Looking at the brain as a tissue….

« There are several degrees of damage to the brain tissue, and the most severe one is necrosis because the tissue is fully dead, there’s nothing there. In the instance where we have necrotic tissue, there is nothing we can do. But in the surrounding tissue, there might be tissue that is not fully dead, that is damaged. In this tissue, we have metabolic dysfunction. The cells in this area have sufficient oxygen supply to stay alive, but they don’t have the full energy needed for the full activation. This is where hyperbaric oxygen can help. The challenge is to be able to demonstrate this. »

Good article interesting interview with dr Efrati 😉 yes my son doctor :

https://www.neurologylive.com/clinical-focus/hyperbaric-oxygen-therapy-offers-hope-post-stroke-cognition-issues

No comments

Just for anybody’s who wants to comment on my blog : I am not confirming ANY comments on it I had too much spam messages and I don’t have time to see all comments which is good or spam … so I delate every day ALL COMMENTS send me

Sorry for your inconvenience but it’s like this

If you want to contact me ( not spam) send me mail:

svetpanuta@gmail.com

And I will see if it’s really professional mail or just a spam ( haw to create my blog and not about nerologie – all spam I put in garbage !!!)

My blog is free I am not gaining money from it I don’t have time for useless comments.

Thanks for understanding

HBOT 2019 Speaker Videos HBOT 2019

I invite you to see all 38 presentations :

HBOT 2019 Speaker Videos

HBOT 2019

As Ted Fogarty posted this I suppose we can all share

On link you can find all speakers from last dr Harch symposium 2019!!!!!

Latest research of Hbot

About Cannabis

About LLLT

And much more

I am shearing but I can’t put my head on everybody’s shoulders

Just try to see yourself!!!!

https://www.youtube.com/playlist?list=PLTOK_IVnJp5lUfDeSn5fVeb9hdpa2a_1g

HBOT 2019 Speaker Videos

https://www.youtube.com/playlist?list=PLTOK_IVnJp5lUfDeSn5fVeb9hdpa2a_1g

Effect of hyperbaric oxygen therapy on chronic neurocognitive deficits of post-traumatic brain injury patients: retrospective analysis

HBOT – What does it do, and how does it treat medical conditions :

The latest seminar by the best experts on healing the brain from Israel, June 2019

https://youtu.be/dyQHztkfiNg

Prof Shai Efrati is the leader in the field of treatment utilising HBOT and achieving what DRUGS can’t.

Israeli Researchers Assaf Harofe find Hyperbaric Oxygen therapy was associated with significant cognitive improvements.

And if we are talking about previous studies with 1.2 ATA on 21% inhaled oxygen (ie, air) cannot be regarded as an inert or sham control!!!!

« In addition to objective evaluations, there are inherent ethical and logistic difficulties in handling the sham control in HBOT trials. HBOT includes two active ingredients: pressure and oxygen. Pressure is needed to increase plasma oxygen, but the pressure change alone may also have significant cellular effects. Additionally, the greatest effect of pressure is in human tissues that are under tight autoregulation pressure control, such as the brain, where the intracranial pressure is normally 0.0092–0.0197 atm.23 24 To generate a pressure sensation, the chamber pressure must be 1.2 ATA or higher. However, such a change in environmental pressure (from 1 ATA to 1.2 ATA) and subsequent tissue oxygenation (with an increase of tissue oxygenation by at least 50%) has a significant biological effect. Thus, sham therapy in previous studies using 1.2 ATA on 21% inhaled oxygen (ie, air) cannot be regarded as an inert or sham control but rather as a lower dose of the active ingredient.4 20 In regards to a possible effect of vasoconstriction of the large blood vessels induced by hyperbaric oxygen—it has been well established that the tissues are saturated by hyperoxia and do not suffer from hypoxia, as the vasoconstriction effect is compensated by increased plasma oxygen content and microvascular blood flow.

