kim

brqwneyesmom, I'm wondering if this remark was in relationship to the findings regarding the corpus callosum or something else? These are a few things that you might want to become familiar with prior to your appointment with the neuro. I would also request a copy of the test results prior to the appt. so you can get a feel for the terms that he will be using and be able to ask specific questions regarding the results. These studies talk about TS with no emphasis on immune function (except possibly the last one with change in myelination). I guess a better place to look might be in regards to changes in corpus callosum relating to autoimmune disease or immune system function? http://www.psychgenetics.com/pt/re/psychge...1?nav=reference Abstract The aim of this study was to investigate the morphology of the corpus callosum (CC) in Tourette syndrome (TS) and attention deficit hyperactivity disorder (ADHD) to determine whether these conditions affect distinct regional differences.Seventy-seven children and adolescents, aged 6 to 16 years, comprised the four research groups--16 patients with TS, 21 patients with TS plus ADHD, 13 patients with ADHD, and 27 unaffected control subjects. A semiautomated, computer-assisted procedure was used to measure the total area, five subregions, centerline length, perimeter, and bending angle of the CC. MRI data were analyzed using several statistical methods, primarily two-tailed analysis of variance to test the effects of TS and ADHD status, while controlling for the influence of age, gender, and total intracranial area (an estimate of brain size). TS was associated with significant increases in the area of four of five subdivisions, the total area, and the perimeter of the CC. ADHD was associated with a significant decrease in the area of the rostral body. There were no interactions between TS and ADHD factors. These findings suggest that the area of the CC is larger in children with TS, and that this difference is independent of age, handedness, intracranial area, and the diagnosis of ADHD. Our findings support hypotheses that the neurobiologic mechanisms in TS and ADHD involve frontal/subcortical circuits. http://www.pubmedcentral.nih.gov/articlere...i?artid=2367151 Corpus callosum The corpus callosum (CC) has been a central focus in studying the biological correlates of TS since the early reports suggesting the presence of abnormal brain lateralization in the disorder. The unilateral character of the initial findings from the basal ganglia—i.e., decreased volumes of the left lenticular nucleus [52] and a loss of the physiological left-greater-than-right asymmetry of the basal ganglia [66]—raised the question of whether individuals with TS would exhibit loss of the normal asymmetric organization of the CNS [75]. In this respect, the CC is a structure of central interest because of the various roles it plays in lateralization of the brain [62]. First, the CC is thought to mirror brain asymmetry and hemispheric specialization [5]. Second, anatomical changes of the CC may represent indirect evidence for alterations in cortical tissue, especially for alterations of the frontal and prefrontal cortical areas, which send widespread, intertwined fibers through the genu and the body of the CC [29]. The first study of the CC in individuals with TS, which included 14 young adults with TS and 14 control subjects, revealed a reduced size of all subregions of the CC in the TS group compared with controls [51]. This study, however, did not include individuals with comorbid ADHD. A second study compared the size of the CC in 16 children with TS, in 21 children with TS-ADHD, in 13 children with ADHD only, and in 21 control children [7]. The group with TS alone had a larger CC on average, whereas the group with comorbid TS-ADHD had an intermediate CC size, and the group with ADHD alone had a reduced CC size. To evaluate the effect of gender on CC size in TS, another study included 10 girls with TS, 9 girls with a comorbid TS-ADHD, and 22 control girls [46]. The absence of differences in CC size across diagnostic groups was interpreted as indicating that differences in the size of the CC in the TS group were restricted to boys. These studies shared the disadvantage of not having realigned midsagittal MR images prior to measuring the CC [59]. The failure to realign midsagittal slices when defining the CC may increase inter-individual differences in measurement of its size, simply because of differences in midline placement of the heads of subjects in the scanner. The most recent study of CC size [58] examined 158 subjects with TS and 121 controls (5 to 65 years of age) in a cross-sectional design using CCs realigned to true midline. Subjects with TS had smaller overall CCs compared with controls. These reductions in size were found to depend significantly on the age of the subject, with smaller CCs present primarily in children with TS compared with healthy control children and larger CCs primarily in adults with TS compared with healthy adults. The sizes of the CC and its subregions correlated with the severity of motor tics, indicating that a smaller CC may have a protective or compensatory function in subjects with TS. Having a smaller CC could therefore represent a compensatory, plastic response to the presence of tics, similar to the postulated role of the larger prefrontal cortex found in children with TS. Furthermore, CC size correlated inversely with volumes of the prefrontal cortex in both the TS and control groups, although the magnitudes of these inverse correlations were significantly greater in the TS group. This exaggeration presumably represented an adaptive or compensatory process in the brains of individuals with TS, given that smaller CCs and larger prefrontal cortices were both associated with less severe tic symptoms. The putative plastic process that produced a smaller CC may have reduced excitatory input from the CC to the inhibitory GABAergic interneurons in the prefrontal cortex [9, 36]. This postulated reduction in numbers of inhibitory GABAergic interneurons would produce enhanced prefrontal output (because the prefrontal cortex receives less transcallosal inhibition), which in turn may increase the suppression of tics (which are themselves mediated through fronto-striatal connections). Over time, the prefrontal cortex may become hypertrophic because of frequent use, thereby enhancing the prefrontal self-regulatory control in persons with TS. As an alternative explanation, a smaller CC in children with TS may signal a less severe form of TS and produce an outcome with fewer tic symptoms, and hence it could have a protective function in the disorder. A larger CC and smaller prefrontal regions, in contrast, would signal the presence of a more severe form of TS. The positive associations of CC size with tic severity in this study do not support this latter alternative; however, its cross-sectional design prevents definitive support for one or the other of the two hypotheses. Findings of smaller CCs in subjects with TS have recently been extended to the fiber tracts that compose the CC as measured by Diffusion Tensor Imaging (DTI) in 20 boys with TS (5 boys with a comorbid ADHD) and 20 control boys (aged 10–18 years) [57]. DTI measurements [6] showed that boys with TS had lower Fractional Anisotropy values in all regions of the CC. The degree of anisotropy depends both on the number of fibers and on the thickness of the myelin sheaths that surround nerve fibers [48]. Recent studies document the correlation of the degree of myelination with changes of anisotropy, as measured by DTI during brain maturation in infants and toddlers [27]. Thus, these DTI findings again point to the presence of reduced interhemispheric connectivity in children with TS. A comorbid diagnosis of ADHD did not influence the findings, as shown by excluding all individuals with ADHD (and with OCD) from statistical analyses. The impetus for examining the CC in TS stemmed from previous reports of reduced structural brain asymmetry of the basal ganglia in patients with TS. The hypothesis of abnormal functional brain lateralization, however, has not been confirmed in subsequent studies or in other reports studying anatomical and functional brain lateralization in TS [41, 54, 55]. Reported findings of morphometric and functional deviations of callosal measures [41, 57, 58] are, however, consistent with findings that implicate prefrontal brain regions in tic suppression in TS [53, 54]. bolding mine http://www.pubmedcentral.nih.gov/articlere...i?artid=1738899 Corpus callosum signal intensity in patients with bipolar and unipolar disorder Conclusions: The findings suggest abnormalities in corpus callosum white matter in bipolar but not unipolar patients, possibly because of altered myelination. Such abnormalities could lead to impaired interhemispheric communication in bipolar disorder.

