HYPERBARIC OXYGEN THERAPY AND AUTISM Giuseppina Benincasa-Feingold, MD HYPERBARIC OXYGEN THERAPY AND AUTISM GIUSEPPINA BENINCASA-FEINGOLD M.D. USAAA 2006 International Conference

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)

BOYLE’S LAW ABSOLUTE PRESSURE AND VOLUME ARE INVERSELY PROPORTIONAL

DALTON’S LAW TOTAL PRESSURE OF A MIXTURE OF GASES IS EQUAL TO THE SUM OF PARTIAL PRESSURES OF THE GASES IN THE MIXTURE

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

CHARLES’ LAW P1V1=P2V2 T1 T2 AS YOU COMPRESS GAS IT GETS HOTTER, CONVERSELY AS YOU DECOMPRESS IT GETS COOLER

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

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

ACUTE EFFECTS OF HBOT WOUND HEALING-ENHANCES FIBROBLAST PROLIFERATION AND COLLEGEN PRODUCTION PROMOTES NEOVASCULARIZATION ACUTE INJURIES- DECREASES EDEMA, IMPROVES REPERFUSION INJURY

ACUTE EFFECTS OF HBOT INFECTIONS-INCREASES PARTIAL PRESSURE OF OXYGEN IN THE TISSUES ACTIVATES NEUTROPHILS INHIBITS THE PRODUCTION OF ALPHA TOXIN BY CLOSTRIDIUM PERFRINGENS

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

TISSUE OXYGENATION MUSCLE- 3 HOURS SUBCUTANEOUS- 4 HOURS ARTERIAL BLOOD – 2 MINUTES

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

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

CONTRAINDICATIONS TO HBOT-ABSOLUTE PNEUMOTHORAX DOXORUBICIN- NOT AT THE SAME TIME BLEOMYCIN-IF GREATER THAN 6 MONTHS OK FOR TX CIS-PLATINUM DISULFIRAM- VASOCONSTRICTION

CONTRAINDICATIONS RELATIVE EMPHYSEMA VIRAL INFECTIONS CONGENITAL SPHEROCYTOSIS OPTIC NEURITIS HISTORY OF SPONTANEOUS PNEUMOTHORAX UNCONTROLLED HIGH FEVER

CONTRAINDICATIONS RELATIVE UPPER RESPIRATORY INFECTION CHRONIC SINUSITIS PLACEMENT OF A STRUT FOR OTOSCLEROSIS

RISKS AND SIDE EFFECTS OF HBOT BAROTRAUMA ALTERNOBARIC VERTIGO FIRE PNEUMOTHORAX O2 TOXICITY-pulmonary 6h @2ATA, CNS, 3h @3ATA

RISKS AND SIDE EFFECTS OF HBOT SEROUS OTITIS VISUAL CHANGES-CHANGES IN REFRACTION- MYOPIA WORSENS, PRESBYOPIA IMPROVES NUMB FINGERS

HYPERBARIC OXYGEN MONOPLACE MULTIPLACE PORTABLE

MULTIPLACE CHAMBER

HBOT MONOPLACE CHAMBER Giuseppina Benincasa-Feingold, MD HBOT MONOPLACE CHAMBER USAAA 2006 International Conference

MONOPLACE CHAMBER HBOT is a medical treatment that saturates the body with 100% pure oxygen under pressure, enhancing the body’s natural healing process.

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.

PORTABLE HYPERBARIC CHAMBER

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.

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.

NEURODEVELOPMENTAL DISORDER EFFECTING 1/166 CHILDREN AUTISM NEURODEVELOPMENTAL DISORDER EFFECTING 1/166 CHILDREN

AUTISM-POSSIBLE MECHANISMS DECREASED CEREBRAL BLOOD FLOW EVIDENCE OF NEUROINFLAMMATION INCREASED MARKERS OF OXIDATIVE STRESS

HYPOPERFUSION SPECT SCANS OF AUTISTIC CHILDREN SHOW HYPOPERFUSION OF SPECIFIC AREAS OF THE BRAIN RESPONSIBLE FOR SOME TYPICAL BEHAVIORS AND SYMPTOMS SEEN IN AUTISM

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

SPECT PRE-TREATMENT AUTISM

SPECT POST-TREATMENT AUTISM

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

AUTISM AND CEREBRAL HYPOPERFUSION NEURONS/ASTROCYTES/VASCULAR CELLS- FUNCTIONAL UNIT WHICH MAINTAINS PROPER BLOOD FLOW AND OXYGENATION OF THE BRAIN

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

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

AUTISM AND INFLAMMATION AUTISTIC CHILDREN HAVE MORE ANTIBODIES TO GLIADIN AND CASEIN PRODUCE MORE PRO-INFLAMMATORY CYTOKINES IMBALANCE OF CD4+ AND CD8+ CELLS

AUTISM AND OXIDATIVE STRESS SERUM GLUTATHIONE LEVELS ARE LOWER IN AUTISTIC CHILDREN OXIDIZED GLUTATHIONE HIGHER IN AUTISTIC CHILDREN

AUTISM AND OXIDATIVE STRESS LOWER SERUM ANTIOXIDANT ENZYME, ANTIOXIDANT NUTRIENT HIGHER PRO-OXIDANT IMPROVEMENT OF SYMPTOMS WITH USE OF ANTI-OXIDANTS

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”

HYPERBARIC OXYGEN INCREASES OXYGEN DELIVERY THUS OVERCOMING THE HYPOXIA CAUSED BY THE CEREBRAL HYPOPERFUSION

HBOT AND NEUROINFLAMMATION HBOT HAS BEEN SHOWN TO HAVE POTENT ANTI-INFLAMMATORY EFFECTS IN VITRO STUDIES- DECREASE THE INFLAMMATORY RESPONSE IN ARTHRITIS, COLITIS

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

STEM CELL MOBILIZATION RECENTLY SHOWN THAT HBOT AT 2.0 ATA AND 100% OXYGEN CAN MOBILIZE STEM/PROGENITOR CELLS FROM BONE MARROW OF HUMANS

MANY QUESTIONS !!!

QUESTIONS HBOT/AUTISM WHO WILL RESPOND? HOW MANY TREATMENTS? WHAT DEPTH TO TREAT AT?