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Case #1 Pediatric Neurology Pearls  8yo boy, with and Obsessive Compulsive (OC) symptoms  Onset of simple tics 2 years prior- sniff, snort, deep CHILDHOOD ACUTE ONSET breathe, tapping fingers, palilalia NEUROPSYCHIATRIC  Some obsessive character to tics, even out SYMPTOMS movements, repeat word a certain #of times to AUDREY FOSTER-BARBER, MD PHD PEDIATRIC BRAIN CENTER OUTPATIENT DIRECTOR, CHILD “make it right” NEUROLOGY RESIDENCY DIRECTOR, VICE CHAIR NEUROLOGY UCSF  In the last month some behavior issues- easy temper, KENDALL NASH, MD PEDIATRIC BRAIN CENTER INPATIENT DIRECTOR, ASSOC. yelling at sib, won’t touch doorknobs or drawer MEDICAL DIRECTOR PHYSICIAN NETWORK DEVT. BENIOFF CHILDRENS HOSPITALS handles  Query- is this PANDAS?

 No ADHD signs or concerns  No recent illness symptoms  Eating and Sleeping well  Throat culture done by Pediatrician, positive for  Doing well at school Group A Strep (GAS), given antibiotics  No seizures  after 10 days of antibiotics tics improved, then worsened again a few weeks later  Tics present for 2 years, vary in severity, often worse with illness or with stress  No change in behavior issues, ocd symptoms

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 PMH- born at term with duodenal atresia, largyngeal  Return to clinic 6 months later with concern for cleft s/p repair “Explosive worsening” of behavior, moody, more  Development- normal milestones, bright child, aa bit OCD symptoms anxious but social and active in sports  Tics not worse, though a few new tics added to his  FH- Mother with Hashimoto’s thyroiditis, history of repertoire anxiety, Father with history of a mood disorder  No associated illness, primary doctor tested for Strep  SH- lives with mother and sibling, parents divorcing by throat culture and mycoplasma by antibodies, both negative  Dx- or chronic disorder, OCD tendency  Did receive a Flu vaccine a few weeks to a month prior

 New stressors- mother with new partner moving in,  6 months later, ongoing CBT with some benefit for with partner’s child behavior and OCD symptoms  Tics still present, wax and wane  Mother would prefer a PANDAS diagnosis, rather  Seen by Integrative Medicine doctor- than a diagnosis of with mood disorder Extensive Testing-zinc, heavy metal, strep culture, MTHFR  “PANDAS seems to have a clear treatment, whereas polymorphism, autoimmune screen (ANA, DS-DNA) all the others would be a chronic disorder” negative  Recommend- cognitive behavioral therapy (CBT), no -myocoplasma IgG+, Lyme Ab equivocal antibiotics -Cunningham panel interpreted as abnormal -treated with 3 months of Azithromycin, patient self d/c’d at 2 months due to GI distress

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Why did PANDAS come up here?

 During the 2 months on antibiotics no tic worsening,  Classic for Childhood Tic disorder- OCD was better already with therapy -tics onset prepubertal, vary in type, wax and wane over time -associated OCD (up to 50 % of patients)  Mother now “not so sure” about a PANDAS -bilineal inheritance (tics, adhd, anxiety, or ocd in both parents) diagnosis, but feels “antibiotics are benign” so will consider them if symptoms worsen (child refused  Family Concerns antibiotic prophylaxis) -FH autoimmune disease -hope for something treatable  Plans to avoid escalation to immune therapy that -difficulty of proving associated infection, of attributing was recommended- IVIg and or pheresis cause/effect of antibiotic therapy -common idea in the lay community, with integrative health  Declined other neurologic work up (MRI and LP) providers because “doing too well”