Hey guy, I ran across this and thought the "Anticholinergic" part interesting. http://www.eliminatesweating.com/hyperhidr..._treatment.html hyperhidrosis Anticholinergic Medications Anticholinergic medications aim to suppress the cholinergic stimulation of the eccrine sweat glands by the sympathetic nerve trunks to eliminate or reduce excessive sweating. Anticholinergic agents such as such as propantheline bromide, glycopyrrolate, oxybutynin and benztropine may be effective in treating hyperhidrosis. However, they can cause significant adverse effects, which include blurry vision, dry mouth and dry eyes, thus limiting their usefulness.

Colleen, Are the bumps flesh colored or inflammed? There is one related condition, Pityriasis Rubra Pilaris, that does mention strep, but most of the pictures look like a lot more of a severe condition than just Keratosis Pilaris. I think some of the google image pictures might be the more striking or dramatic pics. Since keratosis pilaris is so common, it's hard to know whether it's significant or not. I know my youngest son turned orange from head to toe around 1 yr old. I was told by ped that my oldest son had keratosis rash (just looked like a rash, nothing dramatic)on his face at one point, and I have had this infection induced skin thing now. I also just had some red bumps break out on my leg. Before they turned red, they were just flesh colored. I had stopped taking my 3 fish oil per day, when that happened. If there were a higher incidence of this with PANDAS or non PANDAS with tics, would be interesting to know, again for the relationship btwn vit D, A, and possibly fatty acid metabolism? Christie mentioning a mild scalp outbreak of psoriasis with her son during a PANDAS exacerbation, really makes me wonder if there is an overlap here for some. http://emedicine.medscape.com/article/1107742-overview Case reports have described PRP occurring after streptococcal infections http://yourtotalhealth.ivillage.com/kerato...l%3FpageNum%3D2 Keratosis Pilaris Images http://images.google.com/imgres?imgurl=htt...sa%3DG%26um%3D1 http://images.google.com/imgres?imgurl=htt...sa%3DG%26um%3D1 Vit A article http://www.innvista.com/health/nutrition/vitamins/a.htm

Indigo, I know there are a bunch of herbal supplements recommended for clearing strep on Dr. Amy Yasko's forum. I don't know if turmeric/curcumin is one of them or not. I have also seen it recommended for anti inflammatory purposes, but it's ability to selectively inhibit phosphorlase kinase, was research that I found specifically regarding psoriasis and wondered if that property could be helpful in PANDAS situations. As far as I know, it doesn't have any anti bacterial properties (edit article posted below does mention anti bacterial properties), it would work more to shut down a process that is triggered by the strep anti bodies cross reacting with neuronal tissue (big maybe), so it may only be helpful in conjunction with anti biotics? I'm also interested in the gastro effects. My youngest son keeps me on pins and needles with IBS type of symptoms. Here are some more articles. http://www.healthymuslim.com/articles/qvtm...-in-tumeric.cfm http://www.ncbi.nlm.nih.gov/pubmed/1756920...ogdbfrom=pubmed Curcumin: the Indian solid gold.Aggarwal BB, Sundaram C, Malani N, Ichikawa H. Department of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA. aggarwal@mdanderson.org Turmeric, derived from the plant Curcuma longa, is a gold-colored spice commonly used in the Indian subcontinent, not only for health care but also for the preservation of food and as a yellow dye for textiles. Curcumin, which gives the yellow color to turmeric, was first isolated almost two centuries ago, and its structure as diferuloylmethane was determined in 1910. Since the time of Ayurveda (1900 Bc) numerous therapeutic activities have been assigned to turmeric for a wide variety of diseases and conditions, including those of the skin, pulmonary, and gastrointestinal systems, aches, pains, wounds, sprains, and liver disorders. Extensive research within the last half century has proven that most of these activities, once associated with turmeric, are due to curcumin. Curcumin has been shown to exhibit antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anticancer activities and thus has a potential against various malignant diseases, diabetes, allergies, arthritis, Alzheimer's disease, and other chronic illnesses. These effects are mediated through the regulation of various transcription factors, growth factors, inflammatory cytokines, protein kinases, and other enzymes. Curcumin exhibits activities similar to recently discovered tumor necrosis factor blockers (e.g., HUMIRA, REMICADE, and ENBREL), a vascular endothelial cell growth factor blocker (e.g., AVASTIN), human epidermal growth factor receptor blockers (e.g., ERBITUX, ERLOTINIB, and GEFTINIB), and a HER2 blocker (e.g., HERCEPTIN). Considering the recent scientific bandwagon that multitargeted therapy is better than monotargeted therapy for most diseases, curcumin can be considered an ideal "Spice for Life". http://www.ncbi.nlm.nih.gov/pubmed/1841366...ogdbfrom=pubmed Inhibition of Nod2 signaling and target gene expression by curcumin.Huang S, Zhao L, Kim K, Lee DS, Hwang DH. Western Human Nutrition Research Center, United States Department of Agriculture, Agricultural Research Service, Davis, CA 95616, USA. Nod2 is an intracellular pattern recognition receptor that detects a conserved moiety of bacterial peptidoglycan and subsequently activates proinflammatory signaling pathways. Mutations in Nod2 have been implicated to be linked to inflammatory granulomatous disorders, such as Crohn's disease and Blau syndrome. Many phytochemicals possess anti-inflammatory properties. However, it is not known whether any of these phytochemicals might modulate Nod2-mediated immune responses and thus might be of therapeutic value for the intervention of these inflammatory diseases. In this report, we demonstrate that curcumin, a polyphenol found in the plant Curcuma longa, and parthenolide, a sesquiterpene lactone, suppress both ligand-induced and lauric acid-induced Nod2 signaling, leading to the suppression of nuclear factor-kappaB activation and target gene interleukin-8 expression. We provide molecular and biochemical evidence that the suppression is mediated through the inhibition of Nod2 oligomerization and subsequent inhibition of downstream signaling. These results demonstrate for the first time that curcumin and parthenolide can directly inhibit Nod2-mediated signaling pathways at the receptor level and suggest that Nod2-mediated inflammatory responses can be modulated by these phytochemicals. It remains to be determined whether these phytochemicals possess protective or therapeutic efficacy against Nod2-mediated inflammatory disorders. research update with bunch of studies http://www.mdidea.com/products/new/new088research.html psoriasis specific http://www.ncbi.nlm.nih.gov/pubmed/7511111 Curcumin is a non-competitive and selective inhibitor of phosphorylase kinase http://www.ncbi.nlm.nih.gov/pubmed/1106950...ogdbfrom=pubmed Drug-induced suppression of phosphorylase kinase activity correlates with resolution of psoriasis as assessed by clinical, histological and immunohistochemical parameters.

