Hyperbaric Oxygen For Children With Cerebral Palsy

HYPERBARIC OXYGEN THERAPY FOR CEREBRAL PALSY CHILDREN Philip James MB ChB, DIH, PhD, FFOM, Wolfson Hyperbaric Medicine Unit, The University of Dundee, Ninewells Medical School, Dundee DD1 9SY. [<philip@drphilipbjames.freeserve.co.uk>, <p.b.james@dundee.ac.uk>]

To significantly increase the delivery of oxygen delivery to the tissues requires the use of hyperbaric conditions, that is, pressures greater than normal sea level atmospheric pressure. When tissue is damaged the blood supply within the tissue is also damaged and too little oxygen may be available for recovery to take place. Hyperbaric medicine is not taught in most medical schools and is often dismissed by doctors as “alternative” medicine, but it is drugs that are alternative. Some raise fears about toxicity but in practice this is not a problem. More is known about oxygen and its dosage than any pharmaceutical. There is no more important intervention than to give sufficient oxygen to correct a tissue deficiency but, unfortunately, oxygen is only given in hospital to restore normal levels in the blood. The increased pressure has no effect on the body, although the pressure in the middle ear and sinuses in adults has to be equalized.

More oxygen may help many children with cerebral palsy, but it is not a cure. There are some obvious questions to be answered:


Ultrasonic scanning of the brain has shown that in most children the events which cause the development of cerebral palsy (CP) occur at the time of birth 1, although it may be many months before spasticity develops.2 Where does the damage occur? The areas affected in CP are in the middle of the hemispheres of the brain and one side or both sides may involved. These critical areas, called the internal capsules, are where the fibres from the controlling nerve cells in the grey matter of the brain pass down on their way to the spinal cord. In the spinal cord they interconnect with the nerve cells whose fibres activate the muscles of the legs and arms.


Unfortunately, the internal capsules have a poor blood supply, shown by the frequent occurrence of damage to these areas in younger patients with multiple sclerosis and in strokes in the elderly by Magnetic Resonance Imaging (MRI). When any event causes lack of oxygen the blood vessels leak, the tissues become swollen and there may even be leakage of blood. The increased water content, termed oedema, reduces the transport of oxygen. This applies to any tissue, but especially to the brain where a sufficient quantity of oxygen is vital both to the function and, in children, its development. What causes paralysis and spasticity to develop? When the controlling nerve cells in the brain

are disconnected from the spinal cord, the signals to the arms and legs cannot pass and the ability to move is lost. Eventually, because the nerve cells in the spinal cord are separated from the control of the brain, they send an excess of signals to the muscles, causing the uncontrolled contractions known as spasticity. The areas carrying the nerve fibres to the legs are the closest to the ventricles of the brain where the blood supply is poorest3 so the legs are the most commonly affected. The is called diplegia, to indicate that the problem is in the brain and distinguish it from paraplegia where the damage is in the spinal cord.


This is a crucial question that is, at present, not adequately explained or even raised. Children who develop spasticity often appear to develop normally for several months and then lose function gradually. Because in many children there is voluntary movement for a time after birth, the connections must still be intact. Why then are they lost allowing spasticity to develop? The answer almost certainly is due to the failure of the coverings of the nerve fibres, known as myelin sheaths, to develop. This evidence has come from MRI.2 Myelin sheaths envelop the nerve fibres like a Swiss roll in order to increase the speed of impulse transmission. Myelination normally begins about a month before birth and progresses to completion by the age of two. If there is tissue swelling in the mid-brain the delicate cells that form myelin die and the nerve fibres, left exposed, slowly deteriorate with the ultimate development of spasticity.


Loss of function in the brain can be either due to tissue swelling, which is reversible, or tissue destruction, which is not. The recoverable areas can now be identified by a technique called SPECT imaging. The initials stand for Single Photon Emission Computed Tomography. It can demonstrate blood flow which is linked to metabolism of the brain which is, of course, directly related to oxygen availability. By giving oxygen at the high dosages possible under hyperbaric conditions, areas which are not ”dead but sleeping” can be identified. This phenomenon has been discussed for many years in stroke patients and authorities have even stated that the critical parameter is not blood flow it is oxygen delivery.4 Under normal circumstances, blood flow and oxygen delivery are inextricably coupled, but the use of hyperbaric conditions can change this situation. Tissue oedema and swelling may persist in, for example, joints, for many years and SPECT imaging has now revealed that this is true in the brain.5 Suggesting that more oxygen, that is additional oxygen supplied under hyperbaric conditions may be of value generates further questions:


It means a pressure greater than normal sea-level atmospheric pressure. Atmospheric pressure at sea-level varies with the weather and on a high pressure day more oxygen is available to the body. Aches and pains may be worse on a low pressure day because of the reduction of oxygen pressure. A hyperbaric chamber allows much more oxygen to be dissolved in the blood. An indication of the power of this technique is that at twice atmospheric pressure breathing pure oxygen the work of the heart is reduced by 20%. So much can be dissolved in the plasma that life is possible for a short time without red blood cells. The research behind the development of hyperbaric oxygen therapy has been undertaken by doctors involved in aviation, space exploration and diving. This critical information is not yet taught in our Medical Schools, despite many thousands of published articles including controlled studies in many conditions.


Clearly the appropriate time to use of oxygen is at the start of a disease process, not after a delay of months or years. Nevertheless, a course of oxygen therapy sessions at increased pressure has been shown to resolve tissue swelling after the lapse of years. It works by constricting blood vessels and interrupting the vicious cycle where oxygen lack leads to tissue swelling, which then leads to further oxygen deficiency. Although formal studies have yet to be undertaken in children with cerebral palsy there is every reason to believe that exactly the same effect that is seen in stroke patients can occur. Also in children the brain is still developing and therefore the prospects for improvement are very much greater than in adults. Recovery of brain damage in children resulting from cardiac surgery has been documented using X-ray scanning.6


Hyperbaric oxygen therapy is not a miracle cure for children with cerebral palsy, it is simply a way of ensuring the most complete recovery possible. It should be used with exercise programmes, because lack of use in muscles and joints leads to changes that can only be reversed by exercise.


Formal studies are now underway in the USA and Canada and the results of the pilot study in McGill University are now ready for publication. There is a first time for everything. Unfortunately most of the medical research in the UK is funded by the drug industry and the

costs involved are enormous. As the use of oxygen cannot be patented, there is no way that the cost of trials could be recouped and no finance is available for the promotion of the therapy. Because of the great advances made in the use of drugs a climate has been created in which doctors are conditioned to expect a drug-based solution to every disease. Oxygen has been available in Medicine for over a hundred years so it is difficult to accept that it is not being used properly, but over 500 chambers are now operating in the USA and Japan, 1500 in Russia and a similar number in China. As is so often the case much of the original research was undertaken and published in the UK. In many diseases the cost of investigations is often a great deal more than the cost of providing hyperbaric oxygen therapy. MRI and SPECT imaging may allow the benefit to be demonstrated, but they are not in any way therapeutic. There is no better assessor of a child suffering from cerebral palsy than a parent or carer involved in day-to-day hands on care.


The only risk with hyperbaric conditions properly supervised is to the ear drum, just as when aircraft – which are hyperbaric chambers – descend. There are limits to oxygen delivery, for example, the very high pressures used in diving can cause convulsions, but the Chinese have shown that epilepsy is actually treated by hyperbaric oxygen therapy at lower pressures. There is no evidence of either eye or lung toxicity at 1.5-1.75 atm abs.


  1. Pape KE, Wiggleworth JS. Haemorrhage, ischaemia and the perinatal brain. Clinics in developmental medicine. Nos. 69/70 William Heinemann Medical Books, London, 1979.
  2. Dubowitz LMS, Bydder GM, Mushin J. Developmental sequence of periventricular leukomalacia. Arch Dis Child 1985;60:349-55.
  3. Takashima S, Tanaka K. Development of cerebrovascular architecture and its relationship to periventricular leukomalacia. Arch Neurol 1978;35:11-16.
  4. Astrup J, Siesjo BK, Symon L. Thresholds in cerebral ischemia; the ischemic penumbra. Stroke 1981;12:723-25.
  5. Neubauer RA, Gottlieb SF, Kagan RL. Enhancing idling neurones. Lancet 1990;336:542.
  6. Muraoka R, Yokota M, Aoshima M, et al. Subclinical changes in brain morphology following cardiac operations as reflected by computed tomographic scans of the brain. J Thorac Cardiovasc Surg 1981;81:364-69.

Effectiveness of Hyperbaric Oxygen Therapy in Treating Neurological and Motor Dysfunction

Cerebral Palsy- New Study  demonstrates effectiveness of  hyperbaric oxygen therapy in  treating neurological and motor  dysfunction 

By TomFox | Posted May 1, 2014 | Montreal Quebec

Montreal Quebec, April 22, 2014 – A new study published in the current issue of the Undersea and Hyperbaric Medicine Journal demonstrates the beneficial effect of hyperbaric oxygen therapy in addressing motor and neurological dysfunction due to cerebral palsy (CP).

