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We finally saw a top neurologist yesterday. He said my ds did not have PANDAS because his dnase titers where not high enough. I KNOW from everything I have read that he can still have PANDAS without elevated titers. My son has every PANDAS symptom except OCD and urinary issues. The doc did confirm he has chorea so I think he fits the PANDAS criteria. It is my understanding that he has to have OCD and or tics/choreiform movements plus some of the other long list of symptoms, but I have not read about any other patients who do not have OCD. Are there any of you out there? My ds does fixate on what ever activity he is interested to the point of obsession. He is using Star Wars as his current coping mechanism to handle his off the charts anxiety that is keeping him home bound out of school, but he does not have OCD rituals like excessive hand washing, etc type things. I guess I am looking for some assurance as I continue to press for this PANDAS diagnosis. My ds did show improvement with 14 days of augmentin. And when he went off the abx the symptoms came back! So he went back on augmentin 5 days later. I am just starting to see improvement now on his 9th day of augmentin. The neurologist said that said that the abx could not alleviate his symptoms because he did not have an active strep infection, and he said even if they did they would only treat the infection. From everything I have read I know this not to be true - that tons of kids have gotten better long after the strep infection was gone. The neurologist did want to test for almost a dozen other autoimmune diseases, and disorders that have chorea and anxiety as a symptom which could be helpful if I have it wrong and he does not have PANDAS. But I am still trusting my instinct and I am still thinking it is PANDAS. I am trying to get our pediatrician to test his dnase and aso again so we can see if anything as changed and also test for mycoplasma, herpes and mono. I would love any feed back from any of you parents who have been in the trenches much longer than me. Thanks!

I really need support in looking at this--any insights appreciated. This article, co-authored by Dr. Tanya Murphy mentions the possible effects of various antibiotics on autoimmune issues, and the section on Augmentin I am cutting and pasting below-- Is this saying that too much could be a real issue for some kids--making symptoms worse??? Please help me decipher! I tried cutting back on the 2000mg Augmentin, (back by 500 mg) and for 24 hours she was much better--then the next day raging out of control again. Psychotropic effects of antimicrobials and immune modulation by psychotropics: implications for neuroimmune disorders Demian Obregon, Ellisa Carla Parker-Athill, [...], and Tanya Murphy ..."Several antibiotic medications have been known to cause confusion, anxiety and depression and in some instances, psychosis [13]....Although unfavorable in a therapeutic context, these effects are often influenced by age, dosage, blood–brain barrier (BBB) permeability and drug interactions. Research into the mechanisms behind these effects may help to elucidate a therapeutic application. Penicillin for example was known to act on GABA receptors, a mechanism thought to be responsible for many of the side effects [14] '''Although the psychotropic effects of antibiotics are not commonly utilized therapeutically, the commonly associated side effects confirm their potential to influence CNS function. Several antibiotic medications have been known to cause confusion, anxiety and depression and in some instances, psychosis [13]. Although unfavorable in a therapeutic context, these effects are often influenced by age, dosage, blood–brain barrier (BBB) permeability and drug interactions. Research into the mechanisms behind these effects may help to elucidate a therapeutic application. Penicillin for example was known to act on GABA receptors, a mechanism thought to be responsible for many of the side effects [14]. Other classes of antimicrobial compounds, particularly the antimalaria treatment methylene blue and several antituberculosis drugs, have been shown to have monoamine oxidase (MAO) inhibitor (MAOI) properties. Similarly, many psychotropic drugs are known to have significant immunomodulatory effects, particularly agranulocytosis. While these effects are not considered therapeutically useful, it is important to understand, especially in light of recent knowledge of immune CNS interactions, how this interplay affects therapeutic efficacy and how it can be manipulated pharmacologically. Among those compounds with actual psychotropic activity, teasing out whether this activity is due to CNS neuroimmune modulation or resulting from direct effects on neurochemical function is often difficult. Despite these significant limitations, in this review some of the investigations attempting to characterize the dynamics of these compounds with multimodal effects in an effort to better understand their possible roles as preventatives, therapeutics and confounders are explored. From a clinical perspective the understanding of ‘off-target’ effects of antimicrobial agents can be critically important in the case of drug interactions and adverse reactions; however, also important, are mechanistic insights gleaned from existing compounds, whether formally antimicrobial or psychotropic, these can altogether aid in the discovery and development of new therapeutic targets and potentially new future preventatives and treatments. Infection, immune dysregulation & neuropsychiatric disordersAlthough the evidence supporting the role of infection and immune dysregulation in the pathogenesis of neuropsychiatric disorders seems significant, conflicting reports and a lack of clinical research has resulted in some reluctance to accept this as an etiological factor particularly in disorders such as