kim

Thanks Michelle I know how that feels. I am just getting to the point where I can read these things and actually get something out of them the first time around. I find the diagrams really helpful. If you can visualise what they're talking about, it's a lot easier. The abbreviations like DArel throw you too, but when you go back and see that it just means the dopamine release, it gets easier. I have spent an inordinate amt of time at this, though. I probably read all of this stuff quite a while ago, and had no idea what they were talking about either. You just get more familiar as you go. As I was reading back through this, I realised that I hadn't answered any of your questions. I'm sorry I don't think I have anything very useful to add. Again, I think the Cheri used the term "disordered" at one time. Personally, I think that would be a better way of describing it. I think the yeast overgrowth is just one more sign of an immune system that isn't functioning properly. I have read of kids with high ammonia levels related to yeast, inadequate protein digestion, etc. being linked to drunken behavior. Do you see ammonia levels on any of Andrew's test results? Also, with high yeast, kids tend to have depleted levels of some B vitamins. When you start to supplement the B's, it can feed yeast so it can be a cycle, until you get ahead of it. If you have low B's and low magnesium, zinc etc. it can have an effect on how the neurotransmitters function, so yes, yeast overgrowth can make things worse. If there was nothing to suggest that taurine levels weren't already high, yes it should be helpful. We have had a couple of people here, post that their childs levels were super high. Since Andrew had testing, I'm assuming that that isn't a problem. . The only thing that I know about TMJ, is that it is supposed to help with methionine (from homocysteine) conversion. Lithium, i really don't know anything about (except that it's found in rock) Since it isn't checked, there may be a specific reason that your Dr. doesn't want you to use it. Yes, my oldest son uses it. It's very helpful for sleep issues. You can also just open the capsule and use a sprinkle here and there, for calming and help with tics. I would check with your Dr. first though.