CP is a non progressive condition that can be attributed to a neurological injury just prior to or at the time of birth. Affecting more than 2000 children in Quebec, this study confirms the positive results of two previous studies conducted by physicians from Quebec’s Sainte Justine’s hospital.

The concept of using Hyperbaric oxygen to treat brain injury in children with cerebral palsy is not new. For over 25 years, numerous clinical trials have reported significant improvement in study groups worthy of additional study. What makes the current study’s finding’s impressive is the rigorous , methodical, multifaceted comparison of the study design. Standard Intensive Rehabilitation given children with cerebral palsy was compared to groups where hyperbaric oxygen therapy of differing doses HBOT).

Dr. Pierre Marois, a physiatrist from Sainte Justine Hospital in Montreal collaborated on this new study. The clinical trials conducted in India examined 150 children from which 20 received standard intensive rehabilitative therapy only. The remaining 130 children were divided into three different groups distinquished by different doses of

hyperbaric oxygen. His work as a principle investigator in studies since 1998 has helped to document the significant beneficial effects of hyperbaric oxygen in children with Cerebral Palsy. This study found that the children treated in hyperbarics improved three times more than those that received standard intensive rehabilitative therapy. “Some have been able to walk for the first time, others have spoken the first

words of their lives following hyperbaric treatments, says Dr Marois. The current study followed the children for eight months after the completion of treatment and found the improvements “seemed to be permanent “

These results which appear in the Undersea and Hyperbaric Medicine Journal concur with those recently obtained in studies of adults in Israel with residual effects of strokes and traumatic brain injury. “Some patients have begun to use arms or legs that were paralyzed. In viewing images of the brains of these patients, we have seen that areas that previously were completely inactive worked again after hyperbaric treatment , “said Dr. Marois .

With this new study, it becomes clear that this treatment can significantly improve the quality of life of patients , insists Dr. Marois . Hopefully, as evidence continues to accumulate RAMQ will agree to pay for these treatments for children.

Point of Contact: Thomas M. Fox MAS, MS, CHT


Hyperbaric Therapy-Based Multimode Therapy for children with Cerebral Palsy

Title: Hyperbaric Therapy-Based Multimode Therapy for children  with Cerebral Palsy  

Author: Dr. Arun Mukherjee, MD  

Director, UDAAN for the Differently Abled,

A-59 Kailash Colony, New Delhi, India


Cerebral Palsy (CP):  

Abnormalities of tone are an integral component of many chronic motor disorders of  childhood. These disorders result from dysgenesis or injury to developing motor pathways in  the cortex, basal ganglia, thalamus, cerebellum, brainstem, central white matter or spinal  cord. The major damage is to the developing fetal / neonatal brain, mostly affecting the  poorly vascularized Internal Capsule, Descending Cerebro- and Cerebello- Spinal tracts, thus  affecting various motor functions. When the injury occurs in children before 2 years of age,  the term Cerebral Palsy (CP) is often used.

Management of CP  

The classical management of CP is Standard Therapy comprising individualised, need based  and target-oriented Physiotherapy, Occupational therapy, Special Education and Speech  Therapy. These are often offered as exotic management techniques such as Peto technique,  NDT (Neuro-Developmental Therapy), Bobbath technique, etc. Down at heart, they are all  specialised forms of Standard Therapy to derive the best physical and psychosocial outcomes  within the possibilities of neural function left after the original brain injury.  Hoping that these standard therapies alone can solve the problems of the CP child is like  hoping that changing the tyres and lubricating the wheels and axles of a car will make it run  better when its engine is choked with carbon deposits. We need to repair the engine if the  fault is in the engine: it is as simple as that.

There are dozens of papers in world literature, unfortunately not indexed in “Free Internet  Medline” but in other more than 100 “*Lines” in the US National Library of Congress, that  are available only on payment per article, and hence rarely sought out. They carry many  reports on CP children treated with Hyperbaric Oxygen Therapy, showing improvement and  increase in serial GMFM scores over time that were five to ten times faster than that achieved  in the best centres of standard therapies.

UDAAN for the Disabled  

UDAAN for the Disabled is a non-profit organization, recognized and partially aided by the  Government of India. We are offering standard therapies since 1994 to children affected by  various forms of Neurodevelopmental disabilities, in which CP predominates. Since 2001, we  started a research project to study the benefits of HBOT-based multimode therapy of CP. We  have a control batch of CP children that did not receive HBOT, as well as batches that  received HBOT in a Multiplace rigid chamber either at 1.75 ATA (till July 2004) or 1.5 ATA  (after July 2004) with 100% oxygen delivered by an Amron mask. There is a fourth batch  that received mild pressurized air (with no additional oxygen supplementation either with a  Concentrator or oxygen cylinder) at 1.3 ATA using the largest size OxyHealth soft portable  chamber (since 2006).

The study is a prospective open non-randomised study, with batches decided by the parent  based on their own convenience and financial status. It is an ongoing study. Hence, our  database is growing by the year. This article represents data as available till June 2008.

Evolution of existing HBOT based Multimode Therapy for CP in India  June 2001

UDAAN pioneered in India the study of 1.75 HBOT at 100% O2 as supplement to Standard  Therapy (OT + PT + Special Education + Speech Therapy) for CP children.  March 2003

The first UDAAN paper on the use of HBOT in CP (Control 15 vs Test 15) was presented at  the Annual Conference of Indian occupational Therapy Assoc. at Bangalore (Amit Sethi and  Arun Mukherjee) and won the best scientific paper award. This was later reported in  July 2003

3rd Int. Symposium on HBOT & the Brain Damaged Child (Florida): Presented interim data  on 20 CP children given only Standard Therapy vs. 20 matching Test group of 20 CP  Children given additional HBOT (40 sessions of 1.75 ATA with 100% O2). Trend favored  the HBOT group on all parameters.

July 2004

4th Int. Symp. on HBOT …. (Florida): Presented data on 39 CP children given 40 sessions of  HBOT at 1.75 ATA, with statistically significant improvement over the batch given only  Standard Therapy (n=20) .

Dr. Paul Harch advised us to shift down to 1.5 ATA for better results. We did as advised.  July 2006

5th Int. Symp. on HBOT …. (Florida): Presented ongoing long term (6 to 8 months) study  data of 84 CP children given supplemental HBOT (sub-group analysis of 1.5 & 1.75 ATA not  done) Vs. 20 on Standard Therapy alone.

Data on interim pilot study on 7 given 1.3 ATA Hyperbaric Air also shown but not included  in analysis.  

July 2008

6th Int. Symp. on HBOT …. (Torrance CA): Presented data on 128 CP children who  completed at least six months of follow up, after receiving only Standard Therapies (n=20),  or standard therapies supplemented by (a) regular 100% O2 HBOT at 1.75 ATA (n=60), (b)  regular 100% O2 HBOT at 1.5 ATA (n=24), or (c) HB-Air at 1.3 ATA using room air only  (n=24).

Materials and Methods  

Selection Criteria  

Inclusion Criteria  

  • All types of CP in children aged mostly between 1 to 5 years, oldest up to Teen age  • Either Sex
  • Any I.Q. level
  • Pre-HBOT SPECT Scan showing presence of recoverable penumbra in test subjects.  • Those living in Delhi or willing to live in Delhi for 6 – 8 months within reasonable  distance of UDAAN to facilitate daily transportation

Exclusion Criteria  

  • Uncontrolled Epilepsy
  • Uncontrolled Bronchospastic and/or E.N.T. disorders.
  • Any Genetic Disorders
  • Pervasive Developmental Disorders.


Every child received matching Standard Therapy at the same venue by the same group of  therapists, using the same protocol, same equipment, and the same duration of 6 to 8 months. 

  • Batch – A: No hyperbaric therapy
  • Batch – B: 40 sessions of 1.75 ATA HBOT with 100% Oxygen during 1st two months  • Batch – C: 40 sessions of 1.50 ATA HBOT with 100% Oxygen during 1st two months  • Batch – D: 40 sessions of 1.30 ATA HBAT with room air during 1st two months
  1. The Hyperbaric groups also received CP Specific Acupuncture one session a day for 60  sessions as part of multimode therapy, added from 5th month onwards, after giving  HBOT / HBA enough time to exert its effects.
  2. Assessments done every 2 months
  3. Data analyzed for Percentage Change from Basal to 4 and 6 Months.  Physical Assessment  
  • Standard Scales like GMFM scale are always used. We also use other relevant scales  where needed, like Modified Ashworth, BERI VMI, etc. The analytical data is based  on the GMFM Scale.
  • GMFM Measurements: Baseline, 4 months & 6 months, and now-a-days, 8 months  • Statistical evaluation: By a Bio-statistician trained at the prestigious All India Institute  of Medical Sciences, Delhi

Statistical Methods used by our Statistician  

  • Chi Squared Test for Categorical Data
  • Non Parametric Wilcoxon Mann Whitney Test for 2 Groups
  • Non Parametric Krusckal Wallis Test for more than 2 Groups
  • Non Parametric Wilcoxon Signed Rank Test for two different time periods

Assessments other than Physical  

Special Educational and Speech Therapist’s assessments are always a problem in CP due to  combination of intellectual disability & physical impairment in the children.  Hence, based on our long experience with various scales, we developed a modified scale of  22 objective parameters for cognitive changes (Special Education)

Evolved from standard scales like Vineland, Help Check list; RUTTH GRIFFITH; REEL;  FAB & BASIC MR. Each parameter has been divided into 5 achievable grades of  improvement. These grading have been customized to measure smaller differences in  Cognitive skills at 2 month intervals.

