Guest guest Posted February 6, 2008 Report Share Posted February 6, 2008 I have a number of items on HBOT that I will try to find and post. Our local ASA group is planning a talk in Feb on HBOT I need research information for my questions :-) Subject: A consenscus on recommendations on HBTO in autism? A summary of opinions on HBTO usage in autism. I know HBTO has been discussed and was mostly rejected as a valid therapy on this list; I have put down a few arguments here and suggest some aspect to consider before undergoing this therapy- Any comments to add? Lorene From an hypothetical point of view, you can find arguments for and against the use of HBTO. For is to restore a potential brain hypo perfusion (lot of work in France showing hypo perfusion in autism, see e.g. below reference 1). Against is the potential production of oxygen radicals and NO (identified in animal studies but usually under much higher HBOT pressure condition, 3-5 atmospheres, e.g. reference 2, there are many like these though). This is what concerns me most, as you could trigger inflammation with oxygen radical and NO, and triggering further inflammation (see reference 3) in children with autism is potentially a great risk to take- Vargas from s Hopkins University School of Medicine (reference 4) found evidence of brain inflammation in 11 out 11 postmortem brain from children with autism and in all tested Cerebro-spinal fluid samples taken from living patients. If one place brain inflammation behind a proportion of autistic cases (possibly the majority!), one would not like to risk to worsen this. From a practice/clinical point of you, there are more reports of no effects- or side effects in the medical and scientific literature than of positive effects, that is for MS, Cerebral P., epilepsy, to the exception of stroke/ brain damage which tend to have much more favorable reports. No need to say, there are no report of HBTO benefit or lack of benefit in autism. Yet, as far as MS is concerned, and even though a recent Cochrane review (highly respected opinion) concluded there was no proved benefit (reference 5), there are treatment centres all over the place for MS, UK, USA etc; why would they do it if this was not working? Talking to the patients I met in the chamber, I can see though that they were in a critical state of their disease progression; some clearly only had a few more months to live if the picture was to worsen. Would you then try anything that is available? The balance of judgment here is a different one than the one in autism. Reports from these patients to me were that there was some fog lifting, increased energy although at the start of the therapy for about 2 weeks, patients were more tired, but these improvements were reported to be only temporary, hence the need of doing the therapy daily- One man, got actually much more excited about him feeling very good having just started High doses of B6 and Magnesium (have you heard about this somewhere else????). Myself as a parent, I am not inclined at this stage to do this therapy because excessive oxydation could trigger more inflammation and if autism is linked to some kind of brain inflammation (this is for my son the most likely origin to his symptoms of sickness, fever with fits), I do not think that it is wise given the lack of knowledge we have at present. Also, the therapy as a cost (and I do not mean financial which can in some case be enormous though), but cost in time and quality of my relationship with my son. Asking him daily to agree to a long confinement under conditions that were not exactly easy, is asking a lot. You cannot talk with a mask over your face, you have to teach the child to cope with the change of pressure at the start and at the end of the session, this can be very painful (i have experience an atrocious session myself). The session with compression and decompression time was lasting 1h20 minutes, plus the time to be there and traveling, this was taking us a minimum of 2hr 30/day- 2hr30 that cannot be used for other educational therapy. You have to be pretty clear the cost of worth it under these conditions. I know of parents in the Us who would drive early in the morning to arrive to a centre and actually devote their entire day for this therapy and every day- Although this is a personal choice, this may be going beyond what is reasonable? I think my position at present is before I can recommend this to any child to have: 1- Evidence for brain hypo perfusion in the child. 2- Evidence of no brain inflammation 3- Have tried all other therapies before considering HBTO 4- Have in place a suitable monitoring for children at risk of developing epilepsy. 5- Have a strong anti-oxydant therapy in place whilst doing the therapy. References: 1- Ann Neurol. <javascript:AL_get(this, 'jour', 'Ann Neurol.');> 2005 Sep;58(3):466-9. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=16130096> Links <javascript:PopUpMenu2_Set(Menu16130096);> Click here to read <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=16130096 & db=\ pubmed & url=http://dx.doi.org/10.1002/ana.20597> *Autism severity and temporal lobe functional abnormalities.* *Gendry Meresse I* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Gendry+Meresse+I%22%5BAuthor%5D>, *Zilbovicius M* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Zilbovicius+M%22%5BAuthor%5D>, *Boddaert N* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Boddaert+N%22%5BAuthor%5D>, *Robel L* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Robel+L%22%5BAuthor%5D>, *Philippe A* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Philippe+A%22%5BAuthor%5D>, *Sfaello I* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Sfaello+I%22%5BAuthor%5D>, *Laurier L* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Laurier+L%22%5BAuthor%5D>, *Brunelle F* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Brunelle+F%22%5BAuthor%5D>, *Samson Y* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Samson+Y%22%5BAuthor%5D>, *Mouren MC* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Mouren+MC%22%5BAuthor%5D>, *Chabane N* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Chabane+N%22%5BAuthor%5D>. ERM 0205 Institut National de la Sante et de la Recherche Medicale CEA, Service Hospitalier F Joliot, DSV, DRM, CEA, Orsay, France. Two independent studies have described bilateral temporal hypoperfusion in autistic children. Temporal regions are implicated in social perception, language, and " theory-of-mind, " abilities that are impaired in autism. We investigated a putative relationship between cerebral blood flow (rCBF) measured at rest and clinical profile of 45 autistic children (Autism Diagnostic Interview-Revised [ADI-R] scores). A whole-brain covariance analysis was performed. Significant negative correlation was observed between rCBF and ADI-R score in the left superior temporal gyrus. The more severe the autistic syndrome, the more rCBF is low in this region, suggesting that left superior temporal hypoperfusion is related to autistic behavior severity. 