Michelle, I don't think any of these Dr.s know exactly what is going on. I think that they use tests and try to get a child/persons levels of different things as close to "normal" controls as possible. If you read through these three studies, you'll see how confusing and confounding it gets. I have an artcle around here that explains how some of the drugs used to "treat" these disorders aren't smart enough to know what receptor they are supposed to be blocking or stimulating. Some have a higher affiity for specific binding than others, but with many, they just keep trying different meds at different levels, until they find what seems to be helping. That's part of what's making me crazy here. The meds used to treat ADHD they think increase some of the exact things that they think cause tics. I simply can't find any reason to think that these are structural defects. I don't think the problem originates in these area's. Something I wanted to ask you Michelle, do you know what form of phenylalanine was recommended in the amino acid complex that Andrew's Dr. wanted him on? Is it specified? I have been told that I need to get my youngest son's amino acids corrected, to get him to eat more normally. I really have not gotten into all of that yet. This is just something quickly copied from this site. http://www.healingpeople.com/index.php?opt...ia/pg000141.htm Back to neuro transmitters. http://www.nature.com/npp/journal/vaop/ncu...3A1DC9D477C554E Received 23 February 2006; Revised 11 June 2007; Accepted 16 July 2007; Published online 7 November 2007. Top of pageAbstract Tourette syndrome (TS) is a neuropsychiatric disorder with childhood onset characterized by motor and phonic tics. Obsessive-compulsive disorder (OCD) is often concomitant with TS. Dysfunctional tonic and phasic dopamine (DA) and serotonin (5-HT) metabolism may play a role in the pathophysiology of TS. We simultaneously measured the density, affinity, and brain distribution of dopamine D2 receptors (D2-R's), dopamine transporter binding potential (BP), and amphetamine-induced dopamine release (DArel) in 14 adults with TS and 10 normal adult controls. We also measured the brain distribution and BP of serotonin 5-HT2A receptors (5-HT2AR), and serotonin transporter (SERT) BP, in 11 subjects with TS and 10 normal control subjects. As compared with controls, DArel was significantly increased in the ventral striatum among subjects with TS. Adults with TS+OCD exhibited a significant D2-R increase in left ventral striatum. SERT BP in midbrain and caudate/putamen was significantly increased in adults with TS (TS+OCD and TS-OCD). In three subjects with TS+OCD, in whom D2-R, 5-HT2AR, and SERT were measured within a 12-month period, there was a weakly significant elevation of DArel and 5-HT2A BP, when compared with TS–OCD subjects and normal controls. The current study confirms, with a larger sample size and higher resolution PET scanning, our earlier report that elevated DArel is a primary defect in TS. The finding of decreased SERT BP, and the possible elevation in 5-HT2AR in individuals with TS who had increased DArel, suggest a condition of increased phasic DArel modulated by low 5-HT in concomitant OCD. http://www.med.nyu.edu/research/pdf/brasij...e%20in%20TS.pdf A second possibility is a decrease in tonic dopamine levels. We favor this latter concept on the basis of lower levels of CSF HVA (6, 8, 9) and evidence for elevated D2 receptors in some subgroups of Tourette’s syndrome patients (13). If this is indeed the case, how does the decrease in tonic dopamine occur? Diminished tonic dopamine levels could be secondary to a decrease in phasic overflow from the synaptic cleft to the extracellular space, but this is not likely because it conflicts with the observation of an increase in phasic dopamine release. A decrease in tonic dopamine could be secondary to a diminished cortical afferent input, i.e., tonic dopamine release is regulated by cortical glutamatergic afferents (49). To our knowledge, however, postmortem and neuroimaging studies have not identified reduced cortical gray matter volume or abnormal efferent output. Anderson et al. (51) evaluated postmortem 13 brain regions from four Tourette’s syndrome patients and reported lower glutamate levels in the globus pallidus and substantia nigra pars reticulata but not in the putamen. Last, a decrease in tonic dopamine levels could be secondary to an increase in activity of the dopamine transporter, since the reuptake transporter determines the concentration of extrasynaptic dopamine. Hence, we propose that the essential underlying mechanism in Tourette’s syndrome could be an overactive dopamine transporter system. This situation would create reduced levels of extracellular dopamine, higher concentrations of dopamine in the axon terminal, an increase in stimulus-dependent dopamine release, autoreceptor supersensitivity at the presynaptic site, and an increase in sensitivity to low-dose neuroleptics. Several clinical findings in Tourette’s syndrome patients support the overactive dopamine transporter hypothesis. For example, the exacerbation of tics by stimulant medications (52, 53) could be secondary to greater dopamine release from the axon terminal. Environmental stimuli, such as stress, anxiety, and medications, well known to exacerbate tics, have been shown to increase phasic bursts of dopamine. Last, tic suppression with very low doses of neuroleptics (54) may occur because there is less tonic dopamine available for the neuroleptic to block. Future PET studies involving larger numbers of Tourette’s syndrome subjects and using techniques in which measurements of D2 receptors, dopamine transporter, and dopamine release are available for each subject should provide further