UDAAN Study Timeline  

Protocol – Standard Therapy

6 days/week, one-to-one basis, ½ Hr each daily of

  1. Physiotherapy
  2. Occupational Therapy
  3. Special Education
  4. Speech Therapy

Assessment of fitness for Hyperbaric Therapy  

Pre-HBOT SPECT Scan was done in just about every child to show ischemic brain lesion.  Each child had to undergo medical fitness by a pediatrician and an ENT specialist to ensure  safety at hyperbaric conditions. Neurological opinion was sought in children with fits, and  where needed, dose of anti-epileptic therapy was slightly increased during the HBOT phase  to minimize risk of fit relapse.

Protocol Hyperbaric Oxygen Therapy Regimen  

HBOT was done in a multiplace chamber using 15 minutes to pressurize, 15 minutes to  depressurize, and 60 minutes at pressure with 100% Oxygen given through an Amron mask.

The children received one session of HBOT a day x 40 sessions during 1st two months. The  pressure used was 1.75 ATA from 2001 to July 2004, which was subsequently reduced to 1.5  ATA as per guidance received from our mentor, Dr. Paul Harch.

Hyperbaric Air Therapy Regimen  

HBAT was done in a non-ASME-PVHO compliant OxyHealth soft chamber (their largest  chamber size used) as part of our research protocol, at 1.3 ATA using non-enriched room air,  in a dedicated air-conditioned room with filtered air. This batch duplicates the batch wrongly  and repeatedly referred to as “Placebo” by Collet, the lead author of the landmark Canadian  study of HBOT in CP (Collet, J.P., Vanasse, M., Marois, P., Amar, M., Goldberg, J., Lambert, J. et  al. (2001) Hyperbaric oxygen for children with cerebral palsy: A randomized multicentre trial. The  Lancet, 357, 582-586). Each child received one session a day x 40 days during first 2 months.

Protocol of Acupuncture  

One 45-minute session a day for 60 working days, from 5th month onwards, after benefits of  HBOT were observed. A trained qualified Acupuncture Therapist offers it. All usual aseptic  and antiseptic techniques are followed, and no complications have occurred since 2001. We  also use Laser Acupuncture where needed. The therapy is always done in close consultation  with our Occupational Therapy Dept, with reference to case-to-case physical disabilities.


Age Group Cross tabulation  



Control 20 1.0 17.0 16.0 3.5 3.49 3.00 0.78
1.3 24 1.5 9.0 7.5 4.87 2.16 5.00 0.44
1.5 24 1.0 13.0 12.0 4.33 3.14 3.0 0.64
1.75 60 1.0 12.0 11.0 4.22 2.47 4.0 0.24


Non-Parametric Kruskal-Wallis Test: p > 0.06 (NS)

Age Range Cross tabulation  

GROUP  <=2 YR  3-4 YR  5-6 YR  7-8 YR  >8 YR  TOTAL 
Control 8 (40) 9 (45) 2 (10) 0 (0) 1 (5) 20
1.3 4 (16.7) 5 (20.8) 10 (41.7) 3 (12.5) 2 (8.3) 24
1.5 7 (29.2) 9 (37.5) 3 (12.5) 2 (8.3) 3 (12.5) 24
1.75 15 (25) 24 (40) 12 (20) 6 (10) 3 (5) 60


Pearson Chi-Square test: p > 0.02 (NS)

Sex Division Cross tabulation  

Control 7 (35%) 13 (65%) 20
1.3 5 (20.8%) 19 (79.2%) 24
1.5 5 (20.8%) 19 (79.2%) 24
1.75 18 (30%) 42 (70%) 60


Pearson Chi-Square test p > 0.2 (NS)

Conclusion: no significant difference in Age or Sex distribution across the four  groups

Motor Changes, from baseline to 4 & 6 months in GMFM Scores  

GROUP  % CHANGE 0 – 4 MT  

MIN & MAX.  


P = 

% CHANGE 0 TO 6 MT  

MIN & MAX.  


P = 



Min: 1.3; Max 29.9

Mean: 5.99 + 7.6

p < 0.001

Min: 2.5; Max: 59.9

Mean: 11.95 + 15.2

p < 0.001



Min:0.0; Max: 164.1

Mean: 19.41 + 34.1

p < 001

Min: 2.53 Max: 281.5

Mean: 37.3 + 58.5

P < 0.001



Min: 2.44;Max: 194.1

Mean: 22.7 + 33.5

p < 0.001

Min: 4.41; Max: 358.5

Mean 39.1 + 62.9

p < 0.001



Min: 0.58; Max: 59.1

Mean 18.3 + 14.9

p < 0.001

Min: 1.53; Max: 118.5

Mean: 37.1 + 30.0

p < 0.001

1.5+1.75 Min: 0.58; Max: 194.2

Mean 19.9 + 23.3

p < 0.001

Min: 1.53; Max: 358.5

Mean: 37.8 + 30.0

p < 0.001


Non Parametric Test

Wilcoxon Signed Ranks Test

Conclusion: All four groups improved statistically significantly within their own groups.  Comparative GMFM changes  

1.3 vs. Control p < 0.001


p < 0.005


1.5 vs. Control p < 0.001


p < 0.001


1.75 vs. Control p < 0.001


p < 0.001



All three Hyperbaric Groups were significantly superior to Control Group.  Absolute Value Changes in GMFM Scores 

Group 0 mt

Min & Max.

Mean + SD

4 mt

Min & Max.

Mean + SD

6 mt

Min & Max

Mean + SD



Min:12.1; Max: 53.6  Mean: 29.6 + 13.0 Min: 12.5; Max: 54.3  Mean: 31.0 + 12.8 Min: 12.9; Max: 55.0  Mean: 32.4 + 12.3


Min:6.8; Max: 65.5  Mean: 31.2 + 14.7 Min: 20.5; Max: 69.4  Mean: 36.7 + 13.2 Min: 24.0; Max: 71.8  Mean: 38.3 + 13.1


Min: 4.12; Max: 70.8  Mean: 34.7 + 15.4 Min: 12.1; Max: 81.9   Mean 39.6 + 15.2 Min: 18.9; Max: 86.5  Mean: 42.8 + 15.2


Min: 13.5; Max: 81.5  Mean 32.6 + 11.7 Min: 17.4; Max: 63.7  Mean: 37.3 + 10.7 Min: 21.3; Max: 69.2  Mean: 42.10+ 10.3
1.5 +1.75 Min: 4.12; Max: 70.8  Mean 33.3 + 13.1 Min: 12.1; Max: 81.9  Mean: 38.1 + 12.5 Min: 18.9; Max: 86.5  Mean: 42.3 + 12.2


Using these values, the efficacy of 1.3 ATA HBA was compared to the two regular 100%  oxygen based HBOT groups.

The comparative results were as follows, using Non-parametric Mann-Whitney Test:

1.3 ATA HBA vs. 1.5 HBOT:  

 At 4 months, difference not significant (p = 0.467)

At 6 months, difference not significant (p = 0.316)

1.3 ATA HBA vs. 1.75 HBOT  

 At 4 months, difference not significant (p = 0.601)

At 6 months, difference not significant (p = 0.99)

1.3 ATA HBA vs. 1.5 + 1.75 ATA HBOT  

 At 4 months, difference not significant (p = 0.509)

At 6 months, difference not significant (p = 0.126)


Special Education Cognitive tests by Absolute values  

Group 0 mt

Min & Max.

Mean + SD

4 mt

Min & Max.

Mean + SD

6 mt

Min & Max.

Mean + SD



Min: 27; Max: 122

Mean: 48.6 + 27.4

Min: 27; Max: 122  Mean 58.5 + 28.4 Min: 27; Max: 125  Mean: 63.1 + 30.5


Min: 23; Max: 81

Mean: 38.4 + 15.4

Min: 29; Max: 88  Mean: 60.9 + 18.6 Min: 32; Max: 96  Mean: 67.4+ 21.7


Min: 26; Max: 124

Mean: 48.5 + 28.7

Min: 29 Max: 127  Mean 62.9 + 30.8 Min: 30; Max: 128  Mean: 67.6 + 30.7


Min: 26; Max: 128

Mean 48.0 + 28.1

Min: 29; Max: 130  Mean: 67.9 + 32.1 Min: 30 Max: 130  Mean: 75.1+ 33.3
1.5+1.75 Min: 26; Max: 128

Mean 48.1 + 28.1

Min: 29; Max: 130  Mean: 66.4 + 31.6 Min: 30; Max: 130  Mean: 73.1 + 32.6


Based on these values, we tested the changes in the two Hyperbaric Oxygen Therapy groups  as compared to changes in the 1.3 ATA Hyperbaric Air group

The comparative results were as follows, using Non-parametric Mann-Whitney Test:

1.5 ATA HBOT group 

1.5 ATA HBOT group was not statistically superior to the 1.3 ATA HBA group, with p >  0.7 at 4 months and p > 0.7 at 6 months.