2 * *J Neurophysiol. <javascript:AL_get(this, 'jour', 'J Neurophysiol.');> 2000 Apr;83(4):2022-9. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=10758112> Links <javascript:PopUpMenu2_Set(Menu10758112);> Click here to read <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3051 & uid=10758112 & db=\ pubmed & url=http://jn.physiology.org/cgi/pmidlookup?view=long & pmid=10758112> *Effect of hyperbaric oxygen treatment on nitric oxide and oxygen free radicals in rat brain.* *Elayan IM* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Elayan+IM%22%5BAuthor%5D>, *Axley MJ* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Axley+MJ%22%5BAuthor%5D>, *Prasad PV* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Prasad+PV%22%5BAuthor%5D>, *Ahlers ST* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Ahlers+ST%22%5BAuthor%5D>, *Auker CR* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Auker+CR%22%5BAuthor%5D>. Naval Medical Research Center, National Naval Medical Center, Bethesda, land 20889-5607, USA. Oxygen (O(2)) at high pressures acts as a neurotoxic agent leading to convulsions. The mechanism of this neurotoxicity is not known; however, oxygen free radicals and nitric oxide (NO) have been suggested as contributors. This study was designed to follow the formation of oxygen free radicals and NO in the rat brain under hyperbaric oxygen (HBO) conditions using in vivo microdialysis. Male Sprague-Dawley rats were exposed to 100% O(2) at a pressure of 3 atm absolute for 2 h. The formation of 2,3-dihydroxybenzoic acid (2, 3-DHBA) as a result of perfusing sodium salicylate was followed as an indicator for the formation of hydroxyl radicals. 2,3-DHBA levels in hippocampal and striatal dialysates of animals exposed to HBO conditions were not significantly different from controls. However, rats treated under the same conditions showed a six- and fourfold increase in nitrite/nitrate, break down products of NO decomposition, in hippocampal and striatal dialysates, respectively. This increase was completely blocked by the nitric oxide synthase (NOS) inhibitor L-nitroarginine methyl ester (L-NAME). Using neuronal NOS, we determined the NOS O(2) K(m) to be 158 ± 28 (SD) mmHg, a value which suggests that production of NO by NOS would increase approximately four- to fivefold under hyperbaric O(2) conditions, closely matching the measured increase in vivo. The increase in NO levels may be partially responsible for some of the detrimental effects of HBO conditions. 3- * *Neurotox Res. <javascript:AL_get(this, 'jour', 'Neurotox Res.');> 2000 Feb;1(3):197-233. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=12835102> Links <javascript:PopUpMenu2_Set(Menu12835102);> *Reactive oxygen species and reactive nitrogen species: relevance to cyto(neuro)toxic events and neurologic disorders. An overview.* *Metodiewa D* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Metodiewa+D%22%5BAuthor%5D>, *Koska C* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Koska+C%22%5BAuthor%5D>. Institute of Applied Radiation Chemistry, Technical University of Lodz, Poland. media@... Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are formed under physiological conditions in the human body and are removed by cellular antioxidant defense system. During oxidative stress their increased formation leads to tissue damage and cell death. This process may be especially important in the central nervous system (CNS) which is vulnerable to ROS and RNS damage as the result of the brain high O(2) consumption, high lipid content and the relatively low antioxidant defenses in brain, compared with other tissues. Recently there has been an increased number of reports suggesting the involvement of free radicals and their non-radical derivatives in a variety of pathological events and multistage disorders including neurotoxicity, apoptotic death of neurons and neural disorders: Alzheimer's (AD), Parkinson's disease (PD) and schizophrenia. Taking into consideration the basic molecular chemistry of ROS and RNS, their overall generation and location, in order to control or suppress their action it is essential to understand the fundamental aspects of this problem. In this presentation we review and summarize the basics of all the recently known and important properties, mechanisms, molecular targets, possible involvement in cellular (neural) degeneration and apoptotic death and in pathogenesis of AD, PD and schizophrenia. The aim of this article is to provide an overview of our current knowledge of this problem and to inspire experimental strategies for the evaluation of optimum innovative therapeutic trials. Another purpose of this work is to shed some light on one of the most exciting recent advances in our understanding of the CNS: the realisation that RNS pathway is highly relevant to normal brain metabolism and to neurologic disorders as well. The interactions of RNS and ROS, their interconversions and the ratio of RNS/ROS could be an important neural tissue injury mechanism(s) involved into etiology and pathogenesis of AD, PD and schizophrenia. It might be possible to direct therapeutic efforts at oxidative events in the pathway of neuron degeneration and apoptotic death. From reviewed data, no single substance can be recommended for use in human studies. Some of the recent therapeutic strategies and neuroprotective trials need further development particularly those of antioxidants enhancement. Such an approach should also consider using combinations of radical(s) scavengers rather than a single substance. 4- * *Ann Neurol. <javascript:AL_get(this, 'jour', 'Ann Neurol.');> 2005 Jan;57(1):67-81. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=15546155> Links <javascript:PopUpMenu2_Set(Menu15546155);> Click here to read <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=15546155 & db=\ pubmed & url=http://dx.doi.org/10.1002/ana.20315> Erratum in: * Ann Neurol. 2005 Feb;57(2):304. *Neuroglial activation and neuroinflammation in the brain of patients with autism.* *Vargas DL* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Vargas+DL%22%5BAuthor%5D>, *Nascimbene C* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Nascimbene+C%22%5BAuthor%5D>, *Krishnan C* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Krishnan+C%22%5BAuthor%5D>, *Zimmerman AW* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Zimmerman+AW%22%5BAuthor%5D>, *Pardo CA* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Pardo+CA%22%5BAuthor%5D>. Department of Neurology, s Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA. Autism is a neurodevelopmental disorder characterized by impaired communication and social interaction and may be accompanied by mental retardation and epilepsy. Its cause remains unknown, despite evidence that genetic, environmental, and immunological factors may play a role in its pathogenesis. To investigate whether immune-mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme-linked immunosorbent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic patients and determined the magnitude of neuroglial and inflammatory reactions and their cytokine expression profiles. Brain tissues from cerebellum, midfrontal, and cingulate gyrus obtained at autopsy from 11 patients with autism were used for morphological studies. Fresh-frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profiling. We demonstrate an active neuroinflammatory process in the cerebral cortex, white matter, and notably in cerebellum of autistic patients. Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 and tumor growth factor-beta1, derived from neuroglia, were the most prevalent cytokines in brain tissues. CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1. Our findings indicate that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain. 5- Cochrane Database Syst Rev. <javascript:AL_get(this, 'jour', 'Cochrane Database Syst Rev.');> 2004;(1):CD003057. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=14974004> Links <javascript:PopUpMenu2_Set(Menu14974004);> Click here to read <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=14974004 & db=\ pubmed & url=http://dx.doi.org/10.1002/14651858.CD003057.pub2> *Hyperbaric oxygen therapy for multiple sclerosis.* * M* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22+M%22%5BAuthor%5D>, *Heard R* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Heard+R%22%5BAuthor%5D>. Diving and Hyperbaric Medicine, Prince of Wales Hospital, Barker St, Randwick, NSW, Australia. BACKGROUND: Multiple Sclerosis (MS) is a chronic, recurrent and progressive illness with no cure. On the basis of speculative pathophysiology, it has been suggested that Hyperbaric Oxygen Therapy (HBOT) may slow or reverse the progress of the disease. OBJECTIVES: The object of this review was to evaluate the efficacy and safety of HBOT in the treatment of MS. SEARCH STRATEGY: We searched the Cochrane MS Group trials register (July 2002), the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 2, 2002), MEDLINE (January 1966 to October 2002) and the National Library of Medicine (NLM) database (July 2002), along with specialised hyperbaric resources and handsearching of relevant journals and proceedings. SELECTION CRITERIA: All randomised, controlled trials involving a comparison between HBOT and a sham therapy in MS were evaluated. DATA COLLECTION AND ANALYSIS: Two reviewers independently appraised all comparative trials identified, extracted data and scored them for methodological quality. MAIN RESULTS: We identified ten reports of nine trials that satisfied selection criteria (504 participants in total). Two trials produced generally positive results, while the remaining seven reported generally no evidence of a treatment effect. None of our three a priori subgroup analyses placed these two trials in the same group and were therefore unable to account for this difference. Three analyses (of 21) did indicate some benefit. For example, the mean Expanded Disability Status Scale (EDSS) at 12 months was improved in the HBOT group (group mean reduction in EDSS compared to sham -0.85 of a point, 95% confidence interval -1.28 to -0.42, P = 0.0001). Only the two generally positive trials reported on this outcome at this time (16% of the total participants in this review). REVIEWER'S CONCLUSIONS: We found no consistent evidence to confirm a beneficial effect of hyperbaric oxygen therapy for the treatment of multiple sclerosis and do not believe routine use is justified. The small number of analyses suggestive of benefit are isolated, difficult to ascribe with biological plausibility and would need to be confirmed in future well-designed trials. Such trials are not, in our view, justified by this review. *_A few more references of some interest:_* 6- a risk for seizure, but in adult the risk is failry low; 1 in 3,400 about patients. *Central nervous system oxygen toxicity during routine hyperbaric oxygen therapy.* *Hampson N* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Hampson+N%22%5BAuthor%5D>, *Atik D* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Atik+D%22%5BAuthor%5D>. Center for Hyperbaric Medicine, Virginia Mason Medical Center, Seattle, Washington, USA. Hyperbaric oxygen therapy is associated with a recognized risk for clinically apparent central nervous system (CNS) toxicity. The risk for oxygen-induced convulsions during routine hyperbaric treatment of most routine conditions is extremely low. However, reports from the 1980's describing the incidence of CNS oxygen toxicity differ significantly from more recent reports since 1996. This retrospective study was conducted to determine the incidence of hyperbaric oxygen-induced seizures among patients treated at our facility for routine, non-emergent indications. In addition, the period studied was selected to examine the incidence of CNS oxygen toxicity between two brands of oxygen delivery hoods. We reviewed our treatment experience for approximately 10,000 routine patient treatments performed prior to and following a change in the brand of oxygen hoods used. Among 20,328 total patient treatments performed from 1992 to 2001, 6 patients experienced an oxygen-toxic seizure for an overall incidence of 1 in 3,388 treatments (0.03%). No difference in seizure incidence was seen between the two brands of oxygen hoods utilized. We conclude that the incidence of oxygen-toxic seizures in our patient population is approximately three-fold greater than historical reports and in agreement with more recent reports. The reason for this apparent increase in incidence of CNS oxygen toxicity is unknown. 