Introduction

This guide features excerpts from the paper

PANS/PANDAS and Related Inflammatory Brain Conditions Involving the Basal Ganglia: Overarching Principles of Clinical Management

by Dr. Jennifer Frankovich (Stanford University), Dr. Patrick Whelan (UCLA), Dr. Mark Pasternack (Massachusetts General, Harvard), Dr. Kyle Williams (Massachusetts General, Harvard), Dr. Julia Zhang (Tufts), Dr. Gareth Morgan (University of Leicester), Dr. Chris Pittenger (Yale), Dr. Cynthia Wang (UT-Southwestern), Dr. Melissa Silverman (Stanford), Dr. Gail Bernstein (University of Minnesota), Jackie Horgan (Stanford), Dr. Terence Sanger (USC), Dr. John Gaitanis (Tufts), Dr. Juliette Madan (Dartmouth). Additional contents have been reviewed by members of the Neuroimmune Foundation Scientific and Clinical Advisory Board and Board of Directors.

Patient Questionnaire

The Stanford Immune-Behavioral Health Clinic provided Neuroimmune Foundation with a copy of the extensive patient questionnaire they use at intake as a template for physicians wishing to care for patients with PANS and/or research PANS. The questionnaire can be set up in Redcap or a similar platform. To request a copy, please email info@neuroimmune.org. Thank you.

PANS Symptoms and Diagnosis

PANS stands for Pediatric Acute-onset Neuropsychiatric Syndrome. According to the PANS Research Consortium comprised of physicians and researchers from institutions such as Stanford, Yale, Harvard, Columbia, and National Institute of Mental Health, PANS is a clinical diagnosis requiring OCD (Obsessive-Compulsive Disorder) and/or restrictive food intake as well as two or more of the following symptoms:

  • Anxiety
  • Emotional Lability
  • Depression
  • Irritability
  • Aggression
  • Severely oppositional behaviors
  • Behavioral or developmental regression
  • Deterioration in school performance, handwriting, or math skills
  • Sensory abnormalities
  • Sleep disturbances
  • Enuresis
  • Urinary frequency

Identification of the trigger is not required for a diagnosis of PANS. There is no age requirement.

PANS is a diagnosis of exclusion. To exclude other disorders, a comprehensive evaluation including a complete medical and psychiatric history, physical examination, laboratory testing of blood and urine [and possibly, cerebrospinal fluid (CSF)], and selected paraclinical evaluations, such as magnetic resonance imaging, electrocardiogram/echocardio­graphy, electro­encephalography, and polysomnography15 (in severe cases and when autoimmune encephalitis is on the differential diagnosis). Diagnostic recommendations include starting with a broad differential and narrow it to PANS only after eliminating all other possibilities such as Sydenham chorea, autoimmune encephalitis, neuro­psychiatric lupus, and others.7 (p. 201),15

While the acute onset of PANS is a distinguishing factor, it is still important to consider all the causes of OCD and eating restriction given that many autoimmune/inflammatory diseases are associated with OCD and other psychiatric deteriorations (see section “Differential Diagnosis of Neuropsychiatric Deteriorations” below).

PANDAS Symptoms and Diagnosis

PANDAS is the acronym for Pediatric Autoimmune ­Neuropsychiatric Disorders Associated with Streptococcal ­infections. PANDAS is a subset of PANS. Guide­lines for diagnosing PANDAS include:

  • Presence of OCD and/or tics
  • Symptoms begin between age three and puberty
  • Acute-onset and episodic (relapsing-remitting) course
  • Association with Group A Streptococcal (GAS) infection
  • Association with Neurological Abnormalities

The diagnosis of PANDAS does not require comorbid neuropsychiatric symptoms beyond OCD or tics, however, they are often present.

