PANDAS …

Neurobehavioral & Cognitive Disorders

Updated 02.19.2026
Released 11.15.1999
Expires For CME 02.19.2029

PANDAS

Authors: Aravindhan Veerapandiyan MD, Ruthwik Duvuru MBBS

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Editor: Nina F Schor MD PhD

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PANDAS

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Introduction

Overview

Pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS) is a syndrome marked by sudden onset and a relapsing-remitting pattern of obsessive-compulsive symptoms, tics, and other behavioral issues in children with streptococcal infections. The precise incidence and prevalence are unknown, as it is often underdiagnosed due to challenges in establishing the temporal link between group A Streptococcus infection and PANDAS symptoms, along with limited data on the latency period between group A Streptococcus infection and neuropsychiatric symptoms (33) and the absence of disease-specific biomarkers (02). Additionally, similar neuropsychiatric symptoms are often observed in other neurocognitive conditions.

In a retrospective review across three academic primary care populations (2017 to 2019; 95,498 children aged 3 to 12 years), only 13 confirmed cases were identified among 357 potential cases, yielding an estimated annual incidence of 1 per 11,765 children with geographic and temporal variability (128).

Pediatric acute-onset neuropsychiatric syndrome (PANS) is an umbrella term that includes PANDAS and consists of a constellation of rapid-onset, simultaneous neurologic and psychiatric symptoms.

The etiology of PANDAS is thought to involve an immune-mediated, autoaggressive attack on basal ganglia antigens, particularly in the caudate nucleus and putamen, following recent streptococcal infection through molecular mimicry. This relationship remains unproven based on the current evidence. Diagnosis is based on clinical criteria and exclusion of known infectious, metabolic, or structural causes. Immunomodulatory therapy, including plasmapheresis and IVIg, remains highly investigational. Children with potential or diagnosed PANDAS require a multidisciplinary approach.

Key points

	• PANDAS is currently regarded as a subset of pediatric acute onset neuropsychiatric syndrome (PANS), a heterogenous clinical construct lacking validated biomarkers and definitive pathogenic mechanisms.
	• Diagnosis remains clinical and exclusionary, requiring careful differentiation from primary psychiatric disorders and autoimmune encephalitis.
	• Universal testing for a group A streptococcal infection is not recommended; microbiologic testing should be reserved for children with clinical features of streptococcal pharyngitis.
	• Evidence-based psychiatric and behavioral interventions should be initiated promptly and should not be delayed during diagnostic evaluation.
	• Immunomodulatory therapies, including IVIg and plasma exchange, remain investigational and are not recommended for routine use.

Historical note and terminology

Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) refers to a subgroup of pediatric patients with tic or obsessive-compulsive disorders temporally associated with streptococcal infections (132). It was first described in a group of 50 patients with an acute, sudden onset of obsessive-compulsive disorder or tics, and behavioral changes in the context of a previous streptococcal infection. However, the concept of PANDAS originally stemmed from 19th-century published observations of acute onset neuropsychiatric symptoms, which included emotionality, irritability, deterioration in handwriting and attention, and bizarre behaviors (81). Osler reported obsessive-compulsive behaviors in patients with Sydenham chorea. In his accounts, parents reported an abrupt change in character of their children, and in some cases suggested even the possibility of acute-onset psychosis (89). Half a century later, these findings were confirmed by larger case series (17; 25). In 1989, Kiessling described eight patients with tic disorder who had evidence of recent infection with group A beta-hemolytic Streptococcus (GABHS) at the time of their initial presentation or symptom exacerbation (41). That same year, researchers at the National Institute of Mental Health reported on patients with Sydenham chorea who often exhibited obsessive-compulsive symptoms (119) with a fluctuating clinical course (120). These observations have led to the speculation that at least some cases of tic and obsessive-compulsive disorders may have an etiological relationship to GABHS infection. PANDAS may share similar pathogenesis with Sydenham chorea, the scientifically established prototype of GABHS-mediated autoimmune neuropsychiatric disease and a complication of rheumatic fever.

Longitudinal observations identified cases in which the initial onset or exacerbation of tic or obsessive-compulsive symptoms showed temporal correlation with GABHS infections. The first series of such cases appeared in 1995 (01). Initially referred to as Pediatric, Infection-Triggered, Autoimmune Neuropsychiatric Disorders (PITANDs), this entity was eventually renamed PANDAS by Swedo and colleagues in 1998 and has since gained wide recognition under this acronym. Several reviews of the subject are available (114; 111; 126; 32; 44; 82; 94; 103; 81).

Previous cases resembling PANDAS were reported sporadically in the literature. Historically, anecdotal reports have linked an acute onset of tics to chronic sinusitis with bouts of acute sinusitis, including streptococcal etiology (102). A case report from Japan described an 11-year-old boy who was noted to have developed Tourette syndrome approximately ten days after a febrile illness associated with elevated antistreptolysin O antibody titers (46). In an Italian case series of pediatric patients, exposure to streptococcal antigens was associated with an increased incidence of tics (10). Community outbreaks of GABHS infections have reportedly been associated with a 10-fold increase in the number of pediatric patients presenting with tics (42).