1.75 ATA HBOT group 

1.75 ATA HBOT group was not statistically superior to the 1.3 ATA HBA group, with p >  0.7 at 4 months and p > 0.4 at 6 months.

1.5 + 1.75 ATA HBOT group 

The combined 1.5 ATA + 1.75 ATA HBOT group was not statistically superior to the 1.3  ATA HBA group, with p > 0.8 at 4 months and p > 0.6 at 6 months.

Cognitive Percentage Improvement  

Group % Change 0 – 4 mt

Min & Max.

Mean + SD

% Change 0 – 6 Mt

Min & Max.

Mean + SD



Min:0.0; Max: 121.9

Mean: 24.4 + 29.7

Min: 0.0; Max: 165.56

Mean: 34.9 + 41.6



Min:4.9; Max: 157.1

Mean: 65.8 + 40.4

Min: 11.1; Max: 185.7

Mean: 83.6 + 48.2



Min:0.0 Max: 69.3.8

Mean: 34.7 + 20.2

Min: 0.0; Max: 96.6

Mean 47.2 + 26.5



Min: 0.78 Max: 167.7

Mean 49.8 + 42,.3

Min: 1.56; Max: 219.35

Mean: 69.5 + 55.7



Min: 0.0; Max: 167,7

Mean 45.6 + 37.9

Min: 0.0; Max: 219.4

Mean: 63.3 + 50.1


Using these values, the three Hyperbaric groups were compared to the Control groups.  The comparative results were as follows, using Non-parametric Mann-Whitney Test:

1.3 ATA HBA group 

1.3 ATA HBA group was statistically superior to the Control, with p < 0.001 at 0 to 4  months, and p < 0.001 at 0 to 6 months.

1.5 ATA HBOT group 

1.5 ATA HBOT group was statistically superior to the Control, with p < 0.05 at 0 to 4  months, and p < 0.05 at 0 to 6 months.

1.75 ATA HBOT group 

1.75 ATA HBOT group was statistically superior to the Control, with p < 0.005 at 0 to 4  months, and p < 0.005 at 0 to 6 months.



All FOUR Groups showed significant improvement with the therapy received at UDAAN.  However, all three hyperbaric groups were significantly superior to the Control group at both  4 and 6-month follow up.

GMAE Trends  

There was a statistically significant improvement recorded by all three hyperbaric groups as  compared to the control group. No significant difference between the three Hyperbaric  Groups. We may need a much bigger database than 128 CP children to see a significant  difference. We are working towards it with our ongoing study.

The change in GMFM absolute scores after 6 months of therapy was 0.67 in Control, 1.18 at  1.3 ATA, 1.35 at 1.5 ATA and 1.6 at 1.75 ATA. These results are similar to the Lancet study  and show that hyperbaric therapy doubles the improvement rate improvement compared to  non-Hyperbaric therapy regimens, with no significant difference between the individual  hyperbaric regimens used.

Cognitive Trends 

The Cognitive tests done by the Special educators, using our own modified scale based on  available internationally recognized scales adapted to measure smaller changes in Cognitive

improvements, showed no significant difference between the three Hyperbaric Groups. We  may need a still bigger database to come to see a significant difference.

Why the non-significance between HBAT & HBOT  

Let us study with an open mind

Tissue Oxygenation  

The regular HBOT chambers rely on pure oxygen source (oxygen cylinders or piped hospital  supply). They have independent air-cooling mechanisms to maintain a comfortable  temperature inside during the procedure.

Normal tissue fluid Oxygen saturation = 0.3%. Regular HBOT, using a rigid chamber, at 1.5  to 1.75 ATA, with 60 minutes at 100% pure Oxygen, achieves tissue fluid Oxygen saturation  of about 2 to 3 ml /100 ml, representing a 7 to 10 fold rise, or, almost a 700% rise. However,

the use of a hood based close circuit also ensures that there is no inhalation of Carbon  Dioxide. Hence, its level in tissue fluid and blood remains very low.

Carbon dioxide is the most potent stimulator of respiratory effort, besides causing  vasodilatation to ensure normal tissue perfusion, which influences many neuro-endocrine and  other mechanisms in the brain and body.

Thus, a typical HBOT chamber ensures tissue and blood oxygen concentration extremely  higher than physiological levels, combined with intense vasoconstriction induced by highly  unbalanced oxygen (vasoconstrictor) to carbon dioxide (vasodilator) ratio in blood and tissue  fluid.

The low-pressure (1.3 ATA) OxyHealth Soft Hyperbaric chamber used by us compresses  normal room air to 1.3 ATA, to achieve a tissue fluid Oxygen saturation of approximately 0.4  – 0.5 ml /100 ml, or 1/3 rd to ½ fold rise = 33 to 50 % increase. This is achieved by  compressing normal room air that does not have any imbalance in its oxygen to carbon  dioxide ratio, which is what our physiology is used to, in order to maintain physiological  blood vessel patency and other neuro-hormonal regulatory balances within our systems.  Is a 33% rise in tissue Oxygen level enough?

How physiologically significant is a 33% change in our internal milieu of tissue oxygenation  as produced by 1.3 ATA Hyperbaric therapy?

  • Presume that a patient has fever with temperature of 105º F. We use an acetaminophene  (paracetamol) tablet to lower temperature by only 6%. The temperature is now normal.  • A patient develops high diastolic BP of 105 mm Hg. We use an appropriate anti hypertensive drug to lower blood pressure by only 30%. The BP is now normal.  • A patient develops acute respiratory or metabolic derangement, which acidifies his blood  and decrease blood pH to 7.0. We use appropriate IV Fluids, Nutrition and Drugs to  increase the blood pH by 6 %, which brings his blood pH back to about 7.4 or normalNOW, how significant is a 33% change in our internal milieu?  

How could HBAT be non-significantly, though marginally, superior to  regular HBOT on Cognitive parameters?  

Compressed air heats up. While it is no problem in cold climates, it is a big problem in  climate-wise hot countries like India.

When we started using such a low-pressure soft chamber in 2006, besides the additional  problem of keeping the piped air dust free to ensure no problem to the already-weak special  need child as well as prolong the life of the high-efficiency air filters attached to the air  compressors, the high heat developed inside the chamber was intolerable.  We solved this problem by centrally air-conditioning the building to 25º C, and constructing  an enclosed small cabin inside the complex with its own additional air-conditioner that

further cleaned and cooled down the cabin to 16º C. This achieved a physiologically  balanced, clean and comfortable temperature atmosphere inside the soft chamber.  However, we are now realizing that having a centrally closed air-conditioned building does  lead to some degree of carbon-dioxide recirculation. In addition, the further enclosed cabin,  which contains the chamber as well as its compressor, causes a slightly greater carbon dioxide recirculation.

What is the effect of this slightly higher carbon dioxide level on brain physiology?  We were a little surprised to see that though both motor and cognitive changes were  statistically equivalent in all three Hyperbaric groups, there was a statistically non-significant  trend in favor of regular HBOT over low pressure HBAT as far as motor (GMFM) changes  were concerned, whereas in contrast, there was a non-significant trend in favor of low  pressure HBAT as far as cognitive changes are concerned.

In his presentation at the 6th International Symposium on Hyperbaric  Oxygenation and the Future of Healing, July 24 to 26, 2008, Torrance,  California, USA, (www.hbot2008.com) Dr Julian Whitaker, M.D., (IMPROVING  HBOT OUTCOMES BY NORMALIZING C02 LEVELS) suggested that a growing body  of research suggests that breathing 100% O2 at room pressure has adverse  effects and that increasing carbon dioxide (CO2) levels obviates these  effects. Hyperoxia-induced hypocapnia narrows the blood vessels and  reduces blood flow to the brain. It activates regions of the brain that  control autonomic functions and floods the body with potentially harmful  hormones and neurotransmitters.

Studies reveal that the addition of CO2 to the gas mixture greatly  diminishes these responses and could reduce adverse effects of 100% O2.  Standard practice of 100% O2 ventilation needs to be revisited and  methods for reducing hypocapnia explored-both at room pressure and  HBOT. These include modifications to gas mixtures, breathing and  rebreathing devices, and breath holding techniques.

This is what we inadvertently achieved in our enclosed HBAT cabin. The slightly higher  CO2 levels inside the HBAT soft chambers were altering physiology in ways that need  further study, since motor controls are relatively simple brain functions whereas cognitive  and psycho-social behavior are very complex multi-region based neural functions, that are  regulated by a whole host of neuro-endocrine systems, that could be affected by changes in  vascular supply even though they may lie in non-ischemic zones. We must also remember  that the Human Body Physiology works within quite narrow physiological margins, and,  during ill health, nature usually requires only mild to moderate changes in internal  milieu to change the prognosis in favor of the patient.  