Alternative Diagnoses

Regardless of whether a patient has sudden-onset of symptoms meeting criteria for PANS/PANDAS, it is important to consider other psychiatric disorders and other inflammatory brain condition (post-infectious inflammation or other autoimmune condition (see Differential Diagnosis of Neuropsychiatric Deteriorations hyperlink to scroll to that section). Most inflammatory brain conditions present sub-acutely. Additionally, most inflammatory brain conditions in children do not present with MRI findings (since inflammation and most autoimmune processes are microscopic) or have blood markers, so negative findings should be expected. Deep brain processes may not be detected on EEG. For further guidance on inflammatory brain conditions that can cause psychiatric symptoms, see:

Supporting Evidence

Please check the list below to find supporting evidence that your patient has PANS/PANDAS or other related inflammatory basal ganglia disorder

History suggesting propensity to autoimmunity/inflammatory disease (examples):
  • Patient currently has the diagnosis, or has a history of the diagnosis of arthritis, psoriasis, enthesitis, thyroiditis, celiac disease, type 1 diabetes, Behçet’s, inflammatory bowel disease, or other autoimmune/inflammatory condition. Enthesitis, arthritis, or spondylitis most commonly presents with Achilles tendonitis, plantar fasciitis, first MTP pain/tenderness or inflammatory back pain (pain/stiffness worse in morning or with prolonged stationary positions and better with NSAIDs or exercise often starting in adolescence or early adulthood).
  • First-degree family member diagnosed with an autoimmune/inflammatory condition including: arthritis, enthesitis, thyroidi­tis, celiac disease, type 1 diabetes, inflammatory bowel disease, or other autoimmune/inflammatory condition.
  • Patient or first-degree family member diagnosed with an immunodeficiency and/or has difficulty clearing bacterial infections (recurrent sinusitis or otitis media not related to allergies or anatomic problems, hospitalization due to bacterial infection, needing an unusually prolonged course of antibiotics to clear an infection). These patients or first degree family members would typically have hypogammaglobulinemia, poor response to vaccines, and/or B cell development issues (low plasmablasts, class switch, etc.). Immunodeficiency linked to infection clearance issues and autoimmunity.
Laboratory findings of immune dysfunction/inflammation (examples):
  • Monocytosis (based on pediatric reference ranges) as this reflects an active infection or inflammatory process.
  • Elevated immune complexes (elevated C1Q binding or Raji cell assay) which may reflect an autoimmune process or infection.
  • High titers of an autoantibody (histone antibody, thyroid antibodies, ANA, GAD antibody) at least twice separated by 3 months.
  • Iron deficiency +/– anemia in the absence of other risk factors for iron deficiency and iron deficiency anemia
  • Elevated vasculitis blood marker (D-dimer or vWF antigen) at least twice separated by 3 months.
  • Low complement (low C4 +/– low C3)- typically complement is lower in flare and higher in remission.
  • Proteinuria or hematuria reflecting a low grade post-infectious nephritis, not explained by a genetic/familial cause.
  • Cytopenia (leukopenia or thrombocytopenia).
Physical exam evidence of infection, post-infectious inflammation, or chronic inflammation +/– vascular inflammation (examples):
  • Infection/post-infection inflammation/or other active sign of inflammation (e.g., pharyngitis, tonsillitis, adenoiditis, sinusitis, otitis media, uveitis, retinal vasculitis, perianal redness, palatal petechiae) in new-onset case or new-onset flare.
  • Small vessel vasculitis signs (e.g., prominent onychodermal band, periungual redness, splinter hemorrhages, livedo reticularis) in patients with chronic symptoms or flare of chronic symptoms.
  • Arthritis or enthesitis (on physical exam) and symptoms of inflammatory back or joint pain (however, be aware that psychiatric symptoms may be so severe that they overshadow subtle joint symptoms).
    • Pain and stiffness which is worse in the morning or with stationary positions.
    • Pain and stiffness which improves with exercise and/or NSAIDS.
    • Tenderness at joint margins and/or at entheseal points (where tendons and ligaments insert onto bone) in the absence of myofascial tender points which would be consistent with a pain amplification syndrome.
    • MRI or ultrasound showing thickening or enhancement of joint capsule or synovium and/or joint effusions.
Signs suggesting basal ganglia involvement (examples):
  • Neuro exam finding indicating basal ganglia dysfunction: e.g., overflow dystonia, truncal weakness and difficulty holding arms up or overhead, piano playing finger movements when arms/fingers outstretched, positive glabellar sign, darting tongue or tongue fasciculations (Wormian tongue movements), weak grip and/or milkmaid sign, hung-up reflexes, arm or leg movements during standing or sitting Romberg.
  • Eye movements/vision abnormalities consistent with a basal ganglia disorder.
  • MRI (obtained within a few days of symptoms) showing basal ganglia enhancement.
  • Neuropsychiatric symptoms (relating to the basal ganglia functions) which span multiple domains and started simultaneously (e.g., sudden behavior and/or mood change, new and sudden learning difficulties (e.g., loss of math and reading skills) not relating to behavior and mood, movements during REM sleep16–18, dysautonomia, new urinary frequency/incontinence, new movement abnormality pertaining to basal ganglia dysfunction (e.g., handwriting change, tics, etc.), and/or sensory amplification which can be elicited on exam.

