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HYPERBARIC OXYGEN THERAPY AND AUTISM
Giuseppina Benincasa-Feingold, MD HYPERBARIC OXYGEN THERAPY AND AUTISM GIUSEPPINA BENINCASA-FEINGOLD M.D. USAAA 2006 International Conference
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Hyperbaric Medicine Definition Hyperbaric Oxygen:
Hyperbaric Oxygen (HBO2) treatment, in which a patient breaths 100% oxygen while the pressure of the treatment chamber is increased to a point higher than sea level pressure (i.e. > 1 ata)
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BOYLE’S LAW ABSOLUTE PRESSURE AND VOLUME ARE INVERSELY PROPORTIONAL
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DALTON’S LAW TOTAL PRESSURE OF A MIXTURE OF GASES IS EQUAL TO THE SUM OF PARTIAL PRESSURES OF THE GASES IN THE MIXTURE
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HENRY’S LAW THE PARTIAL PRESSURE OF ANY GAS IN A LIQUID IS EQUAL TO THE PARTIAL PRESSURE OF THAT GAS EXERTED ON THE SURFACE OF THE LIQUID IN EQUILIBRIUM
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CHARLES’ LAW P1V1=P2V2 T T2 AS YOU COMPRESS GAS IT GETS HOTTER, CONVERSELY AS YOU DECOMPRESS IT GETS COOLER
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HYPERBARIC OXYGEN THERAPY
CAN A HUMAN BEING SURVIVE BREATHING LESS THAN 21% OXYGEN? YES: AT 7 ATA 3%OXYGEN IS EQUAL TO 21% O2 EXPERIMENT WITH A DOG-BLOODLESS LIFE
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ACUTE EFFECTS OF HBOT CLEARANCE OF OBSTRUCTING GAS BUBBLES-SIZE IN CIRCULATION DECREASED CARBON MONOXIDE POISONING-DISPALCES CO FROM HEMOGLOBIN AND CYTOCHROME C, INCREASES ATP AND DECREASES LACTATE FORMATION
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ACUTE EFFECTS OF HBOT WOUND HEALING-ENHANCES FIBROBLAST PROLIFERATION AND COLLEGEN PRODUCTION PROMOTES NEOVASCULARIZATION ACUTE INJURIES- DECREASES EDEMA, IMPROVES REPERFUSION INJURY
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ACUTE EFFECTS OF HBOT INFECTIONS-INCREASES PARTIAL PRESSURE OF OXYGEN IN THE TISSUES ACTIVATES NEUTROPHILS INHIBITS THE PRODUCTION OF ALPHA TOXIN BY CLOSTRIDIUM PERFRINGENS
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ACUTE EFFECTS OF HBOT IN VITRO- AEROBIC ORGANISMS GROW FASTER WITH INCREASING OXYGEN PRESSURE (1.3 ATA) GROWTH IS INHIBITED AT HIGHER PRESSURE IN VIVO- AEROBES ARE KILLED WITH HBOT
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TISSUE OXYGENATION MUSCLE- 3 HOURS SUBCUTANEOUS- 4 HOURS
ARTERIAL BLOOD – 2 MINUTES
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FREE RADICALS AND HBOT FREE RADICALS TRANSIENTLY INCREASE DURING HBOT
HBOT BLOCKS NEUTROPHIL ADHEREENCE TO ENDOTHELIUM AND RELEASE OF SUPEROXIDE SOD INCREASES AFTER FIRST TREAMENT WITH HBOT
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FREE RADICALS AND HBOT HBOT HAS A QUENCHING EFFECT ON LIPID PEROXIDATION IN EXPERIMENTAL MODELS OF ISCHEMIA /REPERFUSION INJURY, HBOT HAS A SIGNIFICANT BENEFICIAL EFFECT ON SURVIVAL OF TISSUE
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CONTRAINDICATIONS TO HBOT-ABSOLUTE
PNEUMOTHORAX DOXORUBICIN- NOT AT THE SAME TIME BLEOMYCIN-IF GREATER THAN 6 MONTHS OK FOR TX CIS-PLATINUM DISULFIRAM- VASOCONSTRICTION
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CONTRAINDICATIONS RELATIVE
EMPHYSEMA VIRAL INFECTIONS CONGENITAL SPHEROCYTOSIS OPTIC NEURITIS HISTORY OF SPONTANEOUS PNEUMOTHORAX UNCONTROLLED HIGH FEVER
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CONTRAINDICATIONS RELATIVE
UPPER RESPIRATORY INFECTION CHRONIC SINUSITIS PLACEMENT OF A STRUT FOR OTOSCLEROSIS
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RISKS AND SIDE EFFECTS OF HBOT
BAROTRAUMA ALTERNOBARIC VERTIGO FIRE PNEUMOTHORAX O2 TOXICITY-pulmonary CNS,
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RISKS AND SIDE EFFECTS OF HBOT
SEROUS OTITIS VISUAL CHANGES-CHANGES IN REFRACTION- MYOPIA WORSENS, PRESBYOPIA IMPROVES NUMB FINGERS
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HYPERBARIC OXYGEN MONOPLACE MULTIPLACE PORTABLE
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MULTIPLACE CHAMBER
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HBOT MONOPLACE CHAMBER
Giuseppina Benincasa-Feingold, MD HBOT MONOPLACE CHAMBER USAAA 2006 International Conference
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MONOPLACE CHAMBER HBOT is a medical treatment that saturates the
body with 100% pure oxygen under pressure, enhancing the body’s natural healing process.
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HBOT Extremely valuable tool in treatment of multitude acute and chronic disease states and damage from traumatic injury. Oxygen levels in the bloodstream raised up to 10 times normal. As a result, oxygen is more easily delivered to cells and tissues, improving functionality, accelerating healing and controlling infection.
