Wednesday, March 7, 2012

Adult PANDAS: Bare Facts

[Below is a paper a prepared recently for a juried journal. They did not find it pertinent.  They had no idea what this is about and the implications for our health and welfare. I've included the bibliography for patients and parents to take to their, and their children's physicians.  Feel free to critique.  I'll make a comment about this at the end.]

It has been known for more than a century that post-infectious autoimmune physical and neuropsychiatric symptoms can occur. Most well-known are the post-streptococcal infectious autoimmune processes which include rheumatic fever, glomerulonephritis, Sydnenham's Chorea and St. Vitus dance. That the central nervous system is vulnerable to such processes has been acknowledged and understood. 

Over the past 15 years the phenomenon of Pediatric Autoimmune Neurologic and Psychiatric Disorders Associated with Strep, (PANDAS), has been identified around the world1,2. Despite naysayers and nonbelievers the evidence-based clinical data in conjunction with laboratory evidence establishes the existence of this disorder beyond any reasonable doubt.2,3 There remains great confusion as to precisely what neuropsychiatric and/or physical symptoms may be associated with PANDAS4,10; whether or not agents other than Streptococcus cause PANDAS5,6, and what potential laboratory findings may make or support this diagnosis7,8. This leads to further confusion and consternation with respect to diagnostic evaluation, and of greater importance, when, how and what to do to treat the protean manifestations of this disorder.

The question of PANDAS in adults largely has been ignored with uninformed, erroneous comments and statements that adults cannot acquire PANDAS. Hence, they cannot have it.. This paper will present evidence-based clinical research data to prove that adults can have or acquire PANDAS. A broad range of neuropsychiatric and physical symptoms will be described [see table I]. Many of these have been diagnosed as primary problems and treated ineffectively as such. Others have been misdiagnosed and mistreated.  Some simply have been missed [see table II].

A brief discussion of clinical and laboratory diagnostic tools will occur7,9. Comments on the viable treatment options available will be made, again from the perspective of the author's evidence-based clinical research.11,12

Certainly adults can acquire PANDAS. However this would require exposure to a novel infectious agent for that adult. Adult acquisition would, for all intents and purposes, be similar to native Americans and Polynesians falling victim to diseases brought by European explorers. Most commonly adults have had PANDAS for many years but either it has not been considered or it has been misdiagnosed and typically poorly treated as some other neuropsychiatric or physical complaint.

Diagnosis in adults is a logical extension of the diagnosis in children. Thus far the majority of the diagnoses in children are made after the phenomenon has been present for some time. In adults the phenomena have been present for years or decades. Indeed there are an increasing number of reports of acute onset PANDAS in children: Obsessive Compulsive Disorder (OCD); Tourette's and Tics are the most frequent. One familiar with PANDAS immediately considers this diagnosis with acute onset and needs to look for it in patients with other symptomatology [see table III]. In the author's practice innumerable children and adolescents previously diagnosed with Anorexia Nervosa (AN), various anxiety disorders, OCD, Tics and Tourette's, body dysmorphic disorder and quite commonly bipolar disorder (BPD) have been diagnosed with PANDAS, undergone effective treatment and their prior diagnoses disappear. This is of particular importance in BPD, OCD and AN.

The tantrums, outbursts, lability, aggressiveness, ready anger and other symptomatology that leads to the diagnosis of BPD and the treatment thereof in children and adolescents repeatedly has turned out to be PANDAS induced Tourette's, with or without generalized anxiety disorder (GAD) and/or panic disorder (PD). In most of these cases removal of tonsils and adenoids has “cured” the bipolar disorder.11. Patient's have been removed from potent mood stabilizers and atypical antipsychotics as well as [Table II] SSRIs.13  In most cases the patients have Attention Deficit Hyperactivity Disorder (ADHD), usually undiagnosed, which has contributed materially to the overall problems.14 This is an important point which will be elaborated upon further below.

Similarly in adolescent girls with AN,7,15 most of whom have been through months and years of eating disorder treatment, in facilities and hospitals, careful clinical and laboratory examination reveals their true diagnoses to be PANDAS. Most patients with AN have significant symptoms of anxiety and OCD. The OCD symptoms are ego dystonic (OCD is misdiagnosed frequently in patients with ADHD who use obsessive-compulsive mechanisms to bind anxiety–of course this leads to ineffective treatment for the “OCD”). There is an obvious element of body dysmorphic disorder in their preoccupations with weight and image. Again the diagnosis and treatment of the underlying PANDAS which has been driving this constellation of symptoms leads to dramatic resolution of the “eating disorder”, much to the consternation of the devoted eating disorder therapists. And yes, most of these patients have  concurrent ADHD.

This experience with dozens of children and adolescents led the author to examine adults with the same group of diagnoses. It is important to remark at this time that most of the children, adolescents and adults had never done particularly well with any therapeutic intervention for their purported diagnoses [Table II]. Nonetheless examination of adult patients with: OCD; BPD; AN; body dysmorphic disorder; fibromyalgia; and all of the other diagnoses noted in Table I led to the diagnosis of PANDAS. And again, as with the children and adolescents, the putative diagnoses dissolved with proper treatment. Treatment of underlying or concurrent diagnoses of depression, anxiety, ADHD, sleep disorders and so forth then became simple and effective. Elevated anti-DNAase B antibodies plummeted. A 64-year-old woman with a long history of depression, anxiety, poor sleep, fibromyalgia and Systemic lupus erythematosus (SLE) who also had obvious ADHD and periodic limb movement disorder (PLMD) experienced a complete disappearance of her fibromyalgia symptoms after tonsillectomy. Aches and pains went away. Energy improved. Sleep became restorative and attention and mood improved with proper treatment. Anti-DNAase B antibody levels dropped. Her ANA, elevated for many years dropped to a normal level.

This evidence-based clinical research has seen complete resolution of Tics, OCD, GAD/PD/ Tourette's misdiagnosed as BPD and other problems “cured” by the diagnosis and treatment of PANDAS. The outcomes are not perfect. It is obvious that individuals susceptible to PANDAS have a genetic predisposition.16,17,18,19 Very few people with strep throats develop rheumatic fever, glomerulonephritis or the spectrum of neuropsychiatric and physical symptoms driven by an autoimmune response to strep. Those that do develop PANDAS remain susceptible to flares after treatment. This means that exposure to the precipitating agent may cause a brief recurrence of symptomatology. Dependent upon individual circumstances--active infection, exposure without apparent infection and intensity of symptoms--these flares variously are treated with antibiotics and/or corticosteroids or ignored in the knowledge that the flareup will resolve once the antibodies have eliminated the infectious agent and that the source of chronic, subacute infection previously present in the tonsils and adenoids, or sinuses, intestines… has been eradicated. One patient treated from middle school to adulthood knows that she has had a strep exposure when she develops compulsive hand washing again. She knows that this will last about 2 weeks and then stop.

PANDAS is not a single entity. There is no doubt that multiple genetic loci will be identified eventually in individuals susceptible to PANDAS. The variations make different individuals vulnerable to different infectious agents and different symptom clusters. Clearly there is one subgroup that develops a chronic presentation. The author infers that these patients have a chronic viral trigger and/or a genetic subtype wherein the inflamed neurologic tissue continues to generate an autoimmune response regardless of the eradication of the primary infectious agent.20,21,22,23,24

Thus far multiple agents have been identified as precipitants of PANDAS [Table III]. No doubt many others will be determined in the future. Definitive genetic subtypes have not been identified. No specific test is diagnostic of PANDAS. An elevated anti-DNAase B with symptoms is sufficient but not necessary. Elevated mycoplasma, streptozyme, Lyme and many others are also sufficient but not necessary. The fascinating relationship with fibromyalgia and low-level SLE and rheumatoid arthritis (RA) deserves extensive study exploration.

Treatment approaches are controversial. If an antibiotic suppresses symptoms but the symptoms recur after cessation of the antibiotic then, clearly, there is an internal source of chronic subacute infection. Steroids in the acute phase usually exacerbate PANDAS. Plasmapheresis and IVIG are both effective in acute symptomatic relief of symptoms but neither appears definitive or permanent. This suggests either a source of chronic subacute infection, a chronic virus, or inflamed neurologic tissue sufficient to continue to generate an antibody response. 

Many practitioners approach this situation incrementally with long-term antibiotics (which can result in antibiotic allergy, resistant organisms, and pseudomembranous colitis), repeated IVIG (which is not “curative” but provides symptomatic relief for a variable period of time), and plasmapheresis which yields about the same results as the IVIG.

The author has found an aggressive approach most effective. Once the diagnosis is considered, appropriate chemistries and serology must be obtained. Whether or not the chemistries and serology  are  positive a thorough examination for potential sources of chronic subacute infection is warranted. Tonsils and adenoids, sinuses, mastoids, appendix, intestines and colon are all potential nidi. Thus far two patients have been seen with obstipation and multiple symptoms of PANDAS who have improved subsequent to antibiotic therapy for the colonic infection and resolution of the obstipation. One of these patients is a young man who presented with GAD, PD, OCD, ADHD, body dysmorphic disorder and depression who improved subsequent to tonsillectomy only to have a relapse related to a G.I. source which then resolved after effective treatment of that. He truly had PANDAS from top to bottom.

Given the panoply of infectious agents which can precipitate PANDAS there is no single, simple approach to this problem. The most important thing is to think of it, look for it, find it and then treat it.

Adults can get and have PANDAS. More often than not they've had it since childhood. What must the psychiatrist do about this? First and foremost the psychiatrist must not behave as have our peers of prior generations. That means that when anything psychiatric takes on a medical aspect–syphilis, sleep disorders, pain management, seizure disorders, traumatic brain injuries–they turn it over to the “real” doctors. The psychiatrist must go down the list of psychiatric diagnoses extant with specific disregard to the artificial boundaries and parameters of DSM as one begins to look at the specifics of the patient.

Based upon extensive clinical experience there is an obvious overlap between ADHD and PANDAS. And again adult ADHD is not characterized in DSM-IV TR and will be poorly characterized in DSM-V. The psychiatrist must begin to look at each and every diagnosis as potentially symptomatic of something else. Something like PANDAS. Will this be proven correct in a in every case? Of course not.   Will this be proven correct in a startling number of cases? Yes. If you do not think of it you do not look for it and if you do not look for it you do not find it. The author has diagnosed 18 cases of porphyria. Is it contemplated in every case? No. Are there indicators for which to look? Yes.

Psychiatrists must familiarize themselves with all of the available literature on PANDAS which at this time is relatively scant. Never accept anyone else's diagnosis. Think for yourself and peruse the list of symptoms and diagnoses appended to this article and begin to question yourself every time you hear or contemplate these diagnoses.  Question whether or not these may be symptoms of an underlying autoimmune disorder related to  PANDAS.  Learn what labs to order and what history to take with respect to sore throats and ear infections and the timeline for the evolution of various symptoms. The correct diagnosis of PANDAS is a definitive intervention and transformative experience for patients heretofore tormented, disabled, overmedicated and miserable.

It is precisely in circumstances such as these that evidence-based clinical medicine is the determinant of diagnostic accuracy and definitive therapeutic intervention. If each of you were to review your past and present caseload from this perspective the database and knowledge of and this would grow exponentially in less than a year.

Autoimmune phenomena are responsible for a staggering number of NeuroPsychiatric and Medical problems.  With this knowledge the diagnoses, prognoses and lives of hundreds of thousands of patients can be altered and improved in a very short time.

[We've been told that the above does not meet the editorial "needs" of the journal.  I could submit it elsewhere.  But the experience that I and many of my colleagues in private practice have had is that our submissions are rarely published. Without academic affiliations and large bibliographies of our own (having worked their way up from 5th to 4th to 3rd to 2nd to 1st author) we are not credible. Yet, I and dozens of my colleagues with whom I have conferred over decades have had the same experience, usually to see their ideas and research pop up in another journal under the authorship of one of the “jurors” of the journal to which the work was submitted. That is why so many of us self publish. My book, 1st edition copyright 1998 was heavily plagiarized. Hence many of us now post are work on the Internet and self publish on the Internet. Hopefully this article and the appended bibliography will help patients, families and physicians get effective treatment now, rather than having to wait until goombahs at Harvard or the NIH come forward in 2 or 3 years with their startling discovery of the above.]

Table 1.

9      number of patients seen
6                        “
Obsessive Compulsive Disorder
6                        “
Anorexia Nervosa
2                        “
Generalized Anxiety Disorder
16                      “
Panic Disorder
4                        “
4                        “
1                        “
Spastic Dysphonia
1                        “
2                        “
1                        “
Attention Deficit Hyperactivity Disorder
21                      “
Body Dysmorphic Disorder
5                        “
4                        “
Low level Systemic Lupus Erythematosus & Rheumatoid Arthritis associated with Fibromyalgia
3                        “
Periodic Limb Movement Disorder
20                      “
Severe Halitosis
3                        “
Strange Body Odor (perceived by patient & others)--Colonic etiology
2                        “
Bipolar Disorder
7                        “
Intermittent Explosive Disorder (Tourette's)
2                        “
Torsion Dystonia/Spastic Torticollis
2                        “

Table 2.

Acute infection or reinfection (the latter includes acute “flares” with re-exposure after effective treatment)
Noradrenergic/dopaminergic antidepressants
Selective serotonin reuptake inhibitors either by acute akathisia or tachyphylaxis to dopamine blockade
Dopamine blocking agents: atypical antipsychotics, neuroleptics, anti-emetics via acute akathisia, tachyphylaxis to dopamine blockade and exacerbation of extrapyramidal symptoms and dystonia's
Development of antibiotic resistance

Table 3.

Streptococcus, multiple subtypes
Haemophilus influenza
Staphylococcus aureus
Mycoplasma pneumonia
Lyme disease

(Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcus) 
J Child Adolesc Psychopharmacol. 2011 Apr;21 (2):177-82. Epub 2011 Apr 12. 
Pediatric autoimmune neuropsychiatric disorders associated with Streptococcus in identical siblings.
Lewin AB, Storch EA, Murphy TK. 
Rothman Center for Neuropsychiatry, Department of Pediatrics, University of South Florida College of Medicine, St. Petersburg, Florida 33701, USA. 
ABSTRACT: Termed pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (PANDAS), these cases of childhood-onset obsessive compulsive disorder and tic disorders resemble the presentation of Sydenham chorea, in that they have an acute onset following a group A beta-hemolytic streptococcal infection (group A Streptococcus), with accompanying neurological signs, and an episodic or sawtooth course. Familial associations of this subgroup of patients remain understudied. This report provides phenotypic descriptions of three youth with PANDAS as well as their genetically identical siblings (in two cases of twins and one case of triplets). These cases highlight the potential for environmental influences for discordant presentations in genetically identical siblings. Despite identical genetics, presentations showed marked variation across siblings (from a full PANDAS presentation to asymptomatic). Further research into environmentally driven influences such as postinfectious molecular mimicry and epigenetic factors that may influence the manifestation of these pediatric neuropsychiatric disorders will promote our understanding of their prevention and treatment
PMID: 21486169 [pubMed - indexed for MEDLINE
Int J Pediatr Otorhinolaryngol. 2011 Jun;7S(6):872-3. Epub 2011 Apr 3. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS): an indication for tonsillectomy. 
Alexander AA, Patel NJ, Southammakosane CA, Mortensen MM
University of Virginia, Department of Radiology, Charlottesville, VA 22908, USA. 
ABSTRACT: Children with obsessive compulsive disorder or tic disorders that are associated with streptococcal infections (Group A beta-hemolytic) in the oro-pharyngeal region are given the diagnosis of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Tonsillectomy has been reported to resolve the neuro-psychiatric symptoms in these children. We have a 
case of a 9-year-old boy who was seen in our clinic with multiple recurrent streptococcal infections of the oro-pharyngeal cavity. He also exhibited neuro-psychiatric symptoms including agitation, hyperactivity, and tics. These symptoms followed his recurrent infections. Tonsillectomy was performed and in one year followup the patient did not have any recurrent streptococcal infections, and his neuro-psychiatric symptoms resolved completely. Guidelines for medical and surgical management of recurrent strep infections in the face of PANDAS are reviewed. 
PMID: 21466900 [pubMed - indexed for MEDLINEJ 
Neurology. 2011 Jan 18;76(3):294-300. 
Evidence-based guideline update: Plasmapheresis in neurologic disorders: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Cortese I, Chaudhry V, So Yl', Cantor F, Cornblath DR, Rae-Grant A. 
National Institutes of Health, Bethesda, USA. 
Comment in 
Neurology. 2011 Oct 2S;77(17):el0l; author reply el03-4. Neurology. 2011 Oct 25;77(17):e103; author reply el03-4. Neurology. 2011 Oct 2S;77(17):e10S; author reply elOS. Neurology. 2011 Oct 2S;77(17):el01; author reply e103-4. Neurology. 2011 Oct 2S;77(17):el04-S; author reply el0S. Neurology. 2011 Oct 25;77(17):e101-2; author reply el03-4. Neurology. 2011 Oct 2S;77(17):el02-3; author reply el03-4

Neurology. 2011 Oct 25;77(17):el05-6; author reply el06. 
OBJECTIVE: To reassess the role of plasmapheresis in the treatment of neurologic disorders. METHODS: 
We evaluated the available evidence based on a structured literature review for relevant articles from 1995 through September 2009. In addition, due to revision of the definitions of classification of evidence since 
the publication of the previous American Academy of Neurology assessment in 1996, the evidence cited in that manuscript was reviewed and reclassified. RESULTS AND RECOMMENDATIONS: Plasmapheresis is established as effective and should be offered in severe acute inflammatory demyelinating polyneuropathy (AIDP)/Guillain-Barre syndrome (GBS) and in the short-term management of chronic inflammatory demyelinating polyneuropathy (Class I studies, Level A). Plasmapheresis is established as ineffective and should not be offered for chronic or secondary progressive multiple sclerosis (MS) (Oass I studies, Level A). Plasmapheresis is probably effective and should be considered for mild AIDP /GBS, as second-line treatment of steroid-resistant exacerbations in relapsing forms ofMS, and for neuropathy associated with immunoglobulin A or immunoglobulin G gammopathy, based on at least one Class I or 2 Class II studies (Level B). Plasmapheresis is probably not effective and should not be considered for neuropathy associated with immunoglobulin M gammopathy, based on one Class I study (Level B).Plasmapheresis is possibly effective and may be considered for acute fulminant demyelinating CNS disease (Level C). There is insufficient evidence to support or refute the use of plasmapheresis for myasthenia gravis, pediatric autoimmune neuropsychiatric disorders associated with streptococcus infection, and Svdenham 
chorea (Oass III evidence, Level U). 
PMCID: PMC3034395 
PMID: 21242498 [pubMed - indexed for MEDLINEJ 
JAm Acad Child Adolesc Psychiatry. 2011 Feb;50(2):108-118.e3. Epub 2010 Dec 31. 
Streptococcal upper respiratory tract infections and exacerbations of tic and obsessive-compulsive symptoms: a prospective longitudinal study. 
Leckman]F, I<1ng RA, Gilbert DL, Coffey B], Singer HS, Dure LS 4th, Grantz H, Katsovich L, Lin H, 
Lombroso PJ, Kawikova I,Johnson DR, Kurlan RM, Kaplan EL. 
Child Study Center and the Yale Center for Clinical Investigation, Yale University School of Medicine, 230 
South Frontage Road, New Haven, CT 06520-7900, 
OBJECTIVE: The objective of this blinded, prospective, longitudinal study was to determine whether new group A ~ hemolytic streptococcal (GABHS) infections are temporally associated with exacerbations of tic or obsessive-compulsive (OC) symptoms in children who met published criteria for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). A group of children with Tourette syndrome and/or OC disorder without a PANDAS history served as the comparison (nonPANDAS) group. METHOD: Consecutive clinical ratings of tic and OC symptom severity were obtained 
for 31 PANDAS subjects and 53 non- PANDAS subjects. Clinical symptoms and laboratory values (throat cultures and streptococcal antibody titers) were evaluated at regular intervals during a 25-month period. Additional testing occurred at the time of any tic or OC symptom exacerbation. New GABHS infections were established by throat swab cultures and/or recent significant rise in streptococcal antibodies. Laboratory personnel were blinded to case or control status, clinical (exacerbation or not) condition, and clinical evaluators were blinded to the laboratory results. RESULTS: No group differences were observed in the number, of clinical exacerbations or the number of newly diagnosed GABHS infections. On only six occasions of a total of 51 (12%), a newly diagnosed GABHS infection was followed, within 2 months, by an exacerbation of tic and/ or OC symptoms. In every instance, this association occurred in the non- PANDAS group. CONCLUSIONS: This study provides no evidence for a temporal association between GABHS infections and tic/OC symptom exacerbations in children who meet the published PANDAS diagnostic 
PMCID: PMC3024577 [Available on 2012/2/1] PMID: 21241948 [pubMed - indexed for MEDLINEJ 
J Neuroimmunol. 2010 Dec 15;229(1-2):243-7. Epub 2010 Sep 22. 
Maternal history of autoimmune disease in children presenting with tics and/or obsessive- 
compulsive disorder. 
Murphy TK, Storch EA, Turner A, Reid]M, Tan], Lewin AB. 
Department of Pediatrics, University of South Florida, College of Medicine, St. Petersburg, FL 33701, USA. 