Any increase in pressure, even with reduced oxygen percentage, cannot serve as a true placebo, but rather as a low dosage of the active ingredient, further supporting the need for objective data gathered from large cohorts of patients suffering from PCS and treated by HBOT.

Source: https://bmjopen.bmj.com/content/8/9/e023387

Book /Livre

Voilà mon livre « Marc L’invincible » est désormais en ligne et disponible* à l’achat dans la boutique Kindle: ( en français)

https://www.amazon.fr/dp/B07Y34WPXQ

« Marc L’invincible: L’histoire vraie d’une récupération remarquable, après arrêt cardiaque et lésions cérébrales anoxiques », est désormais disponible en livre broché dans la boutique Amazon. Les lecteurs peuvent l’acheter:

https://www.amazon.fr/dp/B07Y4KC5S1

Here is my book « Marc L’invincible » is now online and available * for purchase in the Kindle store: (in French)

I will do English translation ( just give me some time)

Ici lien vers page de Écrivain-biographe basée à Grenoble -Membre des Compagnons Biographes – Julie Lucquet qui à prêter son plume pour raconter notre histoire :

https://www.facebook.com/298833463857319/posts/670782633329065?sfns=mo

We are starting soft hbot for Marc:

I honestly believe that soft chamber can also help in many ways but I think it’s not the best for a period of time right after his injury but on the other hand 100% oxygen has more potential right after an injury from my point of view.

I’ll be honest; I do understand that parents can’t always go to clinics every year, or twice a year for 2 months…. ( in order to do 40 dives).

Just to give you an exemple:

We did four months in Israel’s Hbot back in 2016 ( which was the best thing that could happened to Marc) so it was the period when oxygen 100% helped him mostly and it was more potential because more close to injury in time.

we also did one month in 2017 and then two months in 2018

So in total we did 110hours of hard chamber (1,5ata 100% oxygen) in 3 years.

Both of the two last times, we saw progress which was much less obvious than at his first time in 2016 and it’s totally normal.

So now we are sold on soft chamber: it’s obvious it still helps him but I really think that I would do it now at 1,3 ata without oxygen, not because it’s my favorite protocol, but because it’s safe for home use. In those circumstances it would give less results but everyone is able to do it at home which by the way makes it 50% more oxygen in his plasma that will help him.

So it’s just obvious, we can not escape school every year for 2 months. So I believe that a soft chamber can be THE solution for long term treatment (we are talking years after the acute injury).

And by the way we have some good canadien group testimonials from parents (in french only) who mostly used soft chamber treatments only.

Here’s our chamber installation :

Thanks

Jean-François Tremblay

contact:

www.oxysoins.com

info@oxysoins.com

It was an exeptional experience, very helpful for installation and for all of my questions and just perfectioning training.

(francais):

Nous commençons souple hbot pour Marc:

Honnêtement, j’ai la conviction que la chambre souple peut aussi aider de nombreuses manières, mais j’estime que ce n’est pas la meilleure solution pour une période qui suit immédiatement sa anoxie cérébrale , mais que 100% d’oxygène a au plus de potentiel après son arrêt cardiaque (c’est que de mon point de vue) …après 110h chambre dure 100% oxygene et 1,5 ata on passe à chambre souple à la maison 1,3 ata et sans oxygène et après 3 ans!

Je serai honnête; Je comprends que les parents ne peuvent pas toujours aller aux cliniques chaque année, une ou deux fois par an pendant 2 mois … (pour faire 40 plongées).

Juste pour vous donner un exemple:

On a fait pendant 3 ans En Israël, nous avons Hbot dure (1,5 ata 100% oxygène) –

pendant quatre mois en 2016 (ce qui a été la meilleure chose qui puisse arriver à Marc). C’est donc la période où l’oxygène à 100% l’a aidé le plus, ce qui lui donnait plus de potentiel, car il était plus proche de son anoxie cérébrale dans le temps.

nous avons également fait un mois en 2017 puis deux mois en 2018

Au total, nous avons donc effectué 110 heures de chambre dure (1,5% à 100% d’oxygène) en 3 ans.