http://www.ncbi.nlm.nih.gov/pubmed/17075840 Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis.Funk JL, Frye JB, Oyarzo JN, Kuscuoglu N, Wilson J, McCaffrey G, Stafford G, Chen G, Lantz RC, Jolad SD, Sólyom AM, Kiela PR, Timmermann BN. University of Arizona, Tucson, USA. jfunk@u.arizona.edu OBJECTIVE: Scientific evidence is lacking for the antiarthritic efficacy of turmeric dietary supplements that are being promoted for arthritis treatment. Therefore, we undertook studies to determine the antiarthritic efficacy and mechanism of action of a well-characterized turmeric extract using an animal model of rheumatoid arthritis (RA). METHODS: The composition of commercial turmeric dietary supplements was determined by high-performance liquid chromatography. A curcuminoid-containing turmeric extract similar in composition to these supplements was isolated and administered intraperitoneally to female Lewis rats prior to or after the onset of streptococcal cell wall-induced arthritis. Efficacy in preventing joint swelling and destruction was determined clinically, histologically, and by measurement of bone mineral density. Mechanism of action was elucidated by analysis of turmeric's effect on articular transcription factor activation, microarray analysis of articular gene expression, and verification of the physiologic effects of alterations in gene expression. RESULTS: A turmeric fraction depleted of essential oils profoundly inhibited joint inflammation and periarticular joint destruction in a dose-dependent manner. In vivo treatment prevented local activation of NF-kappaB and the subsequent expression of NF-kappaB-regulated genes mediating joint inflammation and destruction, including chemokines, cyclooxygenase 2, and RANKL. Consistent with these findings, inflammatory cell influx, joint levels of prostaglandin E(2), and periarticular osteoclast formation were inhibited by turmeric extract treatment. CONCLUSION: These translational studies demonstrate in vivo efficacy and identify a mechanism of action for a well-characterized turmeric extract that supports further clinical evaluation of turmeric dietary supplements in the treatment of RA.

Cris, My boys have a BIG strep history, but I have never considered them PANDAS due mostly to lack of abrupt onset. My youngest son does have some OCD, my oldest son only seems to exhibit it during some tic flairs. I have psoriasis, altho I've never paid any attention to it until recently. Just a spot on my elbow and a little at hair line on back of my neck, until I had this full body rash that correlated with infected elbow. My youngest son has some small bumps on one elbow. It doesn't look like psoriasis at this point, but now I'm a little concerned. I was looking at the relationship btwn vit A and D which can be involved in psoriasis ( I believe both the boys and I have a problem in this area) this morning. A deficiency in vit A can be involved here Rhodopsin http://en.wikipedia.org/wiki/Rhodopsin and a vit D deficiency can result in a vit A deficiency (my take so far). Wonder if anyone else thinks this could be involved in photosensitivity and some of these "color" issues? Looks interesting, but I haven't spent enough time, to see if it really makes sense Also, wanted to mention that during a strep infection last year with what I think was an explosive stomach virus at the same time, my youngest son complained of unwanted thoughts and everything "looking green." He was sitting in the Dr.s office looking out the window on a gloomy, cloudy afternoon. He kept insisting everything looked green. He was really really sick. Wanted to ask if anyone has ever noticed anything that looks like "chicken skin," on their children? Again, looking at vit A and D and something called keratosis pilaris. http://en.wikipedia.org/wiki/Keratosis_pilaris didn't know whether to post this on strep/psoriasis, vit d thread or what. If anyone cares to discuss anthing other than the "light" issues, maybe we could move to more appropriate thread.