OBJECTIVES: A commonality across a number of pediatric neuropsychiatric disorders is a higher than typical rate of familial _ and especially maternal - autoimmune disease. Of recent interest, a subtype of obsessive-compulsive disorder (OCD) and tic disorders known collectively as Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (pANDAS) is believed to be secondary to 
central nervous system (CNS) autoimmunity that occurs in relation to group A streptococcal infection. Thus, we hypothesized that a sample of children with OCD and/or tics would have an increased maternal risk for an autoimmune response relative to population norms. We also expected maternal prevalence of various autoimmune diseases to be higher among those participants that met the putative criteria for PANDAS. METHODS: We examined, via structured interview, the medical history of the biological mothers of 107 children with OCD and/or tics. RESULTS: Autoimmune disorders were reported in 17.8% of study mothers, which is significantly greater than the general prevalence among women in the United States (approximately 5%). Further, study mothers were more likely to report having an autoimmune disease if their children were considered "likely PANDAS" cases versus "unlikely PANDAS" cases. CONCLUSIONS: The results offer preliminary support for hypothesized links between maternal autoimmune disease and both OCD / tics and PANDAS in youth. Further research is necessary to clarify these general associations; links to specific autoimmune disease; and relevance of autoimmune disease in other family members (e.g., fathers). 
PMCID: PMC2991439 
PMID: 20864184 [pubMed - indexed for MEDLINEJ 
J Child Adolesc Psychopharmacol. 2010 Aug;20(4):317-31. 
The immunobiology of Tourette's disorder. pediatric autoimmune neuropsychiatric disorders 
associated with Streptococcus. and related disorders: a way forward. 
Murphy TK, Kurlan R, Leckman J. 
Department of Pediatrics and Psychiatry, University of South Florida, St Petersburg, Florida 33701, USA. 
Obsessive-compulsive disorder (OCD) and related conditions including Tourette's disorder (TD) are chronic, relapsing disorders of unknown etiology associated with marked impairment and disability. Associated immune dysfunction has been reported and debated in the literature since the late 80s. The immunologic culprit receiving the most interest has been Group A Streptococcus (GAS), which began to receive attention as a potential cause of neuropsychiatric symptoms, following the investigation of the symptoms reported in Sydenham's chorea (SC) and rheumatic fever, such as motor tics, vocal tics, and both obsessive-compulsive and attention deficit/hyperactivity symptoms. Young children have been desctibed as having a sudden onset of these neuropsychiatric symptoms temporally associated with GAS, but without supporting evidence of rheumatic fever. This presentation of OCD and tics has been termed pediatric autoimmune neuropsychiatric disorders associated with Streptococcus (pANDAS). Of note, SC, OCD, and TD often begin in early childhood and share common anatomic areas-the basal ganglia of the brain and the related cortical and thalamic sites-adding support to the possibility that these disorders might share a common immunologic and/ or genetic vulnerability. Relevant manuscripts were identified through searches of the PsycINFO and MedLine databases using the following keywords: OCD, immune, PANDAS, Sydenham chorea, Tourette's disorder Group A Streptococcus. Articles were also identified through reference lists from research articles and other materials on childhood OCD, PANDAS, and TD between 1966 and December 2010. Considering the overlap of clinical and neuroanatomic findings among these disorders, this review explores evidence regarding the immunobiology as well as the relevant clinical and therapeutic aspects ofTD, OCD, and 
PMID: 20807070 [PubMed - indexed for MEDLINEJ 
Autism Res. 2010 Aug;3(4):147-52. 
Role for antibodies in altering behavior and movement. 
Libbey JE, Fujinami RS. 
Department of Pathology, University of Utah, Salt Lake City, Utah 84132, USA. 
At the past meeting of INSAR, the role of autoimmunity was discussed in an educational session. This article summarizes this discussion. In immune-mediated diseases, antibodies can contribute to the pathogenesis of the disease and are sometimes the force that drives the disease process. This concept has not been established for autism. In autoimmune diseases, such as systemic lupus erythematosus (SLE), antibodies are found to react with double-stranded DNA. These antibodies also cross-react with N-methyl-D aspartate receptors. Many SLE patients suffer neurologic syndromes of the central nervous system (CNS). Similarly individuals 

infected with Group A streptococcus (GAS) have antibodies against the GAS carbohydrate, which cross-react with tubulin and lysoganglioside GMl on neurons. During the acute stage of infection, GAS-infected patients develop Syndenham chorea where the disease process is driven in part by these cross-reactive antibodies. As the antibody levels decrease, the clinical features of Syndenham chorea resolve. In these two immunemediated diseases, antibodies clearly playa role in the pathogenesis of the diseases. There are reports that mothers of individuals with autism have antibodies that react with brain proteins and when these antibodies are passively transferred to pregnant non-human primates or rodents the offspring has behavioral and nervous system changes. It is still not clear whether the antibodies found in mothers of individuals with autism actually playa role in the disease. More studies need to be performed to identify the proteins recognized by the antibodies and to determine how these could affect development, behavior and changes within the CNS
PMID: 20589715 [pubMed - indexed for MEDLINEJ 
TurkJ Pediatr. 2009 Jul-Aug;51 (4):317-24. 
The relationship between group A beta hemolytic streptococcal infection and psychiatric symptoms: a pilot study. 
Cengel-Kiiltiir SE, Cop E, Kara A, Cengiz AB, Uludag AI<, Unal F. 
Department of Child and Adolescent Psychiatry, Hacettepe Universjty Faculty of Medicine, Ankara, Turkey. The aim of this study was to test if children with group A beta hemolytic streptococcal infection (GABHS) are more likely to develop neuropsychiatric symptoms or the syndrome of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection (PANDAS) compared to children with GABHS-negative throat cultures. Children aged 8 to 12 years (n = 81) with upper respiratory tract infection were assessed with the Schedule for Affective Disorders and Schizophrenia for School-Age Children - Present and Lifetime Version, Children's Yale Brown Obsession Compulsion Scale, Yale Global Ti
Severity Scale, Child Behavior Checklist for Ages 4-18, Conners Parent Rating Scale, and State-Trait Anxiety Inventory for Children at baseline and six weeks later. One case of PANDAS was diagnosed and no other differences were observed between groups and time points. It was suggested that GABHS infection may be a triggering factor for PANDAS in some genetically prone individuals
PMID: 19950837 [pubMed - indexed for MEDLINE
I Psychosom Res. 2009 Dec;67(6):547-57
The PANDAS subgroup oftic disorders and childhood-onset obsessive-compulsive disorder. Martino D, Defazio G, Giovannoni G. 
Department of Neurological and Psychiatric Sciences, University of Bari, Italy. 
Diagnosis and treatment of the PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) variant of Gilles de la Tourette syndrome (GTS) and childhood-onset obsessivecompulsive disorder (OCD) are still controversial issues. Most cross-sectional studies confirm a significant association between GTS and the development of an immune response against group A beta-hemolytic streptococcus (GABHS). Moreover, longitudinal retrospective studies suggest that a recent exposure to GABHS might be a risk factor for the onset of tics and obsessive-compulsive symptoms. However, further evidence from longitudinal prospective research is needed to verify whether a temporal association between GABHS infections and symptom exacerbations is a useful and reliable criterion for the diagnosis of PANDAS. In addition, preliminary results suggest that the PANDAS spectrum might be enlarged to include attention deficit/hyperactivity disorder. Although a number of immunological biomarkers have been proposed as markers of the PANDAS variant, at present, none of these has been conclusively proved useful to diagnose and monitor disease course in children with a suspicion of PANDAS. Finally, despite their empirical use in community settings, we still lack conclusive, evidence-based data regarding the usefulness of antibiotic and immunomodulatory treatments in children with PANDAS. Given the relevance of this topic for general pediatric health, additional research efforts to solve all the pending issues and the hottest points of debate are warranted
PMID: 19913659 [pubMed - indexed for MEDUNE] 
Mol Psychiatry. 2010 Jul;15(7):712-26. Epub 2009 Aug 11. 
Passive transfer of streptococcus-induced antibodies reproduces behavioral disturbances in a mouse model of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection. Yaddanapudi K, Hornig M, Serge R, De Miranda], Baghban A, Villar G, Lipkin WI. 

Center for Infection and Immunity and Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY 10032, USA. 
Streptococcal infections can induce obsessive-compulsive and tic disorders. In children, this syndrome, frequently associated with disturbances in attention, learning and mood, has been designated pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). Autoantibodies recognizing central nervous system (CNS) epitopes are found in sera of most PANDAS subjects, but may not be unique to this neuropsychiatric subset. In support of a humoral immune mechanism, clinical improvement often follows plasmapheresis or intravenous immunoglobulin. We recently described a PANDAS mouse model wherein repetitive behaviors correlate with peripheral anti-CNS antibodies and immune deposits in brain following streptococcal immunization. These antibodies are directed against group A beta-hemolytic streptococcus matrix (M) protein and cross-react with molecular targets complement C4 protein and alpha-2-macroglobulin in brain. Here we show additional deficits in motor coordination, learning/ memory and social interaction in PANDAS mice, replicating more complex aspects of human disease. Furthermore, we demonstrate for the first time that humoral immunity is necessary and sufficient to induce the syndrome through experiments wherein naive mice are transfused with immunoglobulin G (IgG) from PANDAS mice. Depletion of IgG from donor sera abrogates behavior changes. These functional disturbances link to the autoimmunity-related IgGl subclass but are not attributable to differences in cytokine profiles. The mode of distupting blood-brain barrier integrity differentially affects the ultimate CNS distribution of these antibodies and is shown to be an additional important determinant of neuropsychiatric outcomes. This work provides insights into PANDAS pathogenesis and may lead to new strategies for identification and treatment of children at risk for autoimmune brain disorders. 
PMID: 19668249 [pubMed - indexed for MEDLIN E) 
Curr Opin Pediatr. 2009 Feb;21 (1):127-30
Pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS): update. 
Shulman ST
The Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. 
PURPOSE OF REVIEW: To review recent developments related to the proposed entity Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococci (so-called 'PANDAS'). RECENT FINDINGS: The relationship between obsessive-compulsive disorder (OCD) or tics/Tourette's syndrome in childhood to antecedent group A streptococci (GAS) is unclear. One recent prospective cohort study found that more than 85% of clinical exacerbations in OCD / tic behavior in patients who met criteria for PANDAS had no relationship to GAS infection. Another study found no correlation between clinical exacerbations and changes in a variety of markers of brain autoimmunity, the proposed pathogenesis of PANDAS. A third recent study concluded that, compared with specialty clinic diagnoses, patients diagnosed with tics or Tourette's by physicians in the community were significantly more likely to be diagnosed with PANDAS without meeting the proposed criteria, most lacked supporting laboratory evidence of GAS infection, and they were more likely to be treated with unjustified short-term to chronic antibiotic and/ or immunomodulatory therapy. SUMMARY: Despite continued research in the field, the relationship between GAS and specific neuropsychiatric disorders (pANDAS) remains elusive. It is possible that GAS infection may be but one of the many stressors that can exacerbate tic/Tourette's or OCD in a subset of such patients. 
PMID: 19242249 [pubMed - indexed for MEDLINE] 
Pediatrics. 2009 Jan;123(1):e171; author reply e171-3. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcus. 
Scolnick B. 
Comment on: Pediatrics. 2008 Aug;122(2):273-8. PMID: 19117840 [pubMed - indexed for MEDLINE] 
Pediatrics. 2008 Aug;122(2):273-8
Pediatric autoimmune neuropsychiatric disorders associated with streptococcus: comparison of 
diagnosis and treatment in the community and at a specialty clinic. 
Gabbay V, Coffey BJ, Babb JS, Meyer L, Wachtel C, Anam S, Rabinovitz B. 
Department of Psychiatry, New York University School of Medicine, New York, New York 10016, USA. 
Comment in: Pediatrics. 2009 Jan;123(1):e171; author reply e171-3. 

OBJECTIVES: This study aimed to examine whether pediatric autoimmune neuropsychiatric disorders associated with streptococcus were appropriately diagnosed in the community and to determine subsequent rates of unwarranted use of antibiotic treatment for tics and obsessive-compulsive symptoms without the identification of an infection. METHODS: The design was a retrospective, cross-sectional, observational study of 176 children and adolescents who were evaluated in a specialty program for tics, Tourette's disorder, and related problems. Previously published diagnostic criteria were used to establish the diagnosis of pediatric autoimmune neuropsychiatric disorders associated with streptococcus in our clinic. RESULTS: 
Subjects were significantly less likely to receive a diagnosis of pediatric autoimmune neuropsychiatric disorders associated with streptococcus at the specialty clinic than in the community. In the community, subjects were significantly more likely to be treated with antibiotics or immunosuppressant medication if they received a diagnosis of pediatric autoimmune neuropsychiatric disorders associated with streptococcus. Of the 27 subjects with a community diagnosis of pediatric autoimmune neuropsychiatric disorders associated with streptococcus who were treated with antibiotics, 22 (82%) were treated without laboratory evidence of an infection; 2 were treated with immunomodulatory medications. CONCLUSIONS: Our results support our hypothesis that pediatric autoimmune neuropsychiatric disorders associated with streptococcus are frequently diagnosed in the community without the application of all working diagnostic criteria. This phenomenon has resulted in unwarranted use of antibiotic treatment for tics/ obsessive-compulsive disorder without evidence 
of laboratory infection. 
PMCID: PMC2770722 
PMID: 18676543 [pubMed - indexed for MEDLINE] 
Pediatrics. 2008 Jun;121(6):1188-97
Streptococcal infection and exacerbations of childhood tics and obsessive-compulsive symptoms: a 
prospective blinded cohort study. 
Kurlan R,Johnson D, Kaplan EL; and the Tourette Syndrome Study Group
University of Rochester School of Medicine, Mt Hope Professional Building, 1351 Mt Hope Ave, Suite 100, Rochester, NY 14620, USA. 
Comment in: Pediatrics. 2008 Nov;122(5):1157; author reply 1157-8. 
OBJECTIVE: If pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections is a unique clinical entity, we hypothesized that children meeting diagnostic criteria would have more clinical exacerbations temporally linked to bona fide group A beta-hemolytic streptococcus infection than matched control subjects (chronic tic and/ or obsessive-compulsive disorder with no known temporal relationship to group A beta-hemolytic streptococcus infection). PATIENTS AND METHODS: Subjects included 40 matched pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections casecontrol pairs who were prospectively evaluated with intensive laboratory testing for group A beta-hemolytic streptococcus and clinical measures for an average of 2 years. Additional testing occurred at the time of any clinical exacerbations or illness. Laboratory personnel were blinded to case or control status and clinical (exacerbation or not) condition. Clinical raters were blinded to the results of laboratory tests. RESULTS: The cases had a higher clinical exacerbation rate and a higher bona fide group A beta-hemolytic streptococcus infection rate than the control group. Only 5 of 64 exacerbations were temporally associated (within 4 weeks) with a group A beta-hemolytic streptococcus infection, and all occurred in cases. The number (5.0) was significantly higher than the number that would be expected by chance alone (1.6).Yet, > /=75% of the clinical exacerbations in cases had no observable temporal relationship to group A beta-hemolytic streptococcus infection. CONCLUSIONS: Patients who fit published criteria for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections seem to represent a subgroup of those with chronic tic disorders and obsessive-compulsive disorder who may be vulnerable to group A betahemolytic streptococcus infection as a precipitant of neuropsychiatric symptom exacerbations. Group A beta-hemolytic streptococcus infection is not the only or even the most common antecedent event associated with exacerbations for these patients. Additional intensive studies are needed to determine whether there is clinical or scientific evidence to support separating out subgroups of tic disorder and/or obsessivecompulsive disorder patients based on specific symptom precipitants. 
PMID: 18519489 [pubMed - indexed for MEDLINE] 
J Trop Pediatr. 2009 Feb;55(1):46-8. Epub 2008 May 22. 
Challenges in the identification and treatment of PANDAS: a case series. Mabrouk AA, Eapen V. 

