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Everything posted by kos_mom

  1. DD had ASO done on 7/18--656. Anti DNaseB 147 (normal <120). Had 103 fever 7/25 with respiratory distress. ER gave her IV Avelox for possible pneumonia and seven days oral Avelox scrip at 400 mg. Also 40 mg steroids for five days with taper finished 8/7. Just learned strep culture done 8/1 came back negative. Could tx with Avelox (which I understand is not particularly effective abx for strep) been enough for culture to go negative? If not, what does negative culture with high titers mean? Much thanks--want to be informed before neuro visit.
  2. So amused by the title of your post. But it hit close to home as well. When my DS was 9 his explanation for what was happening to him was that an alien on another planet was controlling his body. So nice to have a reverse abduction story!
  3. When DS (now 22) was in kindergarten, his teacher told me she thought he may have language delay. We tested him and indeed he had receptive language and processing problems. Perhaps this was PANDAS--he had strep right before entering and had a grimacing thing going on, but not much more. In any case, at the time we thought it was due to having had many ear infections before he was two. I think I read somewhere that ear infections can be a precursor to PANDAS. As I recall, part of the theory of ear infections that are not thoroughly treated soon enough leading to language problems is that sounds become quite uncomfortable during the infection and, for kids, for several more months or so they kind of zone out in the presence of sounds to avoid the discomfort. (It's kind of like hearing everything through an echo box--extrapolating a bit from my adult experience with an ear infection I let go too long.) During that period the neurons for language processing are not connecting the way they should. When DS had an explosion of tics/OCD at 7 and a half we desparately searched for an explanation and ended up at a neuropsych place. With the language problems together with the tics (stereotypical behaviors he called them and was really annoyed when I kept calling them tics), the psych dx'ed him as PDD NOS. I read up (back in those days no internet--had to go search out books)and challenged psych that this could not be something autistic--all those parents knew something was seriously off at age 2 or 3, not suddenly when the kids were almost 8. Finally got a P doc with lots of autistic patients who agreed with me and dx'ed tic-related OCD. (Only tx available was prozac--another story.) I self dx'ed PANDAS when he was 10 and the NIH confirmed the summer he turned 11. In any case, DS did lots of language therapy. What really helped was the summer of third grade when he did Fast Forward--made huge leaps in language progress. If your DD has language problems and has an hx of ear infections it could be PANDAS related but she still may need good language therapy to get those processing neurons to make connections that were missed during ear infections.
  4. Dr. Jory Goodman, who write online articles for Psychology Today, reports good success doing T and A on adults he has diagnosed as having Pandas. Here is a link to one of his articles that describes some of his patients: http://www.psychologytoday.com/blog/attention-please/201107/evil-pandas-part-ii-adult-affliction-treatment I can't comment on our experience as we are just a month out from my DS's T and A. He feels it has made a change for the better.
  5. Don't know if this will be helpful. My DS is 22 (had Pandas from age 6 that ended by the time he was 13 and came back in college twice following strep infections) so I am willing to do anything Dr. L recommends given how much of his life has been disrupted. In his case she noted that he had a strong history of symptom improvement with abx so a T and A in her view was a "no brainer." He also does not have co-infections (as far as we know) and all along has been a pretty textbook case of Pandas.
  6. DD also has nonspecific gastric complaints and feels nauseous a lot. A couple of times a week she does actually throw up--mostly just phlegm, but some food too. She went two weeks last month on just soft foods. She takes Zantac (others use Pepcid, apparently not too much difference) and her PCP added some anti-nausea medication which has reduced symptoms. She is an adolescent and I notice on Dr. K's site that gastric complaints and anorexia (from fear of choking or ensuing gastric pains not from distorted image) are hallmarks of adolescent onset Pandas kids he's seen. The choking thing is a bit different. She'll be sitting watching TV or something not terribly active and suddenly gag and choke--she goes limp for a minute or so and doesn't see to be breathing. I grab her up and start pounding her back and she comes to--I then give her some water and she seems to be able to swallow. This may happen after she's taken a sip of something or not--but she claims to have a problem of excess saliva. This could indicate something wrong with her swallowing function rather than hypersalivation.
  7. DD has no developmental problem that I know of. Her PCP did scrip to weeks ago for swallowing study with a private GI--I hadn't gotten around to it--too much else like ER trip when she had 103 fever, severe chills, and blue lips. PCP's theory is that cyanosis may have resulted from another aspiration episode rather than asthma attack (which she had as well). Amy SLP, in light of what you say, it looks like a good thing we didn't go the GI because a more specialized study may be called for. Am seeing ENT at hospital based practice with her Tuesday--I'll ask him and mention SLP involvement. You guys are the best!
  8. Much thanks to whomever posted the IOCDF notes on Pandas Network. This caught my eye--my DD19 chokes several times a week--pretty scary even as many times as I've seen her do it. Apparently this sometimes happens to her in the middle of the night. I was thinking of posting here to see if anyone else had seen this and if it could be related to PANDAS, but after some consideration decided it was a stretch. And so what do I see in the IOCDF notes on things Dr. Swedo said but: "•A swallowing study may be indicated in the future. •PANS kids can have involuntary muscle movements in the throat that makes it feel like they are choking." Wow! Anyone else's experience with choking would be most interesting. So here's another possible way PANDAS/PANS could be health threatening. DD was hospitalized for six days in May with necrotizing pneumonia--was on really big gun IV antibiotics for 6 days. My MPH sister says her type of pneumonia has a 25% fataity rate in young people. DD's pulmonologist thinks she had aspiration pneumonia--with all her choking/gagging something (and its bacteria) went down her trachea into her lungs instead of her esophagus, leading to the pneumonia.
  9. Thanks all for the validation! Z-Packs it is.
  10. I am so sorry to hear about son. We did not get a chance to do IVIG for my DS--he is now 22, but his first big outbreak was in 1998 when no one could help, even with long term ABX because that was not known as a treatment then. In fact, no one could tell me what was wrong. He eventually got better, but he suffered a much worse outbreak two years later. I would have done IVIG in a heart beat had it been available. And looking back over the years, I think how much better a childhood he could have had with propoer treatment. It came back while he was in college and I have finally got him to a specialist (Dr. L), so I am hoping we can get to a place where he no longer needs to worry about this. If Dr. l suggests IVIG, we'll be at the hospital to do it the next day. I may be inferring too much, but you seem to be questioning whether your DS is severe enough to "deserve" IVIG. Yes, there are kids so bad they cannot get out of bed and maybe your DS is more functional than that. But he has OCD, anxiety, phobias, and tics. Having had to go through this with very little medical help a long time ago, I can tell you the long-term consequences of chronic if not extremely severe PANDAS are very challenging for both the child and his family. You really don't want to have put up with them if you can avoid it. Definitely go for the IVIG in my view.
