Guest guest Posted December 5, 2003 Report Share Posted December 5, 2003 Happy Holidays to all group members We are trying to find answers for our 6 yr. old son on the spectrum. As we wait on Dr. G's list- we managed to get the blood draw completed through our DAN. Wondering if I could ask a couple of questions? My son showed elevated herp6 and am reading more and more about the damage to myelin etc... Does the SPECT scan that Dr. G orders only measure blood flow? or does it also show potential damage to brain areas due to virus etc...? Is Dr. Amen's brain imaging the same as the Spect Scan that Dr. G orders?? As we pursue the anti-viral treatment, just wondering shouldnt we be checking for the permanent damage?.. so worried about this as is numbers were huge! Thanks in advance for any information Reen Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 8, 2004 Report Share Posted February 8, 2004 Unlikely that TLP or FF will improve blood perfusion. These (and have done both) may improve neurological development (build pathways) - hence their effectiveness in receptive and sometimes expressive language. HBOT may well improve oxygenation and has shown by spect to improve perfusion, however Dr Goldberg regards this as highly dangerous as it can over oxygenate and cause damage to areas of the brain that are already over perfused - often the case with our kids. Medical treatments such as protocol do show improvements in spect scans (there are examples in presentations shown on Dr G's website and there have been posts on this list by parents who's children have had a second scan.) It is more likely that the therapies you mention are more effective and hasten improvement in language and behaviour when medical therapy is also used. The Neurospect will also show the result of medical therapy, not language or behaviour therapies. Hope this offers some clarity SPECT scan Hi All, Been lurking for, well, a few years. Anyway, have results of a SPECT scan and shows underdevelopment in the most forward part of both temporal lobes. My child is Aspie/HFA, 8yrs. old, no meds. Expressive/Respective language is biggest issue, followed by TOM and then balance. Was wondering if anyone as experience with therapies that have shown improvement, who have also done SPECT scans. We have done speech therapy for 6yrs., OT for 4yr., some gymnastics, some mood Bell, some biofeedback, most Locutour, most Sentence Master. (wanted to mention too, am big advocate of nutritional supplements - efa's Can now afford to do something like The Listening Program or Fast Forward, HBOT and not sure if I should be looking at something altogether different. Anyone out there with SPECT scans, tried a therapy, showed improvement, then did another SPECT scan? I know everyone's different but you have to start weeding out somewhere. Thank You, Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 8, 2004 Report Share Posted February 8, 2004 Apologize for the confusion. Just posted the links for general information on the topic and as a possible contact. Dr.SpectScanservices@... E-Mail Reviews or Reply to Questions - $75.00 30 minute phone consultation - $225.00 (310) 264-0080 > Hello, > Just finished that presentation while you posted. Didn't see anything regarding HBOT being not recommended for hyperperfusion children. Are referring to slide 37 (Magill University or 3rd International Symposium on Brain Injury & HBOT) > Not being argumentative here, just can't see it documented, meanwhile HBOT advocates say HBOT helps both hyper and hypo and offer " before and after " spect scans as well as documentation that no other therapy was tried. > No hidden agenda, just digging. > Thank you, Responsibility for the content of this message lies strictly with the original author(s), and is not necessarily endorsed by or the opinion of the Research Institute. _____ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 8, 2004 Report Share Posted February 8, 2004 ----Original Message Follows---- From: " petruccione " <petruccione@...> Hello, Just finished that presentation while you posted. Didn't see anything regarding HBOT being not recommended for hyperperfusion children. Are referring to slide 37 (Magill University or 3rd International Symposium on Brain Injury & HBOT) Not being argumentative here, just can't see it documented, meanwhile HBOT advocates say HBOT helps both hyper and hypo and offer " before and after " spect scans as well as documentation that no other therapy was tried. No hidden agenda, just digging. Thank you, --------------------------------------------- Hi, I realize their literature makes the therapy sound positive. When I reviewed the information available I noticed the results were sometimes based on only " one " subject. If I recall....the scans were done shortly after treatment. Unfortunately more is being learned about the mechanisims of reperfusion damage. The damage may not show up until much later. By searching pubmed before I found numerous abstracts discussing damage to child with disorders like Cerebral Palsy. There is so much on oxygen damage that can be found by searching pubmed. Cheryl -------------------------------------------------------------------------------- Teratog Carcinog Mutagen. 2003;Suppl 2:43-52. Oxygen-induced DNA damage in freshly isolated brain cells compared with cultured astrocytes in the Comet assay. Cemeli E, IF, Peers C, Urenjak J, Godukhin OV, Obrenovitch TP, D. Department of Biomedical Sciences, University of Bradford, Bradford, United Kingdom. Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defence mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important, therefore, to identify tools for the quantitative analysis of DNA damage in models of neurological disorders. The aim of this study was to compare the susceptibility of DNA to oxidative stress in cells freshly dissociated from the mouse brain, to that in cultured brain cells. Both primary cultures and a continuous cell line of astrocytes were considered. All cells were treated by xanthine/xanthine oxidase, a superoxide generator or hydrogen peroxide, applied alone or in the presence of the oxygen radical scavengers, superoxide dismutase, catalase, or ascorbic acid. DNA damage, quantified with the Comet assay, was consistent in all the different cell preparations exposed to oxidative stress, and was attenuated in similar ways by superoxide dismutase and catalase, scavengers of superoxide anion and hydrogen peroxide, respectively. The results with ascorbic acid were more variable, presumably because this compound may switch from anti- to pro-oxidant status depending on its concentration and other experimental conditions. Overall, similar responses were found in freshly dissociated and cultured brain cells. These results suggest that the Comet assay can be directly applied to cells freshly dissociated from the brain of rodents, including models of neurological disorders, such as stroke models and animals with targeted mutations that mimic human diseases. Teratogenesis Carcinog. Mutagen. Suppl. 2:43-52, 2003. Copyright 2003 Wiley-Liss, Inc. PMID: 14691979 [PubMed - in process] Stroke. 2004 Feb;35(2):578-83. Epub 2004 Jan 08. Therapeutic window for use of hyperbaric oxygenation in focal transient ischemia in rats. Lou M, Eschenfelder CC, Herdegen T, Brecht S, Deuschl G. Department of Neurology, Christian-Albrechts University of Kiel, Kiel, Germany. BACKGROUND AND PURPOSE: Hyperbaric oxygenation (HBO) is an attractive procedure that has been used frequently in cerebral ischemia. However, depending on the model of cerebral ischemia and HBO protocol, different and conflicting results were obtained in the past. This study was undertaken to reevaluate the effects of single administration of HBO in 2 models of acute cerebral ischemia: transient or permanent focal ischemia in rats. A comparison of the 2 ischemia models was undertaken to search for a putative therapeutic window. METHODS: The intraluminal middle cerebral artery occlusion model (MCAO) was used. The effect of single HBO therapy (3 atm absolute, 60 minutes) on transient or permanent focal ischemia, when applied at different times (3, 6, or 12 hours) after MCAO, was investigated; infarct volume and neurological deficits were assessed at 24 hours and up to 7 days. RESULTS: HBO had neuroprotective effects on transient MCAO when HBO was initiated within the first 6 hours, while it aggravated the ischemic injury histologically and clinically when initiated 12 hours after MCAO. In permanent MCAO, HBO did not reduce tissue damage regardless of the timing of therapy. CONCLUSIONS: HBO is highly efficient in reducing infarct volume and improving neurobehavioral outcome in transient MCAO within the first 6 hours. HBO at later time points (>or=12 hours) is harmful by increasing infarct volume. In permanent MCAO, HBO failed to improve infarct volume and clinical outcome. PMID: 14715976 [PubMed - in process] Resuscitation -- Room Air Appears To Do Less Brain Damage Than Pure Oxygen (September 19, 1998) — When a person's heart stops, standard resuscitation includes treatment with 100 percent oxygen. Now researchers at the University of land School of Medicine and Washington University School of Medicine and Health Sciences report that regular air -- which is 21 percent oxygen -- may be a better choice in some cases, helping prevent neurological damage that can occur after the brain is deprived of oxygen. > full story http://www.sciencedaily.com/releases/1998/09/980919123319.htm Nitric Oxide. 2003 Aug;9(1):18-23. Relationship between protein nitration and oxidation and development of hyperoxic seizures. Chavko M, Auker CR, McCarron RM. Operational and Undersea Medicine Department, Naval Medical Research Center, Silver Spring, MD 20910-7500, USA. ChavkoM@... Recent studies have implicated nitric oxide (NO*) as a mediator of CNS hyperbaric O2 (HBO2) toxicity. One mechanism by which NO* may contribute to HBO2-induced brain toxicity involves a neurotoxic, pro-oxidative action of NO* via the formation of the potent oxidant peroxynitrite (ONOO-). The present study compares: (a) the formation of protein nitrotyrosine as a marker of ONOO- accumulation and ( protein oxidation as an indicator of reactive oxygen species production during HBO2 exposure. Rats were exposed to 5 atm 100% O2 to pre-convulsive exposure or until the occurrence of electroencephalographic (EEG) seizures. After exposures, brains were analyzed for protein nitrotyrosine (NT) and protein carbonyl measurement by Western blot and for superoxide dismutase (SOD) activity by NBT assay. The results show a significant increase in protein NT, exceeding control level by several fold. There was only a slow and non-significant increase in the quantity of oxidized proteins during the pre-convulsive phase of HBO2 exposure. Levels of both protein NT and protein carbonyls were significantly (p<0.05) elevated after seizures. Total SOD activity was not changed during preconvulsive exposures, but was significantly (p<0.05) elevated post-seizures. The specific neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), significantly reduced the increases in seizure-induced protein NT and protein carbonyl and at the same time very effectively (p<0.05) delayed onset of HBO2 seizures. Pre-seizure increases in protein NT might indicate its role in the mechanism of HBO2-induced brain toxicity. This is supported by the observed capacity of 7-NI to inhibit tyrosine nitration and increase time to seizure. PMID: 14559428 [PubMed - in process] J Appl Physiol. 