Unfortunately, a reliable diagnostic test for PANDAS has never been established. This diagnosis has always relied on longitudinal observation of clinical course supplemented by laboratory tests documenting streptococcal infection. The diagnostic criteria for PANDAS proposed by Swedo and colleagues are shown in Table 1 (116):

Table 1. Proposed Diagnostic Criteria for PANDAS

	(1) Presence of a tic disorder and/or obsessive-compulsive disorder
	(2) Prepubertal age (between 3 and the beginning of puberty) at onset
	(3) Abrupt symptom onset or episodic course of symptom severity with dramatic symptom exacerbations. Exacerbations may also occur months to years after the onset. Remissions may not be complete.
	(4) Temporal association between symptom exacerbations and streptococcal infections
	(5) Presence of neurologic abnormalities (eg, choreiform movements, tics, or motor hyperactivity) during periods of symptom exacerbation

The first case series of 50 PANDAS patients was published in 1998 and demonstrated that neuropsychiatric symptoms typically began 7 to 14 days after a suspected GABHS infection (116). Patients had an earlier onset of tics (6.3 years) and obsessive-compulsive disorder (7.4 years) compared to non-PANDAS cases. Comorbid symptoms included emotional lability (66%), personality changes (54%), bedtime fears (50%), and separation anxiety (46%), often linked to GABHS infections; 77% of patients experienced exacerbations associated with positive throat cultures or upper respiratory symptoms. A study of 693 children found that GABHS infections within 0 to 3 months correlated with behavioral changes, including ADHD symptoms (84). In 64 children with recurrent GABHS infections, there was a significant increase in behavioral abnormalities and choreiform movements. A small case series suggested that symptom severity may relate to prior GABHS infections (80). Other behaviors, such as dystonia and myoclonus, have been reported post-GABHS infection, but their connection to PANDAS is unclear (81). On the other hand, a meta-analysis found no significant link between GABHS infections and neuropsychiatric symptom exacerbation in PANDAS (87). A 2025 study by Foiadelli and colleagues measured IL-17 in serum and CSF from children with acute neuropsychiatric disorders and reported higher IL-17 compared to controls (24).

A family history of obsessive-compulsive symptoms has been reported in youth fulfilling PANDAS criteria (83), suggesting a genetic predisposition to these symptoms similar to that observed in young patients with non-PANDAS obsessive-compulsive disorder. At the same time, 25% of mothers of youth with PANDAS had autoimmune disease, compared to 13.4% of mothers of children with non-PANDAS obsessive-compulsive disorder/tics (83b). Anecdotal evidence of a strong family history of tics and accompanying neuropsychiatric features characteristic of PANDAS, which occur in temporal association with GABHS infections, has also been reported (127). On the other hand, clinical presentation among identical siblings may range from typical PANDAS to being completely asymptomatic (58). A Swedish multigenerational study found relatives of probands with severe infections had increased obsessive-compulsive disorder risk that rose with genetic relatedness, and the association remained after accounting for obsessive-compulsive disorder and autoimmune disorders in probands and relatives, suggesting shared genetic factors as an explanation for both severity of infection and incidence of obsessive-compulsive disorder (95).

Cognitive abnormalities in youth diagnosed with PANDAS have been explored (59). In this study, marked impairment in visuospatial recall memory (as assessed using the Rey-Osterrieth Complex Figure Test) was observed despite average to above-average performance on academic and other neurocognitive measures. Group A beta-hemolytic Streptococcus titer elevations were associated with worse performance on tasks assessing neurocognitive and executive abilities (Stroop Color-Word Interference Test), visuospatial memory, and fine motor speed (finger tapping), as well as elevated obsessive-compulsive symptom severity. Another study also found difficulties in visual-motor skills, short memory tasks (Symbol Search subtest of Wechsler Intelligence Scale for Children or Digit Span subtest of Wechsler Intelligence Scale for Children), attention (symbol search subtest of Wechsler Intelligence Scale for Children), and elaboration speed (elaboration of speed index) in patients with PANS, but no statistically significant differences were identified between PANDAS and Sydenham chorea patients (28).

Case reports have linked the onset of PANDAS symptoms not only to streptococcal pharyngitis, but also to dermatological streptococcal infections, including streptococcal perianal dermatitis (12; 124).

The umbrella term “pediatric acute-onset neuropsychiatric syndrome” (PANS) was described more than a decade after PANDAS to expand the spectrum of pediatric neuropsychiatric diseases, which also includes PANDAS.

Although group A Streptococcus remains a hallmark of PANDAS, PANS has been associated with several triggers, including psychosocial trauma, genetic predisposition, and postinfectious autoimmunity. Several infectious agents, including group A Streptococcus, Mycoplasma pneumoniae, and influenza, have been suggested as potential triggers for the syndrome. However, no single agent has been associated with the disease (16; 33).

Table 2. Proposed Diagnostic Criteria for PANS

(1) Abrupt, dramatic onset of obsessive-compulsive disorder or severely restricted food intake (< 48 h)
(2) Concurrent presence of additional neuropsychiatric symptoms, with similarly severe and acute onset, from at least two of the following seven categories:
	(a) Anxiety (b) Emotional lability or depression (c) Irritability, aggression and/or severely oppositional behaviors (d) Behavioral (developmental) regression (e) Deterioration in school performance (f) Sensory or motor abnormalities, including increased sensitivity to sensory stimuli, hallucinations, dysgraphia, complex motor, and/or vocal tics (g) Somatic signs and symptoms, including sleep disturbances, enuresis or urinary frequency
(3) Symptoms are not better explained by a known neurologic or medical disorder, such as Sydenham chorea, systemic lupus erythematosus, Tourette disorder, or others

The key characteristic points are that both PANS and PANDAS have an acute-onset disease with a very short time to peak severity of cardinal symptoms (obsessive-compulsive disease, tics, or food restriction).

Scientific basis

Pathophysiology

The current views on the pathomechanisms of post-streptococcal neuropsychiatric disorders, including the evolving concept of PANDAS, are primarily based on research on Sydenham chorea, the prototype for post-streptococcal central nervous system dysfunction. The diagnosis of Sydenham chorea is sufficient to establish the diagnosis of rheumatic fever in a patient. Interestingly, there is significant overlap of symptomatology between patients with Sydenham chorea and patients with obsessive-compulsive disorder (17; 119; 01). Obsessive-compulsive disorder and tics have been documented in many patients with Sydenham chorea (73). Overlap between obsessive-compulsive disorder and tics is complex because up to two thirds of children with obsessive-compulsive disorder have tics (55), and 20% to 80% of children with Tourette syndrome have obsessive-compulsive disorder (53). These observations have led to speculation that there are similar pathogenetic mechanisms underlying a variety of phenotypically similar diseases, including Sydenham chorea, PANDAS, Tourette syndrome, obsessive-compulsive disorder, acute disseminated encephalomyelitis, and adult-onset tic disorders (32). The final common target believed to be involved in the pathogenesis of these disorders is the basal ganglia and its connections (99; 105). Although broad autoimmune screening is not universally recommended in all suspected cases, a 2024 retrospective cohort of children with PANS reported frequent immune activation and vasculopathy markers during flares and an increased risk of later arthritis and other autoimmune diseases, suggesting that a subset may have broader systemic inflammatory vulnerability (112; 56; 65; 02).