Les deux dernières fois, nous avons constaté des progrès beaucoup moins évidents que lors de sa première fois en 2016 et c’est tout à fait normal.

Nous sommes maintenant commence le chambre souple : c’est évident que peut l’aider toujours, mais je pense vraiment que je le ferais maintenant à 1,3 ata sans oxygène, non pas parce que c’est mon protocole préféré, mais parce que c’est sans danger pour la maison. Dans ces circonstances, cela donnerait moins de résultats, mais tout le monde est capable de le faire à la maison, ce qui lui donne 50% d’oxygène supplémentaire dans son plasma, ce qui l’aidera.

C’est donc évident, nous ne pouvons pas échapper de l’école tous les ans pendant 2 mois. Je pense donc qu’une chambre souple peut être LA solution pour un traitement à long terme (nous parlons des années après anoxie cérébrale).

Et au fait, nous avons de bons témoignages de groupes canadiens de la part de parents qui utilisaient principalement des traitements de chambre souple : https://www.facebook.com/groups/169622703606007/?ref=share

Voici notre installation de chambre:

Merci

Jean-François Tremblay

Si vous voulez contact:

www.oxysoins.com

info@oxysoins.com

Tel france : 0186655685

Ce fut une expérience exceptionnelle, très utile pour l’installation et pour toutes mes questions et pour perfectionner ma formation.

So why Hbot works not always same way in brain injury?

So why Hbot works not always same way in children’s? I am not a doctor I am just a mum like you so please I do analyze my son injury I read a lot but I am not a doctor ( take it just only mum reflection on subject) ok?

It’s very difficult question and I think even best Hbot doctors don’t know exact answer honestly

Let’s say : first of all each brain injury is unique and diferent.

I am trying just analyzing what I can as dates but as I said with anoxic brain injuries we don’t have any studies with spect scans so all this discussion just my personal suppositions ok ?

Ok i post mri of Marc before Hbot and after 80h

We have MRI in January 2016 just some days after anoxic injury

And we have MRI June 2017 after 80h Hbot … but without general anesthesia ( so some artifacts)

Be my guest if any radiology specialist want to make professional hole comparison

1. I think Age of child in the moment of injury play very big role : of child very small ( new born or HIE child for example) smaller is a child at brain injury more fragile his brain ( so same 25 minutes without oxygen will be more devastating on smallest child brain at birth or 1 month age than at 4 years old)

Second why age is important – because if child was already walking / full functioning child before brain injury -so after it will be retraining of his lost functions wile in new born it will be just training ( with less neurons in brain) I think it’s more difficult. But it’s just my opinion.

2. Of cause most important factor : it’s volume of Brain which was damaged!!!!

While there is no way of knowing how much recoverable tissue exists in the days, weeks, and years following brain injury , HBOT can increase cell reproduction and administer oxygen to tissue that was previously cut off from blood flow. The dormant cells surrounding the damaged tissue area, also known as ischemic penumbra, are responsible for much of post-stroke dysfunction. If oxygen therapy can revive these cells, lost functionality may return to the individual.

And this you can say only by MRI and Spect. But again for small children’s I am sorry but MRI don’t give exact informations ( that’s why neurologists don’t like to do MRI for cp children’s too early age …. we can really see at age 4-5 years but before it’s very difficult).

But still : Qualitative assessment of brainstem injury on T1 and T2 images in neonates with HIE may provide information on injury severity and risk of death, but objective quantitative data such as ADC values are lacking. ( if you want to read about read this study:

https://www.ncbi.nlm.nih.gov/m/pubmed/28686592/

These infratentorial areas have high concentrations of excitatory neurotransmitters (e.g., glutamate) and are especially vulnerable to the profound hypoxia-ischemia that is typical in HIE. The cerebellum acts as a satellite system of established cortico-basal ganglia networks in neonates.