clarification of the dopaminergic system in adults with Tourette’s syndrome. Confirmation of a release abnormality in larger numbers of patients with Tourette’s syndrome could, in turn, lead to the development of new tic-suppressing pharmacotherapies. http://www.nature.com/npp/journal/vaop/ncu...3A1DC9D477C554E Received 23 February 2006; Revised 11 June 2007; Accepted 16 July 2007; Published online 7 November 2007. Top of pageAbstract Tourette syndrome (TS) is a neuropsychiatric disorder with childhood onset characterized by motor and phonic tics. Obsessive-compulsive disorder (OCD) is often concomitant with TS. Dysfunctional tonic and phasic dopamine (DA) and serotonin (5-HT) metabolism may play a role in the pathophysiology of TS. We simultaneously measured the density, affinity, and brain distribution of dopamine D2 receptors (D2-R's), dopamine transporter binding potential (BP), and amphetamine-induced dopamine release (DArel) in 14 adults with TS and 10 normal adult controls. We also measured the brain distribution and BP of serotonin 5-HT2A receptors (5-HT2AR), and serotonin transporter (SERT) BP, in 11 subjects with TS and 10 normal control subjects. As compared with controls, DArel was significantly increased in the ventral striatum among subjects with TS. Adults with TS+OCD exhibited a significant D2-R increase in left ventral striatum. SERT BP in midbrain and caudate/putamen was significantly increased in adults with TS (TS+OCD and TS-OCD). In three subjects with TS+OCD, in whom D2-R, 5-HT2AR, and SERT were measured within a 12-month period, there was a weakly significant elevation of DArel and 5-HT2A BP, when compared with TS–OCD subjects and normal controls. The current study confirms, with a larger sample size and higher resolution PET scanning, our earlier report that elevated DArel is a primary defect in TS. The finding of decreased SERT BP, and the possible elevation in 5-HT2AR in individuals with TS who had increased DArel, suggest a condition of increased phasic DArel modulated by low 5-HT in concomitant OCD. http://www.ncbi.nlm.nih.gov/sites/entrez?c...pt=AbstractPlus Grace AA. Department of Behavioral Neuroscience, University of Pittsburgh, PA 15260. A novel mechanism for regulating dopamine activity in subcortical sites and its possible relevance to schizophrenia is proposed. This hypothesis is based on the regulation of dopamine release into subcortical regions occurring via two independent mechanisms: (1) transient or phasic dopamine release caused by dopamine neuron firing, and (2) sustained, "background" tonic dopamine release regulated by prefrontal cortical afferents. Behaviorally relevant stimuli are proposed to cause short-term activation of dopamine cell firing to trigger the phasic component of dopamine release. In contrast, tonic dopamine release is proposed to regulate the intensity of the phasic dopamine response through its effect on extracellular dopamine levels. In this way, tonic dopamine release would set the background level of dopamine receptor stimulation (both autoreceptor and postsynaptic) and, through homeostatic mechanisms, the responsivity of the system to dopamine in these sites. In schizophrenics, a prolonged decrease in prefrontal cortical activity is proposed to reduce tonic dopamine release. Over time, this would elicit homeostatic compensations that would increase overall dopamine responsivity and thereby cause subsequent phasic dopamine release to elicit abnormally large responses http://www.springerlink.com/content/e511014uhj124137/ Takashi Hamamura1 and Toshiki Harada2 (1) Hamamura Clinic, 5-1-17 Kojima Ogawa Kurashiki, Okayama 711-0911, Japan (2) Takahashi Hospital, 2200 Abe Ochiai-cho Takahashi, Okayama 716-0061, Japan Received: 26 September 2006 Accepted: 15 November 2006 Published online: 5 January 2007 Abstract Rationale Aripiprazole is a recently introduced antipsychotic with a unique pharmacological profile, a dopamine partial agonist. Dopaminergic neural transmission has two different components, tonic and phasic, which have different physiological functions, but the effects of aripiprazole on tonic and phasic components are not reported. Objective Studies on antipsychotics including aripiprazole and tonic/phasic dopamine transmission are summarized. Results Antipsychotics exert efficacy without extrapyramidal side effects (EPS’s) when their occupation of dopamine D2 receptors reaches 65–80%. When a “tightly binding” antipsychotic binds 70% of D2 receptors, the remaining 30% are available for endogenous dopamine to bind. These tight antipsychotics suppress dopamine transmission in both tonic/phasic components equally so that similar proportions are kept. Aripiprazole is effective when >90% of D2 receptors are occupied. In this condition, less than 10% of D2 receptors are available for endogenous dopamine to bind; however, EPS’s do not occur because aripiprazole exerts partial dopaminergic agonistic activity. Because the concentration of aripiprazole in the brain is relatively constant and it binds to D2 receptors tightly, the added dopaminergic agonism may show a tonic nature. Thus, aripiprazole suppresses the phasic component relatively more than the tonic component. In contrast, under treatment with “loosely binding” antipsychotics, phasic dopaminergic transmission is relatively preserved. Conclusions Tight antipsychotics suppress both tonic and phasic components equally. Aripiprazole suppresses the phasic component relatively more than the tonic; that is, aripiprazole is a tonic component buster. By contrast, suppression of the phasic component by loosely binding antipsychotics may be relatively weak. An erratum to this article can be found at http://dx.doi.org/10.1007/s00213-007-0716-0 my note... ABILIFY= aripiprazole —