7- Annecdotal report of complication in 2 children with CP- I could not find any annectdotcal reports of improvements, but there are some. *Hyperbaric oxygen therapy for cerebral palsy: two complications of treatment.* *Nuthall G* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Nuthall+G%22%5BAuthor%5D>, *Seear M* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Seear+M%22%5BAuthor%5D>, *Lepawsky M* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Lepawsky+M%22%5BAuthor%5D>, *Wensley D* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Wensley+D%22%5BAuthor%5D>, *Skippen P* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Skippen+P%22%5BAuthor%5D>, *Hukin J* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Hukin+J%22%5BAuthor%5D>. Intensive Care Unit, Children's and Women's Hospital, Vancouver, Canada. There is growing interest in the use of hyperbaric oxygen therapy (HBO(2)) for children with cerebral palsy. Although there is no rigorous evidence to support this management, private hyperbaric centers have been established throughout the United States and Canada. There is likely to be increasing pressure on pediatricians and other health professionals to prescribe HBO(2). We describe 2 children with cerebral palsy who suffered significant morbidity immediately after treatment with hyperbaric oxygen. Both the temporal association and pathologic findings suggest that the hyperbaric treatment is likely to have been responsible for the resulting complications. As with any new therapy, we suggest waiting for the results of a randomized, controlled trial before recommending this treatment. 8- One type of brain infection in children, unlikley linked to the brain inflammation seen in autism, where HBTO was found to be of benefit. Childs Nerv Syst. <javascript:AL_get(this, 'jour', 'Childs Nerv Syst.');> 2006 Jan;22(1):38-42. Epub 2005 May 5. Related Articles, <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed\ _pubmed & from_uid=15875200> Links <javascript:PopUpMenu2_Set(Menu15875200);> Click here to read <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3055 & uid=15875200 & db=\ pubmed & url=http://dx.doi.org/10.1007/s00381-005-1147-z> *Hyperbaric oxygen therapy for the treatment of brain abscess in children.* *Kurschel S* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Kurschel+S%22%5BAuthor%5D>, *Mohia A* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Mohia+A%22%5BAuthor%5D>, *Weigl V* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Weigl+V%22%5BAuthor%5D>, *Eder HG* <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Eder+HG%22%5BAuthor%5D>. Department of Neurosurgery, Medical University, Auenbruggerplatz 29, 8036, Graz, Austria, hans.eder@.... INTRODUCTION: The treatment of brain abscess remains a challenging topic usually involving a multimodal concept. METHODS: We report our experience with hyperbaric oxygen (HBO) therapy in five children presenting with brain abscesses between 1995 and 2002 at the Department of Neurosurgery, Graz. Mean age was 14.8 (range 11-17 years). All abscesses were located supratentorially. One child had a single abscess and one had multilocated abscesses. Two other patients presented with both subdural empyema and brain abscess, one of them showing an epidural empyema as well. In another child, the brain abscess was associated with meningoencephalitis and subdural empyema. In all of them the underlying condition was spread of infection from the paranasal sinuses, except for one, who was immunocompromised due to cytotoxic chemotherapy for acute lymphocytic leukaemia. RESULTS: One single brain abscess and one of the multiple abscesses were drained. All subdural/epidural empyemas were treated surgically. Antibiotics were administered intravenously for 13 to 22 days (mean 22 days). All patients underwent HBO therapy; the number of treatments ranged from 26 to 45 " dives " (mean 30). Treatments were given once daily at 2.2 atmosphere absolutes for 60 min at 12 m. During the hospital stay all improved their clinical condition, with continued regression of abnormalities on magnetic resonance imaging (MRI). In the following weeks, other interventions were performed to treat the origin of the infections. At 6 months follow-up they were all in good clinical condition, either symptom free or with minor residual symptoms. MRI at this time showed no evidence of disease in three, a residual dural enhancement in one and a residual shrunken collection in the child with multilocated abscesses. No recurrence was observed during a mean follow-up of 21 months (range from 7 to 72 months). CONCLUSION: HBO therapy in children with brain abscesses seems to be safe and effective, even when they are associated with subdural or epidural empyemas. It provides a helpful adjuvant tool in the usual multimodal treatment of cerebral infections and may reduce the intravenous course of antibiotics and, consequently, the duration of hospitalization. Multidisciplinary management is recommended to optimize care for these critically ill children. _______ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted February 6, 2008 Report Share Posted February 6, 2008 Thank you very much for the info! >From: Doris and Steve <sjsmith@...