If we talk about MRI of my child ( he had basal ganglia

and thalamus damages) …

In one large study cohort, 60% to 70% of infants who sustained moderate basal ganglia/thalamic injury had cerebral palsy and 35% had developmental quotient less than 70 (40). Cerebral palsy was identified in 98% of infants with severe basal ganglia/thalamic injury 

Before Hbot:

I will post his MRI ( after Hbot a bit father in this article ok?)

3. So here we come fore 3d factor : did child was cooled after brain injury???? I believe that it’s helped to my child ( yes his body temperature was cooled it’s protocol for cardiac arrest but not always for HIE ).

4. Did child had 100% oxygen or just 30% oxygen delivery as Normobaric ? It’s may be has also role to play i think.

( it’s after reading this book I think about )

This lecture is also really good explanation why Hbot is better ( than Normobaric oxygen) we get oxygen in plasma! Lisen at 44minutes :

https://youtu.be/z6qy1hq2zqM

( and by the way I agree about multiple approach with Sherr – before starting Hbot in Israel’s for my son – we did batteries of blood tests and also tubes in ears – in order to protect them against barotraumatisme).

5. And you see naw what I think about Hbot ( we don’t have real agreement between doctors what is the best protocol for brain injury – and what kind brain injury ? By the way ?) TBI or anoxic? ). Parents has some possibilities: 1,5ata 100% oxygen is most used in hard chambers by centers ( sometimes is more pressure but honestly it’s the mostly use regiment for nerology in hard chambers) and I believe that in case of my son really oxygen in Hbot made biggest changes but as I posted before in Hbot conditions contrary to Normobaric 100% oxygen…

« We found that HBO, but not NBO, reduced oxygen and glucose deprivation-induced cell injury, indicating that passive tissue oxygenation (i.e. without vascular support) of the brain parenchyma requires oxygen partial pressure higher than 1 ATA. »

More about read my post in blog:

http://brain-injury-hope.com/2019/04/normobaric-or-hyperbaric/

About other possibilitiy: 1,3ata without oxygen

Of cause first of all it’s the most “ not risky “ protocol for very injured children’s so may be also that’s why a lot doctors prefer start really very-law presssure ( case child brain really very damaged) and if child very small -very fragile.

So do the 1,3ata without oxygen will give same results for anoxic injury as 1,5ata 100% oxygen??? I don’t know 🤷‍♀️

I believe that in acute period use oxygen after anoxic injury just after it is more beneficial than without oxygen….. but it’s consern acute period 2-6-8 months after injury!!!!)

( I am not talking about CP-ok it’s chronic condition already) this we was discussed in study which compared pressures for cp.

http://brain-injury-hope.com/2019/01/study-which-compares-different-pressures-for-cp-in-hbot/

So hope my reflections helps….

So for Marc Sudden cardiac arrest happens to my baby at 4 years old. Because of not diagnosed WPW.

He has cardiac arrest for 25 minutes

I did cpr with fiend ambulance was only after 20 minutes and his heart restarted only after 25 minutes…

He was on the hyperthermic protocol ( cooled)

His child body went through so much:

5 days comas

Blindness for 3 days after coma

He couldn’t talk at all for 2 weeks after ( and restarted very slowly to talk some words)

Wasn’t sitting for 1 month and we was 1 month in Intensive care unit and 4 months in hospital

He had 5 ablations ( for his heart syndrome in 3 years)

He was obliged to learn to do everything again… ( he was just 4 years boy when he has to pass through all this: When My son woke from life support after rewarming his body He had regular heard surveys 24h/24 because of regular SVT , kidney failure, respiratory failure & and he was on a feeding tube as well…. and he was blind and can’t talk….. but constantly crying…..only thing which calm his down a bit was my voice …

He has no memory of what happened but he has PTSD

He couldn’t feed himself

couldn’t stand

couldn’t walk

couldn’t do anything

We passed by phases : wheelchair and walker and he hate both of them….

But yes I am blessed that he is alive.

