HYPERBARIC OXYGEN THERAPY AND AUTISM

GIUSEPPINA BENINCASA-FEINGOLD M.D.

Hyperbaric Medicine

DefinitionHyperbaric 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

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.

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-TREATMENTAUTISM

SPECT POST-TREATMENTAUTISM

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?