Response to Oral Corticosteroid Bursts: An Observational Study of Patients in an Academic Community-Based PANS Clinic. J Child Adolesc Psychopharmacol. 2017 Jul 17.
Brown, K.D., et al. Effect of Early and Prophylactic Nonsteroidal Anti-Inflammatory Drugs on Flare Duration in Pediatric Acute-Onset Neuropsychiatric Syndrome: An Observational Study of Patients Followed by an Academic Community-Based Pediatric Acute-Onset Neuropsychiatric Syndrome Clinic. J Child Adolesc Psychopharmacol. 2017 Jul 11.
Butel, M.J., et al. The developing gut microbiota and its consequences for health. J Dev Orig Health Dis. 2018 Mar 22:1-8.
Burkett, P.R., et al. Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity. J Clin Invest. 2015 Jun;125(6):2211-9.
Calaprice, D., et al. A Survey of Pediatric Acute-Onset Neuropsychiatric Syndrome Characteristics and Course. J Child Adolesc Psychopharmacol. 2017 Jan 31.
Carpentier, A., et al. Clinical trial of blood-brain barrier disruption by pulsed ultrasound. Sci Transl Med. 2016 Jun 15;8(343):343re2.
Chang, K., et al. Clinical evaluation of youth with pediatric acute–onset neuropsychiatric syndrome (PANS): recommendations from the 2013 PANS Consensus Conference. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):3-13.
Chiarello, F., et al. An expert opinion on PANDAS/PANS: highlights and controversies. Int J Psychiatry Clin Pract. 2017 Jun;21(2):91-98.
Cooperstock, M., et al. Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part III—Treatment and Prevention of Infections. J Child Adolesc Psychopharmacol. 2017 Jul, ahead of print.
Cox, C.J., et al. Antineuronal antibodies in a heterogeneous group of youth and young adults with tics and obsessive-compulsive disorder. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):76-85.
Dahm, T., et al. Neuroinvasion and Inflammation in Viral Central Nervous System Infections. Mediators Inflamm. 2016;2016:8562805.
Dale, R.C. Immune-mediated extrapyramidal movement disorders, including Sydenham chorea. Handb Clin Neurol. 2013;112:1235-41.
Dallasta, L.M., et al. Blood-Brain Barrier Tight Junction Disruption in Human Immunodeficiency Virus-1 Encephalitis. Am J Pathol. 1999 Dec;155(6):1915-27.
Das, T., et al. Influence of Calcium in Extracellular DNA Mediated Bacterial Aggregation and Biofilm Formation. PLoS One. 2014 Mar 20;9(3):e91935.
Dasdaq, S., et al. Effects of 2.4 GHz radiofrequency radiation emitted from Wi-Fi equipment on microRNA expression in brain tissue. Int J Radiat Biol. 2015 Jul;91(7):555-61.
DeLong, G.R., et al. Acquired reversible autistic syndrome in acute encephalopathic illness in children. Arch Neurol. 1981 Mar;38(3):191-4.
Ding, H., et al. Molecular Pathogenesis of Anti-NMDAR Encephalitis. Biomed Res Int. 2015;2015:643409.
Ercan, T.E., et al. Mycoplasma pneumoniae infection and obsessive-compulsive disease: a case report. J Child Neurol. 2008 Mar;23(3):338-40.
Ferretti, J.W., et al. Post-Streptococcal Autoimmune Sequelae: Rheumatic Fever and Beyond. Streptococcus pyogenes : Basic Biology to Clinical Manifestations [Internet]. 2016 Feb 10. Oklahoma City (OK): University of Oklahoma Health Sciences Center.
Fiorentino, M., et al. Blood–brain barrier and intestinal epithelial barrier alterations in autism spectrum disorders. Molecular Autism. 2016 Nov 29;7:49.
Frankovich, J., et al. Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part II—Use of Immunomodulatory Therapies. J Child Adolesc Psychopharmacol. 2017 Jul
Frankovich, J., et al. Five youth with pediatric acute-onset neuropsychiatric syndrome of differing etiologies. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):31-7.
Frankovich, J., et al. Multidisciplinary clinic dedicated to treating youth with pediatric acute-onset neuropsychiatric syndrome: presenting characteristics of the first 47 consecutive patients. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):38-47.
Gaughan, T., et al. Rapid Eye Movement Sleep Abnormalities in Children with Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS). J Clin Sleep Med. 2016 Jul 15;12(7):1027-32.
Gerardi, D.M., et al. PANDAS and comorbid Kleine-Levin syndrome. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):93-8.
Ghaziuddin, M., et al. Brief report: autism and herpes simplex encephalitis. J Autism Dev Disord. 1992 Mar;22(1):107-13.