I'm using turmeric as an antiinflam and because there is some research showing that it might be beneficial in controlling psoriasis (down regulating phosphorylase kinase). I have been trying to figure out if this might be helpful in PANDAS cases. I ran across this study (2nd one) and thought the fact that genistein, a component of soy, was capable of inhibiting invasion of strep was interesting. I'm really really not a fan of soy. fed my boys soy infant formula and wish i wouldn't have, but ths was interesting non the less. EA mom, if your reading, I'm wondering if Buster could take a look at this. I know he's very familiar with the Pandas studies and would luv his input here. http://www3.interscience.wiley.com/journal...262209/abstract ABSTRACT Summary To determine whether abnormal activity of a calmodulin-containing enzyme which catalyses phosphorylation reactions may play a pathogenetic role in psoriasis, the presence and activity of phosphorylase kinase (PK) in human epidermis were determined in patients with untreated/active psoriasis (n=10), treated/resolving psoriasis (n= 10), and non-psoriatic controls (n= 10). Biopsies were taken from involved and uninvolved skin for PK, organic phosphorus, and inorganic phosphate estimation, and light and electron microscopy. The enzyme was present in involved and uninvolved skin of every patient in the study. PK activity (units/mg protein) was significantly higher in active psoriasis than in resolving psoriasis and controls. PK activity correlated directly with organic phosphorus levels, and inversely with the extent of cellular glycogenolysis measured by the depletion of glycogen granules within the keratinocytes. The study demonstrates that PK is present in both psoriatic and normal epidermis, with significantly higher levels in active psoriasis. Furthermore, higher levels of PK activity, glycogenolysis and phosphorylation are associated with increased clinical psoriatic activity. We conclude that PK, a calmodulin-containing enzyme, is involved in regulating calcium-dependent phosphorylation events in human epidermis, and disturbance of its activity may play a key role in the clinical manifestations of psoriasis. bolding mine http://jem.rupress.org/cgi/content/abstract/186/10/1633 Regulation of the Phosphorylation of Human Pharyngeal Cell Proteins by Group A Streptococcal Surface Dehydrogenase: Signal Transduction between Streptococci and Pharyngeal Cells By Vijaykumar Pancholi and Vincent A. Fischetti From the Laboratory of Bacterial Pathogenesis and Immunology, The Rockefeller University, 1230 York Avenue, New York, New York 10021 Whether cell-to-cell communication results when group A streptococci interact with their target cells is unknown. Here, we report that upon contact with cultured human pharyngeal cells, both whole streptococci and purified streptococcal surface dehydrogenase (SDH) activate pharyngeal cell protein tyrosine kinase as well as protein kinase C, thus regulating the phosphorylation of cellular proteins. SDH, a major surface protein of group A streptococci, has both glyceraldehyde-3-phosphate dehydrogenase and ADP-ribosylating enzyme activities that may relate to early stages of streptococcal infection. Intact streptococci and purified SDH induce a similar protein phosphorylation pattern with the de novo tyrosine phosphorylation of a 17-kD protein found in the membrane/particulate fraction of the pharyngeal cells. However, this phosphorylation required the presence of cytosolic components. NH2-terminal amino acid sequence analysis identified the 17-kD protein as nuclear core histone H3. Both phosphotyrosine and phosphoserine-specific monoclonal antibodies reacted with the 17-kD protein by Western blot, suggesting that the binding of SDH to these pharyngeal cells elicits a novel signaling pathway that ultimately leads to activation of histone H3-specific kinases. Genistein-inhibitable phosphorylation of histone H3 indicates that tyrosine kinase plays a key role in this event. Treatment of pharyngeal cells with protein kinase inhibitors such as genistein and staurosporine significantly inhibited streptococcal invasion of pharyngeal cells. Therefore, these data indicated that streptococci/SDH-mediated phosphorylation plays a critical role in bacterial entry into the host cell. To identify the membrane receptor that elicits these signaling events, we found that SDH bound specifically to 30- and 32-kD membrane proteins in a direct ligand-binding assay. These findings clearly suggest that SDH plays an important role in cellular communication between streptococci and pharyngeal cells that may be important in host cell gene transcription, and hence in the pathogenesis of streptococcal infection.

Well, I guess the good news would be, if we ever arrange a get together, noone will know who it is with the BO! I was joking in a PM with a member about my husband throwing me over for someone who wears lipstick (lead) drinks tap water and uses a cell phone. I now could probably add no curvature of the spine from excessive laptop use too! A neighbor who was diagnosed with breast cancer was told by her oncologist that the alum in deo contributing to BC was an internet rumor. A few Pub med articles didn't really reassure me a lot. Cheri, about that reaction.....I used to get a rough patch above my eye, when I was younger and used eyeshadow with sparkles. I recently read that those sparkles are alum. I suppose they probably use other material too, but the alum was interesting. I had a bracelet in about 6th grade that said Jesus Christ on it. I would get a horrible rash from it if I wore it too much. I always assemed it was nickle that I was reacting too, but you have to wonder. I don't know about the breast cancer involvement, but look at the language in this study (thinking of this being injected in infants). bolding mine http://www.ncbi.nlm.nih.gov/pubmed/1604599...ogdbfrom=pubmed Aluminium, antiperspirants and breast cancer. 1: J Inorg Biochem. 2005 Sep;99(9):1912-9. Links Aluminium, antiperspirants and breast cancer.Darbre PD. Division of Cell and Molecular Biology, School of Animal and Microbial Sciences, The University of Reading, P.O. Box 228, Whiteknights, Reading, RG6 6AJ, UK. p.d.darbre@reading.ac.uk Aluminium salts are used as the active antiperspirant agent in underarm cosmetics, but the effects of widespread, long term and increasing use remain unknown, especially in relation to the breast, which is a local area of application. Clinical studies showing a disproportionately high incidence of breast cancer in the upper outer quadrant of the breast together with reports of genomic instability in outer quadrants of the breast provide supporting evidence for a role for locally applied cosmetic chemicals in the development of breast cancer. Aluminium is known to have a genotoxic profile, capable of causing both DNA alterations and epigenetic effects, and this would be consistent with a potential role in breast cancer if such effects occurred in breast cells. Oestrogen is a well established influence in breast cancer and its action, dependent on intracellular receptors which function as ligand-activated zinc finger transcription factors, suggests one possible point of interference from aluminium. Results reported here demonstrate that aluminium in the form of aluminium chloride or aluminium chlorhydrate can interfere with the function of oestrogen receptors of MCF7 human breast cancer cells both in terms of ligand binding and in terms of oestrogen-regulated reporter gene expression. This adds aluminium to the increasing list of metals capable of interfering with oestrogen action and termed metalloestrogens. Further studies are now needed to identify the molecular basis of this action, the longer term effects of aluminium exposure and whether aluminium can cause aberrations to other signalling pathways in breast cells. Given the wide exposure of the human population to antiperspirants, it will be important to establish dermal absorption in the local area of the breast and whether long term low level absorption could play a role in the increasing incidence of breast cancer. http://www.ncbi.nlm.nih.gov/pubmed/1882942...ogdbfrom=pubmed [The use of deodorants/antiperspirants does not constitute a risk factor for breast cancer]

This article raises many questions in my mind one being, what of people who don't excrete aluminum as well as others. Does activating this type of response possibly train a developing immune system to respond differently than one that hasn't been exposed to alum? Can anyone believe that they are just getting around to looking at this. http://www3.niaid.nih.gov/news/newsrelease...lum_vaccine.htm Although alum has been used to boost the immune responses to vaccines for decades, no one has known how it works. Another study (which I haven't seen splashed all over the news). http://www.informaworld.com/smpp/content~c...ll~jumptype=rss