2004 Feb;96(2):784-91. Hyperoxia, reactive oxygen species, and hyperventilation: oxygen sensitivity of brain stem neurons. Dean JB, Mulkey DK, RA 3rd, Potter SJ, Putnam RW. Dept. of Anatomy and Physiology, 235C Bio. Sci. Bldg., 3640 Col. Glenn Hwy., State Univ., Dayton, OH 45435. jay.dean@... Hyperoxia is a popular model of oxidative stress. However, hyperoxic gas mixtures are routinely used for chemical denervation of peripheral O(2) receptors in in vivo studies of respiratory control. The underlying assumption whenever using hyperoxia is that there are no direct effects of molecular O(2) and reactive O(2) species (ROS) on brain stem function. In addition, control superfusates used routinely for in vitro studies of neurons in brain slices are, in fact, hyperoxic. Again, the assumption is that there are no direct effects of O(2) and ROS on neuronal activity. Research contradicts this assumption by demonstrating that O(2) has central effects on the brain stem respiratory centers and several effects on neurons in respiratory control areas; these need to be considered whenever hyperoxia is used. This mini-review summarizes the long-recognized, but seldom acknowledged, paradox of respiratory control known as hyperoxic hyperventilation. Several proposed mechanisms are discussed, including the recent hypothesis that hyperoxic hyperventilation is initiated by increased production of ROS during hyperoxia, which directly stimulates central CO(2) chemoreceptors in the solitary complex. Hyperoxic hyperventilation may provide clues into the fundamental role of redox signaling and ROS in central control of breathing; moreover, oxidative stress may play a role in respiratory control dysfunction. The practical implications of brain stem O(2) and ROS sensitivity are also considered relative to the present uses of hyperoxia in respiratory control research in humans, animals, and brain stem tissues. Recommendations for future research are also proposed. PMID: 14715688 [PubMed - in process] : Roper JM, Mazzatti DJ, Watkins RH, Maniscalco WM, Keng PC, O'Reilly MA. Related Articles, Links In vivo exposure to hyperoxia induces DNA damage in a population of alveolar type II epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2004 Jan 16 [Epub ahead of print] PMID: 14729512 [PubMed - as supplied by publisher] : Panayiotidis MI, Rancourt RC, CB, Riddle SR, Schneider BK, Ahmad S, White CW. Related Articles, Links Hyperoxia-induced DNA damage causes decreased DNA methylation in human lung epithelial-like a549 cells. Antioxid Redox Signal. 2004 Feb;6(1):129-36. PMID: 14713344 [PubMed - in process] _________________________________________________________________ Click here for a FREE online computer virus scan from McAfee. http://clinic.mcafee.com/clinic/ibuy/campaign.asp?cid=3963 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 9, 2004 Report Share Posted February 9, 2004 Dr G told me this himself. Certainly it is true that some children can have areas of over perfusion - these are shown as " white " patches on the Neurospect areas of highest perfusion.. - and is the case with my son's neurospect - there are examples in Dr G's presentations which show this. I have not seen clinical data about how much oxygen a brain cell can withstand, except that both Dr G and my local physician have expressed the same concern about HBOT. might be interesting to do a search. SPECT scan Hi All, Been lurking for, well, a few years. Anyway, have results of a SPECT scan and shows underdevelopment in the most forward part of both temporal lobes. My child is Aspie/HFA, 8yrs. old, no meds. Expressive/Respective language is biggest issue, followed by TOM and then balance. Was wondering if anyone as experience with therapies that have shown improvement, who have also done SPECT scans. We have done speech therapy for 6yrs., OT for 4yr., some gymnastics, some mood Bell, some biofeedback, most Locutour, most Sentence Master. (wanted to mention too, am big advocate of nutritional supplements - efa's Can now afford to do something like The Listening Program or Fast Forward, HBOT and not sure if I should be looking at something altogether different. Anyone out there with SPECT scans, tried a therapy, showed improvement, then did another SPECT scan? I know everyone's different but you have to start weeding out somewhere. Thank You, ______________________________________________ Responsibility for the content of this message lies strictly with the original author(s), and is not necessarily endorsed by or the opinion of the Research Institute. Responsibility for the content of this message lies strictly with the original author(s), and is not necessarily endorsed by or the opinion of the Research Institute. Quote Link to comment Share on other sites More sharing options...
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