Differential Diagnosis of Neuropsychiatric Deteriorations

Primary inflammatory brain disorders
  • Autoimmune encephalitis (Hashimoto’s, anti-NMDA receptor, GAD associated, etc.)
  • Demyelinating diseases: Acute disseminated encephalomyelitis (ADEM), multiple sclerosis, neuromyelitis optica, MOG antibody disease, etc.
  • Central nervous system vasculitis
  • Post-infectious neuroinflammatory conditions +/– evidence of systemic inflammation (small vessel vasculitis, arthritis, etc.).
  • Post-COVID neuroinflammatory disease
  • PANS/PANDAS
  • Encephalitis lethargica
  • Sydenham chorea
Neoplastic diseases affecting the brain
  • Paraneoplastic autoimmune encephalitis
  • Primary CNS tumors (glioma, astrocytoma, germ cell tumors, etc.)
  • Lymphoma or leukemia involving the brain
  • Metastatic disease (neuroblastoma, etc.)
  • Langerhans cell histiocytosis
Systemic autoimmune /inflammatory conditions with secondary psychiatric symptoms
  • Neuropsychiatric lupus
  • Sjogren’s
  • Behçet’s
  • Systemic vasculitis
  • Antiphospholipid antibody syndrome
  • Celiac disease
  • Sarcoidosis
  • Autoinflammatory diseases (interferonopathies, hemophagocytic lymphohistiocytosis, FIRES, etc.)
  • Acute necrotizing encephalopathies
  • Medication induced inflammatory condition (e.g., minocycline and other medication hypersensitivity reactions)
Nutritional
  • Vitamin B12 deficiency
  • Cerebral folate deficiency
  • Wernicke’s encephalopathy (thiamin deficiency)
Primary infections of the brain or infectious triggers
  • Parasites (malaria, etc.)
  • Bacteria (Borrelia burgdorferi, Mycoplasma pneumonia, Mycobacterium tuberculosis, Treponema pallidum, Listeria monocytogenes, etc.).
  • Viruses (adenovirus, enterovirus, Epstein-Barr virus, HSV, HIV, influenza, JC virus, measles, rabies, varicella zoster, West Nile virus, coronaviruses, etc.)
Systemic or localized (but not CNS) infections in the setting of a child with atypical neurodevelopmental condition (ADHD, anxiety, autism, developmental delay, etc.)
  • ENT infection (tonsillitis, adenoiditis, otitis media, mastoiditis, abscess, etc.)
  • Other bacterial infections (perianal strep)
  • Severe viral infections (flu, COVID19, adenovirus, etc.)
Metabolic
  • Genetic/inherited: leukodystrophies, mitochondrial diseases, mucopolysaccharidoses, organic acidurias, Wilson’s disease, etc.
  • Hepatic encephalopathy
  • Toxic ingestions or infections with underlying metabolic disorder
Seizure disorders
  • Primary seizure disorders (idiopathic, genetic, or autoimmune)
  • ESES (seizures at night)
  • Underlying primary seizure disorder in the setting of new infection or inflammatory disorder
  • Acute encephalopathy with seizures and diffusion restriction (AESD)
Toxic ingestion/exposure

(+/– underlying psychiatric/atypical neurodevelopment conditions)

  • Recreational drug use (alcohol, marijuana, synthetic cannabinoids, cocaine, opioids, methamphetamines, etc.)
  • Toxic ingestions (ethylene glycol, methanol, inhalants, etc.)
  • Toxic exposures (insecticide, etc.)
  • Medications (metronidazole, cyclosporin, etc.)
  • Chemotherapy
Primary psychiatric disorders – new onset or established

(+/– infection, +/– systemic inflammatory disease, +/– autoimmune encephalitis, +/– social stressor)

  • Autism
  • Obsessive compulsive disorder
  • Anorexia nervosa
  • Avoidant/restrictive food intake disorder (ARFID)
  • Tourette syndrome
  • Transient tic disorder
  • Bipolar disorder
  • Schizophrenia or other psychotic disorder
  • Conversion disorder
  • Psychogenic seizures
Other
  • Trauma (+/– underlying neurodevelopmental challenge, etc.)