Your very welcome! Cheri has worked so tirelessly to advocate for more natural treatments for TS and related disorders, it made me twice as happy to be able to share that! Lyn, glad you found a Dr. that is open to something other than drugs. A neuro that we saw a few years back asked me if I thought that "they" were trying to cover up a cure for TS using vitamins. I wish I would have shot back that no i didn't think "they" were trying to cover it up, because "they" weren't looking. Here are some other studies that you might be interested in reading thru http://www.ncbi.nlm.nih.gov/pubmed/1882594...ogdbfrom=pubmed [Depression-like and anxiety-related behaviour of rats fed with magnesium-deficient diet][Article in Russian] http://www.ncbi.nlm.nih.gov/pubmed/1876739...ogdbfrom=pubmed Spasov AA, Iezhitsa IN, Kravchenko MS, Kharitonova MV. Magnesium (Mg) has been proposed to take part in biochemical dysregulation contributing to psychiatric disorders. [The characterization of central neuromediation in rats fed with magnesium-deprived diet before and after magnesium replenishment] http://www.ncbi.nlm.nih.gov/pubmed/1881943...ogdbfrom=pubmed [Effect of some organic and inorganic magnesium salts on lipoprotein state in rats fed with magnesium-deficient diet] Spasov AA, Iezgitsa IN, Kharitonova MV, Kravchenko MS. Low serum magnesium (Mg) concentrations have been reported in patients with atherosclerosis. http://www.ncbi.nlm.nih.gov/pubmed/1839928...ogdbfrom=pubmed Effect of magnesium chloride and magnesium L-aspartate on seizure threshold in rats under conditions of dietary magnesium deficiency.Spasov AA, Iezhitsa IN, Kharitonova MV, Kravchenko MS. Institute of Pharmacology, Department of Pharmacology, Volgograd State Medical University. farm@vlpost.ru http://www.ncbi.nlm.nih.gov/pubmed/1806216...ogdbfrom=pubmed Vitamin B6 related epilepsy during childhood.Wang HS, Kuo MF. Division of Pediatric Neurology, Chang Gung Children's Hospital, Taipei, Chang Gung University College of Medicine, Taoyuan, Taiwan. wanghs444@cgmh.org.tw http://www.ncbi.nlm.nih.gov/pubmed/1575314...ogdbfrom=pubmed Tocotrienol: the natural vitamin E to defend the nervous system?Sen CK, Khanna S, Roy S. Davis Heart & Lung Research Institute, 473 West 12th Avenue, The Ohio State University Medical Center, Columbus, Ohio 43210, USA. sen-1@medctr.osu.edu Vitamin E is essential for normal neurological function. It is the major lipid-soluble, chain-breaking antioxidant in the body, protecting the integrity of membranes by inhibiting lipid peroxidation. http://www.ncbi.nlm.nih.gov/pubmed/1806216...ogdbfrom=pubmed 1: Chang Gung Med J. 2007 Sep-Oct;30(5):396-401.Links Vitamin B6 related epilepsy during childhood.Wang HS, Kuo MF. Division of Pediatric Neurology, Chang Gung Children's Hospital, Taipei, Chang Gung University College of Medicine, Taoyuan, Taiwan. wanghs444@cgmh.org.tw In some patients without vitamin B6 deficiency, epilepsy can not be controlled without an extra supplement of vitamin B6. The therapeutic role of pyridoxal phosphate (PLP), the active form of vitamin B6, may not be replaced with other forms of vitamin B6 sometimes.

I wonder how many were in this study? http://www.ncbi.nlm.nih.gov/pubmed/1908782...Pubmed_RVDocSum An open study evaluating the efficacy and security of magnesium and vitamin B(6) as a treatment of Tourette syndrome in children][Article in Spanish] García-López R, Romero-González J, Perea-Milla E, Ruiz-García C, Rivas-Ruiz F, de Las Mulas Béjar M. Departamento de Anestesia y Reanimación. Hospital Costa del Sol. Marbella. Málaga. España. drgarcia.anest@telefonica.net BACKGROUND AND OBJECTIVE: We intended to ascertain the effectiveness and safety of oral solutions of magnesium and vitamin B(6) in alleviating the symptoms emerged during clinical exacerbations in children aged 7-14 years suffering from Tourette syndrome (TS). We also aimed to determine the mean and the standard deviation of such an improvement in order to estimate sample sizes in future assays with a control group. PATIENTS AND METHOD: The treatment under investigation was administered to children diagnosed with TS, in accordance with Diagnostic and Statistical Manual of Mental Disorders, fourth edition -IV, under conditions of clinical exacerbation. The effects were scored on the Yale Global Tics Severity Scale (YGTSS) at 0, 15, 30, 60 and 90 days. RESULTS: The total tics score decreased from 26.7 (t0) to 12.9 (t4) and the total effect on the YGTSS was a reduction from 58.1 to 18.8. Both results were statistically significant. With respect to the application of conventional treatment or otherwise, no significant differences were observed. No side effects were seen. CONCLUSIONS: The treatment assayed is safe and effective in reducing the harmful effects of TS in children. Further studies are needed, with a control group, and evaluation of different doses of the drugs.