Department of Pediatrics, School Health Services, Al AID. 
Paediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS), is characterized by childhood-onset obsessive-compulsive disorder (OCD) and Tic disorder that has been found to have a post infectious autoimmune-mediated etiology, where the onset and subsequent exacerbations of symptoms is temporally related to group A beta-hemolytic streptococci (GABHS) infection. In addition to the use of anti-tic and antiobsessional agents, the use of Penicillin during the acute phase and for prophylaxis, tonsillectomy, immunomodulatory therapies such as plasma exchange and intravenous immunoglobulin, etc. have all been reported to improve the symptoms. We describe five cases of neuropsychiatric symptoms triggered by streptococcal infection in an Arab population and highlight the challenges faced by clinicians in the identification and management of PANDAS
PMID: 18499734 [pubMed - indexed for MEDLINEJ 
Cardiac involvement in children with PANDAS. [References]. Segarra, Ana R; Murphy, Tanya K
Journal of the American Academy of Child & Adolescent Psychiatry. Vo1.47(5), May 2008, pp. 603-604. IT ournal; Peer Reviewed Journal) 
The clinical characteristics that define the PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcus) subgroup are the presence of obsessive-compulsive disorder (OeD) and! or tic disorder, prepubertal age at onset, abrupt onset, relapsing-remitting symptom course, association with neurological abnormalities during exacerbations and temporal association between symptom exacerbation and a GAS infection. We report here on 10 cases that we comprehensively evaluated as part of a prospective 
study examining the relationship of GAS to OCD and/or tic symptoms, in which color Doppler 
echo cardiography evaluation was completed in children meeting the PANDAS phenotype. Nine of the 10 children had one or more streptococcal titers that were elevated, and four of the 10 were in a neuropsychiatric exacerbation, and the rest were remitting or remitted. This correlation suggests an acquired or developmental, rather than a congenital, cause of valvular incompetence. The cardiac risk in this series of children with OCD and tics appears to be low and similar to that of the general population. (psycINFO Database Record (c) 
2010 APA, all rights reserved) 
Segarra, Ana R.: Department of Psychiatry, University of Florida, FL, US Murphy, Tanya K.: Department of Psychiatry, University of Florida, FL, US 
What every psychiatrist should know about PANDAS: A review. [References]
Moretti, Germana; Pasquini, Massimo; Mandarelli, Gabriele; Tarsitani, Lorenzo; Biondi, Massimo. Clinical Practice and Epidemiology in Mental Health. Vol.4 May 2008, ArtID 13. 
[journal; Peer Reviewed Journal] 
The term Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections (PANDAS) was coined by Swedo et al. in 1998 to describe a subset of childhood obsessive-compulsive disorders (OCD) and tic disorders triggered by group-A beta-hemolytic Streptococcus pyogenes infection. Like adult OCD, PANDAS is associated with basal ganglia dysfunction. Other putative pathogenetic mechanisms of PANDAS include molecular mimicry and autoimmune-mediated altered neuronal signaling, involving calcium-calmodulin dependent protein (Ca.M) kinase II activity. Nonetheless the contrasting results from numerous studies provide no consensus on whether PANDAS should be considered as a specific nosological entity or simply a useful research framework. Herein we discuss available data that could provide insight into pathophysiology of adult OCD, or might explain cases of treatment-resistance. We also review the latest research findings on diagnostic and treatment. (psycINFO Database Record (c) 2010 APA, all rights reserved) (journal abstract) 
Institution: Department of Psychiatric Sciences and Psychological Medicine, "Sapienza" University of Rome, Rome, Italy 
PANDAS and paroxysms: A case of conversion disorder? [References]. Kuluva, Joshua; Hirsch, Scott; Coffey, Barbara. 
Journal of Child and Adolescent Psychopharmacology. Vol.18(1), Mar 2008, pp. 109-115. [journal; Peer Reviewed Journal] 
Presents a case study of a 16-year-old adolescent Caucasian boy,]. initially referred for consultation regarding Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS). For 

approximately nine months prior to presentation, J. had been experiencing frequent motor and vocal tics punctuated by episodes of violent behavior. These events became so distressful to the patient, his family, and his surroundings that he was forced to leave school and all of his other social activities. Many of J's paroxysmal events were of a violent nature with aggression directed towards other people. Not only does this suggest that these events were neither tics nor seizures, but it also suggests that J. has some difficulty with the modulation of aggression. In addition, given the acute onset of his symptoms and decline in adaptive functioning, one might question whether there had been some trauma that had precipitated the illness
Finally, from a developmental perspective, the timing ofJ's symptom onset cannot be ignored. As it appeared that he was on a trajectory to become a successful athlete and student, the onset of his symptoms put obstacles in his path of continuing with his accomplishments. One may question if, with all of his success, J was on some level quite anxious about responsibility that would come with his advancement in life. Institution: NYU Child Study Center, New York, NY, US Hirsch, Scott: NYU Child Study Center, New 
York, NY, US 
CNS Spectr. 2007 May;12(5):359-64, 367-375. Obsessive-compulsive disorder: boundary issues. Fineberg NA, Saxena S, Zohar J, Craig KJ. 
Postgraduate School of Medicine, University of Hertfordsrure, Gueen Elizabeth II Hospital, Welwyn Garden 
City, UK. 
The boundaries between obsessive-compulsive disorder (OCD) and other neuropsychiatric disorders remain 
unresolved and may well differ from one disorder to another. Endophenotypes are heritable, quantitative traits hypothesized to more closely represent genetic risk for complex polygenic mental disorders than overt symptoms and behaviors. They may have a role in identifying how closely these disorders are associated with another and with other mental disorders with which they share major comorbidity. This review maps the nosological relationships of OCD to other neuropsychiatric disorders, using OCD as the prototype disorder and endophenotype markers, such as cognitive, imaging, and molecular data as well as results from demographic, comorbidity, family, and treatment studies. Despite high comorbidity rates, emerging evidence suggests substantial endophenotypic differences between OCD and anxiety disorders, depression, schizophrenia, and addictions, though comparative data is lacking and the picture is far from clear. On the other hand, strong relationships between OCD, Tourette syndrome, body dysmorphic disorder, hypochondriasis, grooming disorders, obsessive-compulsive personality disorder, and pediatric autoimmune neuropsychiatric disorders associated with streptococcus are likely. Studies designed to delineate the cause, consequences, and common factors are a challenging but essential goal for future research in this area. PMID: 17514081 [PubMed - indexed for MEDLIN E) 
BioI Psychiatry. 2007 Feb 1;61(3):279-84. Epub 2006 Nov 27
Relationship of movements and behaviors to Group A Streptococcus infections in elementary school 
Murphy TK, Snider LA, Mutch PJ, Harden E, Zaytoun A, Edge PJ, Storch EA, Yang MC, Mann G, 
Goodman WK, Swedo SE. 
Department of Psychiatry, College of Medicine, Gainesville, Florida 32610, USA. 
BACKGROUND: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS) research is based on the hypothesis that infections trigger changes in behavior and movement in children. METHODS: We enrolled 693 children (ages 3 to 12 years) into a systematic, longitudinal study. Data were collected monthly for 8 months (October-May) to determine point prevalence of Group A Streptococcal (GAS) infections, tics, behavior, and choreiform movements. Simultaneous throat cultures were obtained, and relational analyses were made between GAS and movement/observation ratings. RESULTS: 
Combined behavior/GAS associations (concurrent with or 3 subsequent months to GAS) revealed a strong relationship, relative risk (RR) of 1. 71 (p < .0001). Detailed analysis revealed that balance/ swaying and nontic grimacing were responsible for a significant proportion of this association (RR = 2.92, P < .0001). A strong seasonal pattern was found, with fall being more significant for GAS infections and observation ratings (p < .0001) compared with winter/spring. Children with repeated streptococcus (n = 64) showed higher rates of behavior and distal choreiform observations (p = .005). CONCLUSIONS: Motor/behavior changes were noted to occur in relationship to positive GAS culture with support that repeated GAS 
increases risk. 

PMID: 17126304 [pubMed - indexed for MEDLINE] 
Tics. anxiety. and possible PANDAS in an adolescent. [References]. Coffey, Barbara; Wieland, Natalie. 
Journal of Child and Adolescent Psychopharmacology. Vol.17(4), Aug 2007, pp. 533-538
[J ournal; Peer Reviewed Journal) 
Presents a case of J, a 16-year-old boy with tics and anxiety symptoms referred by his pediatrician for 
consultation regarding the diagnosis of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (pANDAS). There is no history of hyperactivity or impulsivity in early childhood or currently. J. has always done all of his schoolwork and gets it in on time, including up to the present. However, there have been some problems with attentional functioning in the past, starting in middle school, about which his teachers have apparently been concerned. J. reports that it is difficult for him to concentrate at times now, although he relates this mostly to his tics. J. was evaluated by a child and adolescent psychiatrist 2 months ago. J. has had longstanding treatment with a child psychologist for approximately 5 years. J. describes primarily a supportive psychotherapy, although the mother reports that cognitive behavioral techniques are also used. Given J.'s multiple anxiety, mood, and tic symptoms, he would be a good candidate for more formal cognitive behavioral techniques, including exposure and response prevention, for his anxiety. In 
addition, strong efforts should be made to help J. return to high school. 
JAm Acad Child Adolesc Psychiatry. 2006 Oct;45(10):1171-8. 
Cognitive-behavioral therapy for PANDAS-related obsessive-compulsive disorder: findings from
preliminary waitlist controlled open trial. 
Storch EA, Murphy TK, Geffken GR, Mann G, Adkins J, Merlo LJ, Duke D, Munson M, Swaine Z, 
Goodman WK .. 
Department of Psychiatry, University of Florida, Gainesville, FL 32610, USA. 
OBJECTIVE: To provide preliminary estimates of the effectiveness of cognitive-behavioral therapy (CBT) in treating pediatric obsessive-compulsive disorder (OCD) of the pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS) subtype. METHOD: Seven children with OCD of the PANDAS subtype (range 9-13 years) were treated in a 3-week intensive CBT program conducted at a university clinic. Six of seven children were taking selective serotonin reuptake inhibitor medication(s) upon presentation. Assessments were conducted at four time points: baseline, pretreatment approximately 4 weeks later, posttreatment, and 3-month follow-up. Raters were blind to the nature of the study treatment. RESULTS: Six of seven participants were classified as treatment responders (much or very much improved) at posttreatment, and three of six remained responders at follow-up. Clinician severity ratings, as measured by the Children's Yale-Brown Obsessive-Compulsive Scale and Anxiety Disorder Interview Schedule for DSMIV Child Interview Schedule-Parent version, decreased significantly following intervention, with effect sizes of 3.38 and 2.29, respectively. Self-reported general anxiety and depression symptoms were not significantly reduced. CONCLUSIONS: This study provides preliminary support for CBT in treating the PANDAS subtype of pediatric OCD. This approach is also considered a safe and minimally invasive treatment 
PMID: 17003662 [pubMed - indexed for MEDLINEJ 
J Child Neurol. 2006 Sep;21(9):727-36. 
Autoimmune neuropsychiatric disorders associated with streptococcal infection: Sydenham chorea, 
PANDAS, and PANDAS variants. 
Pavone P, Parano E, Rizzo R, Trifiletti RR. 
Department of Pediatrics, Division of Clinical Pediatrics, University of Catania, Viale Andrea Doria 6, 95125 
Catania, Italy. 
Streptococcal infection in children is usually benign and self-limited. In a small percentage of children, 
prominent neurologic and/ or psychiatric sequelae can occur. Sydenham chorea is the best defined and best recognized. PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection) is a well-defIned syndrome in which tics (motor and! or vocal) and! or obsessive-compulsive disorder consistently exacerbate in temporal correlation to a group A beta-hemolytic streptococcal infection. PANDAS constitutes a subset of children with tics, Tourette syndrome, and obsessive-compulsive disorder. In addition to strictly defined PANDAS, we and others have recognized several PANDAS variants, including adult-onset variant, a dystonic variant, a myoclonic variant, and a "chronic" PANDAS variant. The nosology and classification of these entities are rapidly evolving. The recognition that some pediatric neurobehavioral 

syndromes have infectious and/or immunologic triggers points to important new avenues of disease treatment. In this review, we summarize this complex and rapidly evolving area of clinical research. PMID: 16970875 [pubMed - indexed for MEDLINEJ 
Selective Serotonin Reuptake Inhibitor-Induced Behavioral Activation in the PANDAS Subtype. [References) . 
Murphy, Tanya K; Storch, Eric A; Strawser, Melissa S. Primary Psychiatry. Vol.13(8), Aug 2006, pp. 87-89. Journal; Peer Reviewed Journal) 
Although selective serotonin reuptake inhibitors (SSRI) are an effective and commonly used treatment for pediatric obsessive-compulsive disorder (OCD), their use has come under close scrutiny following reports of adverse reactions. The authors of this case report believe that children with the OCD subtype, pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS), may have increased vulnerability. The following report provides initial data on behavioral activation following SSRI use in 38 children with OCD of the PANDAS subtype. The authors use a particular case to highlight this issue and discuss treatment implications. 
Institution: Department of Psychiatry, University of Florida, Gainesville, FL, US 
Pediatrics. 2005 Jul;116(1);56-60. 
Association between streptococcal infection and obsessive-compulsive disorder, Tourette's syndrome, and tic disorder. 
Mell LK, Davis RL, Owens D. 
Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA. 
OBJECTIVE: Reports have suggested that streptococcal infection may be etiologically related to pediatric autoimmune neuropsychiatric disorders (PANDAS), but there are few good epidemiologic studies to support this theory. Using population-based data from a large West-Coast health maintenance organization, we assessed whether streptococcal infection was associated with increased risk for obsessive-compulsive disorder (OCD), Tourette's syndrome (TS), or tic disorder. METHODS: This is a case-control study of children 4 to 13 years old receiving their first diagnosis of OCD, TS, or tic disorder between January 1992 and December 1999 at Group Health Cooperative outpatient facilities. Cases were matched to controls by birth date, gender, primary physician, and propensity to seek health care. RESULTS: Patients with OCD, TS, or tic disorder were more likely than controls to have had prior streptococcal infection (OR: 2.22; 95% CI: 1.05,4.69) in the 3 months before onset date. The risk was higher among children with multiple streptococcal infections within 12 months (OR: 3.10; 95% CI: 1.77,8.96). Having multiple infections with group A beta-hemolytic streptococcus within a 12-month period was associated with an increased risk for TS (OR: 13.6; 95% CI: 1.93,51.0). These associations did not change appreciably when limited to cases with a clear date of onset of symptoms or with tighter matching on health care behavior. CONCLUSION: These findings lend epidemiologic evidence that PANDAS may arise as a result of a postinfectious autoimmune phenomenon induced by childhood streptococcal infection. 
PMID: 15995031 [pubMed - indexed for MEDLINE] 
Am Fam Physician. 2005 May 15;71(10):1949-54. Evaluation of poststreptococcal illness. 
Hahn RG, Knox LM, Forman TA. 
Department of Family Medicine, University of Southern California, Los Angeles, California, USA. 
Group A beta-hemolytic streptococcal pharyngitis, scarlet fever, and rarely asymptomatic carrier states are associated with a number of poststreptococcal suppurative and non suppurative complications. As in streptococcal pharyngitis,acute rheumatic fever, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and poststreptococcal glomerulonephritis most often occur in children. The hallmarks of rheumatic fever include arthritis, carditis, cutaneous disease, chorea, and subsequent acquired valvular disease. Pediatric autoimmune neuropsychiatric disorders encompass a subgroup of illnesses involving the basal ganglia in children with obsessive-compulsive disorders, tic disorders, dystonia, chorea encephalitis, and dystonic choreoathetosis. Poststreptococcal glomerulonephritis is most frequently encountered in children between two and six years of age with a recent history of pharyngitis and a rash in the setting of poor personal hygiene during the winter months. The clinical examination of a patient with possible 

poststreptococcal complications should begin with an evaluation for signs of inflammation (i.e., complete blood count, erythrocyte sedimentation rate, C-reactive protein) and evidence of a preceding streptococcal infection. Antistreptolysin 0 titers should be obtained to confirm a recent invasive streptococcal infection. Other important antibody markers include antihyaluronidase, antideoxyribonuclease B, and antistreptokinase 
PMID: 15926411 [pubMed - indexed for MEDLIN E) 
J Child Psychol Psychiatry. 2005 Mar;46(3):227-34
Annotation: PANDAS: a model for human autoimmune disease. Swedo SE, Grant PJ. 
National Institute of Mental Health, Bethesda, Maryland 20892-1255, USA. 
BACKGROUND: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections (PANDAS) is a recently recognized syndrome in which pre-adolescent children have abrupt onsets of tics and/or obsessive-compulsive symptoms, a recurring and remitting course of illness temporally related to streptococcal infections, and associated neurologic findings including adventitious movements, hyperactivity and emotional lability. METHODS: Inspired by observations of similar symptoms in children with Sydenham's chorea, a search was undertaken for clinical and laboratory evidence in support 
of the new syndrome. RESULTS: Consistent and predictable clinical findings have been described in a large case series. Magnetic resonance imaging has supported the postulated pathobiology of the syndrome with evidence of inflammatory changes in basal ganglia. Antibasal ganglia antibodies have been found in some acute cases, mimicking streptococcal antigen epitopes. CONCLUSIONS: While PANDAS remains a controversial diagnostic concept, it has stimulated new research endeavors into the possible links between bacterial pathogens, autoimmune reactions, and neuropsychiatric symptoms. 
PMID: 15755299 [pubMed - indexed for MEDLIN E) 
J Neuropsychiatry Clin Neurosci. 2004 Summer;16(3):252-60
A possible association of recurrent streptococcal infections and acute onset of obsessive-compulsive 
Kim SW, GrantJE, Kim SI, Swanson TA, Bernstein GA,Jaszcz WE, Williams KA, Schlievert PM. Department of Psychiatry, University of Minnesota Medical School, Minneapolis, Minnesota, USA. Rheumatic fever is an immunologically mediated disease that follows infection by group A beta-hemolytic Streptococcus (GABHS). In rheumatic fever, antibodies generated against GABHS cross-react with the heart, joints, skin, and other sites, inducing an inflammatory, multisystem disease. Brain tissue-specific antibodies have been demonstrated in a subset of children with Sydenham chorea (a component of the Jones criteria for the diagnosis of rheumatic fever), and most Sydenham chorea patients manifest obsessive-compulsive symptoms very similar to those in traditional obsessive-compulsive disorder. The parallels drawn from the paradigm of Sydenham's chorea to Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) is an area of active controversy. Newly emerging information on the role of GABHS superantigens in the pathogenesis of rheumatic fever is of particular interest. In this article, we review the microbial characteristics of GABHS and the subsequent immune responses to GABHS as a possible etiology of PANDAS. 
PMID: 15377732 [pubMed - indexed for MEDLINE
Mol Psychiatry. 2004 Oct;9(10):900-7
PANDAS: current status and directions for research. Snider LA, Swedo SE
Pediatrics & Developmental Neuropsychiatry Branch, Department of Health and Human Services, Nationa
Institute of Mental Health, Bethesda, MD 20892, USA. 
The recognition of the five ctiteria for PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) by Swedo et al established a homogenous subgroup of children with childhood onset obsessive-compulsive disorder (OeD) and/or tic disorders. The five clinical characteristics that define the PANDAS subgroup are the presence of OCD and/or tic disorder, prepubertal age of onset, abrupt onset and relapsing-remitting symptom course, association with neurological abnormalities during exacerbations (adventitious movements or motoric hyperactivity), and a temporal association between symptom exacerbations and a Group-A beta-hemolytic streptococcal (GAS) infection. These five criteria have been used for the purpose of systematic research on the phenomenology and unique therapies for the 