MRI’s after 80 hours Hbot in Israel:

Videos

M’y son Marc avant hbot juin 2016( main gauche)

https://drive.google.com/file/d/1xI4eNE6pSWY_pgeUgwJ1jXN-W59n-CDB/view?usp=drivesdk

Après 50 hbot: (septembre 2016)

https://drive.google.com/file/d/1yqiFsZ8pGkyapTPBY3qJ4bjUA9D7pOr7/view?usp=drivesdk

Hbot

right – before hbot 1 July 2016

Left – after 15 hours hbot -5 August 2016

https://drive.google.com/file/d/1MX_yGrATtTkk6_fxWmp4q-ARvPqNQXv5/view?usp=drivesdk

PoNS: (started 29 March 2018)

Stairs before Pons (right vidéo septembre 2017)

After 6 months pons (left -September 2018)

https://drive.google.com/file/d/1HBrzFIQ1TA35lQVTAKlux2hz0sxiplZP/view?usp=drivesdk

Pons 6 mois ( left -June 2018/ right – September 2018)

https://drive.google.com/file/d/1Ut7jH8NyZFKG4Dv-4HV96qqBJoVGP1W6/view?usp=drivesdk

pons

https://drive.google.com/file/d/1lvvXrBIKLPVdt76JGljWe3Vr46sm8mWp/view?usp=drivesdk

Stoped using pons from 30 December 2018

So 2 AQM without pons:

AQM 1:(11 January 2019)

Aqm2( 28 January 2019)

Restarted using pons in Russia clinic : 11 February (2 weeks intensive in Moscow clinic with pons): http://brain-injury-hope.com/2019/02/pons-2-clinic-near-moscow/

Aqm 3 (25 February )

I will do 4th AQM in September -October 2019 so hopefully I will get scientific datas for PoNS long therm use ….

If you want more read:

http://brain-injury-hope.com/my-sudden-cardiac-arrest-survivor/

Normobaric or Hyperbaric?

1)Hyperbaric oxygen and hyperbaric air treatment result in comparable neuronal death reduction and improved behavioral outcome after transient forebrain ischemia in the gerbil:

« hyperbaric oxygen may represent a potentially important therapeutic option for post-arrest encephalopathy as well as other forms of brain injury. We also agree that animal studies of global brain ischemia suggest that hyperbaric oxygen may be beneficial with regard to neurologic outcome »

Anoxic brain injury resulting from cardiac arrest is responsible for approximately two-thirds of deaths. Recent evidence suggests that increased oxygen delivered to the brain after cardiac arrest may be an important factor in preventing neuronal damage, resulting in an interest in hyperbaric oxygen (HBO) therapy. Interestingly, increased oxygen supply may be also reached by application of normobaric oxygen (NBO) or hyperbaric air (HBA). However, previous research also showed that the beneficial effect of hyperbaric treatment may not directly result from increased oxygen supply, leading to the conclusion that the mechanism of hyperbaric prevention of brain damage is not well understood. The aim of our study was to compare the effects of HBO, HBA and NBO treatment on gerbil brain condition after transient forebrain ischemia, serving as a model of cardiac arrest.

Source :

https://www.researchgate.net/publication/234042951_Hyperbaric_oxygen_and_hyperbaric_air_treatment_result_in_comparable_neuronal_death_reduction_and_improved_behavioral_outcome_after_transient_forebrain_ischemia_in_the_gerbil

2. this one also :Effects of normobaric versus hyperbaric oxygen on cell injury induced by oxygen and glucose deprivation in acute brain slices

« We found that HBO, but not NBO, reduced oxygen and glucose deprivation-induced cell injury, indicating that passive tissue oxygenation (i.e. without vascular support) of the brain parenchyma requires oxygen partial pressure higher than 1 ATA. »

https://www.google.fr/amp/s/www.researchgate.net/publication/308753914_Effects_of_normobaric_versus_hyperbaric_oxygen_on_cell_injury_induced_by_oxygen_and_glucose_deprivation_in_acute_brain_slices/amp