Gherardi, R.K., et al. Biopersistence and Brain Translocation of Aluminum Adjuvants of Vaccines. Front Neurol. 2015 Feb 5;6:4.
Gillberg, C. Onset at age 14 of a typical autistic syndrome. A case report of a girl with herpes simplex encephalitis. J Autism Dev Disord. 1986 Sep;16(3):369-75.
Goncalves, M.V.M., et al. Pediatric acute-onset neuropsychiatric syndrome (PANS) misdiagnosed as autism spectrum disorder. Immunol Lett. 2018 Nov;203:52-53.
Greer, M.K., et al. A case study of the cognitive and behavioral deficits of temporal lobe damage in herpes simplex encephalitis. J Autism Dev Disord. 1989 Jun;19(2):317-26.
Gulati, G., et al. Anti-NR2 antibodies, blood-brain barrier, and cognitive dysfunction. Clin Rheumatol. 2016 Dec;35(12):2989-2997.
Hacohen, Y., et al. N‐methyl‐d‐aspartate (NMDA) receptor antibodies encephalitis mimicking an autistic regression. Dev Med Child Neurol. 2016 Oct;58(10):1092-4.
Hadjivassiliou, M., et al. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010 Mar;9(3):318-30.
Havas, M. Radiation from wireless technology affects the blood, the heart, and the autonomic nervous system. Rev Environ Health. 2013;28(2-3):75-84.
Hazlett, H.C., et al. Early brain development in infants at high risk for autism spectrum disorder. Nature. 2017 Feb 16;542:348–351.
Herbert, M.R., et al. Autism and EMF? Plausibility of a pathophysiological link part II. Pathophysiology. 2013 Jun;20(3):211-34.
Hirai, N., et al. A new infectious encephalopathy syndrome, clinically mild encephalopathy associated with excitotoxicity (MEEX). J Neurol Sci. 2017 Sep 15;380:27-30.
Hou, J., et al. Viral interactions with the blood-brain barrier: old dog, new tricks. Tissue Barriers. 2016 Jan 28;4(1):e1142492.
Ivanovski, I., et al. Aluminum in brain tissue in autism. J Trace Elem Med Biol. 2019 Jan;51:138-140.
Jain, R., et al. The effect of medical treatments on the bacterial microbiome in patients with chronic rhinosinusitis: a pilot study. Int Forum Allergy Rhinol. 2018 Mar 8.
Jaspers-Fayer, F., et al. Prevalence of Acute-Onset Subtypes in Pediatric Obsessive-Compulsive Disorder. J Child Adolesc Psychopharmacol. 2017 May;27(4):332-341.
Jyonouchi, H., et al. Cytokine profiles by peripheral blood monocytes are associated with changes in behavioral symptoms following immune insults in a subset of ASD subjects: an inflammatory subtype? J Neuroinflammation. 2014 Oct 27;11:187.
Kantarcioglu, A.S., et al. Microbiota-Gut-Brain Axis: Yeast Species Isolated from Stool Samples of Children with Suspected or Diagnosed Autism Spectrum Disorders and In Vitro Susceptibility Against Nystatin and Fluconazole. Mycopathologia. 2016 Feb;181(1-2):1-7.
Kelly, J.R., et al. Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders. Front Cell Neurosci. 2015 Oct 14;9:392.
Khan, Z., et al. Slow CCL2-dependent translocation of biopersistent particles from muscle to brain. BMC Med. 2013 Apr 4;11:99.
Kim, C., et al. Strep and Urinary Frequency: Is There a Connection? New England Section of the American Urological Association, 75th Annual Meeting. 2006 Sep 28-30.
King, L., et al. Intuition: a critical review of the research and rhetoric. J Adv Nurs. 1997 Jul;26(1):194-202.
Kinoshita, M., et al. Targeted delivery of antibodies through the blood-brain barrier by MRI-guided focused ultrasound. Biochem Biophys Res Commun. 2006 Feb 24;340(4):1085-90.
Kirvan, C.A., et al. Streptococcal mimicry and antibody-mediated cell signaling in the pathogenesis of Sydenham’s chorea. Autoimmunity. 2006 Feb;39(1):21-9.
Koffie, R.M., et al. Nanoparticles enhance brain delivery of blood–brain barrier-impermeable probes for in vivo optical and magnetic resonance imaging. Proc Natl Acad Sci U S A. 2011 Nov 15;108(46):18837-42.
Kovacevic, M., et al. Use of Intravenous Immunoglobulin in the Treatment of Twelve Youths with Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):65-9.
Kreuter, J. Nanoparticles and microparticles for drug and vaccine delivery. J Anat. 1996 Dec; 189(Pt 3): 503–505.
Kurlan, R. Tourette’s syndrome and ‘PANDAS’: will the relation bear out? Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Neurology. 1998 Jun;50(6):1530-4.