  11. What would you do? I want to get my dd on abx as fast as possible. A week ago I learned her ASO was 654 and her Anti DNase B was 147 (normal <120). Two days earlier she received IV Avelox for possible pneumonia and was given Avelox 400 mg for seven days. Her PCP felt that was sufficient for the strep. DD didn't get cultured until last Wednesday. I learned from Dr. H at Georgetown that Avelox isn't effective for strep--he recommended Augmentin or a cephalasporin, so I sent message to PCP last night asking for script. No answer--perhaps she is waiting for culture result. DD got scrip of prednisone at same time of Avelox (for asthma) starting at 40 mg for 5 days, then a taper. We are now down to 20 mgs and won't finish until some time next week. I figure she's getting some protection from prednisone, but I am worried about going two or three more days without abx. So I am thinking of: 1) Giving her some of her brother's clindamycine. Scrip was just refilled for 30 days. He has appointment with Dr. L Wednesday and I could sort him out then. or 2)Giving her azithromycin--a dentist friend is wiling to give me several Z packs I could get tomorrow morning. Our medicine chest has plentiful supplies of doxycycline and minocycline, but neither of these look particularly good for strep. I know this self-prescribing is not desirable, but also know PCP while open to Pandas is likely reluctant on the intensive abx front. DD is seeing Dr. H on Tuesday so I could probably get scrip then and possibly bring up briefly with Dr. L Wednesday (DD won't have appointment with her until October 2.) Any advice gratefully accepted.
  12. Nancy, Much thanks--DD has mysterious gastric complaints and won't face the day without taking Zantac first thing. She still has gastric issues, so maybe a night time dose would be helpful.
  13. Thanks Nancy. How often are dosing the Pepcid--once a day or more often? Thanks.
  14. Nancy, Zantac, which my daughter takes,is also an H-2 blocker. Is Pepcid in some way superior and should I switch her to it? Interesting about Atarax. DD once had it prescribed when her allergies were very bad--she used to make a point of reminding me to make sure I put her little red pill out. Maybe she was feeling something from it she wasn't communicating to me--perhaps I can cadge another prescription from her allergist. Thanks, Ko's Mom
  15. My understanding is that these Up to Date articles are the go to place for medical people to learn about/brush up on conditions they are not intimately familiar with. This may explain a lot about why one gets so much resistance from the more generalist doctors, even if they do recognize the Pandas. On the plus side, it does advance longer term abx treatment, however tentatively and circumscribed(although one does need to dig a bit to find it).
  16. This is from Up to Date, which many medical personnel use. A friend sent it to me. More references than one would perhaps like to controversy. PANDAS: Pediatric autoimmune neuropsychiatric disorder associated with group A streptococci Author Michael E Pichichero, MD Section Editors Sheldon L Kaplan, MD Douglas R Nordli, Jr, MD Thomas JA Lehman, MD Deputy Editor Mary M Torchia, MD All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2012. | This topic last updated: Jun 24, 2012. INTRODUCTION — Pediatric autoimmune neuropsychiatric disorder associated with group A streptococci (PANDAS) is a term used to describe a subset of children whose symptoms of obsessive compulsive disorder (OCD) or tic disorders are exacerbated by group A streptococcal (GAS) infection [1]. The hypothesized association between PANDAS and GAS is controversial, as is the limitation of the diagnosis exclusively within the pediatric age group. (See 'Areas of controversy' below.) An overview of PANDAS will be presented below. Other aspects of GAS infection in children, including diagnosis, treatment, prevention, and complications, are discussed separately. (See "Approach to diagnosis of acute infectious pharyngitis in children and adolescents" and "Complications of streptococcal tonsillopharyngitis" and "Treatment and prevention of streptococcal tonsillopharyngitis".) BACKGROUND — Most of the knowledge about PANDAS has been obtained by studying patients with a known tic disorder or long-standing OCD in research facilities and referral centers [1-4]. Investigators at these centers noted an association between Sydenham chorea and OCD [5-7]. Sydenham chorea is a movement disorder characterized by chorea, emotional lability, and hypotonia. It is one of the major clinical manifestations of acute rheumatic fever (ARF). The investigators also identified a subset of children with OCD or tic disorders following GAS infection who did not meet criteria for Sydenham chorea [4,8,9]. This subset is described by the acronym PANDAS [1]. (See "Sydenham chorea" and "Clinical manifestations and diagnosis of acute rheumatic fever".) The diagnostic criteria for PANDAS, which are discussed in greater detail below, include the following [1,10]: Obsessive-compulsive disorder (OCD) and/or tic disorder (Tourette disorder, chronic motor or vocal tic disorder) Pediatric onset (between three years and onset of puberty) Abrupt onset and episodic course of symptoms Temporal relation between group A streptococcal (GAS) infection and onset and/or exacerbation Neurologic abnormalities, such as motoric hyperactivity, choreiform movements, or tics during exacerbations Whether PANDAS is a distinct form of more typical cases of OCD or tic disorder remains controversial; the proposed pathogenesis is also controversial [11-13]. These issues are important because they affect evaluation and management. They are discussed in greater detail below. Areas of agreement — Although PANDAS is a controversial diagnosis, there is general agreement on the following points: GAS is one of several factors that can exacerbate OCD or tic disorder in a subset of patients [1,9,14-17] Children with signs and symptoms compatible with GAS infections should be evaluated for GAS infection [10,12] (see "Approach to diagnosis of acute infectious pharyngitis in children and adolescents", section on 'Diagnostic approach') Children with GAS infection and OCD/tic disorder require standard treatments for these problems (regardless of whether GAS and OCD/tic disorder are causally associated) [10,12] (see 'Management' below) Routine administration of immunomodulatory therapy (eg, glucocorticoids, plasma exchange, intravenous immunoglobulin [iVIG]) is not indicated for children who meet PANDAS criteria [10,12,18] Routine administration of prophylactic antibiotics is not indicated for children who meet PANDAS criteria [10,12] Areas of controversy — Controversies surrounding PANDAS include: Whether PANDAS is sufficiently different from OCD/tic disorder to be considered a separate entity [14,17,19] (see 'Clinical features' below) The nature of the association between GAS and PANDAS (eg, causal versus incidental) and whether it is important to single out GAS among the many other precipitants of OCD/tic disorders [13,14,17,20-23] (see 'Association with GAS' below) Whether PANDAS is an autoimmune disorder [19,20] (see 'Pathogenesis' below) Whether evidence of GAS infection should be sought in children with OCD/tic disorders [11,12,24] (see 'Diagnostic process' below) PATHOGENESIS — The proposed model for pathogenesis of PANDAS suggests that group A streptococcal (GAS) infection in a susceptible host causes an abnormal immune response with resultant central nervous system manifestations. If this hypothesis is correct, there might be a role for prophylactic antibiotics and/or immune modulating therapies in the