PANDAS subgroup as well as studies of the pathophysiology of post-streptococcal OCD and tic disorders. The etiology of OCD and tics in the PANDAS subgroup is unknown, but is theorized to occur as a result of post-streptococcal autoimmunity in a manner similar to that of Sydenham's chorea. The working hypothesis for the pathophysiology begins with a GAS infection in a susceptible host that incites the production of antibodies to GAS that crossreact with the cellular components of the basal ganglia, particularly in the caudate nucleus and putamen. The obsessions, compulsions, tics, and other neuropsychiatric symptoms seen in these children are postulated to arise from an interaction of these antibodies with neurons of the basal ganglia. 
PMID: 15241433 [pubMed - indexed for MEDLINEJ 
J Child Neurol. 2004 May;19(5):387-90
Functional brain imaging in Sydenham's chorea and streptococcal tic disorders. Citak EC, Cucuyener K, Karabacak NI, Serdaroglu A, Okuyaz C, Aydin K. Department of Pediatric Neurology, Gazi University Medical Faculty, Ankara, Turkey. Comment in: J Child Neurol. 2006 Jun;21 (6):544-5. 
Group A streptococcal infections cause a wide range of neuropsychiatric disorders, such as Sydenham's chorea, tics, obsessive-compulsive disorders, and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Structural (computed tomography and magnetic resonance imaging) and functional (positron emission tomography, single-photon emission computed tomography) imaging studies in patients with Sydenham's chorea have suggested reversible striatal abnormalities. The objective of this study was to investigate the cerebral perfusion patterns of the subcortical structures by using hexamethylpropylenamine oxime single-photon emission computed tomography (HMP AO-SPEC1j in seven cases of Sydenham's chorea and two cases of streptococcal tic disorder. HMP AO-SPECT studies revealed a hyperperfusion pattern in two and a hypoperfusion pattern in five of the chorea patients and in two patients with tic disorder. The results are discussed in relation to the duration and severity of the symptoms and the response to therapy. Functional imaging findings can be variable in Sydenham's chorea, and hyperperfusion of the striatum and thalamus could be an indicator of the response to therapy and the severity of symptoms. However, the number of cases so far investigated by either SPECT or positron emission tomography is still too limited to draw any firm conclusions
PMID: 15224712 [pubMed - indexed for MEDLIN E
Pediatrics. 2004 Apr;113(4):907-11. 
The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) subgroup: separating fact from fiction
Swedo SE, Leonard HL, Rapoport JL. 
Pediatrics and Developmental Neuropsychiatry Branch, Intramural Research Program, National Institute of Mental Health, Bethesda, MD 20892, USA. 
Comment on: Pediatrics. 2004 Apr;113(4):883-6. 
PMID: 15060242 [pubMed - indexed for MEDLINEJ 
Pediatrics. 2004 Apr;113(4):883-6. 
The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) etiology for tics and obsessive-compulsive symptoms: hypothesis or entity? Practical considerations for the clinician. 
Kurlan R, Kaplan EL. 
Cognitive and Behavioral Neurology Unit, Department of Neurology, University of Rochester School of Medicine, Rochester, New York 14642-8673, USA. 
Comment in: Pediatrics. 2004 Apr;113(4):907-11. 
Clinicians have been faced with much publicity and contradictory scientific evidence regarding a recently described condition termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS). It has been proposed that children with PANDAS experience tics, obsessivecompulsive behavior, and perhaps other neuropsychiatric symptoms as an autoimmune response to streptococcal infection. We review current scientific information and conclude that PANDAS remains a yetunproven hypothesis. Until more definitive scientific proof is forthcoming, there seems to be insufficient evidence to support 1) routine microbiologic or serologic testing for group A streptococcus in children 

who present with neuropsychiatric symptoms or 2) the clinical use of antibiotic or immune-modifying therapies in such patients. The optimum diagnostic and therapeutic approach awaits the results of additional research studies. 
PMID: 15060240 [pubMed - indexed for MEDLINEJ 
Pediatr Neurol. 2004 Feb;30(2):1 07-10. 
Anti-brain antibodies in PANDAS versus uncomplicated streptococcal infection. Pavone P, Bianchini R, Parano E, Incorpora G, Rizzo R, Mazzone L, Trifiletti RR. Division of Pediatric Neurology, University of Catania, Catania, Italy. 
The objective of this study was to assess brain involvement through the presence of antineuronal antibodies in Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS) and in uncomplicated active Group A streptococcal infection. We compared serum anti brain antibody to human basal ganglia sections assessed by indirect tissue immunofluorescence in two groups: a PANDAS group, comprised of 22 patients (mean age 10.1 years; 20 male, 2 female) who met strict National Institutes of Mental Health diagnostic criteria for PANDAS and had clinically active tics or obsessive-compulsive disorder, or both; and a GABHS control group consisting of 22 patients (mean age 9.1 years; 15 mol/L, 7 female) with clinical evidence of active Group A beta-hemolytic streptococcal (GABHS) infection confirmed by throat culture and elevated antistreptolysin 0 titers but without history or clinical evidence of tics or obsessivecompulsive disorder. We observed positive anti-basal ganglia staining (defined as detectable staining at 1:10 serum dilution) in 14/22 patients in the PANDAS group (64%) but only 2/22 (9%) in the GABBS control group (P < 0.001, Fisher's exact test). These results suggest that antibrain antibodies are present in children with PANDAS that cannot be explained merely by a history of GABBS infection. 
PMID: 14984902 [pubMed - indexed for MEDLINE] 
BioI Psychiatry. 2004 Jan 1;55(1):61-8. 
Detecting pediatric autoimmune neuropsychiatric disorders associated with streptococcus in children with obsessive-compulsive disorder and tics. 
Murphy TK, Sajid M, Soto 0, Shapira N, Edge P, Yang M, Lewis MH, Goodman WK Department of Psychiatry, University of Florida, Gainesville, Florida 32610-0256, USA. 
BACKGROUND: A subgroup of children with obsessive-compulsive and tic disorders are proposed to have an infectious trigger. The purpose of this study was to investigate the relationship between group A streptococcal titers and symptom fluctuations in children with a clinical course resembling that described for pediatric autoimmune neuropsychiatric disorders associated with streptococcus. METHODS: Twenty-five children with obsessive-compulsive disorder and/or tic disorder were evaluated for neuropsychiatric severity and group A streptococcal antibody titers (streptolysin 0, deoxyribonuclease B, and carbohydrate A) at 6-week intervals for> or = six consecutive evaluations (total visits=277). RESULTS: Children with large symptom fluctuations (n=15) were compared with children without dramatic fluctuations (n=10). Comovements of obsessive-compulsive/tic severity and group A streptococcal antibodies were assessed. In subjects with large symptom changes, positive correlations were found between streptococcal titers and obsessive-compulsive severity rating changes (p=.0130). These subjects were also more likely to have elevated group A streptococcal titers during the majority of observations (p=.001). Tic symptom exacerbations occurred more often in the fall/winter months than spring/ summer months (p=.03). CONCLUSIONS: 
Patients with marked obsessive-compulsive/tic symptom changes may be characterized by streptococcal titer elevations and exhibit evidence of seasonal tic exacerbations. 
PMID: 14706426 [pubMed - indexed for MEDLIN E) 
J Child Adolesc Psychopharmacol. 2003 Fall;13(3):209-12. 
Obsessive-Compulsive disorder. Tourette's disorder. or pediatric autoimmune neuropsychiatric disorders associated with Streptococcus in an adolescent? Diagnostic and therapeutic challenges. Gabbay V, Coffey B
New York University Child Study Center, New York University School of Medicine, New York, New York PMID: 14642008 [pubMed - indexed for MEDLIN E) 
Int J Pediatr Otorhinolaryngol. 2003 Aug;67(8):837-40. 14 

PANDAS: pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections--an uncommon. but important indication for tonsillectomy. 
Heubi C, Shott SR. 
Department of Pediatric Otolaryngology, Cincinnati Children's Hospital Medical Center, 3333 Burnet 
Avenue, Cincinnati, OH 45229, USA. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections, also know as "PANDAS," is well described in the neurologic and psychiatric literature. PANDAS is associated with obsessive compulsive disorders (OCD) and tic disorders. The streptococcal infections may trigger an autoimmune reaction that exacerbates these conditions. Recurrent streptococcal tonsillitis is one of the recurrent infections associated with PANDAS. This paper reviews the case reports of two brothers, one with OCD and the other with a tic disorder, both of whom improved significantly after undergoing adenotonsillectomy for treatment of their recurrent tonsillitis. A review of the pathophysiology and 
current understanding of PANDAS is presented. 
PMID: 12880661 [pubMed - indexed for MEDLIN E) 
Curr Opin Neurol. 2003 Jun;16(3):359-65. 
Post-streptococcal autoimmune disorders of the central nervous system. 
Snider LA, Swede SE. 
Pediatrics and Developmental Neuropsychiatry Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA. 
PURPOSE OF REVIEW: Autoimmune disease has long been intertwined with investigations of infectious causes. Antibodies that are formed against an infectious agent can, through the process of molecular mimicry, also recognize healthy cells. When this occurs, the immune system erroneously destroys the healthy cells causing autoimmune disease in addition to appropriately destroying the offending infectious agent and attenuating the infectious process. The first infectious agent shown to cause a post-infectious autoimmune disorder in the central nervous system was Streptococcus pyogenes in Sydenham's chorea. The present review summarizes the most recent published findings of central nervous system diseases that have evidence of a post-streptococcal autoimmune etiology. RECENT FINDINGS: Sydenham's chorea and other central nervous system illnesses that are hypothesized to have a post-streptococcal autoimmune etiology appear to arise from targeted dysfunction of the basal ganglia. PANDAS (pediatric autoimmune disorders associated with streptococcal infections) is the acronym applied to a subgroup of children with obsessive-compulsive disorder or tic disorders occurring in association with'streptococcal infections. In addition, there are recent reports of dystonia, chorea encephalopathy, and dystonic choreoathetosis occurring as sequelae of streptococcal infection. Investigators have begun to isolate and describe antistreptococcal-antineuronal antibodies as well as possible genetic markers in patients who are susceptible to these illnesses. 
SUMMARY: Clinical and research findings in both immunology and neuropsychiatry have established the existence of post-streptococcal neuropsychiatric disorders and are beginning to shed light on possible 
pathobiologic processes. 
PMID: 12858074 [pubMed - indexed for MEDLINE] 
AmJ Psychiatry. 2002 Aug;159(8):1430-2. 
D8/}7 expression on B lymphocytes in anorexia nervosa. 
Sokol MS, Ward PE, Tamiya H, Kondo DG, Houston D, Zabriskie JB. 
Creighton University School of Medicine and Children's Hospital, Omaha, NE 68114, Comment in: Am J Psychiatry. 2003 Jun;160(6):1193-4; author reply 1194. 
OBJECTIVE: The authors' goal was to determine whether D8/17, a rheumatic fever susceptibility trait marker, identifies a possible type of anorexia nervosa: pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS) anorexia nervosa. METHOD: Using immunofluorescence, the authors measured the percentage of D8/ 17 -positive B lymphocytes in the peripheral blood of 16 subjects 7- 21 years old who had not had rheumatic fever but who had possible PANDAS anorexia nervosa. The comparison subjects were 17 psychiatric patients with no eating disorder and no PANDAS characteristics. Subjects were considered D8/17 positive if they had 12% or more D8/17+ cells. RESULTS: There were more D8/17-positive individuals among those with PANDAS anorexia nervosa (81%) than among the comparison subjects (12%). The subjects with PANDAS anorexia nervosa had a higher percentage of D8/17+ cells (mean=27.1 %, SD=17%) than the comparison subjects (mean=5.3%, SD=7.4%). 

CONCLUSIONS: A larger study is needed to determine whether D8/17 serves as a marker for susceptibility to a type of anorexia nervosa. 
PMID: 12153841 [PubMed - indexed for MEDLINEJ 
Mol Psychiatry. 2002;7 Suppl2:S24-5. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections 
Swedo SE. 
Pediatrics and Developmental Neuropsychiatry Branch, National Institute of Mental Health, Bethesda, MD 
PMID: 12142939 [pubMed - indexed for MEDLINE] 
Ann Neurol. 2001 Nov;50(5):588-95. 
Posrstreptococcal acute disseminated encephalomyelitis with basal ganglia involvement and auto- 
reactive antibasal ganglia antibodies. 
Dale RC, Church AJ, Cardoso F, Goddard E, Cox TC, Chong WI(, Williams A, Klein NJ, Neville BG, 
Thompson EJ, Giovannoni G. 
Department of Neurology, Great Ormond Street Hospital National Health Service Trust and Institute of 
Child Health, University of London, UK 
Antibasal ganglia antibodies (ABGA) are associated with Sydenham's chorea and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. We present 10 patients with acute disseminated encephalomyelitis (ADEM) associated with Group A beta hemolytic streptococcal infection. The clinical phenotype was novel, with 50% having a dystonic extrapyramidal movement disorder, and 70% a behavioral syndrome. None of the patients had rheumatic fever or Sydenham's chorea. Enzyme-linked imrnunosorbent assay, Western immunoblotting, and immunohistochemistry were used to detect ABGA. Neurological (n = 40) and streptococcal (n = 40) controls were used for comparison. Enzyme-linked immunosorbent assay results showed significandy elevated ABGA in the patients with poststreptococcal ADEM. Western immunoblotting demonstrated ABGA reactivity to three dominant protein bands of 60,67, or 80 kDa; a finding not reproduced in controls. Fluorescent immunohistochemistry demonstrated specific binding to large striatal neurones, which was not seen in controls. Streptococcal serology was also 
significandy elevated in the poststreptococcal ADEM group compared with neurological controls. Magnetic resonance imaging studies showed hyperintense basal ganglia in 80% of patients with poststreptococcal ADEM, compared to 18% of patients with nonstreptococcal ADEM. These findings support a new subgroup of postinfectious autoimmune inflammatory disorders associated with Group A beta hemolytic streptococcus, abnormal basal ganglia imaging, and elevated ABGA. 
PMID: 11706964 [pubMed - indexed for MEDLIN E) 
Semin Clin Neuropsychiatry. 2001 Oct;6(4):266-76. 
Obsessive compulsive disorder: is there an association with childhood streptococcal infections and 
altered immune function? 
Murphy TK, Petitto JM, Voeller KIZ, Goodman WI(. 
Child Anxiety and Tic Disorder Clinic, McKnight Brain Institute, University of Florida, Department of 
Psychiatry, Gainesville, FL 32610, USA. 
During the last few years, an increased interest in the possibility of immune mediated pathophysiology of 
obsessive compulsive disorder (OCD) and related disorders has been seen. In the late 1980s, the National Institute of Mental Health reported an increase of obsessive compulsive symptoms in patients with Sydenham chorea (SC). Subsequently, a precipitating streptococcal infection in children with sudden onset of OCD symptoms but no chorea led to the coining of PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcus). This association has furthered interest in studying immune parameters in non-PANDAS OCD as well. This article will review the neuropsychiatric findings in OCD and Tourette syndrome (TS) with emphasis placed on PANDAS, and its association with SC, and a review of the existing studies that have assessed immunologic measures in patients with OCD and TS
PMID: 11607922 [pubMed - indexed for MEDLIN E) 
37. Laryngoscope. 2001 Sep;l11 (9):1515-9. 

Pediatric autoimmune neuropsychiatric disorders and streptococcal infections: role of otolaryngologist.
Orvidas LJ, Slattery MJ. 
Department of Otorhinolaryngology, Mayo Clinic, Rochester, Minnesota 55905, USA. 
OBJECTIVE: To increase awareness and understanding of the putative role of streptococcal infection in the development of neuropsychiatric disorders in children and to discuss therapeutic options in this group of patients. METHODS: Case illustration and literature review. RESULTS: Two siblings, one with obsessivecompulsive disorder (OCD) and one with a tic disorder, had tonsillectomy for recurrent streptococcal pharyngitis. At the latest follow-up visit (11 mo postoperatively), both patients exhibited significant improvement in their psychiatric illnesses. We discuss these cases as well as the diagnosis, pathophysiology, and treatment of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). CONCLUSION: PANDAS is an active area of research investigating the relationship between streptococcal infections and the development of obsessive-compulsive disorder or tic disorders (or both) in children. The etiopathogenesis of PANDAS is thought to reflect autoimmune mechanisms and involvement of the basal ganglia of susceptible hosts. Because otolaryngologists evaluate a large portion of pediatric patients with recurrent streptococcal pharyngitis, it is important to be aware of this association and to manage these patients appropriately. 
PMID: 11568599 [pubMed - indexed for MEDLINE] 
J Am Acad Child Adolesc Psychiatry. 2000 Sep;39(9):1120-6. 
Psychiatric disorders in ftrst-degree relatives of children with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Lougee L, Perlmutter SJ, Nicolson R, Garvey MA, Swedo SE. 
Pediatrics and Developmental Neuropsychiatry Branch, NIMH, Bethesda, MD 20892-1255, USA. OBJECTIVE: To determine the rates of psychiatric disorders in the first-degree relatives of children with infection-triggered obsessive-compulsive disorder (OCD) and/or tics (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections; PANDAS). METHOD: The probands of this study were 54 children with PANDAS (n = 24 with a primary diagnosis of OCD; n = 30 with a primary diagnosis of a tic disorder). One hundred fifty-seven first-degree relatives (100 parents [93%) and 57 siblings [100%)) were evaluated for the presence of a tic disorder. One hundred thirty-nine first-degree relatives (100 parents [93%] and 39 of 41 siblings over the age of 6 [95%)) were evaluated with clinical and structured psychiatric interviews to determine the presence of subclinical OCD, OCD, and other DSM-IV Axis I disorders. RESULTS: Twenty-one probands (39%) had at least one first-degree relative with a history of a motor or vocal tic; 6 mothers (11 %),9 fathers (19%), and 8 siblings (16%) received this diagnosis. Fourteen probands (26%) had atleast one first-degree relative with OCD; 10 mothers (19%), 5 fathers (11 %), and 2 siblings 
(5%), received this diagnosis. An additional 8 parents (8%) and 3 siblings (8%) met criteria for subclinical OCD. Eleven parents (11 %) had obsessive-compulsive personality disorder. CONCLUSIONS: The rates of tic disorders and OCD in first -degree relatives of pediatric probands with PANDAS are higher than those reported in the general population and are similar to those reported previously for tic disorders and 
OeD. Further study is warranted to determine the nature of the relationship between genetic and environmental factors in PANDAS. 
PMID: 10986808 [pubMed - indexed for MEDLINE] 
J Child Adolesc Psychopharmacol. 2000 Summer;10(2):133-45. 
Infection-triggered anorexia nervosa in children: clinical description of four cases. Sokol MS
Eating Disorders Program, The Menninger Clinic, Topeka, Kansas 66601, USA. 
BACKGROUND: Anorexia nervosa (AN) is a serious illness with no definitive treatment. Clinical and research evidence led to the hypothesis that some children with AN may have a pediatric autoimmune neuropsychiatric disorder associated with streptococcus (PANDAS), similar in pathogenesis to other hypothesized PANDAS disorders. METHODS: Four youngsters (ages, 11-15 years) with PANDAS AN were treated with an open trial of antibiotics, in addition to conventional treatment. They were evaluated for eating disorder and obsessive-compulsive symptoms, and for weight gain. Evidence of streptococcal infection came from clinical evaluation, throat cultures, and two serological tests: anti-deoxyribonuclease B (anti-DNase B) and anti-streptolysin 0 (ASO) titers. The "rheumatic" marker D8/17 was also measured. This B-cell 