Evidence has increasingly suggested that these disorders are autoimmune in nature and are characterized by the production of potentially pathogenic autoantibodies. Initial studies by Husby and colleagues identified a higher incidence of antineuronal antibodies in patients with Sydenham chorea, indicating a possible link between antibodies against GABHS and neuronal dysfunction through molecular mimicry (37). Subsequent research has detected similar antineuronal antibodies in pediatric patients with obsessive-compulsive disorder and tic disorders, specifically targeting neurons in the basal ganglia (43; 107; 108; 78; 131).

Although circulating antibodies typically do not cross the blood-brain barrier, mechanisms such as the migration of antigen-specific B cells into the CNS and cytokine-induced disruption of the blood-brain barrier may facilitate this process (117). An immunology-based review summarized evidence that Th17 cells and IL-17 may contribute to blood-brain barrier disruption and facilitate CNS entry of cross-reactive antibodies in a post-streptococcal basal ganglia encephalitis model (122; 56). However, studies investigating the presence of antineuronal antibodies have produced mixed results, with some showing higher levels in patients with obsessive-compulsive disorder compared to controls, whereas others found no significant differences (115; 75). Methodological discrepancies in autoantibody detection have contributed to these contrary findings, as many studies utilized complex tissue preparation methods that may not accurately reflect in vivo conditions. Advances in live cell-based methods hold promise for a better understanding of the role of autoantibodies in these disorders. Additionally, the search for alternative immunological markers has been largely unproductive, although a small-scale study indicated a high proportion of D8/17-positive lymphocytes in PANDAS patients (118). Finally, a potential association between a single nucleotide polymorphism in the TNF-alpha gene promoter and PANDAS has been reported, but its significance remains uncertain until further validation is conducted (63).

The potential molecular targets of antineuronal autoantibodies in post-streptococcal neuropsychiatric disorders have been primarily linked to the M protein of GABHS, specifically the M6 and M19 proteins, which are thought to share epitopes with brain structures (37; 08). Comparative studies identified three distinct basal ganglia antigens (40, 45, and 50 kDa) that differentiated patients with Sydenham chorea from those with rheumatic fever and healthy controls (18). Further research showed that circulating antibodies in the CSF of patients with Sydenham chorea cross-reacted with these antigens (19). A proteomic analysis suggested that these antigens are membrane isoforms of enzymes involved in glycolysis and glycogenesis: aldolase C, neuron-specific enolase, and pyruvate kinase M1 (21). Although these enzymes may play a role in local ATP synthesis and modulate ion channels, the pathogenic significance of these autoantibodies in post-streptococcal neuropsychiatric disorders remains unproven. Additionally, the studies conducted did not utilize live cell-based assays, which are now considered the gold standard for autoantibody detection, potentially leading to the identification of nonpathogenic antigen-antibody interactions.

In a cohort of 71 children undergoing lumbar puncture during evaluation for acute or subacute neuropsychiatric deterioration, pleocytosis was not observed in those classified as PANS, whereas CSF abnormalities were reported in a minority (elevated CSF protein in 26% and elevated albumin quotient in 9%), and other markers of intrathecal inflammation (elevated IgG index, oligoclonal bands) were rare. These findings support the approach of reserving lumbar puncture for cases with neurologic red flags or concern for encephalitis, whereas recognizing that mild CSF protein or albumin changes may occur and are not necessarily diagnostic (96).

A pathophysiological model highlights the role of dopamine in immunological mechanisms of disease. Elevated central dopamine levels and modulation of dopamine D2 receptors contribute to neuropsychiatric symptoms by inhibiting regulatory T-cell functions and enhancing B lymphocyte and Th1 cell activity, leading to autoimmune inflammation in the basal ganglia (83). The cross-reactive antibodies in PANDAS patients may affect dopamine D2 receptors (20). Their findings suggest that antibodies targeting GABHS carbohydrate and neuronal surface molecules can activate pathways that increase dopamine production and alter behavior (45; 76). Brimberg and colleagues demonstrated that autoantibodies against D1 and D2 receptors correlated with specific phenotypes in an animal model (07). Recent work extends the dopamine receptor autoantibody hypothesis, reporting differential D1R/D2R autoantibody patterns and receptor signaling effects across cohorts spanning Sydenham chorea and PANDAS or PANS, supporting a basal ganglia encephalitis spectrum model while also underscoring the need for independent replication (70).

Animal models of Sydenham chorea and PANDAS have demonstrated mixed results regarding the role of antineuronal antibodies in neuropsychiatric symptoms (123; 36; 61). Yaddanapudi and colleagues found correlations between repetitive behaviors and motor deficits with anti-CNS antibodies following streptococcal immunization in PANDAS mice (134). Conversely, GABHS-immunized mice showed improved task performance, suggesting normal intelligence before PANDAS onset. Naive mice transfused with serum from GABHS mice exhibited behavioral changes, implicating IgG as the key immunoglobulin involved, as serum depleted of IgG did not induce alterations. Brimberg and colleagues provided novel evidence linking autoantibodies to post-streptococcal neuropsychiatric disorders (07). Rats exposed to GABHS antigen displayed motor abnormalities and increased grooming, with antibody deposition in the striatum and altered dopamine and glutamate levels. Autoantibodies from GABHS rats activated calcium/calmodulin-dependent protein kinase II in neuronal cells, similar to findings in patients. Further characterization identified D1 and D2 receptors as potential autoantigens, with speculation that antibody binding to D2 autoreceptors may enhance dopamine release. Additionally, IgG from GABHS rats reacted with serotonin receptors, suggesting a broader impact on neurotransmission (62). Frick and colleagues demonstrated that sera from patients with well-characterized PANDAS, when infused into the striatum of mice, bound to 80% of cholinergic interneurons, which are implicated in the pathogenesis of tic disorders (26). After treatment with IVIg, patients showed symptom improvement, and their sera no longer contained antibodies with elevated binding to cholinergic interneurons in mice.