History behind PANDAS PANDAS- defined 1998

 1980s- psychiatrists noted subset of patients with  PANDAS- pediatric autoimmune neurologic disorder OCD who had a severe, abrupt onset of symptoms associated with Strep  Temporal association with infectious triggers- strep,  Presence of OCD and or tics- severe, interfere with varicella, mycoplasma, influenza, EBV, Lyme patient’s ability to function  Initially called PITANDS- Pediatric infection  Age of onset 3yo to puberty triggered autoimmune neurologic and psychiatric  Acute onset, episodic (relapsing remitting) disorder  Temporally related to GAS infection  Researchers chose to focus on GAS infection due to  Other associated neurologic (choreiform ease of documentation of infection and connection to movements) and behavioral abnormalities (sleep known molecular mimicry in Sydenham’s Chorea- disturbance, enuresis, anxiety, lability, insomnia) labeled PANDAS Swedo, SE. J Child and Adol Psychpharm, Feb 25(1)’ 2015

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Pediatric Acute onset Neuropsychiatric Defining a GAS infection is tricky Syndrome

 25% of the pediatric population has + strep culture  2013 Consensus meeting without immune reaction (carrier)  Back to the idea that multiple infections can trigger a  ASO and DNAse B titers can remain elevated for months (up to 12 mo in >50 % of kids s/p symptomatic infection) CNS response- PANS  By age 12 years >98% of the population have positive  Mechanism may be molecular mimicry as with Strep titers (pseudo-autoimmune response- Ab to strep also  PANDAS research dx requires flare associated with + reacts to neuronal antigens) culture and antibody evidence of appropriate rise in titer  Assume also other inflammatory mechanisms over time, at least twice (very rarely used clinically- diagnosis most often given with  Primary focus on OCD symptoms, with other single positive culture) associated symptoms secondary- behaviors and Blackburn, J. Seminars in Ped Neuro. 12: 2017 movements

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PANS PANS clinic experience

15  Research clinic, must fulfill research definition exactly  Abrupt, dramatic onset  Behavioral regression  84% documented prior illness, only 17% Strep of OCD or severe food restriction behavior  Deterioration in school  Primary symptom OCD or eating d/o  Concurrent performance  Tics 26%, chorea 15% neuropsychiatric  Sensory and motor  Many with severe compulsions and mood issues, symptoms: 2/7 abnormalities-tics, 1/3 with psychosis  Anxiety chorea  Emotional lability  Higher rate of maternal autoimmune disease,  Somatic symptoms-  Irritability, aggression, strong FH of mood disorder oppositional insomnia, enuresis Chang, K., Frankovich, J. 2015 Journal of Child and Adol Psychopharmacology, 25(1): 2015.

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Diagnostic Assessment for PANS Is the Cunningham panel helpful?

 Recommend full medical and family history, detailed  Serum studies of autoantibodies neuro exam  Sensitivity individual biomarkers for PANS dx  Note mild hypotonia and chorea sometimes seen, no other specific serious neurologic signs or symptoms (no criteria 15-60% seizures, no delirium, no focal findings)  Specificity 28-92%  Strep test, other infectious titers, autoimmune labs  PPV 17-40%  Commercial antibody panel- Cunningham Panel,  NPV 44-74% Moleculara Labs -serum testing, Elisa  Majority of healthy controls had pathologic results -anti- receptor D1 and D2L  Test-retest reliability poor -anti-lysoganglioside GM1 -anti-tubulin  Does not document neuro-inflammation Hesselmark, E. J Neuroimmunol, Nov 15 (312): 2017.

Treatments offered for PANS Do the Treatments for PANS work?

 Cognitive behavioral therapy  Many published papers  SSRI  Systematic review of the literature on PANDAS,  Antibiotics- for acute flare or daily for prevention PANS treatment over 17 years  Steroids  3 large consensus papers- based on expert clinical  NSAIDs experience, no research  Plasma exchange  One large survey of parents  Intravenous Immune globulin  12 treatment studies- only 4 RCTs  Rituximab  65 case series or case reports  Cytoxan  Total 1300 patients (90 in RCTs)  Tonsillectomy, adenoidectomy -Sigra, S. Neurosci and Biobehav Rev. 86:2018.