What this means  

Based on our experience, we believe 1.5 or 1.75 ATA HBOT with 100% O2 is slightly  though Non-Significantly better than 1.3 ATA HB-AIR as regards motor recovery in children  with cerebral palsy while 1.3 ATA HBAT with room air is slightly though Non-statistically  superior to regular 100% oxygen based HBOT for improving cognitive and psycho-social  abilities. Overall, they balance out in improving the prognosis of the child significantly as  compared to children receiving only standard therapy.

1.3 ATA HB-Air is statistically Non-Inferior to 1.5 or 1.75 ATA HBOT with 100% oxygen  though it costs roughly half to provide.

Possibly, more experience with CT-SPECT Fusion Scans could in future show the way as to  which regimen will possibly do cost-effectively better in which brain SPECT Scan pattern,  involving cognitive/temporal lobes or the motor areas of cerebral cortex and internal capsule.


Our experience on tolerance is based on a database of 84 CP children given a minimum of 40  sessions of HBOT at 100% Oxygen and 24 matching CP children treated with a minimum of  40 sessions of 1.3 ATA HBAT using room air, compared to 20 matching CP children  (Control) who received the same Standard Therapy but no Hyperbaric Therapy in any form.  • A few children with recent history of fits had relapse of epilepsy, but its incidence was

similar to the rate of fits in Control children. We stopped therapy for 7 to 10 days, and  could complete the course in all except one child, in the 1.5 ATA group.  • His/her own mother or relation usually accompanies the CP child inside the chamber. No  case of claustrophobia was seen in the children (perhaps due to their cognitive  impairment), though some mothers or relations did have some such problem. Our Nurse  on duty accompanied their children inside the chamber in such cases.

  • There were no significant behavioral problems inside chamber, including some children  with autism, who were not a part of this particular project.
  • We have been doing HBOT since 2001 and HBAT since 2006. During this period, no  deterioration was noticed in any child treated so far.

Chamber problems  

Regular Monoplace HBOT chambers pressurize with 100% oxygen. If they start using room  air to give less costly 1.3 ATA HBAT, the condensing moisture could play havoc with the  inside chamber materials and sealing which were designed to use dry pure oxygen from a  dedicated oxygen source.

The Multiplace chambers simultaneously treat many types of patients, and not just CP.  Different indications require different pressures, often exceeding 1.5 ATA. Hence providing  the less costly 1.3 ATA in such chambers is not cost effective or feasible  Both types of regular HBOT provide 100% pure dry oxygen to the patient. Thus the patient  does not receive physiologically necessary levels of carbon dioxide. Problems associated with  carbon dioxide levels need to be studied in future. There may also be respiratory problems  later on in children receiving dry air for 1.5 hours.

The 1.3 ATA soft HBAT chambers on the other hand, provide the physiological levels of  oxygen and carbon dioxide mixture, and may be better at maintaining intracranial neuro hormonal controls. However, they supply humid air, at least in our setting, which condenses  inside the chambe. The chamber needs to be wiped clean after each round, and aerated  periodically in-between sessions.

Our suggestions for soft chambers:

  1. We normally have a tidal breath volume of 500 ml, and breathe up to about 20 times  per minute. Hence, the chamber must have a flow rate of 10 liters per minute per  person, to ensure normal oxygen supply. Since the chamber normally has a child and  a relation, rarely the nurse also, we need a minimum flow rate of 30 liters/minute.  The Oxyhealth chamber we use has a flow rate of 50 liters/minute.
  2. There should be a dehumidifier inline, before the compressor, with airflow rates  matching that of the compressor. The dehumidified and compressed air can be used  to achieve lower humidity inside the HBAT chamber.
  3. The flexible pipe from the compressor to the chamber is quite long. We could take a  small fridge, and modify it to have an inlet and outlet hole on one wall, through  which the majority of the pipe can be put inside the chamber to be cooled thoroughly  before it opens inside the chamber. That would minimize air-conditioning costs and  even do away with the need for a dedicated room
  4. The HBAT room containing the chamber should have a small exhaust fan, with its air  inlet opening onto a pipe whose other end is brought down to open in a funnel like

fashion close to the twin exhaust valves of the soft chamber. This will reduce the  recirculation of stale air inside the air-conditioned room and chamber and help  maintain the CO2 levels closer to physiologically normal inside the HBAT chamber.  What next?  

  • How many can afford HBOT at its present cost level even in the economically  advanced USA? Not a great many, except in the states where Medicaid has allowed  re-imbursement as a follow up of the Steele child court case in Georgia in 2006.
  • Now think how many can afford costly regular HBOT in India and other similar not  so developed countries which do not have any reimbursement for “experimental  HBOT” in CP children? The soft chambers are “Not ASME-PVHO” compliant.
  • Do we tell them: “Either go in for regular HBOT only, or Get Lost?”  • We need the option of an economical monoplace HBAT chamber that can deliver 1.3  ATA room air at an economical rate, which can run even on a small Electrical  generator (because electricity load-shedding is endemic in countries like ours) with a  dehumidifier AND an air cooling device INLINE.
  • Such an equipment, used by trained personnel under medical supervision, in properly  investigated, selected and adequately followed up cases, should not need permission  from Dept. of Explosives, Dept. of Drugs and the Fire Safety guys because NO  FIRE-SAFETY NORMS ARE VIOLATED AND NO EXPLOSIVE OXYGEN IS  USED.
  • The pressure used in such low pressure chambers is less then the pressure differences  experienced in any commercial airline (0.5 ATA down when ascending and the same  up while descending to land). The pressure increase is equal to that experienced when  diving into a standard swimming pool to a depth of only 10 feet or 3 meters.  Our Dilemma  

What pressure do we recommend to a particular child? That is a hard decision we must take,  especially as the much more affordable 1.3 ATA gives statistically similar benefit at almost  half the cost, which many more parents in the less economically affluent segments can afford.  We would categorically like to clarify that we are NOT RECOMMENDING any particular  chamber, but merely discussing different pressure effects in Indian Children, with their lower  body weight and metabolic activity, with our experience limited to regular HBOT at 1.5 ATA  and 1.75 ATA, and also at 1.3 ATA inside an OxyHealth soft chamber, with their limitations  and benefits, in CP children.

We do not, repeat, DO NOT, advocate the use of 100% Oxygen or an oxygen concentrator  with NON-ASME PVHO chambers, as we have no experience with it nor have any plans to  do so in future.

The mHBOT data we have shown have been with compressed room air only. In fact, the  notice on the side of the chamber clearly states that these chambers are not recommended by  their manufacturer to be inflated with Oxygen.

Our position  

Our data in 128 CP children treated and followed up for 6-8 month is not enough to make an  authoritative recommendation even though our preliminary data suggest that improvements  seen with Hyperbaric Therapy in all it’s three tested forms is very encouraging, and we  should continue the study further.

We believe that we require more supportive data to show that the use of 1.3 ATA may be an  option to parents who cannot afford the higher cost of 1.5 ATA, to get a fair degree of  improvement in the quality of life of their kids. We also need to develop protocols to select  the children who would definitely do better on the low-pressure regimen. It is possible that  the CP child with greater motor dysfunction will be slightly better off with regular HBOT

while the ones with significant cognitive impairment will do better with low pressure HBAT.  Only time will tell us a more definitive answer.

Our ongoing research should have more data on this aspect in another 2 to 3 years.


We have carried out an ongoing open non-randomized controlled prospective study of  management of CP children with intensive one-to-one standard therapies, supplemented in 60  children with 1.75 ATA HBOT, in 24 CP children with 1.5 ATA HBOT and in 24 CP  children with 1.3 ATA HBAT.

The four groups were matching in age, age distribution, sex distribution and initial severity.  They were assessed at 4 and 6 months. Most children also had serial video recordings also.  All three hyperbaric therapy groups induced significant improvement over the Control group  in Cognitive & Speech / Communication parameters within 4 months. The early response as  compared to motor response could be due to the shorter intra-cranial axons responsible,  which re-myelinate faster after HBOT.

The Cognitive and Speech / Communication skill changes appeared to be permanent during  our longer-term follow-up of 6 to 8 months or more.

Improvements in Physical (GMFM) Parameters reach significance after 4th months, though  our clinical impression is that it peaks after 6 to 8 months. The greater response time required  for clinically significant motor achievements could be due to the longer time needed to  remyelinate the long Pyramidal tract from brain to lower spinal motor neurons. The gains in  Physical Controls appear to be permanent

Re-spasticity occurs at limbs due to reduced ability of spastic muscles to lengthen on par with  normal muscles during bone lengthening as per age related growth. Intensive OT/PT till at  least 21 years of age may reduce extent of re-spasticity in those children who are doing it.  We showed at the 5th Symposium on HBOT (Florida) in 2006 that the preferred age for  HBOT in CP is 1-4 years, before brain development, dendritic arborization, synaptic  development, cerebral sphyngomyelin & cholesterol concentrations complete. However,  encouraging statistically significant improvements was also seen older children, due to their  higher level of understanding, cooperation and self-motivation.