alloantigen is associated, in several publications, with poststreptococcal autoimmunity: Rheumatic fever (RF), Sydenham's chorea (SC), and possibly PANDAS obsessive compulsive disorder (OCD) and tic disorders. RESULTS: There was clinical evidence of possible antecedent streptococcal infection in all four patients, two of whom had comorbid OCD, with possible infection-triggered AN. All four had the rheumatic marker: A percentage of D8/17-positive B cells of 28-38%, with a mean of 33% (12% or more is considered positive for the marker). The patients responded to conventional treatment plus antibiotics with weight restoration and decreased eating disorder and obsessive-compulsive symptoms. Three needed to gain weight and did so. CONCLUSIONS: There may be a link between infectious disease and some cases of AN, which raises the 
possibility of new treatment. 
PMID: 10933123 [pubMed - indexed for MEDLINE] 
BioI Psychiatry. 2000 May 15;47(10):851-7. 
On defining Sydenham's chorea: where do we draw the line? Murphy TK, Goodman WK, Ayoub EM, Voeller KlZ. 
Department of Psychiatry, University of Florida, College of Medicine, Gainesville 32610-0256, USA. Sydenham's chorea (SC) is a major manifestation of rheumatic fever characterized by an array of neuropsychiatric symptoms that vary in severity, timing, and character. Some of the same symptoms are seen in Tourette's syndrome and childhood-onset obsessive-compulsive disorder. Genetic vulnerability appears to playa role in all three conditions. The term PANDAS (pediatric autoimmune neuropsychiatric disorder associated with streptococcus) has been introduced to describe a putative subset of obsessive-compulsive disorder and Tourette's syndrome that bears some resemblance to Sydenham's chorea. This article discusses whether PANDAS should be subsumed under Sydenham's chorea, thus expanding the diagnostic boundaries of Sydenham's chorea to include primarily neuropsychiatric presentations now classified as cases of obsessive-compulsive disorder or Tourette's syndrome. We conclude that PANDAS is a useful construct, but that it would be premature to view it as a subset of Sydenham's chorea-whether defined narrowly or broadly. PMID: 10807957 [pubMed - indexed for MEDLIN E) 
Pediatr Infect Dis J. 1999 Mar;18(3):281-2. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS). 
Shulman ST. 
Children's Memorial Hospital, Northwestern University Medical School, Chicago, IL, USA. 
PMID: 10093955 [pubMed - indexed for MEDLINE) 
AmJ Psychiatry. 1998 Feb;155(2):264-71. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical 
description of the first 50 cases. 
Swedo SE, Leonard HL, Garvey M, Mittleman B, AllenAJ, Perlmutter S, Lougee L, Dow S, ZamkoffJ
Section on Behavioral Pediatrics, NIMH, Rockville Pike, Bethesda, MD 20892-1381, USA. 
Erratum in: Am J Psychiatry 1998 Apr;155(4):578. 
Comment in: Am J Psychiatry. 2002 Feb;159(2):320. 
OBJECTIVE: The purpose of this study was to describe the clinical characteristics of a novel group of patients with obsessive-compulsive disorder (OCD) and tic disorders, designated as pediatric autoimmune neuropsychiatric disorders associated with streptococcal (group A beta-hemolytic streptococcal [GABHS]) infections (PANDAS). METHOD: The authors conducted a systematic clinical evaluation of 50 children who met all of the following five working diagnostic criteria: presence of OCD and/or a tic disorder, prepubertal symptom onset, episodic course of symptom severity, association with GABHS infections, and association with neurological abnormalities. RESULTS: The children's symptom onset was acute and dramatic, typically triggered by GABHS infections at a very early age (mean = 6.3 years, SD = 2.7, for tics; mean = 7.4 years, SD = 2.7, for OCD). The PANDAS clinical course was characterized by a relapsing-remitting symptom pattern with significant psychiatric comorbiclity accompanying the exacerbations; emotional lability, separation anxiety, nighttime fears and bedtime rituals, cognitive deficits, oppositional behaviors, and motoric hyperactivity were particularly common. Symptom onset was triggered by GABHS infection for 22 (44%) of the children and by pharyngitis (no throat culture obtained) for 14 others (28%). Among the 50 children; there were 144 separate episodes of symptom exacerbation; 45 (31 %) were associated with documented GABHS infection, 60 (42%) with symptoms of pharyngitis or upper respiratory infection (no throat culture 

obtained), and six (4%) with GABHS exposure. CONCLUSIONS: The working diagnostic criteria appear to accurately characterize a homogeneous patient group in which symptom exacerbations are triggered by GABHS infections. The identification of such a subgroup will allow for testing of models of pathogenesis, as well as the development of novel treatment and prevention strategies. 
PMID: 9464208 [pubMed - indexed for MEDUNE] 
JAm Acad Child Adolesc Psychiatry. 1996 Jul;35(7):913-5. 
Case study: acute basal ganglia enlargement and obsessive-compulsive symptoms in an adolescent 
GieddJN, RapoportJL, Leonard HL, Richter D, Swedo SE. 
Child Psychiatry Branch, NIMH, Bethesda, MD 20892-1600, USA. 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAs) may arise when antibodies directed against invading bacteria cross-react with basal ganglia structures, resulting in exacerbations of obsessive-compulsive disorder (OCD) or tic disorders. This is a report of severe worsening of obsessive-compulsive symptoms in an adolescent boy following infection with group A beta-hemolytic streptococci for whom serial magnetic resonance imaging scans of the brain were acquired to assess the relationship between basal ganglia size, symptom severity, and treatment with plasmapheresis. These data provide further support for basal ganglia-mediated dysfunction in OeD and the potential for immunological treatments in PANDAs patients. 
PMID: 8768351 [pubMed - indexed for MEDLIN E) 
BOOK CHAPTERS (from PsycInfor search) 
We do not have any of the books in the Medical Library collection. 
Immune and endocrine function in child and adolescent obsessive compulsive disorder. [References] . 
Murphy, Tanya K; Yokum, Kelley. 
McKay, Dean [Ed]; Storch, Eric A [Ed]. (2011). Handbook of child and adolescent anxiety disorders. (pp. 505-520). xix, 532 pp. New York, NY, US: Springer Science + Business Media; US. 
(create) This chapter discusses immune and endocrine function in child and adolescent obsessive compulsive disorder (OCD). It begins by examining L. Selling's theory for autoimmune and infection triggered causes of anxiety. It then questions what the pediatric autoimmune neuropsychiatric disorders associated with streptococcus (PANDAS) phenotype looks like. Next, it looks at the role of Group A Strep (GAS) in causing infections. This chapter then explores the links between GAS and OCD /Tics. Support for infection triggered pediatric neuropsychiatric disorders is discussed. Controversies in establishing an infectious trigger are considered. Other topics covered include the best evaluation and treatment options; antibiotics; neurological and cardiac concerns; and, endocrine dysregulation in anxiety. (psycINFO Database Record (c) 2012 AP A, all rights reserved) 
Obsessive-compulsive disorder: Boundary issues. [References]. Fineberg, Naomi A; Saxena, Sanjaya; Zohar, Joseph; Craig, Kevin J. PsycINFO 
Hollander, Eric [Ed); Zohar,Joseph [Ed); Sirovatka, PaulJ [Ed); Regier, Darrel A [Ed). (2011). Obsessive- 
compulsive spectrum disorders: Refining the research agenda for DSM-V. (pp. 1-32). xxiv, 233 pp. Washington, DC, US: American Psychiatric Association; US. 
(from the book) This reprinted article originally appeared in CNS Spectrums, May 2007, Vol. 12(5),359- 375. (The following abstract of the original article appeared in record 2008-15917-004). The boundaries between obsessive-compulsive disorder (OCD) and other neuropsychiatric disorders remain unresolved and may well differ from one disorder to another. Endophenotypes are heritable, quantitative traits hypothesized to more closely represent genetic risk for complex polygenic mental disorders than overt symptoms and behaviors. They may have a role in identifying how closely these disorders are associated with another and with other mental disorders with which they share major comorbidity. This review maps the nosological relationships of OCD to other neuropsychiatric disorders, using OCD as the prototype disorder and endophenotype markers, such as cognitive, imaging, and molecular data as well as results from demographic, comorbidity, family, and treatment studies. Despite high comorbidity rates, emerging evidence suggests 

substantial endophenotypic differences between OCD and anxiety disorders, depression, schizophrenia, and addictions, though comparative data is lacking and the picture is far from clear. On the other hand, strong relationships between OCD, Tourette syndrome, body dysmorphic disorder, hypochondriasis, grooming disorders, obsessive-compulsive personality disorder, and pediatric autoimmune neuropsychiatric disorders associated with streptococcus are likely. Studies designed to delineate the cause, consequences, and common factors are a challenging but essential goal for future research in this area. (psycINFO Database Record (c) 2010 APA, all rights reserved) 
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. [References]
Larson, MichaelJ; Storch, Eric A; Murphy, Tanya K. PsycINFO 
Storch, Eric A [Ed]; Geffken, Gary R [Ed]; Murphy, Tanya K. (2007). Handbook of child and adolescent obsessive-compulsive disorder. (pp. 163-174). xvi, 415 pp. Mahwah, NJ, US: Lawrence Erlbaum Associates Publishers; US. 
(from the chapter) Clinicians and researchers have recently encountered conflicting views and increasing publicity regarding the diagnosis and treatment of a subset of children that present with symptoms of obsessive-compulsive disorder (OeD) and/ot tic disorders as an immune response to a Group A Streptococcus (GAS) infection. Known as Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS), symptoms include an abrupt onset following a GAS infection (e.g., strep throat or scarlet fever), a relapsing-remitting course of illness, and include new onset psychiatric symptoms (e.g., irritability, sudden mood changes, and separation anxiety) in addition to motor/vocal tics and/or obsessions/ compulsions. The prevalence of PANDAS is currently unknown although some estimates suggest that 11 % to 33% of patients with OCD / tics report onset associated with an infection. Difficulties in identification of base-rates and probabilities for encountering the disorder will persist until definitive criteria are established and the validation of PANDAS occurs. This chapter reviews the history, potential etiology, clinical features and the currently accepted treatments for PANDAS. Controversies regarding this disorder are discussed in an effort to encourage critical thought and discussion regarding the potential of infectiontriggered OCD. (psycINFO Database Record (c) 2010 APA, all rights reserved) 


  1. Thank you for the thoughtful commentary on PANDAS. Keep up the good work spreading the word.
    From - a psychologist and mom to a son with PANDAS

    1. I just found out my son who is 9 has Pandas. They have him on a antibiotic for 10 days. Is it possible that I may have it and gave it to him or his dad? So the antibiotic might not work? He has a M.R.I this week and then I meet back with the doctor at the end of the month but its such a long time away. How do we get tested?

    2. My surmise at this point is that PANDAS afflicts genetically pre-disposed individuals. It is probably autosomal dominant but can't be sure. Also cannot conjecture about spontaneous mutation rate. So...he could have been prone to it from either, both or neither of you. Cannot determine this yet.

      Before I answer questions I encourage you to educate yourselves. Besides this article I suggest you read all of my post and importantly all of the commentary appended to them on my Psychology Today blog. The link is at the top of the page. If you do that you will know more about PANDAS that >99% of physicians. Then you will have a better idea of where you and your son are and further options. Then a more focused and specific discussion can ensue. Thanks you, Dr. Goodman.

  2. Dr. goodman. Could you please write the Task Force who is undertaking the DSM 5. They are now taking comments and the addition of pandas would be great.

  3. I have a son that I think has PANDAS. He is 28 years old. I have tried to find treatment for him but because he an adult, his Dr.'s didn't put much effort into helping him. He is also mentally and physically disabled. He had an abscess removed from his head 8 years ago that was caused by the strep bacteria. Since that time he has had excessive OCD about urination and bowel movements. I know that that he has had at least 2 undiagnosed episodes of strep, who knows how many more. I recently read you article about Evil PANDAS in Adults. I was so excited to see that you also think that adults can have PANDAS. I printed the article and also another one you wrote about PANDAS and took them to his Dr. yesterday. He titer tests done several years ago were elevated but because he was post adolescent, the Dr. wouldn't consider him a PANDAS case. I am hoping his Dr. will let him have a T&A. I know this would help him. He had OCD before his operation, but not as severe and it would subside. Thank you so much for putting your research on the Internet.

  4. I hope it helps your son get proper treatment. Dr. Goodman.

  5. Thank you for this valuable information. Our daughter, 36, has just been diagnosed by a consultant in neurology in Coventry, UK. She is a very senior nurse, married with 2 small sons and she suddenly went from being sensitive, caring, intelligent, organised, to being anxious, not sleeping, obsessive, loss of attention, rude and abrupt with people, frequent urination, clapping, foot stamping, screaming, crying etc. After 5 months of hell, she had to move in with her parents as her boys were being affected by her behaviour. For 8 months, we have been through hell whilst she has been passed between psychiatrists, institutionalised in a psychiatric ward for 5 weeks, and given various sedating medication. It was only following an MRI (repeatedly begged for by family and work colleagues and told it was not necessary)that showed global cerebral atrophy disproportionate to her age, that she was investigated by a neurologist. Thank good fortune that this neurologist took such a good history from us, learning about her frequent strep throat infections she had as a child, and carrying out a barrage of tests. After 2 months, one of the tests on her spinal fluid came back positive, and 2 days ago, she was admitted to start a course of immunoglobulins. The neurologist is also considering phrophlactic antibiotics.
    Both my daughter and I work in the NHS so 'know the system'. My daughter has not been able to make her own decisions for a long time and I have had to push on her behalf, with all our family and her colleagues supporting me. I dread to think of what would have become of her had we not pushed. I have recommended to everyone I know to read your blog, to help them understand. Thank you again

    1. Thank you for you comments and nice words. I hope that your daughter does well. If her neurologist or other physicians want to call or email me I'll be happy to share my data and experience. I do not have enough data about your daughter to make comments. Please continue to get the information out there. It's hard enough when most doctor's haven't even heard of PANDAS in children to get them to pay attention to adult PANDAS. The core problem is that it's all too simple and logical, hence it must be simpleminded. Dr. G

    2. P.S. Please see also my posts on PANDAS on There is a link on the right near the top of the page. JG

    3. Thank you for your response. I have written to my daughter's neurologist and her psychiatrist informing them of your blog and your suggestion to contact you if they wish. I do hope they do this.

      On her discharge from hospital, our daughter's neurologist reassured us that we should see improvement in her behaviour over 2-3 weeks. If no real improvement, then he may consider giving a further course of ig. In your experience, what is the rate of improvement and prognosis for adult panda sufferers? CR

    4. Thank you. I have insufficient data to give a good response. Too many variables. Is the infectious agent identified? Is there a nidus of infection generating a continuous response (tonsils, etc). If so has it been eradicated? Those with surgical treatment show improvement in 2-3 weeks if there is not another source. Response to antibiotic and immune therapy is more variable and always begs the questions of etiology, organism(s) and penetration. Dr. Goodman.

    5. Dr Goodman, as we live in the UK and most research and patients are in USA, are you able to advise where/who we can access to get further information, advice, help? The neurologist who is treating our daughter will be leaving soon.
      Thank you

    6. Unfortunately I get this question too often. I do not know anyone in the UK who can help you. In fact there is no formal network of people in the US who can help. Most of us are working on our own. There are some research papers at different centers where one might find it interesting specialist.

      In my bibliography above there is a paper out of the UK about four or five years ago. I tried to email the address included but I was blocked by the national health service. I suggest that you try to track down the authors of this paper in England and see if one of them might be able to help you directly or with a referral.

      Since I'm the only person I know who's doing any work in the area of adult PANDAS it makes it difficult to provide referrals. Good luck and let me know how things work out. Dr. Goodman.

  6. Dr. Goodman,

    I'm curious as to your thoughts about Amantadine in relation to your observations regarding persistent viral triggers as well as ADHD. Have you ever tried Amantadine with your patients and would you consider it a low risk medication? I'm curious about this pharmaceutical as my daughters who have pandas that is under control now present with mild, lingering ADHD symptoms (which completely vanish and the girls are completely neurotypical when on prednisone, but that is not a long term solution.)
    If we examine the genetic kinks in our family trees, we see MS and Parkinson's which are also both treated with Amantadine. This has peeked my curiosity for my girls and I wanted to know if you had any experience using this with your patients. Thanks so much for the article. Kudos, well written!

    1. Please see my reply below. The format can be confusing.

  7. Hi. Interesting issues. Before contemplation of amantadine are my usual queries about search for a nidus of sub-acute infection; titres of various things; surgical options, etc. What are your child's symptoms?

    I avoid all dopaminergic drugs, particularly on a long term basis, except for Parkinson's. Early and continued use, as for RLS causes a marked increase in Parkinson's disease. My conjecture, and it's just that, is that if the symptoms are clearly associated with the basal ganglia and do not show improvement from surgical intervention, antibiotics, and such then I would consider other immunotherapeutic options--IVIG, plasmapheresis, or a unique trial of other immunotherapeutic drugs (i.e. those used for RA). You need to consider the long term risk/benefit ratio of all therapies before you make a decision. Steroids aren't an option, but if they work, what does it tell you?

    BTW, one can also consider a trial of anticholinergic meds in this situation (artane, cogentin, et. al.) which do not carry the long term risks of dopaminergics. Finally, there are reports of NMS with amantadine, particularly in non-Parkinson's patients, so this must be kept in mind. Good luck, Dr. G

  8. Dr. Goodman,
    I have 3 children, ages 14,12,&11 all diagnosed with P.A.N.D.A.S. We are working with the only immunologist in our area who treats this horrific disease. My 12 yr. old also has severe autism and has nocturnal seizures at the onset of strep exposure. There is so little info. on seizures and strep infections. While we are battling this, can you recommend any resources that address this issue? I'm not sure what to do about these seizures,and neurologists I have seen refuse to acknowledge a connection with strep. Thank You. and I apologize if I missed something in your resources.- A sleep deprived Mom

    1. Hello. Thank you for your question. I'm sure this is a difficult situation. First of all let me say that my experience with children who have autism and PANDAS is that they are affected severely. Dramatic changes in behavior, personality and everything else occurs. A very thorough evaluation is necessary. As I always say efforts must be made to find a Nightes of chronic, subacute infection and eradicated if possible. The patients who have undergone tonsillectomy have had a very rough time postoperatively. However eventually they calm down.