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 Bias assessment- moderate to high risk  Overall inconclusive for evidence of efficacy for any  No control groups particular treatment  Unclear randomization -due to lack of consistent disease definition and lack of  Small sample size systemic research  Self selected, self reported  Clear adverse reactions- ranging from mild  Mixed populations- PANDAS and PANS (headache, nausea, GI distress) to serious (increased  Various levels of severity, mixed focus on outcomes psychiatric symptoms, risk of line infection and for OCD vs tics blood clots)  Some with multiple simultaneous treatments  Outcomes primarily short term

Child Neurology Society Editorial Article Recommendations

 Review of the literature on PANDAS and PANS  Acute onset of Psychiatric Symptoms- if healthy child,  Acknowledgement of the pressure to treat even without mild to moderate symptoms: no testing certainty regarding etiology or efficacy  Acute onset Psychiatric Symptoms- if severe, disabling  Caution about the lack of consensus on this controversial then stratify into 2 groups based on presence or absence of dx- no accurate medical diagnostic test to rule in or rule concurrent neurologic signs or symptoms out PANS or PANDAS  Lack of data showing efficacy of any specific antibiotic or -if delirium, seizures, new non-tic movement d/o, immune therapy autonomic symptoms: full neurologic work up  Focus on immune tx distracts from proven therapies- -if only psychiatric symptoms, with no concurrent CBT and SSRIs neurologic symptoms: defer to psychiatry, consider  Risk of missing other neurologic disease based on family history, exam Gilbert, Minnk, Singer. J Peds. ‘Aug, 199: 2018.

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How CAN we know when to evaluate Case #2

 CANS-Childhood Acute Neuropsychiatric Symptoms  11yo girl with GAS pharyngitis, treated with abx -Unusually abrupt onset of severe psychiatric symptoms with concurrent other cognitive, behavioral or neurologic  1 week later behavior change – emotional, anxious, symptoms difficulty sleeping (school stressors)  PCP referred to child neurology for PANDAS  Likely represents multiple mechanisms -postinfectious, autoimmune, neuroinflammatory  2 weeks later began having spells (4 in 24 hours) -toxic  3 ED visits (? non-epileptic spells)  admission for -endocrine expedited work up -metabolic -vascular -psychogenic

Zibordi, Euro jour Ped Neuro. 22:2018.

Orobuccal Dyskinesia (YouTube video Additional History & Clinical Exam of unknown child)

 Withdrawn (decreased speech output), endorsed small abnormal mouth movements  “Type A kid,” but symptoms new and atypical

 Normal vitals and general exam  Normal neurologic exam except:  Mental Status: suddenly agitated, paces around room “I know what’s going on, I have to go home”  Very rare subtle orobuccal dyskinesia (easily could be missed!)

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EEG monitoring Differential Diagnosis

 2 focal seizures (5-10 minutes each) within 1st hour of  Autoimmune encephalitis (e.g. anti-NMDA receptor recording – pretty high burden! encephalitis)  non-convulsive: ipsilateral nose wiping, behavioral arrest with  Infectious encephalitis (e.g. HSV) upward eye deviation, oral and bilateral hand automatisms  CNS involvement of rheumatologic disease (e.g. SLE)  left temporal onset  Metabolic disorder (e.g. mitochondrial)  Initial EEG background  left T7/P3 delta slowing and frequent spike wave discharges,  Brain tumor normal posterior rhythm and sleep  Malformation of cortical development (e.g. focal cortical dysplasia)

Anti-N-methyl-D-aspartate receptor Further Evaluation (NMDAR) encephalitis

 Brain MRI with contrast – normal  Serum labs – no indication of infection or underlying  Antibody-mediated autoimmune encephalitis (AE) rheumatologic disorder  Abs form against extracellular NR1 subunit of  Lumbar Puncture NMDA receptor  6 WBCs (lymphocyte predominant), normal protein/glucose  Known immunologic triggers:   HSV PCR negative Tumor (usually ovarian teratoma)  HSV encephalitis  3 oligoclonal bands  Unknown in about 50% of patients  +NMDAR abs in CSF (and serum)