This sounds an awful lot like PANDAS to me, except the reaction is btwn skin cells and strep. The first study that discusses "peptidoglycan" i believe would implicate N acetylglucosamine in psoriasis related strep reactions, as has been found in PANDAS. Just pulled a couple of excerpts from wiki on peptidoglycan. The first study is dated 2008, so one of the more recent. from wiki http://en.wikipedia.org/wiki/Peptidoglycan Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria, forming the cell wall. The sugar component consists of alternating residues of β-(1,4) linked N-acetylglucosamine and N-acetylmuramic acid residues. Attached to the N-acetylmuramic acid is a peptide chain of three to five amino acids. The peptide chain can be cross-linked to the peptide chain of another strand forming the 3D mesh-like layer. and N-Acetylmuramic acid, or MurNAc, is the ether of lactic acid and N-acetylglucosamine with a chemical formula of C11H19NO8. It is part of a biopolymer in the bacterial cell wall, built from alternating units of N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc), cross-linked with oligopeptides at the lactic acid residue of MurNAc. This layered structure is called peptidoglycan. 2008 http://www.ncbi.nlm.nih.gov/pubmed/1704584...ogdbfrom=pubmed Peptidoglycan: a major aetiological factor for psoriasis?Baker BS, Powles A, Fry L. Department of Dermatology, Faculty of Medicine, Imperial College, St Mary's Campus, London W2 1PG, UK. drbsbaker@aol.com Peptidoglycan (PG), a major cell-wall component of Gram-positive bacteria, has been detected within antigen-presenting cells in various inflammatory conditions, including psoriasis. The additional presence of T-helper 1 cells specific for streptococcal or staphylococcal PG in psoriasis skin lesions implicates PG as an important T-cell stimulator for the disease. PG is a major target for the innate immune system, and associations between genetic polymorphisms of recognition receptors for PG and various auto-inflammatory diseases have been identified. The location of these genes within four linkage sites for psoriasis raises the possibility that an altered innate recognition of PG might contribute to the enhanced T-cell response to the bacterial antigen. These observations suggest that PG is a major aetiological factor for psoriasis and emphasize the importance of PG in bacterial-infection-induced inflammatory disease. 2006 excerpt http://www.ncbi.nlm.nih.gov/pubmed/16493599 Peptidoglycan and peptidoglycan-specific Th1 cells in psoriatic skin lesions.Baker BS, Laman JD, Powles A, van der Fits L, Voerman JS, Melief MJ, Fry L. Department of Dermatology, Faculty of Medicine, St Mary's campus, Imperial College, London, UK. We have previously demonstrated, in psoriatic skin lesions, the presence of a subset of dermal CD4+ T cells that produce interferon-gamma (IFN-gamma) in response to a mixture of cell wall proteins extracted from group A streptococci. However, the identity of the antigen(s) involved is unknown. To investigate the hypothesis that peptidoglycan (PG), the major constituent of the streptococcal cell wall, acts as a T cell activator in psoriasis, we performed in situ analysis to detect antigen-presenting cells containing PG in lesional versus non-lesional skin, and determined proliferation and IFN-gamma responses of lesional skin T cells. Increased numbers of PG-containing cells were detected in the dermal papillae and cellular infiltrates of guttate and chronic plaque skin lesions compared with normal and non-lesional psoriatic skin2002 http://www.ncbi.nlm.nih.gov/pubmed/12443847 CD4+ T-cells from peripheral blood of a patient with psoriasis recognize keratin 14 peptide but not 'homologous' streptococcal M-protein epitope.Kobayashi H, Takahashi M, Takahashi H, Ishida-Yamamoto A, Hashimoto Y, Sato K, Tateno M, Iizuka H. Department of Pathology, Asahikawa Medical College, 2-1-1 Midorigaoka-Higashi, Asahikawa, Japan. Psoriasis has been recognized as an immunologically mediated inflammatory skin disease that has been associated with group A, beta-haemolytic streptococcal infections. Notably cross-reactive autoimmune mechanism, which is mediated by T cells reacting to epitopes that are common to streptococcal M-protein and keratin, has been proposed in psoriasis. In order to investigate this possibility, peptides corresponding to M-protein and human epidermal keratin, which share some amino acid sequence between them, were synthesized and tested for their ability to stimulate T-cells of patients with psoriasis. Among five cases examined, we isolated a CD4(+) T-cell line that recognized the type I keratin (K14)(p168-181) when it was presented by the patient's HLA-DR molecules from a single psoriatic patient, whose MHC allele was HLA-A2/A26, -B27/B16, -DR4/DR8, -DQ8. Further analysis disclosed that the critical peptide recognized by the T-cell line was 10-mer keratin(p171-180) (DLRNKILTAT). However, corresponding M6 protein with homology to K14 did not stimulate the T-cell response and no evidence for cross-reactivity was obtained. The K14-responsive T cell line produced IFN-gamma, but little IL-4 when stimulated with irradiated autologous PBMC pulsed with this peptide. Thus, the finding that human epidermal keratin peptide is immunogenic in a psoriasis patient may provide the evidence that T lymphocytes play an important role in the pathogenesis of psoriasis as an autoimmune disorder participated with Th1 like cells. However, the keratin-responsive T cell line was detected in only one of five cases of psoriasis examined, suggesting that such T cell line appears to be not so popular in psoriatic patients. No evidence for cross-reactivity to streptococcal M protein also suggests that the contribution of streptococci may simply be inducing proliferation of various repertoire of T cells (including K14-responsive T cells) possibly through a superantigen-dependent process. http://www.ncbi.nlm.nih.gov/sites/entrez?D...Search=17344934 Invest Dermatol. 2007 Jun;127(6):1337-42. Epub 2007 Mar 8. Links Increased blood levels of IgG reactive with secreted Streptococcus pyogenes proteins in chronic plaque psoriasis.El-Rachkidy RG, Hales JM, Freestone PP, Young HS, Griffiths CE, Camp RD. Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK. A pathogenic role for Streptococcus (S) pyogenes infections in chronic plaque psoriasis is suspected but poorly defined. We separated cellular and supernatant proteins from S. pyogenes cultures by high-resolution two-dimensional gel electrophoresis, and used immunoblotting to demonstrate the diversity of serum or plasma IgGs that react with elements of the proteome of this bacterium. We have shown that a substantial proportion of IgG-reactive proteins from cultured S. pyogenes are secreted. The total secreted protein fraction, including diverse IgG-binding elements, was subsequently used in an ELISA to measure blood titers of reactive IgG. This ELISA showed that blood samples from patients with chronic plaque psoriasis contained significantly higher titers of reactive IgG than samples from age- and sex-matched healthy controls (P=0.0009). In contrast, neither a standard assay measuring antistreptolysin O titers nor ELISAs measuring titers of IgG reactive with protein fractions from Staphylococcus aureus and Staphylococcus epidermidis, were able to distinguish between blood samples from the two groups. These findings justify the hypothesis that S. pyogenes infections are more important in the pathogenesis of chronic plaque psoriasis than has previously been recognized, and indicate the need for further controlled therapeutic trials of antibacterial measures in this common skin disease. http://www.ncbi.nlm.nih.gov/pubmed/10725825 A 23-year-old man had small desquamative erythematous lesions, round or oval in shape, spread over his entire body, and diagnosed as psoriasis guttate acuta because of clinical and pathological findings. Three weeks before the lesions had started, he was diagnosed as having varicella by his family physician. The psoriatic lesions appeared at the same sites where previously lesions of varicella had appeared. Therefore, VZV infection was regarded as a trigger in this case. We speculate that genetic factors and the change of skin condition are basically involved in the pathogenesis of psoriasis guttate. In addition, one more factor as a trigger is needed to cause the lesions of psoriasis. VZV infection might change the skin condition and induce subsequent immunological disregulation.