      The issue of seizures is to me a no-brainer. In innumerable inflammatory processes including encephalitis, meningitis, lupus, and other autoimmune problems can cause epilepsy. The failure to make a connection is problematic. Certainly the seizure disorder should be treated with appropriate modern anti-seizure medication. To me there would be an obvious cause-and-effect between PANDAS, autoimmune problems, and seizures. This further begs the question of treating the PANDAS. to treat the epilepsy without treating PAMDAS is in my opinion doing half the job. In innumerable auto immune therapies are available and have been discussed in my blog and elsewhere.

      The politics of of the various self-proclaimed authorities in the field who are now busily attacking one another and criticizing one another's treatment approaches including IV IG, plasmapheresis, tonsillectomy, antibiotics, etc. is a divergent from the need to understand that the treatment must be made to fit the patient rather than the patient fit the treatment. If it works it's a reasonable proposition. Nothing works for everybody.

      So from what you tell me I would make a direct connection between an autoimmune attack on the nervous system and the manifestation of the seizure disorder. I have seen patients with both PANDAS and seizures have their seizures improve with treatment of the PANDAS.

      It is difficult to find open-minded inflexible practitioners. It is also difficult, in the present political environment to find practitioners who are willing to think and practice outside of the box under the threat of criticism and assault from some of their colleagues who "don't believe" in these issues and are very threatened by anybody who is the head of four sets her. That's about as much as I can say and hope that it will help you pursue and solve your problems.

    2. I dictate. That should be nidus, not Nighty's!

    3. I'm still trying to into the program to correct the typos

  9. Dr. Goodman,
    We suspect our daughter has PANDAS. She was extremely colicky as a baby and had many strep infections as a child. In 4th grade she had a very sudden onset bladder frequency and leakage problem - literally overnight - and she had never had any problems in that area before. She went to several children's hospitals and no one could explain why it was occurring. So she suffered through. Then she ended up with an eating disorder (AN)a year or so later, and has been struggling terribly with that for many years. (She's 20 now.) I finally convinced her psychiatrist to run some bloodwork (literally begged, as no one else would do it), and she ordered the tests, which showed elevated strep titers. Started abx which decreased D's exhaustion and wanting to die thoughts, but didn't help with the ED. She has been on strong abx (both Augmentin and Azithromycin, high doses) for over 1 1/2 months, and she had her tonsils taken out 3 weeks ago, and she has continued to decline. She complained of being nauseaus today, and on a whim, I took her to dr. for strep test and she tested POSITIVE. (She's been on constant abx for 1 1/2 months!)NOW they are starting her on penicillin. My daughter has been at the end of her rope for a very long time. She just doesn't want to live anymore, between the Anorexia and the horrible, intrusive, OCD thoughts that come from that. She has been unable to work or finish school. Do you have any idea why the abx's are not working? Is there anything else we should be testing for? We are at a complete loss. I don't know how much longer she can go on. Any info would be greatly appreciated.

    1. Hello. Thanks for your comment. Below I will give you my hypotheses and conjectures. Remember that these are not treatment recommendations. First some general observations, most of which I've made before in my book and posts.
      1. there is a strong genetic overlap between PANDAS & ADHD.
      2. Most collect babies actually are manifesting the classic sleep disorder of ADHD with which they are born, periodic limb movement disorder. They cannot initiate or maintain sleep and they can't be put down at night.
      3. Most children with enuresis who do not have anatomical problems, seizures, certain metabolic problems, and in all of those with PLMD, the enuresis is a manifestation of one of the many parasomnias present in periodic limb movement disorder. This also includes sleepwalking, sleep talking, bruxism, kicking around, sweating, and so forth. I have described all of this elsewhere.
      4. Many children with ADHD are misdiagnosed with OCD. This is because they developed a variety of obsessive-compulsive strategies to keep themselves organized. These strategies are ego syntonic and work well for them. However they are misdiagnosed as having excessive compulsive disorder where in the symptoms art ego dystonic and don't ever respond well to the typical treatments for OCD.
      5. There is a disorder of carbohydrate metabolism in ADHD. In many children, it seems more often overtly in girls than boys, this leads to some sort of bulimia. The girls, being more body-conscious than the boys, develop more symptoms that look like anorexia nervosa then do the boys. However it is not true anorexia nervosa and never gets better to the classic eating disorder treatment programs and medications.

      That's, I infer, and I repeat infer and I am not proposing a formal diagnosis, that your daughter likely has always had undiagnosed and untreated attention deficit hyperactivity disorder with periodic limb movement disorder and a variety of the secondary symptoms that involved in such situations. then, she developed pandas. It becomes confusing and difficult to delineate what are symptoms of pandas, untreated ADHD and PLMD, and what are habitual chronic dysfunctional behavior patterns that overlie all of it exacerbated by the obvious intense anxiety that evolves in these situations.

      With respect to the pandas I don't know to which tests you refer; the ASO titre, streptozyme, or anti-DNAase-B antibodies. I meant I really can't comment on the treatment for panda's without more information. Obviously with her tonsils out and on antibiotics that don't work my thinking tends towards the ADHD and the PLMD. Therefore I would take a very close look at the question of undiagnosed ADHD and PLM D and treatment thereof.

      I can't be comprehensive in this response. I wrote an entire book about it. And I'm not trying to make you buy my book, either but that's where it is in best detail. Certainly you can go through my previous writings. Again, I cannot make any formal diagnoses or treatment recommendations here on the web. I do think that pursuing what I believe to be underlying, undiagnosed issues may eradicate most or all of the problem. pandas related issues may have been addressed effectively already and may not really be the problem here. I hope I am making sense. Good luck. Dr. Goodman.

    2. Thanks so much for responding. I'll be looking into your book, for further info.

  10. To the readers: my hands are disabled and I use voice to text programs for my writing. When I do not have someone else proof it for me there are often typographical errors. I apologize for this but I often miss the errors when I do my own proofreading as is common with many writers. Thank you. Dr. Goodman.

  11. Thanks for the post, I hope your son get well soon. I got very good information about sleeping problems.

  12. Hi Dr. Goodman,

    I wrote the above post on 9/21/12 re: Amantadine. I later discussed how my daughters' ADHD symptoms completely disappeared on prednisone tapers, which I am in total agreement with you: not a treatment plan, but diagnostic!

    Totally anecdotal, but I found this blog with several people, some quite mature (who have been in search of relief for ADHD/ADD symptoms their entire lives)have also found incredible clarity and organization while on prednisone for some unrelated condition.

    So, this is THE question; what does this tell us? How do we begin the search to find the underlying cause(s) of neuro-inflammation that is resulting in ADD/ADHD symptoms for some? This could be totally separate from PANS/PANDAS. We are on the east coast, so I have scheduled an appointment with Dr. Nancy O'Hara to try and get to the bottom of this. It's hard to know as a parent that thinking so much clearer and life being so much easier is possible for your kids because you've seen it with your own eyes, but not know how to make that functioning permanent, consistent. I've got to keep digging! It is inquisitive, open-minded physicians like yourself that partner with parents to make this possibility a reality. Keep up the great work! Big Fan

    1. Hi. Sorry for the dilatory response. Corticosteroids are diffuse anti-inflammatory agents. They also affect affect, mood, cognition, etc. ADHD is a spectrum disorder that stands alone but it is exacerbated by PANDAS and a "secondary" form may be induced by PANDAS. So, both situations exist. And it is obvious that any autoimmune problem affects the HPA axis (hypothalamic-pituitary-adrenal) and in some way may diminish natural immune responses including cortisol. It is a long discussion but important. But cortisone is not curative nor viable long term. We'll keep working.

      Dr. Goodman

  13. Dear Doctor Jory F Goodman. I wonder if my case history would be of any interest to you. I am a 67 year old femalestill of beauty and of varied life accomplishments. Life has been rich in sad events but also happy events. However I have suffered chronic health problems since 1991. One morning in February 2011 I awoke feeling shaky. I proceeded to the kitchen where I attempted to fill the kettle with water in order to make some tea but I was overcome by feeling 'odd' unable momentarily to speak when it returned I was stuttering severely.Repeating the first n middle syllable's of every word and sentence. New for me! It is exacerbated by tiredness and extra outside demands on my intellect or extra physical demand. I have frequent headaches when I study or read, my eyesight been checked. Had 6 month's speech therapy. found it helpful. learned to 'slow down my syllable's.Learned to meditate find it helpful. Underwent MRI head scan and CT body scan. Did not show up any underlying cause for sudden onset stutter. The condition started after prolonged malicious bullying towards me and hubby by someone we succesfully won court case against. Unfortunately hubby died 9 days afterwards in November 2009 I nursed my hubby in the preceeding 15 month's and managed legally to keep hubby safe from being maliciously removed from his own home'. During the autumn of the following year I became ill due to a streptococcus bowel infection it took the wind out of my sails for a few months. Then in February 2010,came an uncontrollable stutter. Since 1991 I have a frequent large eruption of a form of the H S., virus it appears just above my right buttock.Treatment being 5x250mg of Acyclovir daily for ten days. Am Aneamic. Suffer frequent Migraine attacks.Start with the appearance of coloured lights and loss of vision then a headache.occasionally have an event where lose 'intelligible speech' for a few seconds, my tongue seems to twist. 16 when it first occurred. During childhood I had a left eye tick when I felt tired. Also had 'Rheumatic pain'. I lived in fear of an Alcoholic father. I was diagnosed with Malnutrition when I fell ill with Pneumonia at seven. Spent a lot of childhood feeling tired with constant rheumatic pains. I wonder if my problems have become exacerbated by physical infections as well as stress and trauma. I have received great kindness and understanding from the medical profession but no one has mentioned the word 'Pandas' to me. Kindest Regards. Susan

    1. Answer: yes. There are several issues here. The emotional (mind) irritates the brain and increase symptoms. Absent a lot of information it appears you have a PANDAS like problem, or a chronic or residual post-viral encephalitic problem, but many issues come to mind. No one really understands speech and language and it is affected by a plethora of factors. I'd need a lot more info to narrow it down. Dr. Goodman

  14. Good evening doctor, I have question.

    I read your paper first at psychology today and was intrigued by your case studies on adults with PANDAS.

    I had OCD when I was a small child(7 or 8), but it went remission for a couple years then came back when I was 17, then left again when I was 24 only to come back again at 26. I'm 27 and have it.

    Would it be possible that I had(and still have) some form of bacterial infection such as PANDAS all these years even though I'm adult now maintaining my OCD? That it the brief periods of relief was only due to it being suppressed by my immune system?

    Secondly which is off topic from the above - Do you think OTC sleep aids could slightly exacerbate the autoimmunity with regards to onset of PANDAS?

  15. I'm going to be seeing a neurologist for the first time on monday to be assessed for this disorder. I am 27 years old but developed a sudden onset of anorexia when I was 18. Now I have severe ocd and haven't responded to any psychiatric intervention within the past 10 years, including ECT. I also am mostly bedridden from severe fatigue, insomnia, non-restorative sleep, and dysautonomia. I did have high titers to: parvo, hhv6, and ebv. I was also positive for coxsackie. With all this, I have been stuck in the CFS "chronic fatigue syndrome" umbrella but have been declining rapidly. The things that differentiate me from other patients are: severe ocd, eating disorders (for years), severe GAD, depression, and add. I truly hope I can get help b/c even with a good therapist and all the meds I take, I am powerless to the ocd. This disorder sounds similar to CFS in this way: an agent or agents (viral and or baterial infection) enter the body, causes auto-immunity, immune system attacks CNS, then the viruses become chronic and the immune system is chronically overactive. I hope I can get help and relief, to say I am miserable is an understatement. I am saddened that many of us CFS'ers are probably mis-diagnosed too, as well as those of us with psychiatric problems. I even went and saw some famous psychiatrists and none mentioned this or were able to help with meds and supplements. Thank-you for this brilliant article. As far as figuring out about bacterial infections and viral, do we need to see an infectious disease doctor? Also, are anti-virals in consideration for treatment?

    - Christiana

    1. Also I should mention I am diagnosed with fibromyalgia, interstitial cystitis, and sleeping disorder.

    2. Another thing, immunomodulators and stimulants make me very very sick. Stimulants actually make me severely fatigued, sleepy, with a very high heart rate, same reaction with immunomodulators like immunovir.

    3. Sorry to hear your complicated story. Obviously one would need ALL of the data and history to try and clear things up. It sounds as though you might need to get off of all meds--carefully and properly--to get a baseline established. THESE ARE NOT TREATMENT RECOMMENDATIONS, just observations.

      You need to be evaluated by someone who understands PANDAS and Neurosomatics and the interplay of all that you describe. Antivirals are a consideration in some cases. Good luck.

    4. Thanks. How do we know if we are seeing the right specialist for this? I am far too ill to do much of any research and had to read your response about 20x's to grasp it even though I have a college degree. Thanks for all you've written in your blog.

    5. Christiana-

      I hope you see this! As a parent of a child with PANDAS I highly recommend that you find a PANDAS expert- someone who is well versed in PANDAS and has seen 1000's of cases. You can go on the ACN forum and ask questions and find out names of respected doctors that are helping our children and adults.

      Here is a link to the ACN forum:

      I recently heard of a 70+ year old woman on the east coast that is being treated for PANDAS. Our doctor, a Dr. Rosario Trifiletti does a large number of blood work to help determine if this is PANDAS. He was also instrumental in helping the girls from Le Roy that were suddenly "overnight" presenting with Tic's etc.

      Good luck in finding a PANDAS expert. A regular neurologist will likely not have the expertise you need and understanding of the various infections to help you get better.

  16. It's depressing, ever since the first connection of strep and children was made and thus PANDAS established, that it has taken 10+ years to really investigate OCD as a possible autoimmune disorder

    According to there seems to be more interest in research on PANDAS. At least a search shows a small increase in clinical trails..

    After reading your article you suggested a possibility of "other infectious agents". Many of the above trails are using antibiotics such as: azithromycin, amoxicillin, erythromycin, etc.

    I'm not knowledgeable of pharmacology or immunology, so I apologize if this is a foolish question to ask, but assuming these drugs above are only targeting strep strains then is there a possibility that the autoimmune disorder link in OCD could be missed because the compounds are only targeting strep type infections? That is to say would these compounds also target the other infectious agents you described your table III or would more trails be needed for this too?

    I'm sorry if that question doesn't make much sense. I'm not sure how to ask it otherwise. I really appreciate your time answering your bloggers and even taking the time to post this article.

    1. I use the eponym PANDAS inclusively; not just strep. Unfortunately, as things evolve politically, control freaks at Harvard will come up with a narrow set of criteria for "PANDAS" exclusive most other cases and the fight will continue one battle at a time.

      Not all OCD an autoimmune problem; many cases are labeled OCD and aren't (obsessive-compulsive compensatory strategies in ADHD, anxiety binding, etc.). OCD must be ego-dystonic.

      Most of the antibiotics you note, and many others, have broad spectrums and kill numerous bacterial strains.

      I have had adult PANDAS patients with anxiety and ADHD respond to tonsillectomy. One improved on augmentin for mycoplasma. So you see it is complex and confusing and needs expert assistance.

    2. Sorry, you must pardon me as I didn't notice my misspellings in my above comment. Luckily for me, you were kind enough to answer my questions about antibiotics and for this I thank you for sparing the time.

      I couldn't help smile at your "Harvard control freak" comment as I had witness this "phenomena" in numerous articles concerning PANDAS. It seems some researchers can't even agree on the name PANDAS or how it should be defined while others such as Dr. Kurlan are too busy criticizing and attacking the concept and the work of Dr. Swedo and others researching PANDAS.

      With so much division, I fear it's at the point of hindering research rather than progressing it. Further more annoying is the fact researchers are not yet considering adults.

      You don't know how grateful I am for you posting your case studies online along with this article about PANDAS in adults. I do hope you will consider another future posts on OCD, as more develops on the autoimmune side of things.

  17. I am a mother of a 3.5 year old boy and I am also a training Child Psychiatrist and researcher at the Institute of Psychiatry in London. I suspect my son just developed PANDAS (6 weeks ago). You say in your article that it can be diagnosed with one blood test - which one do you mean? I would like your advice if possible, but I understand if you are too busy. My email is Best wishes, Paulina

    1. Good evening. No test is diagnostic for PANDAS. Several are suggestive: AntiDNAase-B antibody, streptozyme, Lyme, mycoplasma, CRP, etc. Please read my several posts on PANDAS at the psychology today link on this page, AND please read the extensive commentary and discussions with each one. This will give you a better picture of the problem. Please get back to me if you have questions or concerns.

  18. Dear Dr. Goodman,

    First off, thank you for posting this blog. I am a 24 year old female recent college graduate living in New York City. Since I was 6 years old I have had severe tics (head nodding, eye blinking, leg kicking.) When I was just a few weeks old, I was hospitalized for rhino strep and ever since then, I have had several strep throat infections a year. My mother has noticed that my tics were much worse when I had strep or was under severe stress. My tics have actually gotten worse since I have graduated from college and started my first job. I was recently diagnosed with co-morbid depression anxiety and depression and have since taking a short term medical leave from my job partially due to the tics distracting myself and others from work. I am on Paxil 50mg per day and Topamax 150mg a day (for tics) but nothing seems to be helping. I would like to get back to work and reduce the tics. I have never been diagnosed with PANDAS, yet all of my recent blood tests seems to test high for strep. If you could point me in the right direction or have any words of advice for me, I would be so thankful. I am very much in a lot of pain right now.

    I truly appreciate your help and time!

    1. I've listed the tests I do here and on other posts at the link. I encourage you to read them and the comment sections. Get checked for ant signs of ADHD/PLMD by someone who uses appropriately broad adult criteria and know of the sleep disorder in ADHD. Be detoxed from SSRIs and never go near them again. There are comments, not formal treatment recommendations. Call ENT, Dr. Warren Zager in Philadelphia and explore situation with him. He knows a lot about PANDAS. you'd probably be well off w/o any tonsils/adenoids. Good luck, Dr. G

  19. Dr. Goodman,

    Thank you for your extremely informative posts about PANDAS. I've read/watched all of your posts here and on Psychology Today. My doctor suggested I might have PANDAS; I'd appreciate your input.

    I'm a 33 year-old man. I've suffered from GAD (self-diagnosed) since early adolescence, and Bipolar II Disorder (self-diagnosed), currently in remission, since around age 18. No other obvious psychopathology, other than what follows:

    At age 27, I followed the suggestion of a meditation teacher to "let go of control." Immediately, I started experiencing involuntary muscular contractions (neck flexing; rhythmic contraction and release of facial, stomach, and other muscles throughout the body; sustained teeth clenching) and involuntary repetitive vocalizations (ma ma ma ma ma, da da da da da, wa wa wa wa wa, pee pee pee pee pee, sippy cup sippy cup sippy cup, profanities, nonsense phonemes and nonlinguistic sounds, and the like), and have experienced them ever since, often for hours every day. I have also suffered from chronic fatigue ever since the onset of the involuntary movements and vocalizations. Ironically, the anxiety has decreased and the bipolar tendencies gradually went away ever since the onset of the involuntary contractions and vocalizations.