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Demographics Association with HSV encephalitis

 Female predominance: 81% female  20-30% of patients with HSV encephalitis can  Affects young individuals: 37% < 18 yrs (95% < 45 yrs) develop HSV-induced AE (most commonly anti-  About 50% with a tumor, usually ovarian teratoma (not always, esp > 45)  Sex ratio and detection of ovarian teratoma is age dependent NMDAR encephalitis)  Adults: largely young women, ovarian teratoma common  Occurs within 2 months following HSV infection  Children < 12: sex ratio more equal, ovarian teratoma rare  Similar clinical phenotype Armange et al, Lancet Neurology 2018

VERY IMPORTANT TO TEST FOR ANTI-NMDAR IN CASES OF HSV ENCEPHALITIS RELAPSE!

Titulaer et al, Treatment and prognostic factors for long-term outcome in patients with anti-NMDAR encephalitis: an observational cohort study. Lancet Neurology, 2013.

Clinical Features Initial symptoms by age

 Half of children/young adults have a non-specific viral prodrome Behavior change and seizures are most common presenting  Symptoms- new onset symptoms in all ages  Behavior (psychiatric) and cognitive dysfunction – anxiety, agitation, bizarre behavior, hallucinations, delusions, disordered thinking • Behavior more common in adults  Speech dysfunction • Seizures/movement disorder more common in  Memory deficits children (< 12)  Seizures  Movement disorders: orofacial dyskinesias, choreoathetosis, dystonia, akathisia, rigidity  Decreased level of consciousness  Autonomic instability

 Sleep disturbance also common  Hx in kids: “my child is having tantrums and talking baby talk again” (regression) - not normal! Titulaer et al, Treatment and prognostic factors for long-term outcome in patients with anti-NMDAR encephalitis: an observational cohort study. Lancet Neurology, 2013.

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Poly-symptomatic Disease Findings in anti-NMDAR encephalitis

 87% developed ≥ 4 symptoms  Brain MRI – often normal or shows transient FLAIR within 4 weeks or contrast-enhancing abnormalities in cortical and  1% had only one symptom  Most common: subcortical regions behavior/cognitive changes, memory deficits, speech  CSF – often abnormal with pleocytosis disorder, seizures, movement disorder  EEG – usually focal or diffuse slowing  More sensitive than brain MRI or CSF studies (cell  Children: movement disorder, count/protein) Adults: memory deficits and central  Diagnosis is confirmed with + IgG antibodies to hypoventilation Titulaer et al, Treatment and prognostic factors for NMDAR in CSF or serum  Rare sxs: ataxia and hemiparesis long-term outcome in patients with anti-NMDAR (seen mainly in young children) encephalitis: an observational cohort study. Lancet  CSF testing is important given higher sensitivity (100%) than Neurology, 2013. serum (85%)

What do we know about treatment? Standard Disease Treatment

 No prospective randomized trials  Tumor removal  Observational studies  Immunotherapy  Largest study: retrospective, 501 patients (177 children)  First-line: High-dose steroids, IVIg, plasma exchange  Nearly all (94%) treated with first-line immunotherapy/tumor removal  Typically solumedrol x 5 days AND either IVIg or plasma exchange  53% improved within 4 weeks  Second-line: Rituximab, cyclophosphamide  Of those who didn’t improve, 57% received second-line  Typically start with rituximab in children, but if severe consider immunotherapy  higher likelihood of good outcome (mRS 0-2) dual-therapy  Tenets of treatment:  Questions/challenges  responsive to immune therapy  IVIg versus PLEX?  early treatment better than late  When to move on to second-line therapy?  if no/limited response to first-line therapy move on to second-line therapy  Need novel therapies

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Symptom Management Outcomes

 Goal: minimize morbidity & complications from critical illness  No difference between children and adults