31 Item PANS Symptom Inventory and Ratings

Developed by Gail Bernstein, MD and Tanya Murphy, MD

Symptom 0-None 1-Mild 2-Moderate 3-Severe 4-Extreme
Obsessions
Compulsions
Hoarding
Food refusal/avoidance
Urge to overeat; thinking about eating all the time
Fluid refusal/avoidance
Separation anxiety
Other anxiety/fears/phobias/panic attacks
Mood swings/moodiness
Emotional lability (e.g., inappropriate crying/laughing spells)
Suicidal ideation/behavior
Depression/sadness
Irritability
Aggressive behaviors, violence, and/or rage
Oppositional behaviors
Hyperactivity or impulsivity
Trouble paying attention
Baby talk
Other behavioral/developmental regression (e.g., poor self-care, immature judgement for age)
Worsening of school performance
Worsening of handwriting/copying/art
Cognitive symptoms (e.g., difficulty thinking, foggy brain, memory problems)
Pain (e.g., headaches, abdominal pain, body pain)
Sleep disturbance
Daytime wetting or bedwetting (enuresis)
Urinary frequency (uses restroom frequently)
Bothered by sounds, smells, textures, or lights (sensory amplification)
Hallucinations
Delusions or paranoid thoughts
Tics (movements)
Tics (sounds)

PANS/PANDAS Treatment

In 2017, treatment guidelines for PANS and PANDAS were published in a special issue of the Journal of Child and Adolescent Psychopharmacology (JCAP, 2017). We strongly urge you to review these guidelines as they provide detailed treatment guidelines that are far more robust than can be easily covered here. Authors of the guidelines include physicians and researchers at institutes including Stanford, Yale, Harvard, Columbia, National Institute of Mental Health, and others. They categorized treatments based upon severity.

Treatment for mild to moderate PANS/PANDAS can include:
  • Addressing infections
  • Corticosteroids
  • Anti-inflammatories
  • Therapy
  • SSRIs (please see JCAP for dosing as dose is typically low and and then escalated as tolerated)
Treatment for moderate to severe PANS/PANDAS can include:
  • Addressing infections
  • Corticosteroids
  • Anti-inflammatories
  • Therapy
  • SSRIs (please see JCAP for dosing as dose is typically low and and then escalated as tolerated)
  • IVIG
  • Plasmapheresis
Treatment for severe to extreme PANS/PANDAS can include:
  • Long, tapered corticosteroid courses or repeated high dose IV corticosteroids
  • IVIG
  • Plasmapheresis
  • Rituximab
  • Addressing infections and the above
  • DMARDs