    I have been able to earn a BA in psychology from Harvard and two MAs in psychology, in spite of my symptoms, but I've been completely unable to work for the last two years, due to an increase in the severity of my symptoms. I'm currently applying for SSI/SSDI.

    I find my case difficult to unravel, because it's not clear how much of the symptoms are due to psychodynamic/psycho-spiritual causes, versus purely organic causes (I learned to repress my emotions at a very early age, and had challenging relationships with my parents).

    My symptoms do not seem like ordinary Tourette's: they started in adulthood; are rhythmic in nature (in contrast to the DSM's definition, which defines tics as nonrhythmic); are fully controllable (though when I voluntary suppress them long enough, I become so agitated that I feel compelled to retreat from other people and allow the contractions and babbling to happen); and began during a meditation exercise specifically designed to allow the expression of repressed psychological content, rather than an infection of traumatic event.

    The "episodes" look to me very much like psychogenic non-epileptic seizures (specifically the neck flexing and rhythmic contractions throughout the body), except for the unusual vocalizations, ability to suppress, and complete lucidity I experience.

    Organically: I do have high Anti-DNase B Strep Antibodies (260 U/mL) and high Mycoplasma pneumonia IgG Abs (165 U/mL). Mycoplasma pneumonia IgM Abs is normal (<770) and Antistreptolysin O Ab results are in the normal range (43.8 IU/mL). I'm waiting to hear back about Lyme results (Western Blot, IgG/IgM IFA, and PCR). LDL and VLDL are high, but thyroid and other standard blood work are normal. Also waiting to hear back about cortisol levels, which I suspect are high.

    I also suffer from IBS. Colonoscopy and duodenal biopsy for celiac were negative, but IgA stool testing and IgG blood testing revealed numerous food intolerances (gluten, etc.), which led to a restrictive diet that greatly improved but did not completely cure the IBS.

    I suffered from severe halitosis, starting in adolescence or early adulthood. Last November, I discovered tonsilloliths and received a complete tonsillectomy. My ENT said I had the most tonsilloliths he'd ever seen. The tonsillectomy greatly diminished the halitosis—perhaps even eliminated it—but didn't help with any other symptoms. I don't believe I received a concurrent adenoidectomy. I have suffered from non-allergic rhinitis since early adulthood.

    [Message truncated by character limit—continued in next message.]

    1. [Message continued from previous message.]

      I'll be seeing my primary care physician in a couple of months. In the meantime, I'd be curious to hear your impressions, and whether you think it's worth looking into any additional testing or treatment.

      Specifically, is it worth going back to my ENT and asking him to look for infections in my sinuses and adenoids, and considering an adenoidectomy?

      I've had lots of intestinal testing, so far showing only a bacterial imbalance and elevated food-based IgA antibodies. No parasites. Are there any other tests for chronic intestinal infections—or infections elsewhere in the body—that I might request? Or any treatments I should consider other than probiotics (which I've been taking recently)?

      I'm messaging you on Facebook as well, with a link to a video demonstrating my symptoms.

      I'd schedule an appointment with you, but I don't live very close to you, my insurance is HMO, and I currently have no financial support other than public assistance. If and when I get Medicare or support from my family, I will consider scheduling an appointment with you. Do you take Medicare? Do you do phone or Skype appointments, or just face-to-face? The commute would be difficult, but I could potentially see you in person at least once, if necessary.

      Thanks in advance for any help you might provide.

    2. PS I live in the San Francisco Bay Area. I like my primary care physician—who is the one who first told me about PANDAS and is having me tested—and it sounds like you are the only true expert on adult PANDAS out there, but if there's anyone in my area you'd recommend, I'd be open to suggestions.

      Also, I forgot to mention that I've been seen by multiple psychiatrists and neurologists, and none of them had any definitive diagnoses or anything useful to say. One of the neurologists said my case was fascinating, and suggested I find a neurology researcher at a university to study me, but so far, I haven't found any such researchers who have expressed interest (I'm open to suggestions, should you have any).

      Finally, would you be open to the possibility of a phone consult with my primary care physician, if that ends up seeming like the most appropriate way to proceed?

  20. Dr. Goodman,

    A study was just published that seems to conflict with your suggestion that tonsillectomies and adenoidectomies help with PANDAS. See below for the abstract. Do you know of published research that refutes this?

    Also, since PANDAS is an autoimmune disorder, isn't it possible to suffer from it even if one has no active infection, since the IgG antibodies that stick around after the infection is gone seem to be the source of the PANDAS symptoms?

    Finally, do you have any thoughts about the new Cunningham Panel, available in most states from (I was told it should be available in California in the next month or two)? The panel measures "antibody titers against four neuronal antigens present in the brain," as well as an assay that quantifies "calcium/calmodulin-dependent protein kinase activity using a neuronal cell line to test for functional signaling antibodies against human neuronal cells." It is apparently the most direct way to diagnose PANDAS available.

    Pediatr Infect Dis J. 2013 Mar 20. [Epub ahead of print]
    Tonsillectomies and Adenoidectomies Do Not Prevent the Onset of Pediatric Autoimmune Neuropsychiatric Disorder Associated with Group A Streptococcus.
    Murphy TK, Lewin AB, Parker-Athill EC, Storch EA, Mutch PJ.
    1 Department of Pediatrics, University of South Florida, St. Petersburg, Florida 2 Department of Psychiatry & Behavioral Neurosciences, University of South Florida, Tampa, Florida.
    BACKGROUND:: In children presenting with obsessive compulsive disorder (OCD) and/or tics, especially those with a temporal association with streptococcal pharyngitis (e.g., PANDAS; Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus), there is speculation about whether tonsillectomy/adenoidectomy might improve the child's neuropsychiatric course. Our objective was to examine whether removal of tonsils and/or adenoids impacted streptococcal antibody titers, the timing of onset of OCD and/or tics, and the clinical severity of these symptoms. METHODS:: Study participants (n = 112; average age = 9.2 ± 2.4; 44 female) were recruited as part of a prospective investigation of neuropsychiatric phenomena with temporal association to streptococcal pharyngitis and examined by family history, diagnostic interview, physical examination, medical record review, psychological testing, and streptococcal antibodies and divided into surgical or non-surgery groups. The surgical group consisted of children having previously had a tonsillectomy and/or adenoidectomy (n=32). The remaining children were categorized as non-surgery (N=76). Measures of OCD and tic severity, streptococcal antibody titers, and PANDAS classification were compared between both groups. RESULTS:: There were no significant differences as determined by streptococcal antibody titers, PANDAS classification, and OCD or tic severity between the surgical and non-surgery groups. Most participants had surgery before onset of neuropsychiatric symptoms and surgery did not affect symptomology. CONCLUSIONS:: Streptococcal antibodies and neuropsychiatric symptom severity did not differ on the basis of surgical status. From these data we cannot support that tonsillectomy and adenoidectomy are likely to impact positively the course of OCD/tics or streptococcal antibody concentrations.
    PMID: 23518825 [PubMed - as supplied by publisher]

    1. 1. The new test is very promising, but not definitive. In the area of immunology there are numerous "sero-negative" cases with the diagnosis made on clinical grounds w/ negative labs. Ultimately genetic mapping is needed.

      2.My published research refutes the study you note. The patients I report have had dramatic benefits from surgery. Obviously case selection is critical. The study you cite states that "most" of the surgical cases developed PANDAS some time after surgery. Do they have another nidus of chronic sub-acute infection? What is the causative agent? If it's mycoplasma, Lyme, a virus, etc then surgery is of little or no help. Furthermore, it is very obvious that the Strep tests (which ones, and done at what labs?) are not necessary or sufficient. They may be negative in certain strains of strep, but positive with staph, H.Flu, P.Pneumonia, etc. Hence the study--which gets somebody published--is imprecise, vague and less than helpful. I will not speculate many other elements that may be involved.

    2. Dr. Goodman,

      Thank you for your comprehensive reply. What you say makes sense.

      Could you please provide the citation information for the research you published that you mentioned? I couldn't find it in the abstracts above. A link would nice too, if possible, especially if you can provide access to the full text and not just the abstract, since I don't currently have easy access to journals.

      Also, if you wouldn't mind answering another question: How does one confirm infections in various nidi, such as the adenoids? Culture?

      Thanks again for your help.

    3. Hi.

      Here is the link to my article:

      Infectious nidi are confirmed by CT/MRI (sinus, mastoid, etc.), sometimes direct observation (sinus), rarely by culture (smooth tonsils, sinus polyps, mucoceles, cysts are surface negative), and occasionally by stool culture (overgrowth) or serology (leaky gut). Cultures are the least useful. Culture of surgical specimens or biopsies are critical.

      Indeed, I am a proponent of surgery in appropriate cases. I find the absolutist resistance tiresome, narrow-minded and stupid; not to mention problematic for patients.

    4. Thank you, Dr. Goodman. Very helpful.

      If you wouldn't mind one more follow-up question:

      What is the apparent/potential relationship, if any, between tonsilloliths (aka, tonsil stones) and PANDAS?

      I had a tonsillectomy last year due to tonsillolith-induced halitosis. The ENT said, after the procedure, that I had the most tonsilloliths he had ever seen. Unfortunately, it didn't help with my tics and generalized anxiety, but then again, he did not perform an adenoidectomy, despite my chronic non-allergic rhinitis, so perhaps there is another nidus of infection.

      Also, unfortunately, I don't believe the ENT cultured the removed tonsils. Note that I have antibodies to strep, but I did not experience sore throats on a regular basis.

      I also just discovered that my girlfriend, who suffers from generalized anxiety and dermatillomania, has tonsilloliths, so it makes me wonder what connection there might be, if any, between tonsilloliths and PANDAS.


    5. Hi John Doe,

      I'm from Australia and our situations sound eerily similar. You can email me at narison at gmail dot com

      I have confirmed strep overgrowth in the gut and also test positive to the strep antibodies.


    6. Oh I should mention I am planning on faecal transplant to help fight off strep in my gut. I am having a lot of trouble getting specialist help though even though my GPs believe I have PANDAS. It's unbelievable that in 2013, we may as well be living in the dark ages.

    7. My experience with GI induced PANDAS is that proper bowel cleansing, diet and antibiotics solve the problem. If not then look at the appendix, diverticuli, polyps, cysts or other closed loop or long bowel problems. Fecal transplant won't work if these problems are present. Also, intrinsic leaky gut problems will not be resolved.

    8. Dr Goodman,

      Quick questions if I may ask.

      Why wouldn't a fecal transplant work exactly? Bacteria is very competitive for it's environment and it seems logical that changing the environment to a favorable strain of bacteria would help.


    9. My guess is that it's important to clear out the strep with antibiotics first, detoxify gut, and do things to promote the healing of gut lining (i.e. colostrum?). And then fecal transplant?

  21. Dr. Goodman,

    Good morning, I wonder if you might have advice regarding how best to approach requesting labs/testing for PANDAS? My primary care physician (internal medicine)dismissed my initial request to explore PANDAS after my sleep disorder specialist and OCD therapist both suggested it as a possibility. She cited it being a pediatric disorder of which she is not familiar and does not apply to me as an adult (I attempted providing your article for her review). She referred me to a psychiatrist (pending appt).

    31 yo female with currently diagnosed OCD, impulse control, and hypersomnia--possible depression, social anxiety, ADHD, BDD, bulimia. Childhood strep throat + OCD symptoms; OCD waxed/waned over years -- increasing in severity into adulthood -- finally reported symptoms of OCD, anxiety, sleepiness/insomnia, eating disorder. Experienced many cold/flu/sore throats in past two years and recent pneumonia severely exacerbated above disorders/symptoms. Treated w/ z-pack antibiotics but prednisone taper for asthma issues post-penumonia created roller-coaster for above symptoms. OCD therapist noted resistance to CBT post-penumonia and suggested testing for PANDAS. Currently taking adderall to help w/ daytime sleepiness; ambien to help w/ anxiety for sleep and tapering off wellbutrin (originally prescribed for post-pardum depression and never removed).

    Thank you for your help.

    1. Hi. First I need to apologize for my dilatory response. This page does not notify of new comments and yours just showed up!

      I infer that you have ADHD and PLMD at baseline. If so, Wellbutrin, Adderall and Neurontin are best (the last to correct the sleep disorder of ADHD). Avoid SSRIs.

      People with ADHD seem to be more susceptible to PANDAS than the general population. PANDAS makes everything worse. You have several potential loci of infection and a detailed evaluation is necessary. I do not know where you live but it is best done by someone very familiar with PANDAS who can order the w/u AND interpret the results. I cannot make specific recommendations for evaluation or treatment here. I do encourage you to look at my posts on the link to which include several on PANDAS and one on the sleep disorder. Good luck.

  22. I have a 24 y.o. son suffering from sudden onset OCD in elementary school with hand wringing (choreiform?) movements. There's a significant autoimmune family history.

    The disease is somewhat improved but he's still greatly affected and desparate for help.

    He was never tried on antibiotics (despite his seeing Dr Rapopport and Dr Walkup and my speaking to Dr Swerdo at time of diagnosis). Medicines and cognitive therapy haven't been particularly helpful.

    We'd be extremely grateful if you could offer some suggestions about testing/treatment. Could you point us toward a physician on the East Coast who treats adult "PANDA/ PANS"?

    Thank you!

    1. Sorry to hear about your typical story. Dr. Rosario Trifileti in NYC & Dr. Warren Zager in Philadelphia. Good luck.

  23. I just discovered your blog and I love it. Thank you so much for taking the time to write and share.
    Vancouver Wa

  24. Hello,
    Four years ago exactly, I had a horrific case of Tonsilitis. Approximately a month after I developed severe OCD symptoms mainly the Pure Obsessional kind. Now, as a child I had frequent cases of Strep throat ( at least twice a year for about eight years).
    The sudden on-set of the OCD behavior was out of no where and fierce and has been unrelenting ever since.
    I can't help but come back to the Tonsilitis and Strep causes. I am 33 years old and am not sure what to do. I will be talking with my Primary Care this week and think ordering a CBC to check my Neutrophil Levels which, if decreased have been linked to the pathogenesis of OCD and also have my tonsils examined as well....could be a source of the sub-acute infections???

  25. Dear Doctor, I am a 46 year old woman who had strep multiple times when I was between the ages of 4-8 and have had it as an adult as well. I have had terrible OCD since (my earliest recollections of it) possible 5 or 6 years of age. I always thought I was just cursed with this and there were periods of time over my life where I thought I was just feeling "more secure" with things going on in my life, and during those periods of time the OCD seemed to have gone away. I have also suffered from RLS for more years than I can remember, with it having gotten absolutely terrible over the past few years. Other medical issues I have, and there are many (!!), Hashimoto's thyroiditis, IBS, interstitial cystitis/irritable bladder syndrome, Afib, and over the past few years developed a postive ANA and have all kinds of body aches, etc. Some days I feel like a huge mess! I never had my tonsils out although I remember the doctor told my mother, as I had had it like three times over a 6 month period, that if I got it one more time they would take my tonsils out. I read your article here and I am sitting at work while reading this, but wanted to cry! I thought, could it have been because of my strep??!! Especially the OCD, it has been driving me absolutely CRAZY lately, not one bit of rest from it, I could cry because it is controlling my life. Do you have any thoughts on my situation? Could it be adult form of PANDA's, and if so, who do I go to to try to have them test me for it or whatever it is they do to diagnose it? And can it be cured at my age? If it could be my goodness I would be ecstatic!!

    1. I infer that you may have PANDAS as well as the Neurosomatic Syndrome (described in my book and elsewhere). I do not know where you reside. You can check for referrals through the PANDAS Network online, or see Dr. Richard Harris in Beverly Hills. Good luck.

    2. I live in Connecticut, but I would be more than willing to go out to Beverly Hills :-)
      I will go on the PANDAS Network and see if I can find a doctor close to me. I did see one online, in Darien, CT and he had a good write-up. I don't want to go to the Neurologist I have seen and then they have never heard of this ... I want someone who knows about this because I was so surprised to read about this it sounded like it could be an answer! Thank you.

    3. I'm confused. If this woman were to come all the way to Beverly Hills, why do you recommend she see Dr. Harris, instead of yourself?

      I ask because I'm considering seeing you, Dr. Goodman, for my own possible PANDAS; based on your comment, I'm wondering whether I should see Dr. Harris instead.

    4. I believe it improper to self-refer and insist that people must see me. I finally have a superb immunologist to work with and most patients will see both of us for diagnosis and management. Just a quirk.

  26. Dear Dr Goodman.
    I am 24 years old and had an aso test done for PANDAS. My psychiatrist ordered them because my symptoms were acute and the onset was sudden to where I remember the exact day this started (2 years ago), although more symptoms have surfaced. but I was immediately put on antibiotics and I feel like some things were overlooked. I live in Florida near a center that treats PANDAS but they are a pediatrics center. So I was wondering if you knew if they would consider further test for me even though im not a adolescent.

    1. Here's the problem: I don't know what tests you had done, by whom, or where. So validity is problematic. I don't know if the center you refer to is wonderful or clueless. I cannot evaluate or diagnose or treat in this forum. You are well advised to collate all of your info and see Dr. Rosario Trifiletti in NYC or Dr. Richard Harris in Beverly Hills. I refer all of the immunology work-ups in my practice to Dr. Harris. Good luck.

  27. Dear Dr Goodman
    Sorry for my bad english, it is not my native.
    Can you answer one question to you? Its very very important for my life. Iam 22 years old man. About 7 years i have Chronic tonsillitis (j35 in icd 10), not treated. One year before tonsillitis i developed first OCD symptoms, some little compulsions. They did not affect my life much. But for past few years my OCD became much much worse. I have many intrusive fears. single one, sensomotoric, is just ruining my life. I respond to ssri at max dosage very weak. Actually it just reduces my anxiety from obsessions. I also didnot respond to seroquel augmentation with 300 mg. One med which helped my in past was sulpiride at low dosage (100-150 mg per day). I dont know how it helped, may be cause dopaminergic augmentation which sulpiride produces at low dosage. Main question is: CAN MY OCD (without tics) BE LINKED WITH MY tonsillitis? Sorry for caps. But its very important for me. I have tried several different drugs without big succes and now i am very depressed and dont know what to do. Just give me answer can it all be linked to strep in my tonsils. At least possibility. Thank you!