Carolyn, If it got to the point that it was really intolerable, do you think a cervical collar might work? I had considered that when my oldest son was in the throws of headshaking that I thought was going to really harm him.

Just posted this on the PANDAS forum, but wanted to know if anyone here has any remarks too. Copy of post...... Wondering if anyone has any comments on this. I have a history of heart palpatations. It started in about 6th grade. The first is from the article that browneyesmom posted recently and something that I was trying to get a handle on a while back (the CaM kinases stuff). I found this article when researching my strep induced psoriasis outbreak. I have a few studies on that, will be posting. I'm having a hard time thinking that this is just a coincidence and remember, I have never considered my boys PANDAS due to the lack of "explosive onset." Anyway....... http://www.cpementalhealth.com/content/4/1/13 Other putative pathogenetic mechanisms of PANDAS include molecular mimicry and autoimmune-mediated altered neuronal signaling, involving calcium-calmodulin dependent protein (CaM) kinase II activity. http://www.medicalnewstoday.com/articles/106098.php Study Identifies New Mechanism Linking Activation Of Key Heart Enzyme And Oxidative Stress The UI researchers and colleagues from Vanderbilt University in Nashville, Tenn., focused on calmodulin kinase II, or CaM kinase II, a well-studied enzyme critical to many fundamental processes including heartbeat and thought. Scientists know that CaM kinase's activity is sustained by adding a phosphate group -- a process known as phosphorylation. The new study proves that oxidation -- adding oxygen -- also can sustain the enzyme's activity, and like phosphorylation, the mechanism can be reversed to inactivate the kinase. "Our results suggest that oxidation of CaM kinase is a dynamic and reversible process that may direct cell signaling in health and disease," said Mark Anderson, M.D., Ph.D., UI professor of internal medicine and molecular physiology and biophysics and senior study author. "Because CaM kinase activity is involved in arrhythmias, hypertrophy and heart cell death, this work also provides new insights into a disease pathway in heart that may lead to development of new drugs to treat heart disease."

Wondering if anyone has any comments on this. I have a history of heart palpatations. It started in about 6th grade. The first is from the article that browneyesmom posted recently and something that I was trying to get a handle on a while back (the CaM kinases stuff). I found this article when researching my strep induced psoriasis outbreak. I have a few studies on that, will be posting. I'm having a hard time thinking that this is just a coincidence and remember, I have never considered my boys PANDAS due to the lack of "explosive onset." Anyway....... http://www.cpementalhealth.com/content/4/1/13 Other putative pathogenetic mechanisms of PANDAS include molecular mimicry and autoimmune-mediated altered neuronal signaling, involving calcium-calmodulin dependent protein (CaM) kinase II activity. http://www.medicalnewstoday.com/articles/106098.php Study Identifies New Mechanism Linking Activation Of Key Heart Enzyme And Oxidative Stress The UI researchers and colleagues from Vanderbilt University in Nashville, Tenn., focused on calmodulin kinase II, or CaM kinase II, a well-studied enzyme critical to many fundamental processes including heartbeat and thought. Scientists know that CaM kinase's activity is sustained by adding a phosphate group -- a process known as phosphorylation. The new study proves that oxidation -- adding oxygen -- also can sustain the enzyme's activity, and like phosphorylation, the mechanism can be reversed to inactivate the kinase. "Our results suggest that oxidation of CaM kinase is a dynamic and reversible process that may direct cell signaling in health and disease," said Mark Anderson, M.D., Ph.D., UI professor of internal medicine and molecular physiology and biophysics and senior study author. "Because CaM kinase activity is involved in arrhythmias, hypertrophy and heart cell death, this work also provides new insights into a disease pathway in heart that may lead to development of new drugs to treat heart disease."

Hi Sweetie! It's great to hear to hear from you. I have wondered how you're doing. Sorry to hear about that annoying tic tho. I'm wondering if this is a public or private tic? Are you able to control it around people that you aren't comfortable with? I'm trying to think of something that you could try as a substitution. Something like keeping an orange handy and touching it to your face when the impulse is too strong to overcome? You could tell just say that you feel a cold sore coming on and the oil in the orange skin keeps from emerging. Without having tics myself, I have no idea if this would even remotely satisfy the urge, so forgive me if this is a stupid suggestion. I remember having a buzzing in the back of my legs and some pretty uncomfortable heel pain when I was pregnant. Those hormones probably are acting up. I'm just sorry to hear that you have to deal with this during such an exciting time. You must be getting pretty close to your due date. On the bright side, it sounds like that baby will be well fed! I don't think that tic would have been possible for me, with either pregnancy and I had a heck of a time with nursing. Hoping others that might have personal experience with a socially inappropriate tic will come up with some suggestions for you.

will be interesting to read what Cheri posted when I get a chance. Guy, Guy Hey, I thought your med chart was fabulous! My thoughts on this are the same as with most of the drugs used for movement disorders. Good luck to them. Long term, these things just don't seem to work very well. If my understanding of the term "plastic" is correct, the brain has a great ability to change. If this would work, why wouldn't it happen normally? Too much dopamine.... theoretically, the brain should down (regulate) dopamine receptors (or presynaptic release of dopamine) on it's own in the first place, no? A young friend of mine pops to mind. He was placed on two drugs that worked on blockade of the same receptors. His neuro saw what he was on and asked if the prescribing physician was crazy and made the remark that he would have parkinson's by the time he was 30. Seems the likelyhood of Parkinson's would depend on how many receptors were reduced (or the amount of presynaptic realease possibly increasing the amt of post synaptic receptors), and if they have the ability to return to an altered baseline and "stick" once the med was discontinued, if that's the intention. I suspect that first they are trying to see what happens with continuous use at a certain level, not with the intention of altering pathways then discontinuing drug use. I have to think about TD here too. How is it that long term use of a dopamine antagonist can cause symptoms that are almost indistinguishable from origninal sysmptoms? TD sometimes remits and sometimes it doesn't. Why? Individual levels of brain plasticity makes the most sense to me, and how can that be determined until it's too late? Would luv to hear any of your thoughts on my ramblings Guy!