In addition to above post, wanted to include this here too. http://www.ncbi.nlm.nih.gov/sites/entrez?d...st_uids=1795312 RA Bradley H, Waring RH, Emery P. School of Biochemistry, University of Birmingham, United Kingdom. Patients with rheumatoid arthritis (RA) have a reduced capacity for S-oxidation and formation of drug sulfate conjugates. We investigated S-methylation catalyzed by thiol methyl transferase (TMT) (E.C. 2.1.1.9) as an alternative pathway for metabolism of aliphatic compounds. TMT activity was measured in vitro using red blood cell membrane preparations from 120 patients with RA and 35 controls. Mean values for controls were 10.1 +/- 3 units/mg protein and for RA 3.7 +/- 3 units/mg protein (p less than 0.05). TMT activity was not related to the acute phase response or to drug administration. However, patients with RA with higher TMT activity tended to have higher rheumatoid factor levels. This evidence is consistent with a generalized disturbance of sulfur metabolism in rheumatoid disease.

One thing that may be helpful is to read some basic info on the feingold diet. I'm sure no expert there, but you want to get a little familiar with ammines, phenoyls and salycilates. Sheez, don't know how to spell any of those! http://www.feingold.org/pg-overview.html Faith, I don't think you want to up the consumption of that wine just yet! It sure appears to me, that if it causes an increase in RLS, you want to avoid it. I wanted to ask any of you RLS mom's, do you have actual movement or just sensations? I never had any movements during pregnancy, just felt like an small electrical shocks. Calicat, Cracked me up! Just go for it. No one likes to look like an idiot, I bet they wouldn't question you a bit. I bet most of the MD's wouldn't question it too far. That's the point that they start talking about a referral. Just make sure you use the whole phrase, instead of initials. A lot of these words look really scary, but broken down, they're not that tough.

Cheri, After all of this time, I don't think they fully understand how this works, and the variability from person to person. There is still a lot of credibility to the "older ideas" but.. the same old questions remain. This is a good overview of some of the structures and pathways invoved. Second 1/2 contains PANDAS info. Published 2006 http://jcn.sagepub.com/cgi/reprint/21/8/678.pdf The theory of low phasic dopamine within the axon, resulting in higher tonic supersensitivity reception caught my attention here. The PANDAS summery provides more questions than answers IMHO. I have many articles collected now, that I want to go back thru slowly. I'm just going to post them as I go. This RLS, Parkinson's, tics connection really has my neurons firing. If I short circuit, you guys will be the first to know.

Deedee/All, (Hey Faith, your red wine connection may be here too) I have long suspected a problem with sulfur metabolism with both of my boys. I have posted info from Dr. Amy Yasko here in the past that talks about undersulphated Gags in the GI tract following strep infections. It seems there almost has to be some connection here. Again, I have to think about how much tylenol my kids were given during strep infections, and how my oldest son practically lived on tylenol with codeine after his tonsil removal. I also would give it to them prior to vaccination. (wheres the smiley where you're swatting yourself in the head)? In addition to my above triple post, I'm wondering if you can take a look at this... (bolding and underlining mine). PubMed Citation Articles by Steventon, G. B. Articles by Williams, A. C. NEUROLOGY 1989;39:883 © 1989 American Academy of Neurology Xenobiotic metabolism in Parkinson's disease G. B. Steventon, PhD, M.T.E. Heafield, MB, MRCP, R. H. Waring, PhD, MRCPath and A. C. Williams, MD, FRCP Department of Neurology, Queen Elizabeth Medical Centre, and Department of Biochemistry, University of Birmingham, United Kingdom We studied 68 patients with Parkinson's disease (PD) with probe drugs to determine whether a defect in metabolism might be an etiologic factor and found no difference between patients and controls in their ability to form the 4 hydroxy metabolite of debrisoquin. However, using S-carboxymethyl-L-cysteine, 63.2% (43/68) of PD patients had reduced S-oxidation capacity, while 35.3% (24/68) produced no sulfoxides (controls, 35.2% and 2.5%). When we studied acetaminophen (paracetamol) metabolism, only 29.6% of PD patients excreted >,5% of the dose as the sulfate conjugate; the corresponding figure for controls was 83.9%. These results suggest a deficiency in detoxication pathways involving sulfur metabolism. PD patients may be unusually susceptible to exogenous or even endogenous toxins. Address correspondence and reprint requests to Dr. Williams, Department of Neurology, Queen Elizabeth Hospital, Queen Elizabeth Medical Centre, Edgbaston, Birmingham B15 2TH. UK. Supported by both the Parkinson's Disease Society and the Motor Neurone Disease Association. Received September 2, 1988. Accepted for publication in final form March 27,1989 The majority of this article talks about this problem (or problems resulting from it). I just pulled a couple of excerpts http://www.newtreatments.org/fromweb/sulfur.html Thus, mercury, and any foodstuff that requires or uses up sulfate ions during its metabolism, will make the situation worse. These foodstuffs include foods that supply neurotransmitters, like bananas (serotonin), chocolate (phenylethylamine), and cheese (tyramine), apple juice (and one mother reports her child drank a quart a day!), citrus fruit juices, and paracetamol (Tylenol™). For instance, one or two minutes after a dose of Tylenol™, the entire supply of sulfate in the liver is gone! In fact, any chemicals with a high proportion of phenolic groupings will have this effect, and will enhance the problems referred to above. Many coloring materials, whether of natural or synthetic origin, possess phenolic groupings. Phenol, an organic compound, has other names such as hydroxybenzene. If the PST enzyme is deficient or sulfoxidation is lacking in some 70% to 80% of autistic kids as some say, it behooves mothers to seriously heed the information in this section, and to carefully guard their children from certain obvious sources of trouble. It is interesting to note Dr. Waring's statement that those with the PST/low sulfation problem have central nervous system problems from the toxic amines. For example migraine sufferers usually have low PST activity, and are readily affected by dietary "triggers", especially those with amines. Compounds such as flavonoids (red wine and citrus fruits), aged cheese, beers, chocolate, and strong odors inhibit PST leading to headache in the less resistant. Apple juice, citrus fruits, chocolate, and paracetamol (Tylenol™) were precisely those that were known to precipitate migraine attacks in susceptible individuals. It should be noted that many multivitamin supplements, grapeseed extract, Pycnogenol™, Quercetin, and other antioxidants contain high amounts of flavonoids. Quercetin is found in 78% of the foods. It is useful in hay fever (suppress the histamine release), some forms of cardiovascular disease, and it chelates metals to prevent oxidation. It decreases vascular fragility, but stimulates adrenaline release (decreasing thymus weight), reduces general metabolism (reduces temperature and oxygen consumption), suppresses thyroid activity, inhibits p450 (Phase I) liver enzyme activity, and it is linked with male impotence. From this list of negatives, one can see it should not be used in quantity for long term. and "... dopamine sulphotransferase (ST) activity was inhibited strongly by (+/-)-catechin, (+)-catechin, octyl gallate, tartrazine (yellow #5), and vanillin (synthetic vanilla). Sulphation of the xenobiotic steroid (foreign to the body) 17 alpha-ethinyloestradiol (EE2) was inhibited by vanillin, erythrosin B, and octyl gallate [antioxidant used in margarine]....Vanillin was found to inhibit 50% of liver EE2 ST activity ..."-Common Food Additives are Potent Inhibitors of Human liver 17 Alpha-ethinyloestradiol and Dopamine Sulphotransferases.- Bamforth KJ, Jones AL, Roberts RC, Coughtrie MW, Biochem Pharmacol 1993 Nov 17;46(10):1713-20. There are a number of consequences attributable to PST/sulfate deficiency including effects upon the impaired breakdown and metabolism of classical neurotransmitters such as serotonin and dopamine; impaired breakdown and metabolism of the bile pigments bilirubin and biliverdin; impaired action of the hormone CCK on CCKA receptors which would result in decreased secretion of pancreatic enzymes and of bile from the gall bladder and biliary tract into the intestines. This would result in low uptake of certain vitamins and other nutrients from the intestines; reduced activity of gastrin (and subsequent reduced secretion of stomach acid, mucus, and pepsin in the stomach), and, probably, reduced production of secretin farther downstream. Secretin (esp. at high concentrations) inhibits the histamine releasing action of gastrin and pentagastrin reducing HCl as the stomach empties.