prevention and treatment of PANDAS. However, the hypothesis is as yet unproven. The model for PANDAS pathogenesis is based upon the clinical similarities between Sydenham chorea and PANDAS [1]. The pathogenesis of Sydenham chorea and acute rheumatic fever (ARF) are incompletely understood. However, preceding GAS pharyngitis and an abnormal immune response (in which antibodies directed against GAS antigens cross-react with host antigens in brain and other tissues) are widely accepted as important components. (See "Epidemiology and pathogenesis of acute rheumatic fever", section on 'Molecular mimicry'.) Association with GAS — The association between neuropsychiatric symptoms and GAS infection was evaluated in a case-control study from a large health maintenance organization [9]. The investigators identified 144 patients with obsessive-compulsive disorder (OCD), Tourette syndrome, or a tic disorder (in a population of about 75,000 children) and matched them with one to five control subjects. The following findings were noted: Cases were more likely than controls to have had a GAS infection in the three months before onset of neurologic disease (odds ratio [OR] 2.22, 95% CI 1.05-4.69) Cases were more likely than controls to have had multiple GAS infections during the 12 months before onset of neurologic disease (OR 3.1, 95% CI 1.77-8.96) Prospective studies have confirmed that GAS is associated with the onset or exacerbation of OCD or tic disorder in at least some patients [14,15]. However, the high background rates of GAS infection, GAS carriage, and OCD/tic disorders in prepubertal children make it difficult to establish causality [10,12,13]. (See 'Differential diagnosis' below.) Autoimmunity — The role of autoimmunity in PANDAS is controversial. Support for a role of autoimmunity is provided by reports of response to treatment with immune-modifying therapies, such as glucocorticoids, intravenous immunoglobulin (IVIG), and plasma exchange [4,25,26]. The response to plasma exchange appears to be specific to children with OCD/tic disorders and preceding GAS infection; in an open trial, plasma provided no benefit for children with OCD whose symptom exacerbation did not follow GAS infection [27]. An autoimmune mechanism for PANDAS also is supported by animal studies, as well as studies demonstrating increased antineuronal antibodies in patients with PANDAS compared with patients with OCD/tic disorders but no evidence of GAS infection and patients with GAS infection but without OCD/tic disorder [26,28-30]. However, other studies have been unable to distinguish patients with PANDAS or Tourette syndrome from control patients on the basis of autoantibody profiles [31-34]. The inconsistent findings may be related to methodologic differences [35,36]. Additional observations that conflict with the hypothesis that PANDAS is caused by antineuronal antibodies include: The failure of immunologic markers to correlate with clinical exacerbations in PANDAS patients in a longitudinal case-control study [37] The failure of microinfusion of PANDAS serum into rodent striatum to produce changes in behavior [38] EPIDEMIOLOGY — The incidence and prevalence of PANDAS are not known, although it is rare. In our prospective study [22], only 10 cases were identified among 30,000 throat cultures positive for GAS; since then, the annual incidence has ranged between 0 per 10,000 cultures to 10 per 30,000 cultures, depending upon the strain of GAS and host genetics (unpublished data) [39]. Despite its rarity, some investigators suggest that it may account for ≥10 percent of childhood-onset OCD and tic disorders [40,41]. In the original series of 50 patients, the mean age of onset was 6.3 years for children with tics and 7.4 years for children with OCD [1]. PANDAS was more common among boys and children with a family history of rheumatic fever. CLINICAL FEATURES Working diagnostic criteria — PANDAS is characterized by five working criteria [1,4,10]: Obsessive-compulsive disorder (OCD) and/or tic disorder (Tourette, chronic motor, or vocal tic disorder that meets the DSM-IV diagnostic criteria). (See "Hyperkinetic movement disorders in children", section on 'Tic disorders'.) Pediatric onset (between three years and onset of puberty). Abrupt onset and episodic course of symptoms. (See 'Clinical course' below.) Temporal relation between group A streptococcal (GAS) infection and onset and/or exacerbation. The time frame for the temporal relation was not specified in the original description [1]. Antibody levels to streptolysin O and DNase B remain elevated for several months after an acute infection, complicating the applicability and interpretation of elevated titers [42]. (See 'Laboratory features' below.) Neurologic abnormalities, such as motoric hyperactivity, choreiform movements (elicited through stressed postures, but not present at rest), or tics during exacerbations. Frank chorea (rapid, irregular, and nonstereotypic jerks that are continuous while the patient is awake but improve with sleep) suggests Sydenham chorea. (See "Sydenham chorea".) Some experts have questioned whether the above criteria are useful in distinguishing patients with PANDAS from patients with more typical cases of OCD or tic disorder [11,12,19]. However, observational studies suggest that clinical and laboratory features can distinguish PANDAS from OCD or tic disorder without PANDAS: In a prospective study, 12 children with PANDAS were identified in a primary care practice over a three-year period [15]. All had positive throat cultures at the time of onset of neuropsychiatric symptoms and improvement of neuropsychiatric symptoms with antibiotic therapy. Symptoms resolved completely in four patients within 5 to 21 days after onset, and none of these patients had a recurrence. Recurrent symptoms developed in the remaining children, and each recurrence was associated with a new episode of culture-proven GAS tonsillopharyngitis and amelioration of symptoms with antibiotic therapy. In another study of 109 prepubertal children with tics, OCD, or both, dramatic onset of symptoms, remissions in neuropsychiatric symptoms, a clinical course marked by definite remissions, and remission of neuropsychiatric symptoms during antibiotic therapy were more likely among the 48 children with who met criteria for PANDAS (including positive GAS culture or rising antibody titers at the onset or exacerbation of neuropsychiatric symptoms) than those who did not [43]. Clinical course — The clinical course of PANDAS is characterized by a "sawtooth" pattern with periods of symptom quiescence, followed by exacerbations with abrupt onset and gradual resolution (over weeks to months) [1,4,10,15]. Abrupt onset of OCD/tic disorder symptoms also has been noted in patients without PANDAS [13,44]. Neuropsychiatric exacerbations in children with PANDAS begin at the time of GAS infection or within one to two weeks after GAS infection [1,10,15]. Children with PANDAS and tics occasionally have simultaneous onset of frequent, severe, and varied motor and vocal tics, prompting emergency treatment [10]. This is in contrast to the typical onset of isolated, intermittent, simple motor or vocal tic that has a much more gradual onset and is milder [10,45]. Similarly, children with PANDAS and OCD are described as having an "explosion" of OCD symptoms, reaching clinically significant impairment in 24 to 48 hours [1]. This is in contrast to the typical undulating waxing and waning pattern of OCD symptoms in patients without PANDAS [46,47]. Because fever and other stressors of illness are known to exacerbate OCD and tic disorders, to meet criteria for PANDAS, the exacerbations should