> >Date: 2008/02/06 Wed PM 05:59:32 CST > < > >Subject: [Fwd: Hbot item] > >I have a number of items on HBOT that I will try to find and post. >Our local ASA group is planning a talk in Feb on HBOT >I need research information for my questions :-) > >Subject: A consenscus on recommendations on HBTO in autism? > >A summary of opinions on HBTO usage in autism. > >I know HBTO has been discussed and was mostly rejected as a valid >therapy on this list; I have put down a few arguments here and suggest >some aspect to consider before undergoing this therapy- Any comments to add? > >Lorene > >From an hypothetical point of view, you can find arguments for and >against the use of HBTO. For is to restore a potential brain hypo >perfusion (lot of work in France showing hypo perfusion in autism, see >e.g. below reference 1). Against is the potential production of oxygen >radicals and NO (identified in animal studies but usually under much >higher HBOT pressure condition, 3-5 atmospheres, e.g. reference 2, there >are many like these though). This is what concerns me most, as you >could trigger inflammation with oxygen radical and NO, and triggering >further inflammation (see reference 3) in children with autism is >potentially a great risk to take- Vargas from s Hopkins University >School of Medicine (reference 4) found evidence of brain inflammation in >11 out 11 postmortem brain from children with autism and in all tested >Cerebro-spinal fluid samples taken from living patients. If one place >brain inflammation behind a proportion of autistic cases (possibly the >majority!), one would not like to risk to worsen this. > >From a practice/clinical point of you, there are more reports of no >effects- or side effects in the medical and scientific literature than >of positive effects, that is for MS, Cerebral P., epilepsy, to the >exception of stroke/ brain damage which tend to have much more favorable >reports. No need to say, there are no report of HBTO benefit or lack of >benefit in autism. > >Yet, as far as MS is concerned, and even though a recent Cochrane review >(highly respected opinion) concluded there was no proved benefit >(reference 5), there are treatment centres all over the place for MS, >UK, USA etc; why would they do it if this was not working? Talking to >the patients I met in the chamber, I can see though that they were in a >critical state of their disease progression; some clearly only had a few >more months to live if the picture was to worsen. Would you then try >anything that is available? The balance of judgment here is a different >one than the one in autism. Reports from these patients to me were that >there was some fog lifting, increased energy although at the start of >the therapy for about 2 weeks, patients were more tired, but these >improvements were reported to be only temporary, hence the need of doing >the therapy daily- One man, got actually much more excited about him >feeling very good having just started High doses of B6 and Magnesium >(have you heard about this somewhere else????). > >Myself as a parent, I am not inclined at this stage to do this therapy >because excessive oxydation could trigger more inflammation and if >autism is linked to some kind of brain inflammation (this is for my son >the most likely origin to his symptoms of sickness, fever with fits), I >do not think that it is wise given the lack of knowledge we have at present. > >Also, the therapy as a cost (and I do not mean financial which can in >some case be enormous though), but cost in time and quality of my >relationship with my son. Asking him daily to agree to a long >confinement under conditions that were not exactly easy, is asking a >lot. You cannot talk with a mask over your face, you have to teach the >child to cope with the change of pressure at the start and at the end of >the session, this can be very painful (i have experience an atrocious >session myself). The session with compression and decompression time was >lasting 1h20 minutes, plus the time to be there and traveling, this was >taking us a minimum of 2hr 30/day- 2hr30 that cannot be used for other >educational therapy. You have to be pretty clear the cost of worth it >under these conditions. I know of parents in the Us who would drive >early in the morning to arrive to a centre and actually devote their >entire day for this therapy and every day- Although this is a personal >choice, this may be going beyond what is reasonable? > >I think my position at present is before I can recommend this to any >child to have: > >1- Evidence for brain hypo perfusion in the child. >2- Evidence of no brain inflammation >3- Have tried all other therapies before considering HBTO >4- Have in place a suitable monitoring for children at risk of >developing epilepsy. >5- Have a strong anti-oxydant therapy in place whilst doing the therapy. > >References: > >1- >Ann Neurol. <javascript:AL_get(this, 'jour', 'Ann Neurol.');> 2005 >Sep;58(3):466-9. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=16130096> >Links <javascript:PopUpMenu2_Set(Menu16130096);> > >Click here to read ><http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=16130096 & db\ =pubmed & url=http://dx.doi.org/10.1002/ana.20597> >*Autism severity and temporal lobe functional abnormalities.* > >*Gendry Meresse I* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Gendry+Meresse+I%22%5BAuthor%5D>, >*Zilbovicius M* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Zilbovicius+M%22%5BAuthor%5D>, >*Boddaert N* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Boddaert+N%22%5BAuthor%5D>, >*Robel L* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Robel+L%22%5BAuthor%5D>, >*Philippe A* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Philippe+A%22%5BAuthor%5D>, >*Sfaello I* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Sfaello+I%22%5BAuthor%5D>, >*Laurier L* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Laurier+L%22%5BAuthor%5D>, >*Brunelle F* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Brunelle+F%22%5BAuthor%5D>, >*Samson Y* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Samson+Y%22%5BAuthor%5D>, >*Mouren MC* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Mouren+MC%22%5BAuthor%5D>, >*Chabane N* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Chabane+N%22%5BAuthor%5D>. > >ERM 0205 Institut National de la Sante et de la Recherche Medicale CEA, >Service Hospitalier F Joliot, DSV, DRM, CEA, Orsay, France. > >Two independent studies have described bilateral temporal hypoperfusion >in autistic children. Temporal regions are implicated in social >perception, language, and " theory-of-mind, " abilities that are impaired >in autism. We investigated a putative relationship between cerebral >blood flow (rCBF) measured at rest and clinical profile of 45 autistic >children (Autism Diagnostic Interview-Revised [ADI-R] scores). A >whole-brain covariance analysis was performed. Significant negative >correlation was observed between rCBF and ADI-R score in the left >superior temporal gyrus. The more severe the autistic syndrome, the more >rCBF is low in this region, suggesting that left superior temporal >hypoperfusion is related to autistic behavior severity. > >2 > >* *J Neurophysiol. <javascript:AL_get(this, 'jour', 'J Neurophysiol.