Lancaster, E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016 Jan;12(1):1-13.
Latimer, M.E., et al. Therapeutic plasma apheresis as a treatment for 35 severely ill children and adolescents with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):70-5.
Leclercq, S., et al. Low-dose penicillin in early life induces long-term changes in murine gut microbiota, brain cytokines and behavior. Nature Communications. 2017; 8.
Lionetti, E., et al. Gluten Psychosis: Confirmation of a New Clinical Entity. Nutrients. 2015 Jul 8;7(7):5532-9.
Ludlow, A.K., et al. Understanding the impact of diet and nutrition on symptoms of Tourette syndrome: A scoping review. J Child Health Care. 2018 Mar;22(1):68-83.
Mahony, T., et al. Improvement of psychiatric symptoms in youth following resolution of sinusitis. Int J Pediatr Otorhinolaryngol. 2017 Jan;92:38-44.
Mahony, T., et al. Palatal Petechiae in the Absence of Group A Streptococcus in Pediatric Patients with Acute-Onset Neuropsychiatric Deterioration: A Cohort Study. J Child Adolesc Psychopharmacol. 2017 Apr 7.
Marcello, A., et al. Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS): An Evolving Concept. Tremor Other Hyperkinet Mov (N Y). 2013 Sep 25;3. pii: tre-03-167-4158-7.
Marquet, F., et al. Noninvasive, Transient and Selective Blood-Brain Barrier Opening in Non-Human Primates In Vivo. PLoS One. 2011;6(7):e22598.
Mason, R. Expanding Diagnostic Vision with Medical Intuition. Alternative and Complementary Therapies. 2009 Mar 19; 6(6).
Mink, J., et al. Acute postinfectious movement and psychiatric disorders in children and adolescents. J Child Neurol. 2011 Feb;26(2):214-7.
Muir, K.E., et al. A case report of obsessive-compulsive disorder following acute disseminated encephalomyelitis. Pediatrics. 2013 Sep;132(3):e771-4.
Murphy, T.K., et al. Cefdinir for recent-onset pediatric neuropsychiatric disorders: a pilot randomized trial. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):57-64.
Murphy, T.K., et al. Characterization of the pediatric acute-onset neuropsychiatric syndrome phenotype. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):14-25
Murphy, T.K., et al. A Double-Blind Randomized Placebo-Controlled Pilot Study of Azithromycin in Youth with Acute-Onset Obsessive-Compulsive Disorder. J Child Adolesc Psychopharmacol. 2017 Mar 30.
Murphy, T.K., et al. Pediatric acute-onset neuropsychiatric syndrome. Psychiatr Clin North Am. 2014 Sep;37(3):353-74.
Nadeau, J.M., et al. A pilot trial of cognitive-behavioral therapy augmentation of antibiotic treatment in youth with pediatric acute-onset neuropsychiatric syndrome-related obsessive-compulsive disorder. J Child Adolesc Psychopharmacol. 2015 May;25(4):337-43
Orefici, G., et al. Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS). Streptococcus pyogenes: Basic Biology to Clinical Manifestations [Internet]. Oklahoma City (OK): University of Oklahoma Health Sciences Center; 2016-. 2016 Feb 10.
Orlovska, S., et al. Association of Streptococcal Throat Infection With Mental Disorders: Testing Key Aspects of the PANDAS Hypothesis in a Nationwide Study. JAMA Psychiatry. 2017 Jul 1;74(7):740-746.
Pall, M.L. Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression. J Chem Neuroanat. 2016 Sep;75(Pt B):43-51.
Parker-Athill, E.C., et al. Cytokine correlations in youth with tic disorders. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):86-92.
Pearlman, D.M., et al. Anti-basal ganglia antibodies in primary obsessive-compulsive disorder: systematic review and meta-analysis. Br J Psychiatry. 2014 Jul;205(1):8-16.
Pihtili, A., et al. Evidence for the Efficacy of a Bioresonance Method in Smoking Cessation: A Pilot Study. Forsch Komplementmed. 2014;21(4):239-45.
Plioplys, A.V., et al. Anti-CNS antibodies in childhood neurologic diseases. Neuropediatrics. 1989 May;20(2):93-102.
Rawls, W.E., et al. Encephalitis associated with herpes simplex virus. Ann Intern Med. 1966 Jan;64(1):104-15.
Sahyouni, R., et al. Effects of concussion on the blood–brain barrier in humans and rodents. Journal of Concussion. 2017 Jan 1; 10.1177/2059700216684518
Sai, Y., et al. Clinical diagnosis and treatment of pediatric anti-N-methyl-D-aspartate receptor encephalitis: A single center retrospective study. Exp Ther Med. 2018 Aug;16(2):1442-1448.