have an association with GAS infection, documented by culture or serology to qualify as a possible case [1]. Laboratory features — Diagnosis of PANDAS requires a temporal relation between GAS infection and the onset and/or exacerbation of neuropsychiatric abnormalities [1,10]. GAS infection is confirmed by: Positive throat or skin culture or rapid antigen detection test for GAS at the beginning of a PANDAS exacerbation, or Clinically significant rise in antistreptococcal antibody between the onset of symptoms and four to six weeks later. It is important to obtain anti-DNase B as well as anti-streptolysin O titers since anti-DNase B titers are elevated in approximately 80 percent of PANDAS cases, whereas ASO titers are significantly elevated in 20 to 50 percent of cases [15]. Some authorities suggest repeat cultures and/or serology when children with suspected recurrent episodes of PANDAS are well to exclude streptococcal carriers [1,10,48]. DIAGNOSTIC PROCESS — PANDAS is a clinical diagnosis. It may be suspected in children with an abrupt onset of neuropsychiatric symptoms, recent group A streptococcal (GAS) infection, and remission of neuropsychiatric symptoms with antibiotic therapy. The obsessive-compulsive disorder (OCD)/tic disorder and acute GAS infection should be treated as outlined below. Patients with suspected PANDAS should be monitored for recurrence of neuropsychiatric symptoms and/or GAS infection because approximately 50 percent have second episodes [15]. (See 'Management' below.) We suggest that children who present with abrupt onset of OCD/tic disorder be evaluated for GAS infection. Diagnosis of PANDAS requires prospective evaluation with documentation of an episode of neuropsychiatric symptoms associated with evidence of GAS infection. Evidence of GAS is provided by [1,10,48]: A positive throat or skin culture or rapid antigen detection test for GAS, or A rise in antistreptococcal antibody (ASO and/or anti-DNase titers (twofold or greater) Demonstration of negative throat culture or declining antistreptococcal antibody titers during remission of neuropsychiatric symptoms is helpful in distinguishing GAS carriers [1]. The diagnostic process described above is that which is outlined by investigators at the National Institutes of Mental Health (NIMH) [1,10]. They maintain that the risk of acute rheumatic fever mandates the detection and appropriate treatment of GAS infections, including mildly symptomatic infections and infections in which neuropsychiatric manifestations are the only symptoms. (See "Treatment and prevention of acute rheumatic fever".) However, this process is not endorsed by all experts [11,12]. Until a causal relationship between PANDAS and GAS infection is established, the American Heart Association (AHA) Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee does not recommend routine laboratory testing for GAS to diagnose PANDAS in children with OCD/tic disorders [11]. The evaluation of children with pharyngitis in the absence of neuropsychiatric manifestations is discussed separately. (See "Evaluation of sore throat in children" and "Approach to diagnosis of acute infectious pharyngitis in children and adolescents", section on 'Diagnostic approach'.) DIFFERENTIAL DIAGNOSIS — The major considerations in the differential diagnosis of PANDAS are obsessive-compulsive disorder (OCD)/tic disorder in a child with coincident or intercurrent episodes of group A streptococcal (GAS) or a child with GAS carriage and Sydenham chorea [1,10,12,49]. Tic disorder or OCD — Both neuropsychiatric symptoms and GAS are common in prepubertal children. OCD occurs in 1 to 2 percent of school-age children and transient motor tics in as many as 25 percent [50-52]. GAS accounts for 15 to 30 percent of all cases of pharyngitis in children between the ages of 5 and 15 years. Prospective surveillance identified GAS carriage in 2.5 percent of well children and 4.4 percent of children with URI (including a sore throat) [53]. (See "Approach to diagnosis of acute infectious pharyngitis in children and adolescents", section on 'Group A streptococcus' and "Antibiotic failure in the treatment of streptococcal tonsillopharyngitis", section on 'Streptococcal carriage'.) Strict adherence to the diagnostic process described above should help to distinguish between PANDAS and coincidental simultaneous occurrence of these problems [10]. Documenting negative throat culture and/or stable antistreptococcal antibody titers during remission helps to exclude GAS carriage. (See 'Diagnostic process' above.) Sydenham chorea — Sydenham chorea is a movement disorder characterized by chorea, emotional lability, and hypotonia. Neuropsychiatric manifestations that may be present in Sydenham chorea also may occur in PANDAS patients (eg, OCD, separation anxiety, hyperactivity, adventitious movements) [6,49,54]. (See "Sydenham chorea".) NATURAL HISTORY — The natural history of PANDAS was described in a prospective case-control study of 40 children with PANDAS and 40 children with obsessive-compulsive disorder (OCD)/tic disorders but no evidence of group A streptococcal (GAS) infection [14]. Throat cultures were obtained once per month, and streptococcal antibody titers were measured at least once every three months, for two years; testing for GAS also was performed during exacerbations. Case subjects were treated with standard therapies for their neuropsychiatric symptoms and received prompt antibiotic therapy for GAS infections. Prophylactic antibiotics and immune modulating therapy were not administered. Laboratory personnel were blinded to the status of the patient (case versus control and exacerbation versus routine monitoring), and clinical raters were blinded to the laboratory results. The following observations were made: Forty neuropsychiatric exacerbations (clinically significant worsening for ≥5 days unrelated to a change in medication) occurred in 21 case patients (0.56 exacerbations per person year), and 25 neuropsychiatric exacerbations occurred in 14 control subjects (0.28 exacerbations per person year). These rates were lower than expected. Only five neuropsychiatric exacerbations occurred within four weeks of GAS infection; all of these occurred in PANDAS patients. This was greater than the number expected by chance (1.6). However, in a subsequent similarly designed study by the same group, no neuropsychiatric exacerbations occurred within two months of newly diagnosed GAS infection in 31 PANDAS patients who were followed for 25 months [17]. The majority of exacerbations in PANDAS patients (87.5 percent) had no relation to GAS infection. Definite or probable GAS infection was more frequent among cases than controls (0.43 versus 0.13 infections per person-year, relative risk 2.76, 95% CI 1.4-5.3). These observations and those from other studies suggest that a subgroup of patients with tics/OCD may be vulnerable to GAS as a precipitant of neuropsychiatric symptoms, but the majority of exacerbations have other triggers [14,17,22]. In addition, PANDAS has a relatively benign clinical course when neuropsychiatric exacerbations and GAS infection are treated with standard therapies. (See 'Management' below.) MANAGEMENT — The management of children with PANDAS centers on providing standard therapies for group A streptococcal (GAS) infection and obsessive-compulsive disorder (OCD)/tic disorder [10,12]. Antibiotic therapy — Antibiotic therapy is indicated for the treatment of acute streptococcal infection as diagnosed by a positive throat or skin culture or rapid antigen detection test [10]. GAS infection — We recommend that children with positive culture or rapid antigen detection test for