<wbr>');> >2000 Apr;83(4):2022-9. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=10758112> >Links <javascript:PopUpMenu2_Set(Menu10758112);> > >Click here to read > <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3051 & uid=10758112 & db=\ pubmed & url=http://jn.physiology.org/cgi/pmidlookup?view=long & pmid=10758112> > *Effect of hyperbaric oxygen treatment on nitric oxide and oxygen > free radicals in rat brain.* > >*Elayan IM* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Elayan+IM%22%5BAuthor%5D>, > *Axley MJ* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Axley+MJ%22%5BAuthor%5D>, > *Prasad PV* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Prasad+PV%22%5BAuthor%5D>, > *Ahlers ST* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Ahlers+ST%22%5BAuthor%5D>, > *Auker CR* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Auker+CR%22%5BAuthor%5D>. > >Naval Medical Research Center, National Naval Medical Center, > Bethesda, land 20889-5607, USA. > >Oxygen (O(2)) at high pressures acts as a neurotoxic agent leading > to convulsions. The mechanism of this neurotoxicity is not known; > however, oxygen free radicals and nitric oxide (NO) have been > suggested as contributors. This study was designed to follow the > formation of oxygen free radicals and NO in the rat brain under > hyperbaric oxygen (HBO) conditions using in vivo microdialysis. Male > Sprague-Dawley rats were exposed to 100% O(2) at a pressure of 3 atm > absolute for 2 h. The formation of 2,3-dihydroxybenzoic acid (2, > 3-DHBA) as a result of perfusing sodium salicylate was followed as > an indicator for the formation of hydroxyl radicals. 2,3-DHBA levels > in hippocampal and striatal dialysates of animals exposed to HBO > conditions were not significantly different from controls. However, > rats treated under the same conditions showed a six- and fourfold > increase in nitrite/nitrate, break down products of NO > decomposition, in hippocampal and striatal dialysates, respectively. > This increase was completely blocked by the nitric oxide synthase > (NOS) inhibitor L-nitroarginine methyl ester (L-NAME). Using > neuronal NOS, we determined the NOS O(2) K(m) to be 158 ± 28 (SD) > mmHg, a value which suggests that production of NO by NOS would > increase approximately four- to fivefold under hyperbaric O(2) > conditions, closely matching the measured increase in vivo. The > increase in NO levels may be partially responsible for some of the > detrimental effects of HBO conditions. > >3- > >* *Neurotox Res. <javascript:AL_get(this, 'jour', 'Neurotox Res.');> >2000 Feb;1(3):197-233. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=12835102> >Links <javascript:PopUpMenu2_Set(Menu12835102);> > >*Reactive oxygen species and reactive nitrogen species: relevance to > cyto(neuro)toxic events and neurologic disorders. An overview.* > >*Metodiewa D* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Metodiewa+D%22%5BAuthor%5D>, > *Koska C* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Koska+C%22%5BAuthor%5D>. > >Institute of Applied Radiation Chemistry, Technical University of > Lodz, Poland. media@... > >Reactive oxygen species (ROS) and reactive nitrogen species (RNS) > are formed under physiological conditions in the human body and are > removed by cellular antioxidant defense system. During oxidative > stress their increased formation leads to tissue damage and cell > death. This process may be especially important in the central > nervous system (CNS) which is vulnerable to ROS and RNS damage as > the result of the brain high O(2) consumption, high lipid content > and the relatively low antioxidant defenses in brain, compared with > other tissues. Recently there has been an increased number of > reports suggesting the involvement of free radicals and their > non-radical derivatives in a variety of pathological events and > multistage disorders including neurotoxicity, apoptotic death of > neurons and neural disorders: Alzheimer's (AD), Parkinson's disease > (PD) and schizophrenia. Taking into consideration the basic > molecular chemistry of ROS and RNS, their overall generation and > location, in order to control or suppress their action it is > essential to understand the fundamental aspects of this problem. In > this presentation we review and summarize the basics of all the > recently known and important properties, mechanisms, molecular > targets, possible involvement in cellular (neural) degeneration and > apoptotic death and in pathogenesis of AD, PD and schizophrenia. The > aim of this article is to provide an overview of our current > knowledge of this problem and to inspire experimental strategies for > the evaluation of optimum innovative therapeutic trials. Another > purpose of this work is to shed some light on one of the most > exciting recent advances in our understanding of the CNS: the > realisation that RNS pathway is highly relevant to normal brain > metabolism and to neurologic disorders as well. The interactions of > RNS and ROS, their interconversions and the ratio of RNS/ROS could > be an important neural tissue injury mechanism(s) involved into > etiology and pathogenesis of AD, PD and schizophrenia. It might be > possible to direct therapeutic efforts at oxidative events in the > pathway of neuron degeneration and apoptotic death. From reviewed > data, no single substance can be recommended for use in human > studies. Some of the recent therapeutic strategies and > neuroprotective trials need further development particularly those > of antioxidants enhancement. Such an approach should also consider > using combinations of radical(s) scavengers rather than a single > substance. > >4- > >* *Ann Neurol. <javascript:AL_get(this, 'jour', 'Ann Neurol.');> 2005 >Jan;57(1):67-81. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=15546155> >Links <javascript:PopUpMenu2_Set(Menu15546155);> > >Click here to read > <http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=15546155 & db=\ pubmed & url=http://dx.doi.org/10.1002/ana.20315> > Erratum in: > >* Ann Neurol. 