    1. Yes, it is quite possible. You are well advised to see a true PANDAS expert.

    2. Wow, many thanks for fast reply, Dear Doctor!
      Bad news that I am not sure that there is true pandas expert EVEN across whole my country. But you gave me a hope. So Iam gonna to explore all presented information about pandas, by you ofc, and probably others. And i will do blood test, ASLO and anti-DNAase B. Also will collect some other indications for T&A and will do it. Can I ask one more question to you? You believe that PANDAS suffers should avoid SSRI. That "PANDAS related "OCD" involves disturbance of dopaminergic neurons". Can you explain this statement? I respond well to sulpiride low dosage, which blocks dopamine autoreceptors and cause some surge in dopamine. Another argument for my PANDAS probably. Thank you!

  28. Hi. I have insufficient information to make definitive observations, and, respectfully, cannot do a treatise on SSRIs and PANDAS, etc. here. I do not know where you live. On the East coast there is Dr. Rosario Trifiletti in NYC. On the West coast I work with Dr. Richard Harris (immunologist). I cannot refer to people I do not know, or at least know a lot about. You might be well advised to gather your data and see one of the few authorities. I am not soliciting you. I just do not know where to send you.

    1. Dear Doctor!
      I am not asking for treatment recommendation! I just wonder - what is PANDAS pathogenesis? You write that PANDAS involves disturbance of dopaminergic neurons. Is it true? Can you tell more about it, doctor? Or recommend some book, article about it. I am very interested. Sorry if i miss something or dont understand. Thank you very much!

    2. I encourage you to go to the link on this blog to There I have 3 posts, all of which have extensive commentary. Please read those, and then go to PANDAS Network on Facebook. This is the best and swiftest way to educate yourself.

  29. Hello Dr.,
    Thank you so much for your research and for the time you spend to reply on our comments.
    I'm a 32 year old female, I had a sudden very acute OCD on the night of February 25th 2014. I thought I lost my mind because everything obsessed me. All the things we do spontaneously scared me.. Like taking a shower, putting close on, sun rise! It got worse with time that I couldn't see or hear anything couldn't read or watch TV and most of all I couldn't be by myself because I was so scared. I went from being an outgoing happy self confident successful girl with no past traumas at all and a very happy childhood to someone withdrawn anxious and for some period Depersonalized! I've kept thinking that my mind wasn't functioning the way it should! I knew something got suddenly very wrong. Ofcourse I left my job, my BF and went back to live with my parents. I've been to many psychiatrists and non of them knew what I had, they said it's an accumulation of stress that Led to this, or that I hate myself! Nothing convinced me until I got to a dr. Who asked me if I had any recent step infection. In fact at the end of December until mid January I have had 3 very severe consecutive tonsilis infections. I've took three antibiotic courses for 10 days each and each time I finish the course I relapsed. Augmenting, amoxicillin and finally Levaquin. My gland got huge after the third course and I have photos and tests of all three infections. Strep was negative but dr. said maybe because of the previous antibiotic course and I've responded quickly to antibiotics in all three episodes until the relapse. Neutrophils and WBC were very high. One month later I started the horrible symptoms. I've had frequent streps as a child but never developed any post infection symptoms. I've been tormented so much since February. The Dr. I saw put me on SSRi low dose and it did help a lot. I can read now, go out, I've got rid of many obsessive thoughts. But the thing is that I just don't feel that I'm back to my old self, I still need to put an effort to exist which was totally spontaneous. Can you please let me know if there is anything I could do to get my brain to function as it was before feb 25th? Should I undergo a tonsils removal? What's the long term outcome for my case? Will I be able to work and continue my life as normal people do?
    Your reply is much appreciated. Thank you so much Dr.

  30. I forgot to mention Dr. That I'm not in the US nor Europe and I have no access to any PANDAS specialist. Thanks

    1. Hello. Obviously this sounds like PANDAS. I do not know where you are. Typically you would need a proper immunologic work-up, both for PANDAS specific items and broader immune problems frequently found in PANDAS individuals. The results of this evaluation would determine the best forms of immune therapy.

      I infer that you would likely do better without your tonsils/adenoids. Long-term antibiotics may be used but not with out potential risks. Short-term corticosteroids often are helpful.

      I encourage you to read all of my PANDAS posts in (see link on this page) and ALL of the comments and discussions. It will give you a better database with which to work.

      Nothing I wrote here is diagnostic or therapeutic, just observations. Ultimately it may serve you well to assemble as much data as you can, maybe get your tonsils out, and find your way to a consultation with someone in N. America. Good Luck. Dr. Goodman

    2. Thanks so much dr. for your swift reply. I have read all your posts and comments about the disease and found them very informative and helpful. I'm currently in Lebanon and unfortunately there are no PANDAS specialists around. I just want to take your opinion in few things:
      1- if I remove my tonsils is there any risk that my symptoms worsen as a consequence to post surgery antibodies formation?
      2-If SSRI are fairly working for me, could it be a cure on the long term?
      3- what tests should I do to determine if antibodies are still forming and what immunology treatment works best for me?

      Again, I'm so thankful for all your effort to help all us overcome this horrible disease. God bless you!

    3. Hi.
      1. If you have T&A need pre-op antibiotics for a few weeks. Expect a flare from the release of bacteria during surgery. That requires antibiotics and sometimes corticosteroids. It will settle down.

      2. I hate SSRIs. Short term benefits usually wear off. But I'm not in possession of all of the data.

      3. I am a NeuroPsychiatrist and Psychopharmacologist. I work with a superb immunologist. I make initial diagnoses and handle many of the meds but pass the further immunologic work-up and treatment to him.

      I do not know what else to tell you. I can refer to colleagues in Texas, NYC and Beverly Hills.

    4. Can't thank you enough doctor. Went to ENT today and he agreed that I should get my tonsils out. He put me on Penicillin 1000mg x2 a day and corticostroid .,25x2 a day for 4 weeks before surgery. Please let me know if you agree on that dosage. So grateful for all your help.

    5. This appears to be quite reasonable. Good luck.

    6. Hi Dr., a quick update since my last post. Since I started the antibiotics and corticosteroid few weeks ago I feel much better, and my tonsils reduced significantly in seize. I wish I took those medicines long time ago. Although SSRI were helpful, but those medicines almost got me back to my old self. I have scheduled T&A next week and I will write an update after the surgery. Again thank you so much Dr. for all your help.

  31. Hello, a quick update after my surgery that I did on Sep 27. I feel way better, I actually had an acute hidden inflammation despite the fact that I took Penicillin 2000mg a day for 5 weeks before my surgery. The tonsils analysis showed: "Bacterial focal acute inflammation on chronic tonsillitis with lymphoid hyperplasia."
    Right after my surgery I started Augmenting 1000 x2 a day and continued Dexametazone 0.25x2 a day. I experienced a mild flare of my old symptoms especially the first 2 nights. However, I do feel well now and I think it's the best choice that I made to do the tonsillectomy. My question to you Dr. Is this : I stopped the Augmentin after 10 days and continued the corticosteroid, now I feel that I'm having very mild flares after stopping the antibiotics. I don't know if it is psychological. Should I continue the antibiotics for some more time and when to stop the Dexametazone?

    Thank you so much!

  32. Dr,

    Would you consider resubmitting your work (along with updated and most recent case studies) to another journal?

    The NIH only sponsors research of PANDAS in pediatrics. Currently the funding isn't available to investigate adults hence the lack of referrence.

  33. Thank you for your enquiry. There are several impediments to a further revised article. First amongst them is a virtual certainty of rejection. I and my colleagues have been plagiarized numerous times. The odds of the publication of a comprehensive article with review of the literature, scores of cases, and scholarly discussion are very poor. The political nature of the journals and academia is that they would rather table something like this in favor of a skimpy report of three cases from some of their chums at any important medical center. For the most part this is how they operate all the time.

    Secondly it is very time consuming. To proceed at this point would involve the coordination of my colleagues in immunology and ENT. None of us have much free time. Nor have we yet come upon a graduate student or medical student with the motivation to get involved.

    Personally I am absorbed with my practice, clinical research, and most intensively with the further development of a new family of molecules I have invented and patented with more than 25 neuroscience and somatic indications. This has been and remains enormously time-consuming and complicated.

    I and many of my colleagues find it more useful to post our observations and information immediately on the Internet rather than wait six months or longer turnaround time from a journal. This is not about money. It is about efficiency and effectiveness. Certainly there is some ego involvement. It would not be purposeful to proceed without the necessary immunological and surgical input from my colleagues because the database has expanded so much over the past two years or so. Bluntly put, if the editors of a meaningful journal approached me with a request to do what you suggest and a strong probability of publication then my colleagues and I would jump on the opportunity and get it done. Thank you.

  34. Dear Dr. Goodman,

    I have suffered from severe, life dominating OCD for almost 9 years. It started getting severe at age 20, and I am now 29 years old. I seemed to be somewhat obsessive as a child/adolescent as well.

    Diagnoses: Blood work shows elevated Strep B, extremely elevated EBV, mycoplasma, Bartonella, and diagnosed with Lyme (diagnosed by a top Lyme disease physician with IgeneX laboratory testing).

    I just had my tonsils removed 3 months ago, convinced ENT to do it after reading your posts. It has not made a difference yet, but I am holding on to hope after reading it could take up to 6 months to work in comments. Recent prednisone burst for bad cough proved to relieve my anxiety greatly. As for antibiotics, Zithro caused terrible anxiety, Tindamax for Lyme seems either neutral or might help a little. Taking Augmentin right now for seasonal respiratory infection, doesn't seem to be helping, maybe making OCD worse.

    Questions: Is there ANY hope for me this late in the game? I've heard repeatedly that IVIG looses success rate the older you get. Are there any other treatment methods you know of besides IVIG and steroids?

  35. I have an insane amount of ocd, anxiety, sleeping problems etc etc. I had strep throat a few times growing up and have taken loads of antibiotics.

    I'm getting tests done to see if I have strep in my intestinal tract

    I plan on doing a fecal transplant soon.

    How effective would it be to get a fecal transplant to kill strep in my intestinal tract?

    What else should I do? I'm very desperate.


  36. Dear Readers. I receive numerous enquiries every day on this blog, other blogs, by mail, email and telephone. The distress and suffering many of you experience is frustrating to me. However I cannot practice medicine in these venues. The stories I hear, and the data received are always incomplete. It remains that a thorough history, revive of data and an examination, usually with further work-up as determined on a case-by-case basis is necessary.

    I do not solicit patients here. But, wherever you are, you need to see an expert. This is not always convenient, and rarely inexpensive; just necessary.

    Attempts at video medicine are complicated by state laws, insurance companies and licensing boards. Hence I cannot continue to attempt to correspond and advise in a fragmentary manner. I will continue to post data as I have it. The Physicians who know and treat PANDAS are well known on the Internet and by the PANDAS network. Try to see one of us. That is your best resource. Thank you.

  37. Are there any clinical trials open to study adults who think they have had PANDAS since childhood? I'd be interested in being included in one.

    1. Not to my knowledge. You have to stick with the frontiersmen.

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  39. Dear doctor Goodman,

    I have been suffering from depression and severe anxiety and panic attacks and weird symptoms and I am so sure that inflammation and an infection have something to do with because I will get attacks were it feels like my brain is on fire. Anyway, I am Belgian. Would you happen to know any doctor in Belgium who is open to testing these kind of things ?

    1. Ah I saw your response to a British commenter. So you probably don't know any Belgian neurologist either.

    2. The more I am reading about this the more I am thinking that there must be a connection. I had a lot of various throat and lung infections as a child and I think I have periodic limb movement disorder or at least I move excessively during sleeping according to family and friends. I am going to ask my doctor to look at my blood;

    3. Sorry, do not know anyone in Belgium.

  40. Hello Dr.Goodman,
    I'm finding it very difficult to find a doctor who treats Adult Pandas, I live in Tampa, Fl and Dr.Storch is well known for Pandas here but does not treat adults. Is it that most Doctors do not believe Adults can have have it or there are just not enough of you out their to cover adults, very frustrating?

    1. Good morning. 1) most doctors haven't heard of PANDAS; 2) most who have heard of it do not know what it is or what to do about it; 3) most who do understand the problems and try to treat it limit themselves to the "acknowledged " groups for fear of persecution for the provision of unnecessary treatment for "non-existent" disorders; 4) it is very difficult to do alone. As a psychiatrist I need an immunologist an an ENT and an ID. They all get rattled with accusations by other doctors who do not know PANDAS but whose patients have attacked them for missing it. Finally, and it needs to be said, those of us who do treat PANDAS get tired of the incessant pounding and demands of patients and families who expect us to know everything about this evolving illness and to CURE it. We understand the anguish and frustration, and the displacement and projection, but it is not helpful and appropriate. When a patient or relative happens to be rather Borderline, or worse, it creates havoc in the practice. As knowledge grows and spreads there will be more doctors engaged. Just a brief response for you.

  41. Hello dr. I would really appreciate if you can answer me even with a yes or no.
    I have posted on your blog last year August 14, I have recovered completely from Pandas after tonsils removal and antibiotics and corticosteroids, thanks to your guidance and advice, can't thank you enough. However three months ago I was traveling for my honeymoon and I got a cut in my foot, it got infected, and I took antibiotics and it healed, however, since then I have terrible insomnia, no OCD, just can't sleep, while I always slept like a baby even when I had the severe panda episode. I have tried everything from Remeron to Valium but nothing is working, finally in taking Lunesta, but would not get more than 3-4 hours max. My question is do you think this is a panda relapse, or just a severe insomnia case. My mind is peaceful when I go to bed, and empty of thoughts but can't fall asleep. Please let me know what you think, and although I don't live in the states but I can come see you if necessary. Thank you so so much.

  42. Hello, I am a 45 year old woman who has had PANDAS my entire life. I am a classic case, like the patient in this article. I really want to see the researchers turn their attention to the adults like me, as we have suffered far longer with chronic illness, misdiagnoses and lack of effective treatment! Plus you may be able to learn more about us, by looking at blood as well as brain scans during acute flares! I am in a flare right now, having been diagnosed with mycoplasma, and I am 100% certain that my basal ganglia would be inflamed if you can a PET scan today. My ADHD symptoms have been off the charts, anxiety through the roof, irritability/explosiveness CRAZY (my poor family!!). Got on wrong antibiotic for first 4 days but finally realized it and switched yesterday. Also got a shot of steroids and am feeling so much better!! Please study the adult's! We can teach you not only about the illness, but the adaptive mechanisms associated with this chronic illness. I am also a psychotherapist and have clients who are adults with this illness.

    Please help!

    1. Thank you for your comment. Sorry to hear of your distress.

      There are a few of us pushing forward. But the resistance, denial and often hostile derision of the "mainstreamers" is exhausting. It is very important that every patient and family member post their stories; bring info to their often ignorant MD's, and advocate aggressively for themselves.

  43. Dr. Goodman...what are your thoughts on laser tonsil ablation for a persistent high ASO titer/ throat inflammation in a 28 year old female? Biggest symptoms are deep muscle aches and anxiety. I am trying to avoid a full tonsillectomy in fear of post-op complications. Thank you.

  44. Cannot make a treatment recommendation here but would tell my patients either to remove all tonsillar tissue or don't bother...

  45. Dr. Goodman, thank you for the incredible work you are doing. Can you explain why you discourage SSRI's for Pandas? Do you work with the Cunningham panel. Thank you!

  46. SSRIs, all of them, cause dopamine blockade which induces akathisia and numerous other serious side-effects. This cause insomnia via Alpha-intrusion. They cause EPS. The normal brain, let alone the PANDAS afflicted brain do not need or like this.

    The Cunningham panel may be helpful in some cases but in my opinion is not diagnostic of PANDAS. Almost every area of the brain is susceptible to inflammation and the panel identifies antibodies to the basal ganglia. More general tests can find inflammation. When found more specific tests for immune deficiencies are done and immunotherapy begun.

    In PANDAS the issues are:

    1. Think of it
    2. Look for it
    3. Identify the infectious agent and try to eradicate it chemically and surgically
    4. Stimulate, support and/or augment the immune system
    5. Anticipate and suppress flares
    6. Avoid foolish pharmacotherapy

    There you have it.

    1. The above comment is from Dr. Goodman. We are having problems with the web site. Thank you.

  47. Dr. Goodman, my 25 year old who still has PANDAS flares has Anthem Blue Cross Select HMO. Do you take this type of insurance?

    1. You must call my office. Staff can answer questions about insurance.

  48. Dr. Goodman, I have an 8 year old daughter recently diagnosed with PANDAS> Major behavior change began about a year and half ago. She has tested positive for Myco Pneumonia, CMV, and Lyme. My question is how common is PANDAS with siblings? My family has had many diagnosis recently and I can't help but wonder if there is more to it. I have a 6 year old who has many difficult behaviors...ADHD type, some oppositional/negative bxs, very poor eater and within the past 4 months has had mono, tested positive for myco pneumonia and has developed molluscum on his legs. My older son, 12 was recently diagnosed with a goiter and we are getting thryoid tested. He also had an active mcyo infection. I myself was also just diagnoses with Hashimotos. I am feeling like the overall health of our family is not good, and am wondering if I should push further for testing for PANDAS on at least the younger sibling? Any suggestions would be greatly appreciated. Would running the Cunningham on siblings be useful? My daughter was elevated on all 5 tests. Thank you for any insight!!!Thank you. Jenni Batalucco

  49. It is obvious that there is a genetic predisposition to PANDAS. It is obvious then that there will a proclivity towards PANDAS in families; they share similar genetic profiles. PANDAS is an autoimmune/immune deficiency problem. You have Hashimoto's. I would check everyone for PANDAS. Cunningham panel is fine but I have never needed it. Search for etiology/source and remove/eradicate it. Use effective strategies to stimulate/boost or assist immune system. There you have it.

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  52. Dr. Goodman, I have had OCD, anxiety, and depression all my life. I also have Lyme Disease. I'm severe now with the OCD/anxiety/depression at the age of 46 to where I can hardly leave home. I'm allergic to most meds I've tried. I seem to respond to meds that affect glutamate like Lamictal, but I'm allergic. She won't try Riluzole and Memantine, which I'm curious to try. I just learned about PANDAS and wonder if I might have that going on. My psychiatrist doesn't know what to do for me and recommend ECT because I'm so severe I have felt suicidal for year, but I'm not sure that would help ECT (do you think it might?). Are there any other doctors like you closer to Ohio? Kim

  53. Dr. Goodman, me again. I wanted to add I also have Candida, leaky gut, and a rare condition called colonic inertia where my colon is partially paralyzed. Therefore I can't have treatment for candida because when I kill any candida, even with probiotics, the dead candida turns into a gluey mucus (biofilm?) that will NOT come out no matter what I do, even with enemas, Dr. Schulze formula 1 and 2, etc... Is there any hope for me to feel better from this severe OCD/anxiety/depression? I have felt suicidal for many years and need relief. I get relief from Lamictal and also did from Anafranil, but I'm allergic to those. Many years ago Prozac helped me, then it stopped. I had ECT 21 years ago and it helped me several months after my last treatment. But I read that ECT can cause glutamate in the brain to rise, and I seem to benefit from meds that lower or block glutamate. I don't even know where to start. My mind races and I can't think straight. I need help really bad.

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