GAS be treated with antistreptococcal therapy (whether or not they have neuropsychiatric symptoms). Antimicrobial therapy is administered to reduce the severity and duration of signs and symptoms, including suppurative complications, reduce the incidence of nonsuppurative complications (eg, acute rheumatic fever), and reduce the risk of transmission. Treatment of GAS pharyngitis is discussed separately. (See "Treatment and prevention of streptococcal tonsillopharyngitis".) PANDAS subgroup — There are no randomized controlled trials of antibiotic treatment of children suspected of having PANDAS syndrome. In a prospective study that identified 12 children with abrupt onset of neuropsychiatric symptoms and evidence of recent GAS infection, antistreptococcal (penicillin or cephalosporin) therapy was associated with prompt symptom resolution in all cases [15]. Antistreptococcal therapy also was associated with prompt resolution of symptoms in the six patients who developed recurrent symptoms associated with GAS infection. The mean time to resolution of symptoms was shorter among children treated with cephalosporin than with penicillin (14 versus 5 to 6 days). Whether prompt antimicrobial treatment of GAS infection prevents the development of neuropsychiatric symptoms is not known [21,22]. We suggest that children with suspected PANDAS (ie, abrupt onset of neuropsychiatric symptoms and evidence of recent GAS infection) be treated with antimicrobial therapy, even if the episode of GAS was already treated (given the failure rates for penicillin and amoxicillin therapy). (See "Treatment and prevention of streptococcal tonsillopharyngitis", section on 'Selection'.) The author of this topic review suggests therapy with a cephalosporin rather than a penicillin. Several alternative regimens are listed below: Cefadroxil (30 mg/kg per day in one dose for 10 days) Cephalexin (30 mg/kg per day in two divided doses for 10 days) Cefuroxime (30 mg/kg per day in two divided doses for 10 days) Cefpodoxime (10 mg/kg per day in two divided doses for five days) Cefdinir (14 mg/kg per day in two divided doses for five days) Neuropsychiatric therapy — Children with OCD and/or tic disorders should receive standard neuropsychiatric treatment for these disorders (whether or not the children have evidence of recent GAS infection) [10,12]. Treatment of neuropsychiatric symptoms should not be delayed pending confirmation of PANDAS (eg, documenting rise in antistreptococcal antibodies or while monitoring for a second episode). The neuropsychiatric manifestations of children in the PANDAS subgroup respond to treatment with standard pharmacologic and behavior therapies [10]. OCD symptoms generally respond to a combination of pharmacotherapy (typically a selective serotonin reuptake inhibitor) and cognitive behavior therapy. Motor and vocal tics can be treated with a variety of medications. (See "Tourette syndrome", section on 'Management'.) Immune modulating therapy — Immune modulating therapies include glucocorticoids, plasma exchange, and intravenous immunoglobulin (IVIG). If PANDAS is an autoimmune disorder (and this remains controversial), immunomodulatory treatments might be beneficial. We recommend not treating children who meet criteria for PANDAS with immune modulating therapies outside of the research setting [10]. Immune modulating therapy may be an alternative for severely ill patients who have not responded to standard therapies. In such cases, consultation with a specialist in the treatment of neuropsychiatric and/or autoimmune disorders is recommended. The potential benefits of treatment with plasma exchange or IVIG compared with placebo were evaluated in a randomized controlled trial in 29 children who met PANDAS criteria and were severely affected [25]. Symptom severity was rated at baseline, and at 1 and 12 months after treatment. Significant improvement in symptoms from baseline was noted in the treatment groups at one month; improvements were maintained at one year, although psychotropic medications were decreased or discontinued in only 7 of 13 patients who required them at baseline. Adverse effects, which occurred in approximately two-thirds of patients in the treatment groups, included nausea, vomiting, headache, and dizziness. Limitations of the trial included the lack of a control for plasma exchange, open treatment of controls after the one-month follow-up (making it impossible to exclude the possibility of spontaneous improvement in the control group at the 12-month follow-up), lack of correlation between therapeutic response and rate of antibody removal, and poorly understood mechanism of therapeutic benefit [19,25]. A subsequent open trial of plasma exchange in children with OCD who did not meet PANDAS criteria failed to demonstrate a benefit [27]. This finding suggests that the effects of plasma exchange in children with OCD may be limited to those with preceding GAS infection, lending support to the autoimmune hypothesis. (See 'Autoimmunity' above.) Referral indications — Referral to a specialist (neurologist, psychiatrist, mental health provider) for treatment of OCD/tic disorder may be indicated for children who meet criteria for PANDAS. (See 'Neuropsychiatric therapy' above.) Referral to a rheumatologist/immunologist also may be warranted for patients with severe symptoms that are unresponsive to standard therapies. PROGNOSIS — The long-term outcome of children who meet criteria for PANDAS is not known. Cases of carditis (as occurs in patients with Sydenham chorea) have not been reported [12]. Unrecognized PANDAS and untreated PANDAS may result in an increased risk of progression to lifelong obsessive-compulsive disorder (OCD) and tic disorders [55]. PREVENTION — If the proposed pathogenetic model for PANDAS described above is correct, it might be possible to prevent PANDAS by preventing group A streptococcal (GAS) infection. Whether the prompt treatment of GAS infection prevents the development of neuropsychiatric symptoms is not known [21,22]. Recognition of the sentinel PANDAS episode and its prompt treatment may impact the likelihood of a recurrence and prevent kindling (eg, repeated stimulation of autoantibodies that target brain tissue, which eventually results in permanent destruction of the brain cells and permanent disability in the form of obsessive-compulsive [OCD] or tic disorder). (See 'PANDAS subgroup' above.) GAS infection — Measures to prevent GAS infection include early recognition and prompt initiation of antistreptococcal therapy and taking steps to decrease transmission. School-age children with sore throat or unexplained fever should be evaluated for GAS infection and treated with antibiotics if throat culture or rapid antigen detection test is positive. (See "Approach to diagnosis of acute infectious pharyngitis in children and adolescents" and "Treatment and prevention of streptococcal tonsillopharyngitis".) To prevent transmission of GAS infection, children with GAS pharyngitis or skin infection should stay home from school or child care until they have received 24 hours of appropriate antimicrobial therapy [23]. They should avoid close contact with other children during this time. Prophylactic therapy — Prophylactic antibiotics prevent recurrences of acute rheumatic fever and Sydenham chorea [49]. (See "Treatment and prevention of acute rheumatic fever" and "Sydenham chorea".) If, as hypothesized, the pathogenesis of PANDAS is similar to that of acute rheumatic fever and Sydenham chorea, then prophylactic antibiotics might be expected to prevent recurrences of PANDAS as well. However, the pathogenesis of PANDAS has not been established, and the role of