2005 Feb;57(2):304. > >*Neuroglial activation and neuroinflammation in the brain of > patients with autism.* > >*Vargas DL* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Vargas+DL%22%5BAuthor%5D>, > *Nascimbene C* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Nascimbene+C%22%5BAuthor%5D>, > *Krishnan C* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Krishnan+C%22%5BAuthor%5D>, > *Zimmerman AW* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Zimmerman+AW%22%5BAuthor%5D>, > *Pardo CA* > <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed\ _Abstract & term=%22Pardo+CA%22%5BAuthor%5D>. > >Department of Neurology, s Hopkins University School of > Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA. > >Autism is a neurodevelopmental disorder characterized by impaired > communication and social interaction and may be accompanied by > mental retardation and epilepsy. Its cause remains unknown, despite > evidence that genetic, environmental, and immunological factors may > play a role in its pathogenesis. To investigate whether > immune-mediated mechanisms are involved in the pathogenesis of > autism, we used immunocytochemistry, cytokine protein arrays, and > enzyme-linked immunosorbent assays to study brain tissues and > cerebrospinal fluid (CSF) from autistic patients and determined the > magnitude of neuroglial and inflammatory reactions and their > cytokine expression profiles. Brain tissues from cerebellum, > midfrontal, and cingulate gyrus obtained at autopsy from 11 patients > with autism were used for morphological studies. Fresh-frozen > tissues available from seven patients and CSF from six living > autistic patients were used for cytokine protein profiling. We > demonstrate an active neuroinflammatory process in the cerebral > cortex, white matter, and notably in cerebellum of autistic > patients. Immunocytochemical studies showed marked activation of > microglia and astroglia, and cytokine profiling indicated that > macrophage chemoattractant protein (MCP)-1 and tumor growth > factor-beta1, derived from neuroglia, were the most prevalent > cytokines in brain tissues. CSF showed a unique proinflammatory > profile of cytokines, including a marked increase in MCP-1. Our > findings indicate that innate neuroimmune reactions play a > pathogenic role in an undefined proportion of autistic patients, > suggesting that future therapies might involve modifying neuroglial > responses in the brain. > >5- > >Cochrane Database Syst Rev. <javascript:AL_get(this, 'jour', 'Cochrane >Database Syst Rev.');> 2004;(1):CD003057. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=14974004> >Links <javascript:PopUpMenu2_Set(Menu14974004);> > >Click here to read ><http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3058 & uid=14974004 & db\ =pubmed & url=http://dx.doi.org/10.1002/14651858.CD003057.pub2> >*Hyperbaric oxygen therapy for multiple sclerosis.* > >* M* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22+M%22%5BAuthor%5D>, >*Heard R* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Heard+R%22%5BAuthor%5D>. > >Diving and Hyperbaric Medicine, Prince of Wales Hospital, Barker St, >Randwick, NSW, Australia. > >BACKGROUND: Multiple Sclerosis (MS) is a chronic, recurrent and >progressive illness with no cure. On the basis of speculative >pathophysiology, it has been suggested that Hyperbaric Oxygen Therapy >(HBOT) may slow or reverse the progress of the disease. OBJECTIVES: The >object of this review was to evaluate the efficacy and safety of HBOT in >the treatment of MS. SEARCH STRATEGY: We searched the Cochrane MS Group >trials register (July 2002), the Cochrane Central Register of Controlled >Trials (The Cochrane Library, Issue 2, 2002), MEDLINE (January 1966 to >October 2002) and the National Library of Medicine (NLM) database (July >2002), along with specialised hyperbaric resources and handsearching of >relevant journals and proceedings. SELECTION CRITERIA: All randomised, >controlled trials involving a comparison between HBOT and a sham therapy >in MS were evaluated. DATA COLLECTION AND ANALYSIS: Two reviewers >independently appraised all comparative trials identified, extracted >data and scored them for methodological quality. MAIN RESULTS: We >identified ten reports of nine trials that satisfied selection criteria >(504 participants in total). Two trials produced generally positive >results, while the remaining seven reported generally no evidence of a >treatment effect. None of our three a priori subgroup analyses placed >these two trials in the same group and were therefore unable to account >for this difference. Three analyses (of 21) did indicate some benefit. >For example, the mean Expanded Disability Status Scale (EDSS) at 12 >months was improved in the HBOT group (group mean reduction in EDSS >compared to sham -0.85 of a point, 95% confidence interval -1.28 to >-0.42, P = 0.0001). Only the two generally positive trials reported on >this outcome at this time (16% of the total participants in this >review). REVIEWER'S CONCLUSIONS: We found no consistent evidence to >confirm a beneficial effect of hyperbaric oxygen therapy for the >treatment of multiple sclerosis and do not believe routine use is >justified. The small number of analyses suggestive of benefit are >isolated, difficult to ascribe with biological plausibility and would >need to be confirmed in future well-designed trials. Such trials are >not, in our view, justified by this review. > >*_A few more references of some interest:_* > >6- a risk for seizure, but in adult the risk is failry low; 1 in 3,400 >about patients. > >*Central nervous system oxygen toxicity during routine hyperbaric oxygen >therapy.