PANDAS. Evidence from other disorders, however, point to a role for infection and potentially more importantly, the resulting immune disruptions in precipitating neuropsychiatric symptoms. In schizophrenia there is increasing evidence to support the role of specific pathogen exposure and resulting immune activation in precipitating the neuropsychiatric symptoms observed clinically. Several studies have alluded to a possible role for Toxoplasma gondii, a parasite commonly found in cat feces and of immense concern for pregnant women and is thought to infer increased risk for the disorder, possibly precipitating clinical symptoms. There have been findings of increased seroprevalence of toxoplasma antibodies in schizophrenic patients as well as observations that the parasite may affect dopamine signaling, a pathway commonly disrupted in schizophrenia [15,16]. The strong association of neuropsychiatric symptoms in autoimmune disorders and the mounting evidence to suggest antigenic mimicry as a central mechanism in infection-mediated neuropsychiatric symptoms strengthens the hypothesis of immune involvement, mediated by infection, in the appearance and progression of some neuropsychiatric disorders. In Grave's disease – an autoimmune disorder characterized by the production of excess thyroid hormones due to thyroid receptor autoantibody – anxiety, panic disorders and OCD are often associated and, in some rare cases, psychosis-like symptoms have also been reported [12,17]. Antimicrobial agents with psychotropic effects The role of the immune system and, more importantly, its dysregulation in neuropsychiatric disorders has not only hinted at a potential pathological mechanism but may also provide new therapeutic alternatives. Antimicrobial agents are an appealing class of compounds owing to their inherent immunomodulatory properties. In addition, several of these compounds have been shown to have direct CNS effects, which may further hint to their efficacy in the treatment of some neuropsychiatric disorders, particularly those with an established or proposed immunological component. β-lactams: penicillinβ-lactams are a class of antibiotic compounds with a cyclic amide ring, a β-lactam, as a core component of their molecular structure. While penicillin, named after the genus of the original producing mold, is the most prominent derivative, other members include cephalosporins, monobactams and carbapenems. β-lactams’ antimicrobial activity is attributed to the structure and activity of the β-lactam ring connected to a thiazolidine ring that binds and inhibits bacterial transpeptidase, thereby disrupting peptidoglycan synthesis necessary for the formation of the bacterial cell wall and, thus, preventing cell division. Other penicillin target proteins include holing-like proteins in the cell membrane of certain bacteria [18]. While primarily utilized for their antimicrobial activity, β-lactam antibiotics were found to promote the expression of the glutamate transporter GLT1 and have a neuroprotective role in vivo and in vitro when used in models of ischemic injury and motor neuron degeneration, suggesting significant neuroprotective properties [19]. Azithromycin (AZM) and penicillin have been utilized in the treatment of PANDAS, with observations of improvement in neuropsychiatric symptoms after 2–6 weeks of antibiotic treatment [20]. Although eradication of chronic latent, undetected GAS may be responsible for these observations via lowering antigenic load and immune activation, the potential for pleotrophic effects is possible given the effects on glutamate, immunomodulation and neuroprotection outside its antimicrobial actions. Given the potential role of glutamatergic therapies in OCD, depression, TBI, neurodegenerative disorders and schizophrenia, CNS-permeable β-lactams could be expected to exhibit efficacy in these neuropsychiatric disorders but further study is needed. In a recent study investigating the effects of cephalosporin in a mouse model of major depressive disorder, ceftriaxone, of the cephalosporin family, was shown to exhibit antidepressant properties increasing glutamate uptake, thought to be impaired in major depressive disorder [21]. Clavulanic acidClavulanate is a β-lactamase inhibitor commonly used in conjunction with amoxicillin to overcome antibiotic resistance provisioned by β-lactamase production by some bacteria, but has no significant antibacterial activity when used alone, despite containing a β-lactam ring. This structural similarity, however, is integral to its inhibitory mechanism allowing it to irreversibly bind to and inactivate bacterial β-lactamase [22]. Clavulanate readily crosses the BBB and has demonstrated anxiolytic properties in rodents and nonhuman primates [22]; a mechanism possibly due to increased dopamine release [23] or due to its possible effects on glutamate transmission through N-acetyl-l-aspartyl-l-glutamate (NAAG) peptidase inhibition. Specifically, clavulanate through NAAG-peptidase inhibition may decrease glutamate, enhance NAAG stability and consequently lead to greater metabotropic glutamate (mGlu)3 receptor (mGlu3R) activation. Known agonists of mGlu3R appear to display anxiolytic, antidepressant and neuroprotective properties in animals [24]. Moreover, mGlu3R activation is associated with reductions in glutamate release from the presynaptic neurons and decreased excitotoxic glutamate-mediated neuron damage [25]. Further, NAAG-mediated mGlu3R activation on glial cells appears to lead to release of trophic factors [26,27]. In accord, clavulanate enhances TGF-β release from glial cells possibly due to it's ability to inhibit NAAG peptidase [28]. Through reductions in glutamate, enhancements in dopamine and trophic factors, clavulanate displays significant potential as an antidepressant and anxiolytic agent. Phase IIb clinical trials for major depressive disorder are pending [23].