prophylactic antibiotics is unknown. Potential adverse effects of prophylactic antibiotic therapy include diarrhea, pseudomembranous colitis, candida infections, and increased rates of antibiotic resistance [56]. In the author’s experience, prophylactic antibiotics are an option to aid in the diagnosis of PANDAS and prevent symptom recurrences. The clinical course during prophylaxis may help provide insight into the disease for the patient/family and clinician: remission of neuropsychiatric symptoms helps to establish the diagnosis of PANDAS, whereas recurrence of neuropsychiatric symptoms during prophylaxis excludes the diagnosis. However, other experts recommend against the use of prophylactic antibiotics for children with PANDAS [10,11]. The prophylactic regimen is the same as that for acute rheumatic fever (amoxicillin 250 twice per day orally, or [for penicillin allergic children] a macrolide [eg, azithromycin 5 mg/kg orally once per day, maximum dose 250 mg]). Antibiotic prophylaxis is generally continued for one winter season, coinciding with the peak seasonal occurrence of GAS (about six months). Prophylaxis is discontinued if neuropsychiatric symptoms do not improve or the child has a recurrence of neuropsychiatric symptoms. In the only placebo-controlled trial, an equal number of GAS infections occurred in the penicillin and placebo groups; failure to achieve adequate prophylaxis against GAS prohibited drawing conclusions regarding efficacy of PANDAS prevention [57]. A subsequent study compared rates of streptococcal infections and neuropsychiatric symptom exacerbation before and during 12 months of prophylaxis with penicillin or azithromycin [3]. Prophylaxis was associated with fewer episodes of GAS infection and fewer neuropsychiatric exacerbations compared with baseline. However, the lack of a placebo group, and other design problems (eg, small numbers, inadequate blinding, nonstandardized definition of exacerbation, failure to exclude GAS carriage), make these results difficult to inconclusive [58]. SUMMARY AND RECOMMENDATIONS PANDAS (pediatric autoimmune neuropsychiatric disorder associated with group A streptococci) is a term used to describe a subset of children whose symptoms of obsessive-compulsive disorder (OCD) or tic disorders are exacerbated by group A streptococcal (GAS) infection. The hypothesized association between PANDAS and GAS is controversial. (See 'Background' above.) PANDAS is characterized by five working criteria (see 'Clinical features' above): OCD and/or tic disorder Pediatric onset (between three years and onset of puberty) Abrupt onset and episodic course of symptoms Temporal relation between GAS infection and onset and/or exacerbation Neurologic abnormalities or tics during exacerbations We suggest that children who present with abrupt onset of OCD/tic disorder be evaluated for GAS infection (Grade 2C). (See 'Diagnostic process' above.) Diagnosis of PANDAS requires prospective evaluation with documentation of an episode of neuropsychiatric symptoms associated with evidence of GAS infection (positive throat or skin culture, rapid antigen detection test, or rising antistreptococcal antibody titers). (See 'Diagnostic process' above.) We recommend that children with positive culture or rapid antigen detection test for GAS be treated with antistreptococcal therapy (Grade 1A). (See 'GAS infection' above and "Treatment and prevention of streptococcal tonsillopharyngitis".) We suggest that children with abrupt onset OCD and/or tic disorders and evidence of GAS infection (ie, those with possible PANDAS) be treated with antistreptococcal therapy (Grade 2C). They should receive standard neuropsychiatric treatment for OCD/tic disorder if the symptoms do not remit after antibiotic therapy. (See 'PANDAS subgroup' above and 'Neuropsychiatric therapy' above.) We recommend not treating children who meet criteria for PANDAS with immune-modulating therapies outside of the research setting (Grade 1B). (See 'Immune modulating therapy' above.) Prophylactic antibiotics are an option to aid in the diagnosis of PANDAS and prevent symptom recurrences. The clinical course during prophylaxis may provide insight into the disease for the patient/family and clinician: remission of neuropsychiatric symptoms helps to establish the diagnosis of PANDAS, whereas recurrence of neuropsychiatric symptoms during prophylaxis excludes the diagnosis. (See 'Prophylactic therapy' above.) Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1 Swedo SE, Leonard HL, Garvey M, et al. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. Am J Psychiatry 1998; 155:264. 2 Swedo SE. Sydenham's chorea. A model for childhood autoimmune neuropsychiatric disorders. JAMA 1994; 272:1788. 3 Snider LA, Lougee L, Slattery M, et al. Antibiotic prophylaxis with azithromycin or penicillin for childhood-onset neuropsychiatric disorders. Biol Psychiatry 2005; 57:788. 4 Allen AJ, Leonard HL, Swedo SE. Case study: a new infection-triggered, autoimmune subtype of pediatric OCD and Tourette's syndrome. J Am Acad Child Adolesc Psychiatry 1995; 34:307. 5 Swedo SE, Rapoport JL, Cheslow DL, et al. High prevalence of obsessive-compulsive symptoms in patients with Sydenham's chorea. Am J Psychiatry 1989; 146:246. 6 Swedo SE, Leonard HL, Schapiro MB, et al. Sydenham's chorea: physical and psychological symptoms of St Vitus dance. Pediatrics 1993; 91:706. 7 Asbahr FR, Negrão AB, Gentil V, et al. Obsessive-compulsive and related symptoms in children and adolescents with rheumatic fever with and without chorea: a prospective 6-month study. Am J Psychiatry 1998; 155:1122. 8 Swedo SE, Leonard HL, Kiessling LS. Speculations on antineuronal antibody-mediated neuropsychiatric disorders of childhood. Pediatrics 1994; 93:323. 9 Mell LK, Davis RL, Owens D. Association between streptococcal infection and obsessive-compulsive disorder, Tourette's syndrome, and tic disorder. Pediatrics 2005; 116:56. 10 Swedo SE, Leonard HL, Rapoport JL. The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) subgroup: separating fact from fiction. Pediatrics 2004; 113:907. 11 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; 119:1541. 12 Kurlan R, Kaplan EL. The pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) etiology for tics and obsessive-compulsive symptoms: hypothesis or entity? Practical considerations for the clinician. Pediatrics 2004; 113:883. 13 Shulman ST. Pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS): update. Curr Opin Pediatr 2009; 21:127. 14 Kurlan R, Johnson D, Kaplan EL, and the Tourette Syndrome Study Group. Streptococcal infection and exacerbations of childhood tics and obsessive-compulsive symptoms: a prospective blinded cohort study. Pediatrics 2008; 121:1188. 15 Murphy ML, Pichichero ME. Prospective identification and treatment of children with pediatric autoimmune neuropsychiatric disorder associated with group A streptococcal infection (PANDAS). Arch Pediatr Adolesc Med 2002; 156:356. 16 Leslie DL, Kozma L, Martin A, et al. Neuropsychiatric disorders associated with streptococcal infection: a case-control study among privately insured children. J Am Acad Child Adolesc Psychiatry 2008; 47:1166. 17 Leckman JF, King RA, Gilbert DL, et al. Streptococcal upper respiratory tract infections and exacerbations of tic and obsessive-compulsive symptoms: a prospective longitudinal study. J Am Acad Child Adolesc Psychiatry 2011; 50:108. 18 PANDAS Information. Pediatrics and Developmental Neuroscience Branch National Institutes of Mental Health. intramural.nimh.nih.gov/pdn/web.htm (Accessed on September 07, 2011). 19 Singer HS. PANDAS and immunomodulatory therapy. Lancet 1999; 354:1137. 