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PORTABLE HYPERBARIC CHAMBER
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Pediatric Experience with HBOT
More than 80 articles detail the treatment of infants and children with HBOT. CO poisoning, radiation-induced sequelae, purpura fulminans, wound healing, peripheral ischemia secondary to DIC, necrotizing infections. Few side effects reported. Ventilated children are at greater risk for problems.
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Studies on HBOT caveats
Animals are not humans Healthy volunteers are not ill patients Different responses to different pressures Very few animal or human studies have been done at 1.5 ATA.
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NEURODEVELOPMENTAL DISORDER EFFECTING 1/166 CHILDREN
AUTISM NEURODEVELOPMENTAL DISORDER EFFECTING 1/166 CHILDREN
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AUTISM-POSSIBLE MECHANISMS
DECREASED CEREBRAL BLOOD FLOW EVIDENCE OF NEUROINFLAMMATION INCREASED MARKERS OF OXIDATIVE STRESS
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HYPOPERFUSION SPECT SCANS OF AUTISTIC CHILDREN SHOW HYPOPERFUSION OF SPECIFIC AREAS OF THE BRAIN RESPONSIBLE FOR SOME TYPICAL BEHAVIORS AND SYMPTOMS SEEN IN AUTISM
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HYPOFERFUSION AND AUTISM
TEMPORAL REGION-language comprehension and auditory processing, obsessive desire for sameness, impairment of communication and social interaction THALAMUS-repetitive, self-stimulatory and unusual behaviors such as resistance to change AMYGDALA-impairment in processing facial expressions and emotions
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SPECT PRE-TREATMENT AUTISM
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SPECT POST-TREATMENT AUTISM
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AUTISM-CEREBRAL BLOOD FLOW
DOPPLER OF AUTISTIC CHILDREN SHOWED THAT THERE IS DECREASED BLOOD FLOW AND INCREASED MIDDLE CEREBRAL ARTERY RESISTANCE UPON AUDITORY STIMULATION, NEUROTYPICAL CHILDREN SHOWED OPPOSITE FINDINGS
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AUTISM AND CEREBRAL HYPOPERFUSION
NEURONS/ASTROCYTES/VASCULAR CELLS- FUNCTIONAL UNIT WHICH MAINTAINS PROPER BLOOD FLOW AND OXYGENATION OF THE BRAIN
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AUTISM AND CEREBRAL HYPOPERFUSION
RECENT STUDY SHOWED EVIDENCE OF NEUROINFLAMMATION AND ASTROGLIAL ACTIVATION IN AUTISM. IT IS POSSIBLE THAT THIS MAY AFFECT THE CONTROL OF BLOOD FLOW REGULATED BY ASTROCYTES
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AUTISM AND NEUROINFLAMMATION
AUTOPSY OF AUTISTIC CHILDREN-inflammation of middle frontal gyrus, anterior cingulate gyrus and cerebellar hemispheres CSF- living children showed “prominent proinflammatory profile” AUTOANTIBODIES- to brain elements and neuron specific antigens such as myelin basic protein
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AUTISM AND INFLAMMATION
AUTISTIC CHILDREN HAVE MORE ANTIBODIES TO GLIADIN AND CASEIN PRODUCE MORE PRO-INFLAMMATORY CYTOKINES IMBALANCE OF CD4+ AND CD8+ CELLS
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AUTISM AND OXIDATIVE STRESS
SERUM GLUTATHIONE LEVELS ARE LOWER IN AUTISTIC CHILDREN OXIDIZED GLUTATHIONE HIGHER IN AUTISTIC CHILDREN
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AUTISM AND OXIDATIVE STRESS
LOWER SERUM ANTIOXIDANT ENZYME, ANTIOXIDANT NUTRIENT HIGHER PRO-OXIDANT IMPROVEMENT OF SYMPTOMS WITH USE OF ANTI-OXIDANTS
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IDLING NEURON THEORY CEREBRAL HYPOPERFUSION CAUSES HYPOXIA WHICH IN TURN CAUSES ELECTRICAL FAILURE. WORSENING OF HYPOXIA LEADS TO ION PUMP FAILURE AND EVENTUALLY CELL DEATH. CELLS WHICH HAVE ELECTRICAL FAILURE BUT RETAIN ION PUMP ABILITY- IDLING- “ISCHEMIC PENUMBRA”
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HYPERBARIC OXYGEN INCREASES OXYGEN DELIVERY THUS OVERCOMING THE HYPOXIA CAUSED BY THE CEREBRAL HYPOPERFUSION
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HBOT AND NEUROINFLAMMATION
HBOT HAS BEEN SHOWN TO HAVE POTENT ANTI-INFLAMMATORY EFFECTS IN VITRO STUDIES- DECREASE THE INFLAMMATORY RESPONSE IN ARTHRITIS, COLITIS
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HBOT AND OXIDATIVE STRESS
NEUTRAL EFFECT OF HBOT ON OXIDATIVE STRESS RISE IN ANTIOXIDANT ENZYME-SOD FOUND 24h AFTER HBOT WITHOUT A DROP IN GLUTATHIONE
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STEM CELL MOBILIZATION
RECENTLY SHOWN THAT HBOT AT 2.0 ATA AND 100% OXYGEN CAN MOBILIZE STEM/PROGENITOR CELLS FROM BONE MARROW OF HUMANS
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MANY QUESTIONS !!!
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QUESTIONS HBOT/AUTISM
WHO WILL RESPOND? HOW MANY TREATMENTS? WHAT DEPTH TO TREAT AT?
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