* > >*Hampson N* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Hampson+N%22%5BAuthor%5D>, >*Atik D* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Atik+D%22%5BAuthor%5D>. > >Center for Hyperbaric Medicine, Virginia Mason Medical Center, Seattle, >Washington, USA. > >Hyperbaric oxygen therapy is associated with a recognized risk for >clinically apparent central nervous system (CNS) toxicity. The risk for >oxygen-induced convulsions during routine hyperbaric treatment of most >routine conditions is extremely low. However, reports from the 1980's >describing the incidence of CNS oxygen toxicity differ significantly >from more recent reports since 1996. This retrospective study was >conducted to determine the incidence of hyperbaric oxygen-induced >seizures among patients treated at our facility for routine, >non-emergent indications. In addition, the period studied was selected >to examine the incidence of CNS oxygen toxicity between two brands of >oxygen delivery hoods. We reviewed our treatment experience for >approximately 10,000 routine patient treatments performed prior to and >following a change in the brand of oxygen hoods used. Among 20,328 total >patient treatments performed from 1992 to 2001, 6 patients experienced >an oxygen-toxic seizure for an overall incidence of 1 in 3,388 >treatments (0.03%). No difference in seizure incidence was seen between >the two brands of oxygen hoods utilized. We conclude that the incidence >of oxygen-toxic seizures in our patient population is approximately >three-fold greater than historical reports and in agreement with more >recent reports. The reason for this apparent increase in incidence of >CNS oxygen toxicity is unknown. > >7- Annecdotal report of complication in 2 children with CP- I could not >find any annectdotcal reports of improvements, but there are some. > >*Hyperbaric oxygen therapy for cerebral palsy: two complications of >treatment.* > >*Nuthall G* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Nuthall+G%22%5BAuthor%5D>, >*Seear M* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Seear+M%22%5BAuthor%5D>, >*Lepawsky M* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Lepawsky+M%22%5BAuthor%5D>, >*Wensley D* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Wensley+D%22%5BAuthor%5D>, >*Skippen P* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Skippen+P%22%5BAuthor%5D>, >*Hukin J* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Hukin+J%22%5BAuthor%5D>. > >Intensive Care Unit, Children's and Women's Hospital, Vancouver, Canada. > >There is growing interest in the use of hyperbaric oxygen therapy >(HBO(2)) for children with cerebral palsy. Although there is no rigorous >evidence to support this management, private hyperbaric centers have >been established throughout the United States and Canada. There is >likely to be increasing pressure on pediatricians and other health >professionals to prescribe HBO(2). We describe 2 children with cerebral >palsy who suffered significant morbidity immediately after treatment >with hyperbaric oxygen. Both the temporal association and pathologic >findings suggest that the hyperbaric treatment is likely to have been >responsible for the resulting complications. As with any new therapy, we >suggest waiting for the results of a randomized, controlled trial before >recommending this treatment. > >8- One type of brain infection in children, unlikley linked to the brain >inflammation seen in autism, where HBTO was found to be of benefit. > >Childs Nerv Syst. <javascript:AL_get(this, 'jour', 'Childs Nerv >Syst.');> 2006 Jan;22(1):38-42. Epub 2005 May 5. Related Articles, ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubme\ d_pubmed & from_uid=15875200> >Links <javascript:PopUpMenu2_Set(Menu15875200);> > >Click here to read ><http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3055 & uid=15875200 & db\ =pubmed & url=http://dx.doi.org/10.1007/s00381-005-1147-z> >*Hyperbaric oxygen therapy for the treatment of brain abscess in children.* > >*Kurschel S* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Kurschel+S%22%5BAuthor%5D>, >*Mohia A* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Mohia+A%22%5BAuthor%5D>, >*Weigl V* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Weigl+V%22%5BAuthor%5D>, >*Eder HG* ><http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubme\ d_Abstract & term=%22Eder+HG%22%5BAuthor%5D>. > >Department of Neurosurgery, Medical University, Auenbruggerplatz 29, >8036, Graz, Austria, hans.eder@.... > >INTRODUCTION: The treatment of brain abscess remains a challenging topic >usually involving a multimodal concept. METHODS: We report our >experience with hyperbaric oxygen (HBO) therapy in five children >presenting with brain abscesses between 1995 and 2002 at the Department >of Neurosurgery, Graz. Mean age was 14.8 (range 11-17 years). All >abscesses were located supratentorially. One child had a single abscess >and one had multilocated abscesses. Two other patients presented with >both subdural empyema and brain abscess, one of them showing an epidural >empyema as well. In another child, the brain abscess was associated with >meningoencephalitis and subdural empyema. In all of them the underlying >condition was spread of infection from the paranasal sinuses, except for >one, who was immunocompromised due to cytotoxic chemotherapy for acute >lymphocytic leukaemia. RESULTS: One single brain abscess and one of the >multiple abscesses were drained. All subdural/epidural empyemas were >treated surgically. Antibiotics were administered intravenously for 13 >to 22 days (mean 22 days). All patients underwent HBO therapy; the >number of treatments ranged from 26 to 45 " dives " (mean 30). Treatments >were given once daily at 2.2 atmosphere absolutes for 60 min at 12 m. >During the hospital stay all improved their clinical condition, with >continued regression of abnormalities on magnetic resonance imaging >(MRI). In the following weeks, other interventions were performed to >treat the origin of the infections. At 6 months follow-up they were all >in good clinical condition, either symptom free or with minor residual >symptoms. MRI at this time showed no evidence of disease in three, a >residual dural enhancement in one and a residual shrunken collection in >the child with multilocated abscesses. No recurrence was observed during >a mean follow-up of 21 months (range from 7 to 72 months). CONCLUSION: >HBO therapy in children with brain abscesses seems to be safe and >effective, even when they are associated with subdural or epidural >empyemas. It provides a helpful adjuvant tool in the usual multimodal >treatment of cerebral infections and may reduce the intravenous course >of antibiotics and, consequently, the duration of hospitalization. >Multidisciplinary management is recommended to optimize care for these >critically ill children. > >_______ > > Sincerely, Juarez, M.S., Marriage and Family Therapist Quote Link to comment Share on other sites More sharing options...
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