oops..double post

Deedee, I'm sorry to hear that your Mom has PD. I hope it isn't causing her too many difficulties. I'm wondering if you have ever done any research on Parkinson's? I'm looking at a couple of studies that suggest impaired detox capabilities again, which makes perfect sense to me, but I'm not sure what the latest research shows. I can understand impaired detox in older people a lot easier than in all of these young children. http://www.springerlink.com/content/kg6t175225302775/

Deedee, I'm sorry to hear that your Mom has PD. I hope it isn't causing her too many difficulties. I'm wondering if you have ever done any research on Parkinson's? I'm looking at a couple of studies that suggest impaired detox capabilities again, which makes perfect sense to me, but I'm not sure what the latest research shows. I can understand impaired detox in older people a lot easier than in all of these young children. http://www.springerlink.com/content/kg6t175225302775/

emma, I bought a bottle of now brand. It only states inositol also. 500 mg capsule. $7.99 for 100.

I think this study offers important info on the both RLS and tics. It just takes such an incredible amt of time, to get something really useful out of it. I know it's there, but I'm getting all clogged up with info that I can't interpret or get so sidetracked trying, that I lose the origial basic information that I went searching for! http://archneur.ama-assn.org/cgi/reprint/61/5/641.pdf another thing I want to add. I posted earlier about dopamine appearing at normal levels, unitl a challenging agent was added. I got thinking, that it wowuld be interesting to know what that challenging agent was. I thought i remembered it being formalin (or close). I just quickly typed that in Wiki. It looks like it's formaldehyde. Very interesting. I hope this is accurate info, as I'm doing this on the run, as usual I know some vaccine contain formaldehyde. I would love to spend some time looking for other sources (air, foods....I think diet soda's have a role here, especially at higher temperatures?