Contradictory evidence also exists. Morris-Berry and colleagues measured ELISA optical densities for three antibodies (N-acetyl-beta-D-glucosamine, tubulin, and dopamine D2 receptor) in PANDAS, Tourette syndrome, and healthy controls (77). There were no significant differences among the groups. Additionally, no changes in anti-tubulin and anti-D2 receptor antibody levels were observed in PANDAS patients before, during, and after exacerbations. Loiselle and colleagues demonstrated no behavioral changes when sera from patients with PANDAS and Tourette syndrome were infused into the striatum of rats (61).

Regardless of autoimmune mechanisms, a subgroup of tic disorder patients might manifest an enhanced immune response to GABHS exposure. Bombaci and colleagues compared circulating antibody reactivity in a group of children with chronic tic disorders without evidence of GABHS infection, a group of children with documented GABHS pharyngitis, and a smaller control group of healthy children. The antigens were different in the tic and pharyngitis group when compared with the tic-only group. Although these preliminary findings need to be further investigated using an adequate sample size that includes children diagnosed with PANDAS and obsessive-compulsive disorder, these data suggest the presence of an enhanced immunological response of tic disorder patients to a wide range of GABHS antigens. Previous evidence had shown that youngsters with Tourette syndrome and obsessive-compulsive disorder may have a higher average annual rate of new GABHS infections per subject per year compared to healthy peers (64). In line with this, patients with tics or obsessive-compulsive symptoms are more likely to have had a GABHS infection in the 3 months before neuropsychiatric symptom onset (69). Subsequent work has shown persistently raised anti-streptolysin O levels in sera of 60% of non-selected children with tic disorders, in the absence of a clear link between symptom exacerbations and recent GABHS infections (66). Additional evidence is also accumulating on possible intrinsic abnormalities in the regulation of immune responses in children with Tourette syndrome. These include reduced percentages of T regulatory lymphocytes (40), which are crucially involved in immune tolerance mechanisms and protect against autoimmunity, and possible abnormalities of immunoglobulin subtype profile (eg, IgA dysgammaglobulinemia) (39; 06), which can also predispose to both upper respiratory infections (explaining the higher rate of GABHS infections in these patients) and to autoimmunity. Finally, GABHS infections might interact with psychosocial stress in predicting future short-term tic severity in patients with tic disorders (60).

Imaging studies have been done on patients with PANDAS to identify structural and functional changes. Magnetic resonance imaging volumetric studies showed involvement of the basal ganglia in PANDAS. In patients with Sydenham chorea, enlargement of the caudate, putamen, and globus pallidus was noted (30). Structural and functional MRI studies have demonstrated abnormalities of the basal ganglia and associated corticostriatal or corticothalamic pathways in patients with obsessive-compulsive disorder (67; 93; 74; 34). More evidence is necessary to support basal ganglia volumetric changes in the acute phase of post-streptococcal neuropsychiatric disorders. Differences in characteristics of the gray and white matter were described in patients with PANDAS when compared with controls (09).

SPECT studies have demonstrated increased perfusion in some patients with Sydenham chorea (54; 03; 31). In patients with obsessive-compulsive disorder, SPECT studies reveal perfusion abnormalities in the fronto-subcortical regions (51; 13). A PET study has explored ongoing neuroinflammation using a tracer for activated microglia (C-[R]-PK11195) in 17 children with PANDAS, which showed an increased binding potential value in the caudate and lentiform nuclei bilaterally in PANDAS and in bilateral caudate nuclei only in Tourette syndrome. To date, this study represents the first and only evidence of ongoing neuroinflammatory changes in youth with PANDAS.

Diffusion tension imaging measures and cortical features such as thickness, volume, curvature, and gyrification have not shown any significant differences between patients with PANDAS and healthy controls (09).

Differential diagnosis

Table 3, which is adapted from the study by Murphy and colleagues, provides a list of alternative causes that may present with the PANS phenotype and that, therefore, need to be differentiated from PANDAS (81).

Table 3. Differential Diagnosis

	(1) Autoimmune encephalitis or encephalopathy: acute disseminated encephalomyelitis, Sydenham chorea
	(2) Infectious encephalitis
	(3) Neuropsychiatric lupus
	(4) Antiphospholipid antibody syndrome
	(5) Emotional trauma or stress
	(6) Metabolic or mitochondrial disorders (MELAS, Cerebral folate deficiency)
	(7) Acute onset of obsessive-compulsive disorder, anxiety disorder, tic disorder
	(8) Tourette syndrome
	(9) Sydenham chorea

PANDAS is a very different category from autoimmune encephalitis. These two conditions have different diagnostic criteria, diagnostic work-up, and treatment modalities.

Pediatric autoimmune encephalitis presents with acute/subacute onset (3 months or less) and neurologic or psychiatric symptoms in previously healthy children. Symptoms may include altered mental status, focal neurologic findings, cognitive difficulties, movement disorders (except tics), psychiatric symptoms, and seizures (not explained by a previously known epilepsy or other condition) in the setting of paraclinical evidence of neuroinflammation (14).