Our data suggests that a minimum of 4 months, preferably 6 months, of follow up is needed  to show significant cognitive, and later, motor improvements.

Just as a normal child needs up to 4 years for his full Neuro-development, so does a CP child  given HBOT, whose “TIME” starts six months after completing HBOT, when remyelination  is complete.

How many HBOTs?  

We suggest that parents carry on intermittent HBOT (40 sessions at a time) as long as the  GMFM development curve shows significant upward deviation (more than about 1 point per  month).

Our Final Conclusion  

CP is a multifactorial ischemic brain pathology with motor deficiencies, besides variable  degrees of cognitive, sensory, communication and visual deficiencies.

Based on the data we have gathered so far, we feel that in the medical intervention therapy of  CP children receiving intensive Standard Therapy with supplemental Hyperbaric Therapy  gives a statistically significant benefit as compared to children receiving only similar  Standard Therapy.

Also that 1.3 ATA Low pressure Hyperbaric Air Therapy is Statistically Not Inferior to  Regular HBOT at 1.5 / 1.75 ATA using 100% oxygen.

Further study over the next 2 to 3 years may shed more light on this evidence.

Causes of Cerebral Palsy Oxygen Therapy in the Neonatal Period Treatment of Cerebral Palsy with HBOT Conclusions

An entry from K.K. Jain’s Textbook Of Hyperbaric Medicine

Cerebral palsy is a chronic neurological disorder that can be due to several causes of brain damage in  utero, in the perinatal period, or postnatally. Hyperbaric oxygen has been shown to be useful in treating  children with cerebral palsy. This topic is discussed under following headings:

Causes of Cerebral Palsy 

Oxygen Therapy in the Neonatal Period Treatment of Cerebral Palsy with HBOT Conclusions 

Causes of Cerebral Palsy The term cerebral palsy (CP) covers a group of non-progressive, but often changing, motor impairment  syndromes secondary to lesions or anomalies of the brain arising in the early stages of development.  Between 20 to 25 of every 10,000 live-born children in the Western world have the condition (Stanley et  al 2000). Problems may occur in utero, perinatal, and postnatal. Infections, traumatic brain injury, near drowning and strokes in children suffering from neurological problems come under the heading of  cerebral palsy. Diagnosis of cerebral palsy resulting from in utero or early perinatal causes may be made  immediately after birth, but more commonly occurs between 15 and 24 months. It is possible that CP may  be misdiagnosed for years because specific symptoms may show up very late in childhood. Some of the  possible causes of Cerebral Palsy and are listed in Table 21.1.

Although several antepartum causes have been described for CP, the role of intrapartum asphyxia in  neonatal encephalopathy and seizures in term infants is not clear. There is no evidence that brain  damage occurs before birth. A study using brain MRI or post-mortem examination was conducted in 351  full-term infants with neonatal encephalopathy, early seizures, or both to distinguish between lesions  acquired antenatally and those that developed in the intrapartum and early postpartum period (Cowanet  al 2003). Infants with major congenital malformations or obvious chromosomal disorders were excluded.  Brain images showed evidence of an acute insult without established injury or atrophy in (80%) of infants  with neonatal encephalopathy and evidence of perinatal asphyxia. Although the results cannot exclude  the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, the  data strongly suggest that events in the immediate perinatal period are most important in neonatal brain  injury. These findings are important from management point of view as HBOT therapy in the perinatal  period may be of value in preventing the evolution of cerebral palsy.

Oxygen Therapy in the Neonatal Period Following World War II, oxygen tents and incubators were introduced, and premature infants were given  supplementary oxygen to improve their chances of survival, with levels up to 70% being given for  extended periods. Epidemics of blindness due to retrolental fibroplasia followed in the 1950s, which led to  a restriction of the level of supplemental oxygen to 40%. A reduction in the incidence of blindness  followed, which appeared to confirm the involvement of oxygen in the development of the retinopathy.  The link between the use of recurrent supplemental oxygen and the rise of retinopathy was rapidly  accepted, even though it was suggested that retrolental fibroplasia was produced by initially  preconditioning a child to an enriched oxygen environment and then suddenly withdrawing the same: The  disease occurred only after the child’s removal from the high oxygen environment (Szewczyk 19 51). It  was also noted that retinopathy developed upon the withdrawal from the high level of oxygen, and that  probably the best thing to do was to return the child to the oxygen environment (Forrester 1964). Under  these circumstances, in many of the patients, the results were encouraging, and vision returned to

normal. A slow reduction of oxygen and final return to the atmospheric concentration for several weeks  was all that was needed to restore the vision. Thus, there is no rational basis for withholding oxygen  therapy in the neonatal period. As mentioned in other chapters of this textbook, retrolental fibroplasia is  not associated with HBOT. It is unfortunate that nearly all affected newborns today are deprived of  appropriate oxygen therapy because of the fear that it will cause retrolental fibroplasia (see Chapter 31).  Some observations indicate that since the practice of administration of high levels of oxygen has been  abandoned, there is a rise in the incidence of cerebral palsy as compared to previous levels.

Treatment of Cerebral Palsy with HBOT 

The use of hyperbaric oxygenation in the pediatric patient was relatively common in Russia (see Chapter  28) . HBOT has been used in Russia for resuscitation in respiratory failure, for cranial birth injuries, and  for hemolytic disease of the newborn. HBOT was reported to reduce high serum bilirubin levels and  prevent development of neurological disorders. In cases of respiratory distress, delayed use of HBOT  (12-48 h after birth) was considered useless. However, early use (1-3 h after birth) led to recovery in 75%  of cases. The Italian physicians began treating the small fetus in utero in 1988 demonstrating a reduction  of cerebral damage. Patients were hospitalized before the 35th week and hyperbaric treatments were  given every 2 weeks for 40 min at 1.5. The fetal biophysical profile showed a remarkable improvement as  soon as the second treatment.

At the conference “New Horizons for Hyperbaric Oxygenation” in Orlando, Florida, in 1989, results were  presented of HBOT therapy of 230 Cerebral Palsy patients who had been treated in the early stages  since 1985 in Sao Palo, Brazil (Machado 1989). Treatment consisted of 20 sessions of 1 h each at 1.5  ATA (100% oxygen), once or twice daily in a Vickers monoplace chamber. A few of the children had  exacerbation of seizures or developed seizures. The results showed significant reduction of spasticity:  50% reduction in spasticity was reported in 94.78% of the patients. Twelve patients (5.21%) remained  unchanged. However, follow-up included only 82 patients, and 62 of these (75.6%) had lasting  improvement in spasticity and improved motor control. The parents reported positive changes in balance  and “intelligence with reduced frequency of seizure activity.” Results of a continuation of this work in  Brazil were presented by in 2001 at the 2nd International Symposium on Hyperbaric Oxygenation and the  Brain Injured Child held in Boca Raton, Florida, to include 2,030 patients suffering from childhood chronic  encephalopathy that had been treated since 1976, 232 of whom were evaluated with long-term follow-up;  age ranged from 1 to 34 years. The improvements were noted as follows: 41.81% decreased spasticity,  18% noted global motor coordination improvement. Improvements were also noted in attention: 40.08%,  memory, 10.77%, comprehension, 13 .33%, reasoning, 5.60%, visual perception, 12.93%, sphincter  control, 6.46%. It was concluded from this study that HBOT therapy should be instituted as early as  possible in such cases.

Another presentation at the 2nd International Symposium was a study by Chavdarov, Director of the  Specialized Hospital for Residential Treatment for Rehabilitation of Children with Cerebral Palsy in Sofia,  Bulgaria, where HBOT had been considered an important part of the management of children with CP  since 1997. This study included 50 children with distribution of various types as follows: spastic Cerebral  Palsy (n = 30), ataxic/hypotonic cerebral palsy (n = 8), and mixed cerebral palsy (n = 12). Measurements  included motor ability, mental ability, functional development, and speech. Overall psycho-motor function  (single or combined) improved in 86% of the patients following 20 HBOT sessions at 1.5-1.7 ATA lasting  40-50 min once daily.

The first North American case of Cerebral Palsy treated with HBOT was in 1992. The case was presented  by Paul Harch at the Undersea and Hyperbaric Medical Society meeting in 1994 (Harch 1994). In 1995,  Richard Neubauer began treating Cerebral Palsy using HBOT. Because of the growing worldwide  anecdotal reports, a small pilot study of HBOT therapy in cerebral palsy children was conducted in the UK  in 1995, which showed similar improvements in a group of seriously brain-injured children and led to the  foundation of the Hyperbaric Oxygen Trust, a charity to treat Cerebral Palsy and the brain injured  children. The Trust, which has since changed its name to Advance, has treated over 350 patients, though  no scientific appraisals have been published. Positive anecdotal reports of its use in cerebral palsy  started to accumulate. As more HBOT treatment clinics for Cerebral Palsy opened in the United States

and Canada, further studies were conducted. It is estimated that over 5000 children with Cerebral Palsy  have been treated worldwide with HBOT.