PANS Sub-Groups and Corresponding Treatment Considerations

Sub-Group Treatment Considerations
Relapsing-remitting with full resolution Patients in this category typically have less severe episodes, less frequent episodes, and return to a good baseline between episodes. These patients typically do not progress to a chronic-static course. Most of the episodes/flares last weeks to a few months thus psychotropics and aggressive immunomodulation are not warranted. These patients should be managed with CBT with considerations of NSAIDS or brief (5 day) corticosteroid bursts (akin to the treatment of asthma exacerbations) to treat the flares. However, it is not known if the benefits of NSAIDS and corticosteroids outweigh the risks. As described above, addressing trauma and underlying infections is essential. Steroids may prolong elimination of triggering infections.
Patients with Primary Chronic Symptoms The vast majority of cases of PANS are relapsing-remitting with initial episodes lasting 4 weeks-4 months. For patients with a high burden of symptoms (with no or little signs of an improving trajectory) by 6 months likely have one of the following situations: ongoing infection or autoimmune/inflammatory condition (arthritis or other autoimmune condition) or an underlying neurogenetic/neuroimmunogenetic condition, or a combination of these factors. Primary chronic cases are rare but may represent a good portion of families who participate in blogs or frequent clinics and ERs due to the high level of burden and tremendous mental anguish suffered by these patients and families. These cases benefit from a multidisciplinary team approach for a thorough and coordinated evaluation and treatment planning. Essential subspecialists include: psychiatrist with expertise in OCD and other behavior disorders, behavioral therapist, social work support, neurodevelopmental specialist. Subspecialists to consult include: infectious disease expert, rheumatologist, immunologist, geneticist with expertise in neurogenetics/neuroimmunogenetics.
Relapsing-remitting worsening baseline +/– eventual progression to secondary chronic. A subgroup of patients with PANS have a relapsing-remitting course but do not return to baseline between episodes. These patients tend to have more severe flares and take longer to recover from each flare. They may also suffer from more frequent flares and stacked-flares. Evaluation for underlying immunodeficiency and autoimmune/rheumatological conditions may need to be explored and consultation with psychiatrists which can help stabilize the brain so the child will be more robust (and not deteriorate) with the usual barrage of childhood infections. As with primary chronic PANS, these patients benefit from having a multidisciplinary approach including clinicians with expertise in neurodevelopmental disorders and neuroimmunogenetics.
Patients with frequent relapses and frequent infections Patients with underlying immunodeficiencies (which composes a small subset of patients with PANS) may have a harder time clearing infections and thus may have more PANS episodes than immunocompetent patients with PANS50,51. Addressing the underlying immunodeficiency may help minimize the frequency and severity of relapses.
Patients with frequent relapses with signs/symptoms of autoimmunity and/or arthritis Since immunodeficiency causes “frustrated inflammation” (i.e., difficulty clearing infections thus overactivation of inflammation pathways) and predisposes to the development of autoimmunity and other inflammatory diseases, patients with immunodeficiency and frequent infections and/or PANS relapses should be evaluated for secondary autoimmune conditions.

PANS and PANDAS FAQs

Laboratory tests guide treatment and help differentiate between PANS and PANDAS, however, there are no lab tests that determine whether or not an individual has PANS. PANS is strictly a clinical diagnosis.

Clinicians often order the following tests:

  • Throat culture or culture of peri-anal region
  • ANA titer
  • ASO titer
  • Anti-DNase B titer
  • Streptozyme
  • Lyme Western Blot in Lyme endemic areas
  • Comprehensive Metabolic Panel
  • Quantitative immunoglobulins (IGG, IGA, IGE, IGM)

Negative titers or negative strep culture do not rule out PANS, while positive lab values do not rule PANS or PANDAS in. Presence of strep simply distinguishes between PANS and PANDAS.

Individuals with PANS and PANDAS often have relapsing and remitting symptoms. Some are symptom free for months or years or may even have only one PANS/PANDAS episode. There is currently no cure for PANS and no treatment that helps all patients. 

The strict criteria requiring abrupt onset of symptoms was designed to expedite research of a homogenous group of patients. There is mounting evidence of immune dysregulation and inflammation contributing to a number of neuropsychiatric illnesses. Stanford, a leader in research and treatment of PANS, reported in this study that only 40% of patients they treated at that point had lightening-like onset. Research on PANS is constantly evolving. More research is needed in this area.

The first onset of symptoms often occurs between the ages of three and twelve. However, diagnosis of PANS is not limited to a specific age range.

It is important to realize that criteria in both PANS and PANDAS was established primarily so that scientists could more quickly elicit answers by focusing their research efforts on a relatively homogenous and well-defined group. 

Yes. Autism and PANS/PANDAS are not mutually exclusive. 

These references and other publications are included on our Publications page.