Autoimmune encephalitis symptoms tend to be more persistent, whereas PANDAS is characterized by a relapsing-remitting course. Most children with autoimmune encephalitis have cognitive impairment, whereas many children with PANDAS show normal cognition.

Diagnostic work-up

Each patient should have a tailored exam and diagnostic approach.

Careful history and physical examination. Symptom onset, severity, functional impact, and medical and social history, including stressors and potential triggers, should be assessed. Patients with pre-existing mental health problems might have exacerbations related to an underlying condition rather than a new syndrome, such as PANDAS. Recent infections, including group A Streptococcus infections, and treatments should be noted. A review of previous medical history and school notes might be helpful to get a sense of prior neurocognitive functions or developmental evaluations.

Neurologic examination. Most children with PANDAS have a normal, nonfocal neurologic examination. They may present with tics, inattention, and choreiform movements, which is different than chorea. Generalized chorea should prompt evaluation for Sydenham chorea.

Children with PANDAS usually have normal cognition, although they may have some impairment in school performance due to inattention, obsessive-compulsive disorder, or anxiety. After a detailed history and neuropsychological exam, a formal neurocognitive evaluation might be considered in selected cases.

Significant memory and cognitive deficits may suggest autoimmune encephalitis or other organic brain pathologies.

Psychiatric assessment. A detailed evaluation by a psychiatrist or a psychologist is necessary to rule out other disorders that present with similar neuropsychiatric symptoms.

Laboratory work-up. A phased approach is recommended to prevent an unnecessary diagnostic work-up.

Diagnostic test for S pyogenes. Universal testing of all patients with acute-onset neuropsychiatric syndrome is not recommended due to a lack of evidence. Current guidelines recommend diagnostic testing for group A Streptococcus only for children with pharyngitis consistent with streptococcal infection.

Further work-up. An additional work-up is recommended if there are any focal neurologic signs or symptoms and signs that may indicate autoimmune encephalitis. This work-up may include EEG, MRI brain, lumbar puncture, blood tests (inflammatory markers), neurocognitive evaluation, and autoimmune panel.

Treatment. The treatment of patients with PANDAS is still a subject of considerable controversy, as it is complicated by a lack of well-designed trials. As previously noted, more research is needed to identify the best possible treatments for patients with PANDAS.

Psychiatric and behavioral interventions. Current consensus emphasizes that children presenting with obsessive-compulsive disorder, tics, and other acute neuropsychiatric symptoms should receive prompt, disorder-specific psychiatric care. Treatment should not be delayed while evaluating possible PANS or PANDAS. Cognitive behavioral therapy and SSRIs are considered first-line therapies for obsessive-compulsive disorder symptoms in this population (33).

Obsessive-compulsive disorder is characterized by repetitive behaviors (compulsions) and intrusive, unwanted thoughts (obsessions) that individuals are compelled to engage in. The emergence of obsessive-compulsive disorder in children can be particularly distressing, and when it is accompanied by PANDAS, it frequently results in severe and intense symptoms. PANDAS is defined by the abrupt onset of neuropsychiatric symptoms subsequent to a streptococcal infection, which encompasses a variety of behavioral changes, tics, and obsessive-compulsive disorder (98). In this context, the complexity of obsessive-compulsive disorder requires the implementation of effective treatment methods to enhance quality of life and outcomes.

Cognitive behavioral therapy is a psychotherapeutic approach that is structured and time-limited, and it examines the connection between thoughts, emotions, and behaviors. In this context, exposure and response prevention (ERP) has exhibited substantial efficacy in the management of obsessive-compulsive disorder symptoms. ERP involves the systematic exposure of patients to stimuli that induce anxiety, while simultaneously instructing them to refrain from engaging in their typical compulsive behaviors. This method employs classical conditioning principles to mitigate anxiety through systematic desensitization (90). ERP has been consistently demonstrated to be effective in the treatment of obsessive-compulsive disorder, including in children with PANDAS, according to research. Micali and colleagues demonstrated that compared to children who received standard treatment, those who underwent ERP experienced substantial reductions in the severity of their obsessive-compulsive disorder (72). Olatunji conducted a follow-up study on children and adolescents with obsessive-compulsive disorder, which revealed that participants who received structured CBT, including ERP, had superior long-term outcomes compared to those who did not (109; 88). The significance of ERP in the treatment of obsessive-compulsive disorder associated with PANDAS is emphasized by these findings.

Although ERP is effective on its own, its integration with pharmacological treatments, particularly selective serotonin reuptake inhibitors (SSRIs), has demonstrated improved treatment outcomes for obsessive-compulsive disorder. Sertraline and fluoxetine are examples of SSRIs that are frequently employed to mitigate anxiety and compulsive behaviors. When implemented in conjunction with ERP, they generate a synergistic effect that results in enhanced symptom relief when contrasted with either approach alone (125). The meta-analysis conducted by Skapinakis and colleagues demonstrated that the integration of CBT and SSRIs leads to a significantly greater reduction in obsessive-compulsive disorder symptoms than either treatment when administered independently (109). The inflammatory processes associated with PANDAS may require a comprehensive treatment strategy, which is why this dual approach is particularly relevant for children (68). Clinicians should exercise caution when prescribing SSRIs to children with PANDAS, as they may exhibit heightened sensitivity to these medications, necessitating gradual titration and close monitoring.

Treatment for group A Streptococcus infection. Although throat cultures remain the gold standard due to their greater sensitivity, clinicians frequently use rapid antigen detection tests (RADTs) to confirm the presence of group A Streptococcus (02). Following a positive outcome, recommendations for guidelines call for a 10-day course of antibiotics, such as penicillin or amoxicillin, to eradicate the infection and perhaps minimize the related neuropsychiatric symptoms (29).