20 Kaplan EL. PANDAS? PAND? Or both? Or neither? Assessing a (possible?) temporal or pathogenetic relationship with the Group A "streptococcal diseases complex". Contemp Pediatr 2000; 18:81. 21 Luo F, Leckman JF, Katsovich L, et al. Prospective longitudinal study of children with tic disorders and/or obsessive-compulsive disorder: relationship of symptom exacerbations to newly acquired streptococcal infections. Pediatrics 2004; 113:e578. 22 Perrin EM, Murphy ML, Casey JR, et al. Does group A beta-hemolytic streptococcal infection increase risk for behavioral and neuropsychiatric symptoms in children? Arch Pediatr Adolesc Med 2004; 158:848. 23 American Academy of Pediatrics. Group A streptococcal infections. In: Red Book: 2012 Report of the Committee on Infectious Diseases, 29th, Pickering LK (Ed), American Academy of Pediatrics, Elk Grove Village, IL 2012. p.668. 24 Gilbert DL, Kurlan R. PANDAS: horse or zebra? Neurology 2009; 73:1252. 25 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; 354:1153. 26 Tucker DM, Leckman JF, Scahill L, et al. A putative poststreptococcal case of OCD with chronic tic disorder, not otherwise specified. J Am Acad Child Adolesc Psychiatry 1996; 35:1684. 27 Nicolson R, Swedo SE, Lenane M, et al. An open trial of plasma exchange in childhood-onset obsessive-compulsive disorder without poststreptococcal exacerbations. J Am Acad Child Adolesc Psychiatry 2000; 39:1313. 28 Hoffman KL, Hornig M, Yaddanapudi K, et al. A murine model for neuropsychiatric disorders associated with group A beta-hemolytic streptococcal infection. J Neurosci 2004; 24:1780. 29 Church AJ, Dale RC, Lees AJ, et al. Tourette's syndrome: a cross sectional study to examine the PANDAS hypothesis. J Neurol Neurosurg Psychiatry 2003; 74:602. 30 Pavone P, Bianchini R, Parano E, et al. Anti-brain antibodies in PANDAS versus uncomplicated streptococcal infection. Pediatr Neurol 2004; 30:107. 31 Singer HS, Hong JJ, Yoon DY, Williams PN. Serum autoantibodies do not differentiate PANDAS and Tourette syndrome from controls. Neurology 2005; 65:1701. 32 Singer HS, Loiselle CR, Lee O, et al. Anti-basal ganglia antibodies in PANDAS. Mov Disord 2004; 19:406. 33 Morris CM, Pardo-Villamizar C, Gause CD, Singer HS. Serum autoantibodies measured by immunofluorescence confirm a failure to differentiate PANDAS and Tourette syndrome from controls. J Neurol Sci 2009; 276:45. 34 Brilot F, Merheb V, Ding A, et al. Antibody binding to neuronal surface in Sydenham chorea, but not in PANDAS or Tourette syndrome. Neurology 2011; 76:1508. 35 Dale RC, Church AJ, Candler PM, et al. Serum autoantibodies do not differentiate PANDAS and Tourette syndrome from controls. Neurology 2006; 66:1612; author reply 1612. 36 Rippel CA, Hong JJ, Yoon DY, et al. Methodologic factors affect the measurement of anti-basal ganglia antibodies. Ann Clin Lab Sci 2005; 35:121. 37 Singer HS, Gause C, Morris C, et al. Serial immune markers do not correlate with clinical exacerbations in pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. Pediatrics 2008; 121:1198. 38 Loiselle CR, Lee O, Moran TH, Singer HS. Striatal microinfusion of Tourette syndrome and PANDAS sera: failure to induce behavioral changes. Mov Disord 2004; 19:390. 39 Pichichero M, Rochester General Hospital, 2011, personal communication. 40 Giuliano JD, Zimmerman A, Walkup JT, Singer HS. Prevalence of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection by history in a consecutive series of community referred children evaluated for tics. Ann Neurol 1998; 44:556. 41 Cardona F, Orefici G. Group A streptococcal infections and tic disorders in an Italian pediatric population. J Pediatr 2001; 138:71. 42 Johnson DR, Kurlan R, Leckman J, Kaplan EL. The human immune response to streptococcal extracellular antigens: clinical, diagnostic, and potential pathogenetic implications. Clin Infect Dis 2010; 50:481. 43 Murphy TK, Storch EA, Lewin AB, et al. Clinical factors associated with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Pediatr 2012; 160:314. 44 Singer HS, Giuliano JD, Zimmerman AM, Walkup JT. Infection: a stimulus for tic disorders. Pediatr Neurol 2000; 22:380. 45 Pichichero ME. The PANDAS syndrome. Adv Exp Med Biol 2009; 634:205. 46 Swedo SE, Rapoport JL, Leonard H, et al. Obsessive-compulsive disorder in children and adolescents. Clinical phenomenology of 70 consecutive cases. Arch Gen Psychiatry 1989; 46:335. 47 Leonard HL, Swedo SE, Lenane MC, et al. A 2- to 7-year follow-up study of 54 obsessive-compulsive children and adolescents. Arch Gen Psychiatry 1993; 50:429. 48 Perlmutter SJ, Garvey MA, Castellanos X, et al. A case of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. Am J Psychiatry 1998; 155:1592. 49 Bottas A, Richter MA. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Pediatr Infect Dis J 2002; 21:67. 50 Snider LA, Swedo SE. Pediatric obsessive-compulsive disorder. JAMA 2000; 284:3104. 51 Zohar AH. The epidemiology of obsessive-compulsive disorder in children and adolescents. Child Adolesc Psychiatr Clin N Am 1999; 8:445. 52 Snider LA, Seligman LD, Ketchen BR, et al. Tics and problem behaviors in schoolchildren: prevalence, characterization, and associations. Pediatrics 2002; 110:331. 53 Pichichero ME, Marsocci SM, Murphy ML, et al. Incidence of streptococcal carriers in private pediatric practice. Arch Pediatr Adolesc Med 1999; 153:624. 54 Murphy TK, Goodman WK, Ayoub EM, Voeller KK. On defining Sydenham's chorea: where do we draw the line? Biol Psychiatry 2000; 47:851. 55 Dale RC, Heyman I, Giovannoni G, Church AW. Incidence of anti-brain antibodies in children with obsessive-compulsive disorder. Br J Psychiatry 2005; 187:314. 56 Scolnick B. Pediatric autoimmune neuropsychiatric disorders associated with streptococcus. Pediatrics 2009; 123:e171; author reply e171. 57 Garvey MA, Perlmutter SJ, Allen AJ, et al. A pilot study of penicillin prophylaxis for neuropsychiatric exacerbations triggered by streptococcal infections. Biol Psychiatry 1999; 45:1564. 58 Budman C, Coffey B, Dure L, et al. Regarding "antibiotic prophylaxis with azithromycin or penicillin for childhood-onset neuropsychiatric disorders". Biol Psychiatry 2005; 58:917; author reply 918.
  17. Re: this line-- "Another thing I have noticed is that it only happens when we are home, this makes me believe this is psychological in nature." I would not be quick to dismiss as psychological. My DS had big time tics and OCD and was pretty good at holding everything in during school only of ourse to have a huge outbreak once he got home. If anything was psychological about that it was him using mind over matter and probably every bit of psychic energy to restrain himself during school. I also did ERP with him and he later told me that when we initially did it, he would go afterwards and hide himself in a closet where he frentically ticced.
  18. DD doesn't like the test of prednisone so I split with a pill splitter and insert into empty gel caps I bought at Whole Foods. This works great and perhaps could be done with probiotics that have a bad taste but which you find effective.
  19. I don't know him, but wanted to say that my DD's new PCP spent a number of years at JHU in rheumatology befoe going into private practice a couple of years ago--she seems very open to Pandas, although the test will really come when I see if she is willing to give long-term antibiotics. I think Singer in neurology is the JHU loci of Pandas naysaying--it could be it doesn't spill over to all the disciplines. Perhaps you could call the immunology and allergy clinic and ask if they deal with Pandas--occasionally one gets someone who is willing to chat. Just curious--why no vaccine challenge? Concern it could worsen the Pandas?