  1. Swedo SE, Leonard HL, Garvey M, et al. Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infections: Clinical Description of the First 50 Cases. Vol 155.; 1998.
  2. Premraj L, Kannapadi NV, Briggs J, et al. Mid and long-term neurological and neuropsychiatric manifestations of post-COVID-19 syndrome: A meta-analysis. J Neurol Sci. 2022;434. doi:10.1016/j.jns.2022.120162
  3. Schou TM, Joca S, Wegener G, Bay-Richter C. Psychiatric and neuropsychiatric sequelae of COVID-19 – A systematic review. Brain Behav Immun. 2021;97:328-348. doi:10.1016/j.bbi.2021.07.018
  4. Rogers JP, Chesney E, Oliver D, et al. Psychiatric and neuropsychiatric presentations associated with severe coronavirus infections: a systematic review and meta-analysis with comparison to the COVID-19 pandemic. Lancet Psychiatry. 2020;7(7):611-627. doi:10.1016/S2215-0366(20)30203-0
  5. Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain Behav Immun. 2020;87:34-39. doi:10.1016/j.bbi.2020.04.027
  6. Calabria M, García-Sánchez C, Grunden N, et al. Post-COVID-19 fatigue: the contribution of cognitive and neuropsychiatric symptoms. J Neurol. 2022;269(8):3990-3999. doi:10.1007/s00415-022-11141-8
  7. Swedo SE, Frankovich J, Murphy TK. Overview of Treatment of Pediatric Acute-Onset Neuropsychiatric Syndrome. J Child Adolesc Psychopharmacol. 2017;27(7):562-565. doi:10.1089/cap.2017.0042
  8. Xu J, Liu RJ, Fahey S, et al. Antibodies from children with PANDAS bind specifically to striatal cholinergic interneurons and alter their activity. Am J Psychiatry. 2021;178(1):48-64. doi:10.1176/appi.ajp.2020.19070698
  9. Frick LR, Rapanelli M, Jindachomthong K, et al. Differential binding of antibodies in PANDAS patients to cholinergic interneurons in the striatum. Brain Behav Immun. 2018;69:304-311. doi:10.1016/j.bbi.2017.12.004
  10. Zheng J, Frankovich J, McKenna ES, et al. Association of Pediatric Acute-Onset Neuropsychiatric Syndrome With Microstructural Differences in Brain Regions Detected via Diffusion-Weighted Magnetic Resonance Imaging. JAMA Netw Open. 2020;3(5):e204063. doi:10.1001/jamanetworkopen.2020.4063
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  12. 12.Kumar A, Williams MT, Chugani HT. Evaluation of Basal Ganglia and Thalamic Inflammation in Children With Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infection and Tourette Syndrome: A Positron Emission Tomographic (PET) Study Using 11C-[R]-PK11195. J Child Neurol. 2015;30(6):749-756. doi:10.1177/0883073814543303
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  14. Swedo SE. Sydenham’s Chorea: A Model for Childhood Autoimmune Neuropsychiatric Disorders. JAMA. 1994;272(22):1788-1791. doi:10.1001/jama.1994.03520220082035
  15. Chang K, Frankovich J, Cooperstock M, et al. Clinical evaluation of youth with pediatric acute-onset neuropsychiatric syndrome (PANS): Recommendations from the 2013 PANS consensus conference. J Child Adolesc Psychopharmacol. 2015;25(1):3-13. doi:10.1089/cap.2014.0084
  16. Santoro JD, Frankovich J, Bhargava S. Continued Presence of Period Limb Movements During REM Sleep in Patients With Chronic Static Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS). J Clin Sleep Med. 2018;14(7):1187-1192. doi:10.5664/jcsm.7222
  17. Gaughan T, Buckley A, Hommer R, et al. Rapid eye movement sleep abnormalities in children with Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS). J Clin Sleep Med. 2016;12(7):1027-1032. doi:10.5664/jcsm.5942
  18. Gagliano A, Galati C, Ingrassia M, et al. Pediatric acute-onset neuropsychiatric syndrome: A data mining approach to a very specific constellation of clinical variables. J Child Adolesc Psychopharmacol. 2020;30(8):495-511. doi:10.1089/cap.2019.0165
  19. Thienemann M, Murphy T, Leckman J, et al. Clinical Management of Pediatric Acute-Onset Neuropsychiatric Syndrome: Part i – Psychiatric and Behavioral Interventions. J Child Adolesc Psychopharmacol. 2017;27(7):566-573. doi:10.1089/cap.2016.0145