Although antibiotics are clearly used to treat acute streptococcal infections, there are contradictory data about the effectiveness of prophylactic antibiotic use in preventing later neuropsychiatric flare-ups in PANDAS. According to Garvey and colleagues, penicillin prophylaxis did not significantly reduce the incidence of clinical exacerbations, which raises issues regarding the worth of extended antibiotic treatments in this patient population (29). Likewise, Sigra and colleagues and the American Academy of Pediatrics agree that inadequate data exist to justify long-term antibiotic prophylactic action for PANDAS (104; 02). Thus, current recommendations underline the need for ongoing research to clarify long-term management strategies and advise concentrating on quick identification and treatment of acute group A Streptococcus infections instead of routine extended antibiotic use (33).

Immunomodulatory or immunosuppressive treatment. This is the most controversial area of treatment for PANDAS. Aggressive immunomodulatory therapy in the form of plasma exchange and intravenous immunoglobulin has been used for symptoms associated with PANDAS. However, many experts are skeptical about the use of immunomodulatory treatment given the lack of CNS inflammation and autoimmunity. A randomized, controlled trial of 20 pediatric patients that studied the effects of IVIg or plasma exchange versus placebo in the treatment of obsessive-compulsive disorder and tic disorders showed promising results (92). In the treatment of obsessive-compulsive symptoms, treatment resulted in a 45% (IVIg) to 58% (plasma exchange) decrease in symptoms. In the treatment of tic disorders, plasma exchange showed a 49% decrease in symptoms. On the contrary, Hoekstra and colleagues demonstrated no improvement in tic symptoms in a randomized trial using IVIg versus placebo in an older series of patients ages 14 to 53 years (35). It is important to recognize that both IVIg and plasma exchange therapy are not without potentially serious side effects. Even though a 12-patient case series with moderate/severe PANDAS showed a benefit of IVIg treatment in clinical practice (47), a randomized controlled study in 2016 revealed no significant difference between the IVIg and placebo groups in 35 children with a PANDAS diagnosis (133). In a retrospective series of 12 children with relapsing-remitting PANS treated with an immunomodulatory dose of IVIg, improvement was observed in at least one cognitive or functional domain in 11 of 12 patients, most commonly involving memory and sensory-motor or visual-motor integration. Treatment response was reported regardless of the duration of illness before IVIg initiation. A subset of patients demonstrated baseline hypogammaglobulinemia requiring ongoing immunoglobulin replacement, underscoring the importance of evaluating for underlying immune deficiency and individualizing risk-benefit discussions. Given the small sample size, retrospective design, absence of controls, and variable testing intervals, these findings should be interpreted with caution (23).

The American Academy of Pediatrics emphasizes that these therapies should be considered investigational and, if pursued, should occur only within specialized multidisciplinary programs or research protocols. Anti-inflammatory therapy (NSAIDs and corticosteroids) is commonly used in practice, but evidence remains limited and largely nonrandomized. Observational data suggest possible reductions in flare duration, and placebo-controlled trials are still needed (33). Due to a lack of evidence regarding autoimmunity and potential side effect profiles, immunotherapies are not usually recommended.

Discussion

The clinical definition of PANDAS has been the object of intense debate throughout the past 15 years (50), opposing two main different views, with some authors arguing that PANDAS may not exist and the connection between obsessive-compulsive disorder or tic disorder and streptococcal infection is merely coincidental, and others supporting the existence of this entity. Recent reviews and a 2024 Delphi consensus continue to describe PANDAS as an overlapping, heterogeneous, and controversial clinical entity supporting continued nosological reappraisal and standardization efforts rather than a single, universally accepted PANDAS construct (33). Undoubtedly, GABHS infection is very common in children, and evidence of recent GABHS infection is likely found by chance in large numbers of children. Furthermore, obsessive-compulsive disorder occurs in 1% to 2% of school-age children (135), and transient tic disorders can be detected in 10% to 25% of early school-age children (110). The complex behavioral spectrum exhibited in the acute phase by children diagnosed with PANDAS, summarized above, encompasses several features that have been previously reported during the acute phase of illness in patients with Sydenham chorea (117) as well as in patients with acute rheumatic fever without chorea (71). This has led some to hypothesize that PANDAS could represent a neuropsychiatric presentation of rheumatic fever in the absence of florid chorea. However, this hypothesis was soon refuted, mainly due to the absence of other rheumatic features in the vast majority of children diagnosed with PANDAS. More than other features, the lack of echocardiographic changes suggesting carditis is strikingly different from Sydenham chorea patients, in whom the frequency of carditis ranges between 30% and 80% of cases (111; 101). Other authors, however, have shown subtle echocardiographic changes in children with tic disorders, although it is unclear how many of these had PANDAS (11). One of the biggest problems in the routine clinical application of Swedo and colleagues’ working criteria for PANDAS is the need to obtain serial measurements of serological markers (eg, anti-streptolysin O, anti-DNAse B antibodies, or preferably both) and correlate them with the severity of behavioral symptoms. Indeed, it has been clarified that serological streptococcal markers may show several different temporal fluctuation patterns across different individuals, depending on the type of exposure to the pathogen and the degree of immune activation in the host (38). This minimizes the clinical significance of single-time-point cultures and antibody measurements. Simultaneously increased levels of ASO and anti-DNAseB were shown in patients with PANDAS compared to controls (15). However, positive results only indicate exposure to the streptococcal infection, and they do not differentiate between the carrier state and an acute infection (22). A 2024 Delphi consensus reiterates that group A Streptococcus exposure markers are supportive at best, titers peak weeks after infection and can remain elevated for months, and single time point values are insufficient to establish PANDAS; at most, they contribute to diagnostic suspicion, with greater interpretive weight given to serial patterns alongside microbiologic confirmation (33).