Calicat, Honestly, I woud really be surprised if symptoms of RLS are not an important clue here. It's really interesting to look into all of the pathways that can go haywire. You have neurotransmitters, but you also have secondary messangers, synthesis of proteins, the energy componenet of the cell (mitochondria/ATP) etc. It has occured to me, almost since the beginning of trying to understand some of the issues involved here, that low levels of something, can result in a hypersensitivity at some point, as Cheri recently commented on. Our bodies are amazing in the fact that they will compensate for low levels, sometimes by forming extra receptors to grab what is available. I only recently learned of tonic and phasic dopamine, but that's for another thread, anyway, I don't think it's normal that our legs have abnormal sensations during this process The abnormal influx of calcium into a cell, is known to be involved in exaggerated exocytosis. It seems rather obvious that something is disrupted in this process, in Moms that experience RLS or during the late stage of pregnancy. None of this means that vitamin or mineral deficiencies, toxic substances, illness, etc are not implicated. It may simply suggests that we may have a genetic vulnerability to any one of these things. If RLS symptoms are improved by the use of dopamine agonists, what might that imply for a child with TS ? Is there any reason to believe that by stimulating dopamine production at some point in development, that we might avoid the hyper responsiveness? Does the problem even stem from dopamine production, or is it simply the most obvious endpoint? Dopamine also modulates other catecholamines. I will post some links under the dopamine thread, as soon as I have more time. If ATP is involved is an area that we as Mom's have experienced, then add Faith's remark+adult TS with reduced levels of cAMP, it seems there may be something important here. ATP and cAMP (cyclic adenosine monophosphate) are a real treat to try to get any kind of a handle on, I'm really struggling! http://en.wikipedia.org/wiki/Adenosine_triphosphate Good page to start if you want to weed through. You have to click on the clickable part of this paragraph to get to cAMP This is the study that I mentioned. You have to remember that new testing methods have shown some of the things in these older studies to not be exactly as previously thought. A good example, dopamine appeared to be at usual levels until a stimulating agent was used in some of the later studies. They found a lot higher levels in patients as compared to controls when a stimulating agent was used. http://www3.interscience.wiley.com/cgi-bin...678840/ABSTRACT Brief Communication Tourette's syndrome: A neurochemical analysis of postmortem cortical brain tissue Harvey S. Singer, Dr., MD 1 2 *, In-Hei Hahn, BA 1, Edward Krowiak, BA 1, Eric Nelson, BA 3, Timothy Moran, PhD 3 1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 2Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 3Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD *Correspondence to Harvey S. Singer, Department of Neurology, Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21205 Abstract Postmortem frontal, temporal, and occipital regions of the brain from adult patients who had a diagnosis of Tourette's syndrome were analyzed for neurochemical alterations. In 3 of 4 TS-affected brains, the concentration of adenosine 3,5 -monophosphate (cyclic AMP) was reduced in all brain regions evaluated. This diminution in cyclic AMP was not associated with a significant change in the activity of the synthesizing enzyme, adenylate cyclase. No significant differences were identified for the neurotransmitter-synthesizing enzymes choline acetltransferase and glutamate decarboxylase. Concentrations of dopamine, norepinephrine, and the serotonin metabolite 5-hydroxyindoleacetic acid were not altered. Postsynaptic receptor-binding activity for muscarinic cholinergic ([3H] quinuclidiny1 benzilate) and beta receptors ([125I]iodocyanopindolol) showed no generalized impairment. It is suggested that symptoms of Tourette's syndrome might be related to an abnormality within a second messenger system. Received: 17 July 1989; Revised: 10 October 1989; Accepted: 11 October 1989

third post in this thread Faith, read this study http://www.blackwell-synergy.com/doi/pdf/1...96.1998.00381.x read page 392 last 2 paragraphs on the right. I can't get those paragraphs to copy for some reason, but this is helpful too. ATP is increased in social drinkers, but not alcoholics. Notice the remark about increase in catecholimines in the alcoholic group. Hummmm lots more to consider. The problem is, you have to keep reversing all of this stuff. I have one study copied where 3 adult patients with TS, postmortem were found to have low levels of ATP across all brain regions. For anyone reseach minded, I'd be happy to dump my note pad to see if anyone can help make sense of it all.