  20. Thanks for all the replies. The pneumonia was major--she was in hospital for six days: they still were treating very seriously in our two trips to the ER this month. She has been on steroids as on both trips she also had major asthma attacks (her lips were blue the second time). The first time she was given 60 mg of prednisone for 6 days and the second time 40 mg for 5 days, with a taper ordered by her PCP, which we started today. I didn't see an improvement the first time, but clearly she was coming down with something, culminating in 103 fever last Wednesday. Since her Wednesday trip to the ER, I have begun to see a real change for the better in mood starting Saturday, although her energy level remains very low and she continues to spend much of her day in bed. They didn't identify the pneumonia pathogen--in fact they said they were alternating their two big gun IV antibiotics to ensure as much as possible was covered. Interesting about the Avelox and hallucinations--didn't know that. Hers are longstanding so I don't think they are related, but I will definitely be on the alert as she is still on Avelox. Her ANA is fine. Her Babesia test was with an LLMD we saw briefly three years ago. He also tested for Lyme and said it was negative, but then added sometimes you have it and it doesn't test positive. (Yikes! Would really prefer not to have to deal with Lyme--controversy over treatment for that seems exponentially higher than that for Pandas/PANS!) I am adding streptozyme titer and strep serotype testing to my list. For Dr. L, I was planning to put the relevant results together in a short list and show it to her at the end for a recommendation. I think I can get another doctor to prescribe on the basis of what she says.
  21. My DS saw Dr. L in June--she suggested DD 19 be evaluated. Appointment not until October 2, but as she is quite nonfunctional now (always feeling unwell, ongoing gastric problems, pains in in legs and back, increasingly agoraphobic--rarely leaves house and is mostly in her room, very little appetite, two asthma attacks this month, in addition to severe pneumonia in May, as well as minor OCD and severe insect phobia, also occasional seizures and mysterious nonpsychotic hallucinations both visual and auditory for years) I wanted to do as much as I could in advance. Her new adult PCP seems interested in possible Pandas, but knows little about it. I have a few questions I hope someone can answer. DD's abnormal tests results from July 17: ASO 656 (Range 0-169) Anti DNase B 147 (Range 0-120) Note: She has not been tested for strep for three years and has significant recent abx history. May 9 to 17, 5 day Z pack for pneumonia. May 11-May 15 IV vancomycin and cefepime in hospital for necrotizing pneumonia. May 16-May 26 Avelox 400 mg. July 4-14 Avelox 400 mg for possible pneumonia flare. 7 day Avelox 400 mg again starting July 26 for same reason. IgE 197 (Range 5-159) CRP 22.42 (Rheumatological range 0-10, cardio range 0-3) Iron 47 (53-190) (Has problem with too frequent periods) Normal test results from tests showing up on Pandas Network and IOCDF sites : thyroid, vitamin D, IgA, IgM, and IGg. Question 1: Does this all look consistent with Pandas? Question 2: What other tests should I get? From Pandas network, looks like EBV, Mycoplasma pneumonia, Western Blot, Herpes Simplex, Stapholococus, CD4, and IgG subclasses 1,2,3 (what about 4?) She's had EBV, so I am not sure if there is any point in testing (she does get sweats and chills almost every night though). I also read testing for CMV, but she's tested positive for that in the past. In addition she once tested positive for Babesia--should I get that re-tested? Question 3: Should I get her ASO and anti-Dnase tested again? It's been two weeks since last test. If not now, when? Question 4: DS has post T and A appointment with Dr. L on August 8. Any views on previewing DD test results with her then for opinions on abx teatment pending October 2 appointment? Other option for early treatment would be to have her P doc, who is at NIH but sees patients on the side and knows Swedo and colleagues, consult with his NIH colleagues for a recommended course of action. Much thanks for any advice.
  22. Kimflow, Thanks for the message of urgency, whether this is post T and A flare or new strep from his sister. (He has long history of symptomless strep that cultures positive.) I am wondering whether its worth culturing to see if this is new strep and whether it would be beside the point to get ASO, antDnase B. Ko's Mom
  23. Ds's tics changed over the course of a post-strep out break and also changed from one outbreak to another. One outbreak was purely tics, another purely OCD, and others a combination of the two.
  24. DS, 22, has had Pandas since he was 6. No incidents during high school, but came back twice in college after strep. We saw Dr. L in June, who recommended T and A, which he had three weeks ago with Dr. H. Pending operation, Dr. L gave him clindamycin 300 mg 3 X day. After oral amoxicilling following T and A, I had him continue the clindamycin but we ran out. I called Friday for a refill but Dr. L was out and I was told to call back Monday. After T and A he told me he thought he still needed the antibiotic, but would not admit to OCD (too old to tell me?). Yesterday, DD 19 told me he came to her for some makeup to cover up redness on his hands. This is old OCD, almost BDD, where he thinks his hands are so red people are staring at them. Needless to say, he has a bit of pinkness on his knuckles that is absolutely nothing out of the ordinary. (When he had this two years ago at college, he finally admitted to me suicidal ideation--I had to fly up to his college and put him in ER to get temporary psych admission.) Yesterday and today, I have noticed him muttering to himself and today random exclamations of *******, a racist term. Am feeling sickening sense of deja vu. A few days ago I noticed a red rash on the back of his neck extending into upper back,perhaps 3 inches by 2--still there, but fading a bit. Was worried about strep but he agreed to go to PCP for strep only if it got worse. (I was being too dramatic.) Then saw a small rash on his back and another small one on his chest. In June, Dr. L suggested DD get evaluated, but next opening not until beginning of October. In meantime, tried to get ball roling with her new PCP. She has rheumatology background and is not dismissive of Pandas (relief as she has JHU training) but also knows little about it. DD's results came in Friday. ASO at 684 and antiDnase B at 146 (upper limit on test 125). (Don't have exact numbers as copying machine broken--was going to get tomorrow to post for advice on further testing.) DD hasn't been tested for strep for nearly two years, but brother had it last September. PCP thinks Pandas definite possibility. DD was in ER Wednesday for chills and high fever (103) with severe asthma attack (lips turned blue). I tried to get ER to test for strep but they didn't see need as glands and throat seemed fine (I did say family history of symptomless strep that tests positive). ER of course not ideal place to argue and they were much more focused on asthma and concern about recurrence of pneumonia (she was hospitalized six days in May for necrotizing pneumonia). They did a bunch of blood tests and found nothing; Xray showed "no clear sign of pneumonia." Nonetheless they gave her IV Avelox and prescription for seven days of Avelox 400 mg. What is next best step for DS (will try to sort out DD tomorrow)? Go to Pandas friendly ped (he referred us to Dr. L) tomorrow for strep culture and ASO, anti-Dnase B tests? Call Dr. L's office for abx refill (not sure clindamycin best choice at this point)? (He has post-op appt with her August 8--not sure how responsive she is between appts.) Wait until Wednesday when he has follow up T and A appt with Dr. H? Am feeling acute time pressure--DS scheduled to go back to college August 20--he can't afford to mess up another semester because of this wretched disorder. Much thanks for any and all advice. Ko's Mom
  25. I'd check for both narcolepsy and epilepsy--perhaps absence seizures? I have come across information that some epilepsy is autoimmune, which I find fascinating but haven't been able to get much information on it other than it is much less responsive to antiepileptic medications. My dd has been dx'ed with epilepsy and had a fair amount of breakthrough seizures on her AEDso I didn't fuss much when she reached a point where she strongly refused to take it. (Doctors are aghast at this, but at least she doesn't drive.) We are looking into possible PANDAS. It is pretty common to have more than one autoimmune condition--I think one could say having one autoimmune condition increases the likelihood of having another.
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