Nevertheless, in real practice, and particularly in community clinics, the diagnosis of PANDAS has often been formulated based on a cross-sectional association between streptococcal markers and behavioral symptoms, which may well be coincidental (27). It is, therefore, not completely surprising that multicenter longitudinal studies comparing children with a diagnosis of PANDAS to children with non-PANDAS tics or obsessive-compulsive symptoms failed to detect a higher number of streptococcus-linked clinical exacerbations and immune marker profiles in either of the two patient groups (49; 106; 52). Despite their high rate of clinical assessments, suggesting a robust longitudinal observation, patients diagnosed with PANDAS in these studies might have been clinically different from patients with PANDAS described by Swedo and colleagues in their original report. This potential heterogeneity generated by the application of Swedo and colleagues’ working criteria by different clinicians in different settings raised the suspicion that such criteria may lack validity and reliability, requiring a revision (121).

One first useful approach to overcome this hurdle is to search for specific phenomenological features, different from those highlighted by Swedo and colleagues’ criteria, which might help in differentiating PANDAS from non-PANDAS clinical look-alikes. A study done by Bernstein and colleagues identified specific clinical characteristics of children with PANDAS compared to a group of children with non-PANDAS obsessive-compulsive disorder (04). They described patients with PANDAS as more likely to present with separation anxiety, urinary urgency (but not enuresis), hyperactivity, impulsivity, deterioration in handwriting, and decline in school performance. Additionally, total and vocal tics were noted to be more severe in children with PANDAS. Murphy and colleagues examined 109 children with tics, obsessive-compulsive disorder, or both with personal and family history, diagnostic interview, physical examination, medical record review, and measurement of baseline levels of streptococcal antibodies (85). Children with PANDAS were more likely than non-PANDAS to have had a dramatic onset, definite remissions, remission of neuropsychiatric symptoms during antibiotic therapy, a history of tonsillectomies/adenoidectomies, ADHD comorbidity (61% vs. 31%), evidence of group A streptococcal infection, and clumsiness. This last observation is particularly striking in that it confirms Bernstein and colleagues’ findings, as well as earlier observations from Swedo’s team, of worse performance on fine motor tasks (including drawing and writing) during the acute phase of PANDAS. It also fits nicely with the behavioral regression and oppositionality that these patients are thought to display.

Despite these attempts to better characterize specific clinical features of the PANDAS phenotype, this concept is currently undergoing substantial nosological reappraisal. The rationale behind this derives from different points of concern, some of which have been highlighted above. First of all, tics and obsessive-compulsive disorder can fluctuate without any evidence of GABHS infection or change in antibody titer. In patients with Tourette syndrome, tics are known to worsen during periods of stress or illness. Hence, exacerbations with streptococcal infection may represent a nonspecific stress response (48). Moreover, there is anecdotal evidence suggesting tic exacerbation after Mycoplasma pneumoniae (79) or other types of infection (01) and raised anti-Mycoplasma antibody response in Tourette syndrome patients (79). Murphy and colleagues intriguingly highlight a clinical overlap between the neuropsychiatric manifestations of Lyme disease in children and PANDAS/PANS (81). The Delphi’s consensus explicitly states that no circulating antibody or biomarker is pathognomonic for PANS or PANDAS. The Autoimmune Brain Panel is described, but the consensus concludes that its sensitivity and specificity and clinical utility remain unclear in pediatric patients, even if it might provide ancillary information in selected cases (33). Without a specific biological marker or radiographic feature of disease, the entity of PANDAS may be nonspecific. The proposed diagnostic criteria suggested by Swedo may not be specific for PANDAS and encompass features of numerous other disease processes. On the other hand, proponents of PANDAS suggest that a substantial number of cases of patients with tic disorder and obsessive-compulsive disorder are in fact PANDAS, based on a common pathway involving the basal ganglia and their respective circuitry. Successful treatment of symptoms with immunomodulatory therapy further supports the concept of PANDAS as an immune-mediated autoaggressive disease. A genetic predisposition has been suggested for both obsessive-compulsive disorder and tic disorder (91; 129). Environmental causes may also play a role, and the genotypes of individuals may be important in determining the response to the environmental stimuli, rather than being a primary cause of the illness. A second relevant point of concern is related to the diagnosis of group A streptococcal infections, which may not be straightforward. The growth of this pathogen from throat specimens may indicate a carrier state rather than a recent infection, and serial antistreptococcal antibody measures are required to distinguish between the two. At the same time, antistreptolysin O antibodies are not specific to group A streptococci but may also rise with exposure to group C and G streptococci. The temporal latency between an inciting group A streptococcal infection and the onset of PANDAS is also not well defined; for a neuropsychiatric entity with well-established post-streptococcal etiology, such as Sydenham chorea, this may be as long as 6 months, and it is currently uncertain if and why this latency should be shorter for PANDAS. As summarized above, moreover, some clinical features such as the abrupt, dramatic onset and the co-occurrence of specific behavioral features other than tics and obsessive-compulsive symptoms are not included in the working criteria by Swedo and colleagues. Finally, the phenomenological distinction between chorea in Sydenham chorea and “choreiform movements” described by Swedo and colleagues in PANDAS seems mainly based on the severity of the hyperkinetic symptoms rather than by a qualitative difference. These observations formed the rationale beyond the proposal of broader concepts such as childhood-onset acute neuropsychiatric syndrome (CANS) and pediatric acute neuropsychiatric syndromes (PANS), theoretically encompassing also the PANDAS phenotype. Recent work has focused less on revising Swedo-era criteria per se and more on improving reliability via validated structured symptom instruments for PANDAS screening and longitudinal tracking, reflecting persistent concerns about heterogeneity and cross-setting diagnostic inconsistency (05).

In summary, the diagnosis of PANDAS and related conditions is purely clinical, and it requires a complete medical, neurologic, and psychiatric history; a thorough physical examination; a series of laboratory tests (to exclude other causes); and a comprehensive neuropsychological assessment. Serum and CSF autoimmune antibodies may be considered based on the clinical presentation and the need to exclude autoimmune encephalitis. Given its poor specificity, a Cunningham Panel is not routinely recommended (97).