Published Clinical Trials 

In 1999 the first pilot study in the use of HBOT in Cerebral Palsy was published (Montgomery et al 1999).  This study involved 23 children (10 female, 15 male; age range 3.1 to 8.2 years) with spastic diplegia.  Absence of previous surgical or medical therapy for spasticity was one of the prerequisites for inclusion  as well as a 12-month clinical physiotherapy plateau. The study was performed at McGill University  Hospital’s Cleghorn Hyperbaric Laboratory in a monoplace chamber at 1.75 ATA (95% oxygen) for 60 min  daily and at the Rimouski Regional Hospital in a multiplace chamber ( 60 min at 1.75 ATA twice daily) for  20 treatments in total. Assessments, pre- and post-treatment, included gross motor function  measurement (GMFM), fine motor function assessment (Jebsen’s Hand Test), spasticity assessment  (Modified Ashworth Spasticity Scale) as well as parent questionnaire and video analysis. Results  following treatment were an average of 5.3% improvement in GMFM and a notable absence of  complications or clinical deterioration in any of the children. “Cognitive changes” were observed, but  these were nonspecific. Video analysis was also positive. The obvious flaws of this study were the lack of  placebo control and the application of two different HBOT protocols. The assessment tools utilized also  had inherent variations. Montgomery achieved improvement in Cerebral Palsy children using 20  treatments at 1.66 ATA oxygen (1.75 ATA 95% O2)/60 min), but the children experienced rapid  regression of neurological gains after cessation of treatment. The number of treatments was inadequate  as the authors of this chapter had recommended 40 treatments at 1.5 ATA/60 min, because consolidation  of the gains does not occur until 30 to 35 treatments. This first study, however, provided useful data  regarding the potential efficacy of HBOT therapy and provided the justification for a larger controlled,  randomized study.

The results of just such a prospective, hyperbaric-air controlled, randomized multicenter study have been  published “with intriguing results” (Collet et al 2001). This study included 111 Cerebral Palsy children  (ages 3-12 years) that were randomized into two groups: receiving either 1.75 ATA 100% oxygen or 1.3  ATA room air (the equivalent of 28% oxygen at 1 ATA) for 1 h for a total of 40 treatments. Gross and fine motor function, memory, speech, language, and memory were assessed. Improvement in global motor  function was 3% in the hyperbaric air group and 2.9% in the hyperbaric-oxygen-treated group. Although  the results were statistically similar in both groups, the HBOT-treated group had a more rapid response  rate in the more severely disabled children. Cognitive testing was performed on a subset of the preceding  study to investigate the effect of HBOT on cognitive status of children with CP (Hardy et al 2002). Of the  111 children diagnosed with CP (aged 4 to 12 years), only 75 were suitable for neuropsychological  testing, assessing attention, working memory, processing speed, and psychosocial functioning. The  children received 40 sessions of HBOT or sham treatment over a 2-month period. Children in the active treatment group were exposed for 1 h to 100% oxygen at 1.75 atmospheres absolute (ATA), whereas the  sham group received only air at 1.3 ATA. Children in both groups showed better self-control and  significant improvements in auditory attention and visual working memory compared with the  baseline. However, no statistical difference was found between the two treatments. Furthermore, the  sham group improved significantly on eight dimensions of the Conners’ Parent Rating Scale, whereas the  active treatment group improved only on one dimension. Most of these positive changes persisted for 3  months. No improvements were observed in either group for verbal span, visual attention, or processing  speed. Unfortunately, the Collet study increased the pressure to 1.75 ATA of 100% oxygen for 60 min (40  treatments) and to 1.3 ATA in the control group breathing air for 60 min, i.e., a 30% increase in oxygen for  the controls. This dose of HBOT had not been used previously in Cerebral Palsy patients and was  possibly an overdose (Harch 2001) and likely inhibited the HBOT group’s gains. Evidence for this was  seen in the GMFM data where five of the six scores increased in the HBOT group from immediate post  HBOT testing to the 3-month retest versus three of six scores in the controls. Some of the negative  effects of 1.75 ATA likely had worn off by this time. Results of the Collet study showed significant  improvements in both groups, but no difference between groups. The serendipitous flaw in the study was  the 1.3 ATA air control group, which also improved significantly. This underscored the fact that the ideal  dose of HBOT is unknown in chronic pediatric brain injury, but it suggested that oxygen signaling may  occur at very low pressures. Mild HBOT therapy can be effective in improving SPECT as well as attention

and reaction times (Heuser & Uszler 2001). Therefore, the beneficial effect in patients described by Collet  and colleagues is probably related to the beneficial effects of slightly pressurized air rather than to the act  of participating in the study. In addition a biphasic sham pressurization, which is highly recommended for

a control group, was not used in this study. The duration of this study was only 2 months. Perhaps this  length of time is not sufficient for evaluating neuropsychological effects of HBOT in a chronic neurological  condition.

The controversy regarding this study will undoubtedly take a long time to resolve, but it has already  begun to raise some very important issues and some very important questions about the validity of “mild”  HBOT (1.3-1.35 ATA air or the same pressure supplemented with oxygen concentrator). The first issue is  that 1.3 ATA ambient air was not an inert or true placebo, but had a real effect on the partial pressure of  blood gases and perhaps other physiological effects as well. Compressed air at 1.3 ATA increases the  plasma oxygen tension from 12.7 kPa (95 mmHg) to 19.7 kPa (148 mmHg), and the increase of a  concentration of a reactive substrate by 50% is substantially notable. Rather than answer the question of  effectiveness of HBOT in CP the Collet study and its offspring Hardy (2002) substudy confused the  scientific community not familiar with hyperbaric oxygen. The unequivocal finding of these studies is that  both pressure protocols achieved statistically significant objective neurocognitive gains, a phenomenon  that cannot be attributed to placebo. This reinforced the findings of the other non-controlled studies in the  chronic category above, and was strengthened by the studies using functional brain imaging as surrogate  markers (Harch 1994a, Neubauer 2001, and Golden et al 2002).

Unpublished Studies 

The Cornell Study 

Upon the urging of interested parents, Dr. Maureen Packard of Cornell University in New York City  agreed to perform such a study. This study was randomized to immediate and delayed (6 months later)  treatment with HBOT (the delayed treatment group to serve as an untreated control group). Age range  was 15 months to 5 years with moderate to severe Cerebral Palsy and patients were given 40 1-h  sessions at 1.5 ATA, once a day, 5 days a week for 4 weeks. The study population included 26 children  with cerebral palsy secondary to prenatal insults, premature birth, birth asphyxia, and post-natal  hemorrhage. The average age of enrollment was 30 months. Nine patients presented with cortical visual  impairment. Assessment was neurodevelopmental, Bayley II (cognitive), Preschool Language Scale,  Peabody Motor Scale, Pediatric Evaluation of Disabilities Inventory(PEDI), parental report of specific skills  including mobility, self-care and social interaction. Final assessments were available on 20 subjects. The  only side effects of the study were barotrauma in nine children requiring placement of a ventilation tube or  myringotomy.

Assessments were performed at four time points: enrollment (Tl), after the immediate group had received  treatment (T2), prior to the delayed groups’ HBOT therapy 5 months after enrollment (T3), and after the  delayed groups’ treatment (T4). There was a significant difference (p < 0.05) in the improvement of scores  on the mobility sub-domains for the time period T2 minus Tl in favor of the immediately treated group. For  the period T4 minus T3 there was a trend favoring the recently treated delayed group and a trend in the  social function subdomain in the more recent treated group. Parental diaries over the month of treatments  demonstrated 83% marked improvement in mobility, 43% marked increase in attention, and 39% marked  increase in language skills. Overall, there was some improvement in mobility in 91%, in attention in 78%,  in language in 87%, and in play in 52%. One family saw no improvement and six families minimal  improvement for a total of 30%. Five families (22%) reported major gains in skills, and 11 families  reported modest gains (48%). Four of the nine children with cortical visual impairment had improvement  in vision noted by families, vision therapists, and ophthalmologists. There was no statistical difference in  Peabody or Bayley II scores on blinded assessment.

Their conclusions at 6-month post-interview were that although changes in spasticity may diminish over  time, improvements in attention, language and play were sustained. ‘”This increase in attention is  particularly important for children must be aware’ in order to learn. This represents a direct impact on  cognitive functioning. The main differences between HBOT and traditional therapies are the rapid gains

over time and the impact on cognitive skills, which, in general are not improved by physical, occupational  and speech therapies.” This study was presented At the University of Graz, on 18 November 2000.