FBguy, This looks like an article that has some good info on raw vs cooked garlic. I was under the impression that pressed, than eaten immediately was the most beneficial. I only read the first couple of paragraphs but I'll be interested to read the rest too. I'm wondering if you think that the onset of Lyme's correlates to the onset of your tics or any neuro problem? edit: guess including the link might be a good idea! http://www.healthy.net/asp/templates/Inter...view&Id=173

Hi Pat, Bonnie's Bontech vits contain 300 mgs of mag taurate per 10 capsules. It lists 75% under daily value. The suggested use for 35-66 lbs is 10 to 14 capsules. 67-89 lbs is 15 to 19 capsules. Hope that gives you something to go on. Also, many sites will say to give 2 to 1 ratio of calcium to magnesium. Some sites will say to give equal amts. Bontech contains equal amts (300 mgs of calcium per 10 capsules, however it only lists 30% under daily value, so I'm assuming she is leaving the rest to diet) Which ever you decide, I don't think long term supplementing of one without the other is a good idea as they need each other to avoid becoming deficient in either.

Betty, I looked at this the other nite but was too tired to really understand what I was reading or post. What I was thinking was that one of the articles said that the antibiotic and the magnesium occupy or compete for the same site? If that's the case, wouldn't the magnesium that's circulating in your system naturally just be absorbed after the the antibiotic is absorbed? In a long term antibiotic situation I guess one could become deficient. The Keflex that I'm taking interfers with vit K and I have been on a fairly high dose, 2nd 10 day round. I have bruising if I scratch the rashy spots. Wouldn't surprise me if I have always been vit K deficient to some extent, as I have always bruised easily. Anyway here are a couple of sites that show nutrient/drug interactions. http://www.invitehealth.com/page.htm?PG=DrugDepletion http://www.chiro.org/nutrition/ABSTRACTS/N...tibiotics.shtml http://www.vitacost.com/Healthnotes/Drug/Azithromycin.aspx edit... As I was checking the links to make sure they work, I noticed that the 3rd one said that azith may deplete vit K also. I guess any anti biotic that wipes out healthy gut flora (which aids in the actual production of some of these vits) is probably capable of depleting essential nutrients.

It appears I have my own autoimmune issue, quite possibly involving strep and vit D. New Years day I spent 6 hours in emergency with the most hideous full body rash that you could ever imagine. It seems I had an infection triggered (most likely strep) case of psoriasis or eczema. The biopsy came back excema, but I think the specimen was taken from a place where too much healing had taken place or something. From everything that I have read, this is Psoriasis! Anyway, I'm on my 2nd round of Keflex 500 mgs 4 x a day. Was on Prednasone 20 mgs 2x's a day for 10 days. I'm about 80% clear, but what a $%*^* this has been! I find this just a bit too coincidental for comfort, in light of the boys history of strep and tics. Been finding some very interesting info on one of the psoriasis forums. Also, prior to this outbreak I had been taking about 1200 mgs of vit D3. Vit D is a big player in the treatment of psoriasis. At this point, I'm not sure if it contributed to this outbreak, or helped in the way that it seems to be clearing more quickly than what some people experience. If anyone has a family history of psoriasis or excema and wants more info or details, as always, happy to share! This study has lots of interesting tid bits http://iai.asm.org/cgi/content/full/76/9/3837

abbe, thought this was an interesting study http://physiolgenomics.physiology.org/cgi/...t/full/31/3/441

http://www.ageofautism.com/2009/01/his-nam...tial-facil.html MSG and Autism

I ran across this last week and wanted to encourage everyone to read through at least some of these reports (i read them all, you can also click on reply and read what remarks were made in response). How horrifying is this? I have to think of our infants that were repeatedly vaccinated and the heavy amts of thimerosal that the kids btwn the early 90's thru early early 2000 were given in addition. Now these girls CAN TELL what they're feeling and sadly it seems most still don't want to hear. Please be aware that this vaccine is slated to be added to the schedule for BOYS in the near future. Here is the link to page one http://www.medications.com/se/gardasil?page=1 This is an excerpt from a particularly horrendous post on page two http://www.medications.com/se/gardasil?page=2 another site with links to study info http://www.cynthiajanak.com/2008071doctorsstory.html http://www.argusleader.com/apps/pbcs.dll/a...1#pluckcomments Lawsuits will target Gardasil

Judy, There is some discussion about potassium bicarbonate on the TS forum that you might want to read through. http://www.latitudes.org/forums/index.php?showtopic=3497 I guess I'm wondering if there is a chance that his potassium was low prior to the illness that caused the mesenteric adenitis or if they figured it was low due to the vomiting? I had never heard of Mesenteric adenitis before but after looking it up, I'm wondering if they ever determined what type of infection caused it? I know your grandson had a slight fever and stiff neck when this whole thing started. They gave him the chicken pox shot and tics and behaviors became very intense. He also tested positive for lupus antibodies (scanned some old posts, even though I remember your little guys story quite well). What I don't remember is if he ever tested positive for strep during the onset. For anyone who is not familiar with this condition that may have some idea's to help Judy, here is a little info http://emedicine.medscape.com/article/411043-overview Pathophysiology Mesenteric adenitis is most frequently caused by viral pathogens, but other infectious agents have been implicated, including Yersinia enterocolitica, Helicobacter jejuni, Campylobacter jejuni, and Salmonella or Shigella species.1, 2, 3 An association with streptococcal infections of the upper respiratory tract, particularly the pharynx, has been reported. In younger children and infants, concurrent ileocolitis may be present; this finding suggests that the lymph node involvement may occur in reaction to a primary enteric pathogen. http://en.wikipedia.org/wiki/Hypokalemia Hypokalemia refers to the condition in which the concentration of potassium in the blood is low. The prefix hypo- means low (contrast with hyper-, meaning high). Kal refers to kalium, the Neo-Latin for potassium, and -emia means "in the blood." Normal serum potassium levels are between 3.5 to 5.0 mEq[1]; at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+-ATPase pump. and A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of vomiting, diarrhea, excessive perspiration, or losses associated with surgical procedures