Resolution

Despite increasing recognition, robust epidemiologic estimates of PANDAS incidence and prevalence remain unavailable (33). Unfortunately, in the wake of gaining further information on the accuracy of novel potential biomarkers like antidopamine receptor antibodies, at present, there are no diagnostic tests available that positively establish the diagnosis of PANDAS. So far, diagnosing PANDAS has been challenging, especially in the community setting, due to the difficult application of the Swedo criteria in a routine clinical setting (see Discussion). In a retrospective cross-sectional observational study done by Gabbay and colleagues, 31 of 176 patients were diagnosed with PANDAS by community physicians (27). However, 19 of these failed to meet the criteria of Swedo and colleagues (listed in Table 1), most with no laboratory confirmation of GABHS infection; furthermore, seven of the 145 patients not diagnosed were found to meet the PANDAS criteria at a specialty clinic. This demonstrates significant overdiagnosis as well as underdiagnosis of PANDAS in the community setting (103). In an Italian PANDAS cohort, routine inflammatory markers were generally unremarkable (CRP negative in all, ESR elevated in a small minority), throat cultures were negative at assessment, and ASO elevation was common but not differentiating, as elevated ASO titers were also frequent in controls, underscoring the limited specificity of ASO alone for case identification. Complement abnormalities were observed in a substantial subset (overall complement alterations in 42%), including reduced C3 in 31% and reduced C4 in 12% of patients. Cytokine profiling showed that more than half had elevated serum TNF-alpha, and the authors discuss a potential mechanistic link between inflammatory cytokines and blood-brain barrier permeability, while emphasizing that larger studies are needed to confirm group differences and clinical correlations (57). Considerable controversy exists as to what clinicians should do when they see a patient with an acute onset of tic disorder or obsessive-compulsive disorder. It is prudent to evaluate the patient for streptococcal infection by a throat culture. Although the information provided by antistreptolysin O and antideoxyribonuclease B may not help to detect active infection, serum antibody titers may correlate with recurring symptoms.

The definition of clinical concepts such as pediatric acute neuropsychiatric syndromes (PANS) and childhood-onset acute neuropsychiatric syndrome (CANS) aims to overcome the current limitations in the diagnosis of post-streptococcal acute neuropsychiatric disorders. In contrast to CANS and the former PANDAS criteria, tics lost central relevance in PANS; this is partially due to the general character of tics, which fluctuate over time, sometimes markedly and more intensely than obsessive-compulsive symptoms, often depending on the exposure to different contextual factors, which may include infections, amongst others. Nevertheless, tics are acknowledged amongst the motor abnormalities that may constitute accompanying symptoms to either of the two core features of PANS. Another difference between these two concepts is the central relevance given in PANS to anorexia, which constitutes, together with obsessive-compulsive disorder, a primary criterion. These differences notwithstanding, CANS and PANS represent highly similar concepts. If the common approach underlying both concepts is to be taken forward in the attempt to identify the features of a “post-streptococcal” subtype of CANS/PANS, then additional, preliminary efforts to homogenize the two concepts are necessary. On the other hand, pursuing clinical subtyping of the two concepts independently would generate great confusion for clinicians and might lead to a lack of future development and clinical application for both CANS and PANS.

Treatment of a child with antibiotics for an abrupt onset of tics and obsessive-compulsive disorder in the absence of a negative throat culture is not recommended. Likewise, one does not treat elevated antistreptolysin O or antideoxyribonuclease B titers alone. On the other hand, a patient with new-onset Sydenham chorea meets criteria for rheumatic fever and should be appropriately treated. Until data providing the efficacy of antibiotic prophylaxis are available, continuous treatment with antibiotics for fluctuating tic or obsessive-compulsive disorder symptoms is not recommended. It appears reasonable to treat symptoms of potential PANDAS cases with conventional treatment for obsessive-compulsive disorder and tic disorder until new data show the usefulness of other therapeutic interventions directed against GABHS or autoimmune mechanisms. Immunomodulatory therapies should be considered experimental until further clinical trials clearly show their efficacy, particularly considering their potentially serious adverse effects (130; 100).

Health misinformation is highly prevalent across social media platforms, with systematic reviews demonstrating frequent dissemination of inaccurate or misleading medical claims that may influence patient beliefs and healthcare utilization. In the context of pediatric neuopsychiatric syndromes such as PANDAS and PANS, online misinformation may amplify parental concern, promote unvalidated diagnostic testing, and increase demand for investigational therapies despite limited supporting evidence. Clinicians should anticipate these concerns and provide clear, evidence-based counseling to mitigate potential harm (113).

As our comprehension of the basic science of tic disorders, obsessive-compulsive disorder, and movement disorders increases, perhaps a better understanding of PANDAS will be established. It is hoped that many of the controversies existing today with regard to the diagnosis and treatment of PANDAS will be resolved by well-designed, prospective clinical trials.

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PANDAS

Also Relevant

Sydenham chorea
Tourette syndrome

PANDAS …

PANDAS

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Table 1. Proposed Diagnostic Criteria for PANDAS

Table 2. Proposed Diagnostic Criteria for PANS

Scientific basis

Pathophysiology

Differential diagnosis

Table 3. Differential Diagnosis

Diagnostic work-up

Discussion

Resolution

References

Contributors

Authors

Editor

Former Authors

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PANDAS

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Table 1. Proposed Diagnostic Criteria for PANDAS

Table 2. Proposed Diagnostic Criteria for PANS

Scientific basis

Pathophysiology

Differential diagnosis

Table 3. Differential Diagnosis

Diagnostic work-up

Discussion

Resolution

References

Contributors

Authors

Editor

Former Authors

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Upadacitinib

Ataxia-telangiectasia

Cryptococcal meningitis

GM2 gangliosidoses

Developmental delay in children: evaluation and management

Neonatal opioid withdrawal syndrome

Guillain-Barre syndrome in children

Levacetylleucine

This is an article preview.
Start a Free Account
to access the full version.