Calicat, I have been intensely studying ATP recently in regards to TS. Your remark about restless legs during pregnancy, hit me out of the blue, while I was getting ready to pull out of the driveway! I had to come back in, and see if there was a connection. I too had buzzing in my legs during pregnancy. I wondered if I was getting MS . Without getting too technical...look at this study. ATP-Dependent Ca2+ Transport Is Up-Regulated during Third Trimester in Human Syncytiotrophoblast Basal Membranes. Articles Pediatric Research. 48(1):58-63, July 2000. STRID, HILJA; POWELL, THERESA L. Abstract: In late gestation, Ca2+ transport across the human placenta must increase in response to the demands of accelerating bone mineralization of the fetus. This is an ATP-dependent transport against a concentration gradient across the basal or the fetal-facing plasma membrane of the syncytiotrophoblast. The aims of the present study were to determine the relationship between ATP-dependent Ca2+ transport and gestational age in the third trimester and to identify the specific isoforms of plasma membrane Ca2+ ATPase (PMCA) present in human syncytiotrophoblast. Basal membrane vesicles were isolated from normal placentas and from placentas obtained from preterm deliveries with no other complications (32-37 wk of gestation). We studied the uptake of 45Ca2+ into basal membrane vesicles in the absence and presence of ATP by using rapid filtration techniques. Western blot was used to assess the protein expression of the PMCA isoforms 1-4. Isoforms 1 and 4 of PMCA were identified in basal membrane of human placenta. The ATP-dependent Ca2+ transport increased linearly during the third trimester (r = 0.571, p = 0.0015, n = 28). However, PMCA protein expression was unaltered during the same period of gestation. Our results show that PMCA in the fetal-facing plasma membrane of the human syncytiotrophoblast is markedly activated toward the end of pregnancy. We suggest that these changes are critical in supplying the rapidly growing fetus with sufficient Ca2+ for bone mineralization. Thank you thank you for that remark! If I piece anything together here, I'll post.

You know what's really interesting, RLS is thought to be more associated with low dopamine transmission. The prescription drug Requip increases dopamine levels. It's thought to be more of a Parkinson's like syndrome. Parkinson's is related to the death of dopamine neurons. It's confusing how adhd (which is treated with stimulant meds) Parkinson's (again stimulant med) and TS can all occur in the same person/family.

I always llike to look at how these drugs work now, when somesone comments on them. Wiki says dramamine is an anticholinergic. I was just reading about 5HT earlier (another anti nausea medication). It blocks a certain serotonin receptor. Interesting to learn why some of these things make symptoms worse sometimes. these are just from wiki......on dramamine Anticholinergic http://en.wikipedia.org/wiki/Anticholinergic H1 antihistamine http://en.wikipedia.org/wiki/Antihistamine Dimenhydrinate (marketed under brand names Dramamine, Gravol and Vertirosan) is an over-the-counter drug used to prevent motion sickness. http://en.wikipedia.org/wiki/Dimenhydrinate

Michele, Just curious, where are you at with treatment with Nystatin? Have you finished, or still giving it?

Hi everyone! Tamiflu, flu vaccination, or naturally occuring illness, could have implications depending upon the genetic expression of the immune system, it appears to me. Just consider the effect tamiflu seems to be causing in some people and what we are seeing in regards to illness, whether viral or bacterial, etc. It probably will not be the same for each person, but it would be interesting to do a thread on this, and see how many we see with increase or decrease with each phase of illness. Neither of my boys (that i can ever remember) "ticced" during what I would call the acute phase of an illness. Before or afterwards, yes. I think this article may offer some idea's is this area. Maybe during the acute phase, some problematic genes were underexpressed in my boys, and are overexpressed in others. http://vir.sgmjournals.org/cgi/reprint/87/6/1677.pdf In order to clarify the mechanism of the host response to influenza virus, gene-expression profiles of peripheral blood obtained from paediatric patients with influenza were investigated by oligonucleotide microarray. In the acute phase of influenza, 200 genes were upregulated and 20 genes were downregulated compared with their expression in the convalescent phase. Interferon-regulated genes, such as interferon-induced protein with tetratricopeptide repeats 2 (IFIT2) and vipirin, were strongly upregulated in the acute phase. Gene ontology analysis showed that immune response genes were highly overrepresented among the upregulated genes. Gene-expression profiles of influenza patients with and without febrile convulsion were also studied. In patients with febrile convulsion, 22 genes were upregulated and five were downregulated compared with their expression in patients without febrile convulsion. These results should help to clarify the pathogenesis of influenza and its neurological complications.

http://www.nytimes.com/aponline/us/AP-Silenced-Genes.html WASHINGTON (AP) -- Remember biology class where you learned that children inherit one copy of a gene from mom and a second from dad? There's a twist: Some of those genes arrive switched off, so there is no backup if the other copy goes bad, making you more vulnerable to disorders from obesity to cancer.