The United States Army Study on Adjunctive HBOT 

Treatment of Children with Cerebral Anoxic Injury 

Shortly after the previous studies were begun, the US Army conducted a small study on functional  outcomes in children with anoxic brain injury. Baseline and serial evaluations showed improvement in  gross motor function and total time necessary for custodial care in nine children with Cerebral Palsy.  Eight volunteer (parental) subjects with varying degrees of Cerebral Palsy and one near-drowning victim  were included in this investigation. Of the Cerebral Palsy cases studied, the mean age was 6.4 years  (range 1.0- 16.5 years), and the near drowning patient was 5.6 years of age seen 1 year post incident.  Pretreatment evaluation included gross motor function ( GMPM, lying, rolling, crawling and kneeling,  sitting, standing and walking, running, and jumping), the Modified Ashworth Scale (MAS) for spasticity,  rigidity, flexion/extension, the Functional Independence Measure for Children (WeeFIM) regarding self care, sphincter control, transfers, locomotion, communication and social cognition, video, 24-h time  measure, parental questionnaire, and single photon emission computerized tomography (SPECT)  scanning. Testing was conducted every 20 treatments with the exception of SPECT and parental  questionnaire which were completed at 40 and 80 sessions.

All subjects received 80 HBOT treatments in a multiplace chamber (100% oxygen) at 1.75 ATA (60 min  for each session) daily (Monday to Friday) for 4 months. Each patient served as his or her own control as  compared to the baseline scores. Improvements in GMFM in the categories of lying and rolling, crawling  and walking, sitting and walking, running and jumping were statistically significant (p < 0.05) . The total  time necessary for parental care also showed a statistically significant improvement (p < 0.03%) in  reduction of custodial time required. In the parental questionnaire, overall improvement was indicated  through the end of the study, including other assessments not included in the survey. Three children  demonstrated improved swallowing function and were able to ingest a variety of liquids and foods; there  was reduction in strabismus in two subjects, nystagmus was resolved in one participant, and one patient  experienced complete resolution of a grade 3 vesicoureteral reflux, obviating the need for surgery.  Unfortunately, the SPECT scan results were omitted due to multiple technical and procedural problems.

Overall improvement was 26.7% at 30 treatments, up to 58.1% at 80 treatments. Their conclusions were  that HBOT therapy seemed to effect overall improvement in Cerebral Palsy (with little response in the  near-drowning case), although the optimum number of treatments remained undetermined, since the  improvements were noted at the end of the study. They advised further research and follow-up studies to  determine the true potential of HBOT for children with anoxic injury and Cerebral Palsy.

Ongoing Studies in Hyperbaric Oxygen Therapy  Treating Cerebral Palsy 

Studies of the use of mild HBOT, hyperbaric air, supplemental oxygen, and higher pressures of HBOT  must be continued to eventually determine the ultimate benefits for cerebral palsy and to identify the  subgroups of patients who may benefit from each. Investigations of mild HBOT therapy are currently  ongoing in Russia, the United States, and South America. Up to April 2003, the Ocean Hyperbaric  Neurologic Center (Fort Lauderdale, Florida) has treated over 600 children suffering from Cerebral Palsy  and brain injury. Analysis of these cases has not yet been completed. Another 200 children with Cerebral  Palsy and a large variety of neurological disorders have been treated at the Harch Hyperbaric Center in  New Orleans (Louisiana, USA). One case is shown here as an example.

HBOT in the Management of Cerebral Palsy  Case Reports 

Patient 1: Cerebral Palsy

The patient is a 2-year-old boy whose twin died in utero at 14 weeks. He was delivered at term by  vacuum extraction and developmental delay was detected at the age of 4- 5 months. He was diagnosed  as a case of cerebral palsy. At 2 years of age SPECT brain imaging was performed and showed a  heterogeneous pattern of cerebral blood flow. The patient underwent a course of twice daily, 5 days/week  HBOT treatments in blocks of 50 and 30 treatments. At the conclusion of treatments he showed  improvement in spasticity, speech, chewing/swallowing, cognition, and ability to sit in his car seat and  stroller for prolonged periods. Repeat SPECT brain imaging showed a global improvement in flow and  smoothing to a more normal pattern consistent with the patient’s overall clinical improvement. The two  SPECT scans are shown side by side in Figure 21.1. Three dimensional reconstructions of the two scans  are shown in Figures 21.2 and 3.

Patient 2: Cerebral Palsy 

The patient is an 8-year-old boy with a history of cerebral palsy. He had spastic diplegia secondary to  premature birth from a mother with eclampsia. Patient was delivered by emergency Cesarean section at  27 weeks when his mother developed seizures. APGARS scores were 7 and 8. The patient spent 5  months in the hospital primarily because of feeding problems. The patient did not achieve normal  milestones and developed infantile spasms at 2 years of age. Baseline SPECT brain imaging (Figure  21.4) showed a mildly/moderately heterogeneous pattern and reduction of blood flow. Three hours after a  single HBOT session at 1.5 ATA for 60 min, repeat SPECT showed global improvement and smoothing to  a more normal pattern in Figure 21.5. The patient underwent a course of 80 HBOT sessions (1.5 ATA/60  min) over the next 6 months in two blocks of treatment (twice daily, 5 days/week x 40, then once-daily 5  days/week x 40), and showed improvement in his impulsive inappropriate behavior, motor function,  vision, and constipation. Repeat SPECT brain imaging reflected these neurological gains (Figure 21.6),  showing generalized improvement in cerebral blood flow and pattern. Three-dimensional surface  reconstruction of Figures 21.4, 21.5, and 21.6 are presented in Figures 21.7, 21.8, and 21.9, respectively.  While there is a global increase in blood flow, the most significant relative increase in flow is to the  temporal lobes as shown in the three-dimensional figures.

All SPECT brain imaging was performed on a Picker Prism 3000 at West Jefferson Medical Center. All  scans were identically processed and three dimensional thresholds obtained by Phillip Tranchina.  Pictures of the scans in the above figures were produced by 35 mm single frame photography under  identical lighting and exposure conditions.


SPECT brain imaging transverse images of baseline pre-HBOT study on the left and after 80 HBOT  treatments on the right. Note the global increase in flow and change from heterogeneous to the more  normal homogeneous pattern. Slices begin at the top of the head in the upper left corner and proceed to  the base of the brain in the lower right corner of each study. Orientation is standard CT: the patient’s left  is on the viewer’s right and vice versa with the patient’s face at the top and the back of the head at the  bottom of each image. Color scheme is white, yellow, orange, purple, blue, black from highest to lowest  brain blood flow.

Figure 21.2

Three-dimensional reconstruction of baseline SPECT study in Figure 21.1 (study on left side). Note  reduction in flow to both temporal lobes, inferior frontal lobes, and the brainstem (central round structure  between the temporal lobes below the large colored area-frontal lobes).

Figure 21.3

Three-dimensional reconstruction of SPECT after 80 HBOT treatments (right hand study in Figure 21.1)  Note the increased flow to the temporal lobes, inferior frontal lobes, and brainstem.


Sagittal slices of baseline SPECT brain imaging through the center of the brain. Note the heterogeneous  pattern of blood flow. Slices proceed from the right side of the head in the upper left corner to the left side  of the head in the lower right corner. The front of the brain (face) is on the left side and the back of the  brain (back of the head) is on the right side of each slice.


Sagittal slices of SPECT three hours after a single 1.5 ATA/60 min HBOT treatment. Note the generalized  increase in flow and smoothing to a more normal pattern.

Figure 21.6

Sagittal slices of SPECT after 80 HBOT treatments. Note the marked increase in flow and smoothing of the pattern compared to the baseline in Figure 21.4.


Three-dimensional surface reconstruction of SPECT in Figure 21.4. Note reduction in flow to the temporal  lobes and coarse appearance of flow to the surface of the brain.

Figure 21.8

Three-dimensional surface reconstruction of SPECT in Figure 21.5. Note improvement in flow to the  temporal lobes and slight smoothing of flow to the surface of the brain.


Three-dimensional surface reconstruction of SPECT in Figure 21.6. Note improvement in flow to the  temporal lobes and slight smoothing of flow to the surface of the brain.


Cerebral palsy is the result of a large variety of causes, and it is difficult to design trials with subgroups of  patients with similar pathomechanisms. The results of several studies have been presented including one  controlled study that did not show improvement in neuropsychological status. A large number of patients  have been treated, and some have been followed up for long periods to document improvement that can

be correlated with imaging studies. Cognitive improvement is usually seen by the 40th treatment in  patients with chronic neurological disorders such as Cerebral Palsy (Golden et al 2002). Controlled  studies of HBOT in CP should continue, but they may not resolve all the issues. The extensive  experience of open clinical studies with some good results cannot be ignored. In a condition where there  is nothing else to offer, HBOT therapy is considered to be worth a trial. The concept of personalized  medicine as described in Chapter 38 can be applied to HBOT treatments in Cerebral Palsy. One cannot  recommend a standard protocol, but the ideal treatment schedule should be determined for each patient  including the pressure, dose, and duration of treatment. It may be possible to identify responders early on  in the treatment. Although molecular diagnostic procedures may be used in the investigation of patients  with Cerebral Palsy, genotyping and gene expression studies have not yet been done as a guide to  treatment but this is a promising field for future investigation (Jain 2003i).