Samsel, A., et al. Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies. Surg Neurol Int. 2015 Mar 24;6:45.
Shet, A., et al. Immune Response to Group A Streptococcal C5a Peptidase in Children: Implications for Vaccine Development. J Infect Dis. 2003 Sep 15;188(6):809-17.
Sifra, S., et al. Treatment of PANDAS and PANS: a systematic review. Neuroscience & Biobehavioral Reviews. 2018 Mar;86:51-65.
Singer, H.S., et al. Moving from PANDAS to CANS. The Journal of Pediatrics. 2012 May; 160(5):725-731.
Song, Y., et al. Effects of acute exposure to aluminum on blood-brain barrier and the protection of zinc. Neurosci Lett. 2008 Nov 7;445(1):42-6.
Spartz, E.J., et al. Course of Neuropsychiatric Symptoms After Introduction and Removal of Nonsteroidal Anti-Inflammatory Drugs: A Pediatric Observational Study. J Child Adolesc Psychopharmacol. 2017 Jul 11.
Spindler, K.R., et al. Viral disruption of the blood-brain barrier. Trends Microbiol. 2012 Jun;20(6):282-90.
Swedo, S.E., et al. Clinical Presentation of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections in Research and Community Settings. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):26-30
Swedo, S.E., et al. Identification of children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections by a marker associated with rheumatic fever. Am J Psychiatry. 1997 Jan;154(1):110-2.
Swedo, S.E., et al. Overview of Treatment of Pediatric Acute-Onset Neuropsychiatric Syndrome. J Child Adolesc Psychopharmacol. 2017 Jul 19.
Tanaka, S., et al. Autoantibodies against four kinds of neurotransmitter receptors in psychiatric disorders. J Neuroimmunol. 2003 Aug;141(1-2):155-64.
Tang, J., et al. Exposure to 900 MHz electromagnetic fields activates the mkp-1/ERK pathway and causes blood-brain barrier damage and cognitive impairment in rats. Brain Res. 2015 Mar 19;1601:92-101.
Theoharides, T.C., et al. Neuro-inflammation, blood-brain barrier, seizures and autism. J Neuroinflammation. 2011 Nov 30;8:168.
Thienemann M., et al. Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part I-Psychiatric and Behavioral Interventions. J Child Adolesc Psychopharmacol. 2017 Jul 19.
Tohidpour, A., et al. Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit. Front Cell Infect Microbiol. 2017 Jun 20;7:276.
Tona, J.T., et al. Impact of PANS and PANDAS Exacerbations on Occupational Performance: A Mixed-Methods Study. Am J Occup Ther. 2017 May/Jun;71(3):7103220020P1-7103220020P9.
Toufexis, M.D., et al. Disordered eating and food restrictions in children with PANDAS/PANS. J Child Adolesc Psychopharmacol. 2015 Feb;25(1):48-56.
Tuchscherr, L., et al. Staphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection. EMBO Mol Med. 2011 Mar;3(3):129-41.
Vitaliti, G., et al. A new clinical feature associated with familial early-onset of dystonic-guttural tics: An unusual diagnosis of PANDAS. J Pediatr Neurosci. 2014 Jan;9(1):79-81.
Wang, Hsiuying. Anti-NMDA Receptor Encephalitis. Int J Mol Sci. 2017 Jan 18;18(1). pii: E193..
Yaddanapudi, K., et al. Passive transfer of streptococcus-induced antibodies reproduces behavioral disturbances in a mouse model of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Mol Psychiatry. 2010 Jul;15(7):712-26.
Zong, S., et al. Neuronal Surface Autoantibodies in Neuropsychiatric Disorders: Are There Implications for Depression? Front Immunol. 2017 Jul 5;8:752.
Blaylock, Russell L. Excitotoxins: The Taste That Kills. Health Press, 1996.
Cahalan, Susannah. Brain on Fire: My Month of Madness. Simon & Schuster, 2013.
Campbell-McBride, Natasha. Gut and Psychology Syndrome: Natural Treatment for Autism, Dyspraxia, A.D.D., Dyslexia, A.D.H.D., Depression, Schizophrenia. 2010.
Chutkin, Robin. The Microbiome Solution: A Radical New Way to Heal Your Body from the Inside Out. Avery, 2016.
Lambert, Beth, et al. Brain Under Attack: A Resource for Parents and Caregivers of Children with PANS, PANDAS, and Autoimmune Encephalitis. Answers Publications, 2018.
Maloney, Alison Beth. Saving Sammy: A Mother’s Fight to Cure Her Son’s OCD. Broadway Books, 2010.
Weiss, Melanie S. In a Pickle Over PANDAS. First Edition Design Publishing, 2015.