Tracey, I'm wondering if you could answer a question for me? After the CP vax, do you remember your son showing any signs (even slight) of loss of coordination or muscle weakness?

Tracey, The only thing I can relate to the chicken pox vax and strep, is the possibility of staph or strep infection following the chicken pox lesions becoming infected by one of those things, which of course doesn't apply in your situation. IMHO, what your son is experiencing could be from either thing. The vax or strep. Has your son had confirmed strep in the past? If not, the symptoms may not have shown up as quickly as they may have, in a child who has had strep repeatedly. The other scenerio could be, where the two things (as in a strep infection followed by a live viral injection) triggerd this. I wish I knew if a viral panel, that may show abnormally high varicella titers would help? Maybe one of the nurses on our forum could comment on that. What a coincidence I found you, and you had found us, only hours before! I've been trying to stay out of the conversation, as I tend to "go off" in too many directions. I knew some of the wonderfully specific posters, would be of most help. Anyway, welcome. for anyone who would like to read the thread that I'm referring to....... http://www.mothering.com/discussions/showthread.php?t=800381 I had PMed Tracey and Caryn had already led her here!

2nd case from autism omnibus proceedings http://www.ageofautism.com/2007/11/its-hard-out-he.html

I see the recipe that Caryn posted has plantain leaf listed. I meant to share this, this past summer but didn't seem to get around to it. If you use google image, you can find a picture of a plantain plant. They grow right in most yards. You can find them near sideways, driveway borders etc. This plant is like a miracle for people who are allergic to bee stings. I have a very stubborn friend, who would not go to a Dr. for a horribly swollen hand. The swelling extended up to her elbow with a red line spreading up the arm. I was having a fit, so I got on the computer, found this "natural remedy" and we tried it. The bees had stung her 2 days prior. I didn't think it would be able to remove any toxins, but it worked. By the next day her arm was 80 % better. She said the pain started to diminish almost as soon as the leaves hit her skin. That night she took some of the leaves, put them in a food processor with a little liquid green tea, sort of made a paste and slept with it on the bites. She had a friend who has the same reaction, use it when he was stung on the neck, he had no reaction. I had my husband use it on a steam burn. It was your typical painful steam burn (as we were learning how to can tomatoes from the same friend who had the bee reaction...ahhh the joys of eating healthier ) I ran out, got a few leaves, rinsed them, beat them with a butter knife handle....and the burn never even blistered. The next day it was just a flat red mark. It has anti inflammatory properties, and removes much of the sting, almost immediately. Really cool plant.

Michelle, I hope you didn't take my post as any kind of encouragement to try ANY medication for ADD. The only point was, that maybe by increasing low levels of amino acids, some which may result in increased levels of dopamine, that you may improve ADD symptoms as dopamine is involved in focus and attention. Cheri was absoultly right in the statement about ritalin bringing out tics in some children who never exhibited them before, but that's ritalin not substances that come naturally from dietary sources, or that our body manufactures itself. I know other parents have shyed away from amino acid supplementation, for fear of the possibility of increasing tics. I just think it's important that we share, discuss all aspects that anyone can think of. Then discuss your thoughts with your Dr! I'm truly overjoyed to hear of his improvement!

This is one study that I found really interesting regarding dopamine. Again, reading these studies is kind of like a ping pong match! http://www.med.nyu.edu/research/pdf/brasij...e%20in%20TS.pdf Excerpt...bolding mine The difference in relative dopamine release in the putamen between Tourette’s syndrome and comparison subjects approached significance when the less sensitive constrained method of analysis was used. Although the change in dopamine release appears unrelated to age, tic severity, and OCD, whether it is associated with other symptoms, such as ADHD, remains unclear. Dopamine transporter density, measured by SPECT, has been shown to be greater in adults with ADHD than in healthy comparison subjects (39). Although global tic severity ranking did not correlate with the degree of dopamine release, potential explanations include the small number of study subjects and characteristics relating to tics, i.e., their natural variability, possible improvement over time, and exacerbation by external factors such as stress, anxiety, fatigue, or the presence of infection