 Psychosis/agitation/delirium  During hospitalization: 75% are admitted to ICU  Delirium precautions  At 2 yrs, 81% of patients “good” outcome (mRS 0-2), 6%  Clonidine/dexmedetomidine  Low-dose anti-psychotics only with caution (risk of NMS) died  Sleep disruption   Melatonin, clonidine, others Improvement up to 18 months after symptom onset  Movements  Predictors of good outcome  Difficult to treat - goal is to minimize morbidity (self-harm, rhabdo), not to stop the movements  Earlier treatment with immunotherapy/tumor removal  Benzodiazepines, others  No need for ICU stay  Vigilant attention to oral care Titulaer et al, Treatment and prognostic factors for long-  Seizures  12% relapse in first 2 yrs term outcome in patients with anti-NMDAR encephalitis: an observational cohort study. Lancet Neurology, 2013.  Consider avoiding levetiracetam given risk of worsening irritability  Dysautonomia/hypoventilation  NEOS score (1-5) -> associated with functional status at 1 year  Cardio-respiratory monitoring Balu et al, Neurology 2019

Clinical Approach to Diagnosis of Autoimmune Encephalitis (Graus et al, Lancet Neurol 2016) Case #3

 Goal: early treatment  Graus criteria validated  10yo boy with recent onset MRI-negative focal epilepsy before ab test returns in separate cohort of  Presents to ED with new spells of non-stereotyped children (Ho et al, Dev Med and Child Neuro 2017) extremity movements, gait instability, and  29 patients anti-NMDAR, anxiety 74 other encephalitides  EEG: non-epileptic movements  Graus anti-NMDAR  Dx: non-epileptic spells, conversion disorder (for the gait), and criteria 90% sensitive anxiety disorder and 96% specific  Parents bring him back to ED couple days later with  Median time to meet worsening anxiety (“I’d rather be dead”) and episode of criteria 2 weeks “shaking with LOC”  Transferred for further evaluation/cEEG monitoring

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Additional HX & Clinical Examination Diagnostic Evaluation/Outcome

Family reported (and patient endorsed) fidgety leg  EEG monitoring: movements, spells of stiffening, and  Very frequent focal seizures  Normal background initially, transitioned to diffuse slowing withdrawal/anxiety over past few weeks -> atypical  Brain MRI with contrast  normal Examination:  CSF  Normal vitals and general exam  2 WBC, normal glucose and protein  Normal neurologic exam except:  Screen for tumor - negative  Distressed, readily brought to tears in between spells, “please help me”, fluent but decreased speech output  Fulfilled 4/6 sxs for Graus criteria – empiric RX started  Subtle leg akathisia  +NMDAR ab in CSF and serum  Several beats ankle clonus bilaterally  Complete recovery after first-line therapy, no relapse

Take-Home Points Take-Home Points

 PANDAS/PANS remains a controversial diagnosis, and  Anti-NMDAR encephalitis is a severe antibody- treatments are unproven mediated disease responsive to immunotherapy and  Children with concurrent onset of acute psychiatric and clinically recognizable neurologic symptoms deserve a full neurologic diagnostic  Young children initially present with movement evaluation disorder or seizures more often than adults, and  Treatment should include evidence based psychiatric young girls/boys nearly equally affected care (CBT and SSRIs)  In all patients, important to probe about  Antibiotics or immune modulation treatment should be behavior/psych symptoms, changes in speech, subtle discussed on a case by case basis, ideally based on abnormal movements, “spells”  we need to ask, objective findings of infection or neuro-inflammation listen, and promptly evaluate when indicated  CANS/Childhood Acute Neuropsychiatric Symptoms have a much broader differential diagnosis  Goal is early therapy to improve outcome

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Thank you

 For your attention!  For our collaborators  Emmanuelle Waubant  Carla Francisco  Jeffrey Gelfand  Michael Wilson  Bennett Leventhal  Khyati Brahmbatt  Josep Dalmau

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