  20. Cooperstock MS, Swedo SE, Pasternack MS, Murphy TK. Clinical management of pediatric acute-onset neuropsychiatric syndrome: Part III—Treatment and prevention of infections. J Child Adolesc Psychopharmacol. 2017;27(7):594-606. doi:10.1089/cap.2016.0151
  21. Frankovich J, Swedo S, Murphy T, et al. Clinical management of pediatric acute-onset neuropsychiatric syndrome: Part II—use of immunomodulatory therapies. J Child Adolesc Psychopharmacol. 2017;27(7):574-593. doi:10.1089/cap.2016.0148
  22. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009;119(11):1541-1551. doi:10.1161/CIRCULATIONAHA.109.191959
  23. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group a streptococcal pharyngitis: 2012 update by the infectious diseases society of America. Clin Infect Dis. 2012;55(10):1-17. doi:10.1093/cid/cis629
  24. Murphy TK, Brennan EM, Johnco C, et al. A Double-Blind Randomized Placebo-Controlled Pilot Study of Azithromycin in Youth with Acute-Onset Obsessive-Compulsive Disorder. J Child Adolesc Psychopharmacol. 2017;27(7):640-651. doi:10.1089/cap.2016.0190
  25. Garvey MA, Perlmutter SJ, Allen AJ, et al. A pilot study of penicillin prophylaxis for neuropsychiatric exacerbations triggered by streptococcal infections. Biol Psychiatry. 1999;45(12):1564-1571. doi:10.1016/S0006-3223(99)00020-7
  26. Snider LA, Lougee L, Slattery M, Grant P, Swedo SE. Antibiotic prophylaxis with azithromycin or penicillin for childhood-onset neuropsychiatric disorders. Biol Psychiatry. 2005;57(7):788-792. doi:10.1016/j.biopsych.2004.12.035
  27. Frankovich J, Thienemann M, Rana S, Chang K. Five youth with pediatric acute-onset neuropsychiatric syndrome of differing etiologies. J Child Adolesc Psychopharmacol. 2015;25(1):31-37. doi:10.1089/cap.2014.0056
  28. Kovacevic M, Grant P, Swedo SE. Use of intravenous immunoglobulin in the treatment of twelve youths with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Child Adolesc Psychopharmacol. 2015;25(1):65-69. doi:10.1089/cap.2014.0067
  29. Brown KD, Farmer C, Freeman GM, et al. Effect of Early and Prophylactic Nonsteroidal Anti-Inflammatory Drugs on Flare Duration in Pediatric Acute-Onset Neuropsychiatric Syndrome: An Observational Study of Patients Followed by an Academic Community-Based Pediatric Acute-Onset Neuropsychiatric Syndrome Clinic. J Child Adolesc Psychopharmacol. 2017;27(7):619-628. doi:10.1089/cap.2016.0193
  30. Brown K, Farmer C, Farhadian B, Hernandez J, Thienemann M, Frankovich J. Pediatric Acute-Onset Neuropsychiatric Syndrome Response to Oral Corticosteroid Bursts: An Observational Study of Patients in an Academic Community-Based PANS Clinic. J Child Adolesc Psychopharmacol. 2017;27(7). doi:10.1089/cap.2016.0139
  31. Perlmutter SJ, Leitman SF, Garvey MA, et al. Therapeutic plasma exchange and intravenous immunoglobulin for obsessive-compulsive disorder and tic disorders in childhood. Lancet. 1999;354(9185):1153-1158. doi:10.1016/S0140-6736(98)12297-3
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  33. Spartz EJ, Freeman GM, Brown K, Farhadian B, Thienemann M, Frankovich J. Course of Neuropsychiatric Symptoms after Introduction and Removal of Nonsteroidal Anti-Inflammatory Drugs: A Pediatric Observational Study. J Child Adolesc Psychopharmacol. 2017;27(7):652-659. doi:10.1089/cap.2016.0179
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  36. Latimer ME, L’Etoile N, Seidlitz J, Swedo SE. Therapeutic plasma apheresis as a treatment for 35 severely Ill children and adolescents with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Child Adolesc Psychopharmacol. 2015;25(1):70-75. doi:10.1089/cap.2014.0080
  37. Demesh D, Virbalas JM, Bent JP. The role of tonsillectomy in the treatment of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS). JAMA Otolaryngol – Head Neck Surg. 2015;141(3):272-275. doi:10.1001/jamaoto.2014.3407
  38. Murphy TK, Lewin AB, Parker-Athill EC, Storch EA, Mutch PJ. Tonsillectomies and adenoidectomies do not prevent the onset of pediatric autoimmune neuropsychiatric disorder associated with group A streptococcus. Pediatr Infect Dis J. 2013;32(8):834-838. doi:10.1097/INF.0b013e31829062e2
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