Out of scope of practice or just politics Part 2
By Boris Prilutsky
|As I explained in the previous blog, when massage Magazine removed my article, without allowing me to reply to those complaints, my partner wrote Karen Manahan editor in chief an emotional personal e-mail. The text is below.
As you know, I am Boris Prilutsky’s business partner, as well as providing technical support.
You might not know this, but among a multitude of bad things that has happened in the former Soviet Union, there were actually rare diamonds of good things. One of those diamonds was Medical and Sports Massage, to which the Soviet Machine devoted huge scientific efforts and human resources.
The reason for this was simple. The Soviet Union was, generally speaking, a closed society and the only change for its people to compare themselves against the West was through sport, Olympic Games, Bolshoi ballet etc. The Olympic gold was the way to show to all people inside the Soviet Union and outside it that the Soviet System is superior to the West and thus making the Soviet life superior as well.
Why was Medical and sports Massage making such a difference? Simple. Because the main problem with athletic performance is athlete’s susceptibility to injuries. In other words, an athlete could have huge potentials, but if s/he’s injured, s/he cannot compete. Side effects of vigorous exercise not only precondition athletes, for sports related injuries, but also wouldn’t allow performing to maximum potentials.
Still, people during those times heard the rumors about it, and the profession of massage therapists was very prestigious and required many years (7 years) of extensive medical studies. People who became such therapists always worked in the hospital environment among doctors or, like Boris, worked with Olympic teams.
You see, Boris learned all these protocols long times ago and although he learned them from scientists who invented and tested them, he is not a scientist himself.
For example, the concussion protocol was invented in 1963 by Professor Alexander Dembo, when one of the most famous Soviet boxers, had developed post-concussion encephalopathies. Since that time, Boris uses these protocols very successfully in his practice. However, it is pointless to ask him for references. Again, this information was classified. You actually might find some publications in some old Soviet scientific magazines, but it has never been published in English.
In America, massage was a hugely underdeveloped field, because since 1920’s America took a course to chemically produced medications. With time, this field became a very profitable enterprise, and for its proponents, it was not necessary to develop competitive fields. Thus, for a long time, massage in America was looked by the American public as something borderline prostitution or luxury for rich people.
Today, there is a change for the better, but unfortunately, instead of finding out what was done in massage science in other countries, America is going through the hard times of reinventing the wheel.
Well, the US was very good to us and we want to give it back with whatever we can. In the case of Boris – this is his knowledge. If you only knew how many doctors are sending him their patients to try the last time if the surgery could be avoided because in many cases this is exactly what happen? Is this occurs because Boris is some kind of a magician? No, because he knows many scientifically designed protocols and knows very well how to use them. Can references do this?
Thus, I gather the people who bad mouthed Boris, are simply gullible. A knowledgeable person always objects on a quintessence but the other kind objects on technicalities. Why do they need to see the references, because he’s going to read them? No, it just gives them a comfortable feeling that what he’s reading must be scientific.
Ten years ago I was completely incapacitated by frequent life-threatening panic attacks. Pills only made me drowsy. It was Boris who treated me with Medical Massage. When, after the first session, my blood pressure dropped from 200/100 to 160/85, that made me a believer. That’s why I decided to help him, and in the end, he offered me a partnership. Because he is a person with the big heart and it makes me sad when he is so utterly misunderstood and put down.
All the best to you in your future endeavors,
I didn’t know about this letter, and most likely didn’t have to know about my partner’s private affairs. However, a few weeks ago, Karen told Michael that she is planning to publish his letter in massage Magazine March issue and Michael come back to me with this news. We both agree, if massage Magazine will not allow me to publish the reply to Michael’s letter, then we shall request from massage magazine, not to publish his letter.
My partner, Michael, learn from me quite a bit about the history of Medical Massage in general and especially about the secrecy behind Soviet propaganda that used Olympic Games to prove that the Soviet system is much superior to the West. As a matter of fact, Medical and Sports massage played a crucial role in allowing Soviet Olympians from the 60s to 80s to win the most of the Olympian gold. Yet much of Michael have presented in his emotional reaction letter, needs a clarification. Otherwise, readers of massage Magazine will remember only that: ”Again, this information was classified. You actually might find some publications in some old Soviet scientific magazines, but it has never been published in English.”
Pertaining to the late Soviet period of Medical Massage development his description is pretty accurate. However, for the sake of this discussion I should point out that the general history of medical massage is not a secret at all. On the contrary, it is quite well known. I was trained on this fundamental principles and have all the necessary references.
It goes back to the 18th century, when British physician Dr.Head published, his, what we now call, Dr.Head’s zones. During a very long time, observing hundreds of patients, Dr.Head paid attention that in many cases of chronic internal organs diseases, skin within somatic distal components, develop changes in a form of higher skin density, a local low threshold of pain, etc. The great clinical value of his observation soon became obvious. When he performed skin massage in these areas he not only eliminated these abnormalities in the skin but also have had a tremendous healing impact on diseased internal organs. I believe that Dr.Head was the first one who have established visceral somatic reflex concept as well as somatovisceral reflex concept, which allowed to professor Sherback in 1937 to go further and to develop the concept and hands-on techniques of segment reflex massage as we practice it today.No doubt, that Professor Zabludovsly (1913) remarkably advanced massage therapy as a powerful clinical tool and, I would say, that in many cases, it became the most powerful methodology for treatment.
Professor Zabludovsly (1913) was the first one who explained the reflex effect on arterial circulation in non-massaged extremity. The phenomenon was confirmed later by many experimental and clinical studies (Guthberson, 1933; Ebel and
In 2003, at Beverly laboratory of Vascular Studies, I repeated Professor Zabludovsly’s protocol. In Medical Massage Vol.2 text, Dr.Ross Turchaninov extended on this experiment. We have provided him with all post-experimental data. Please keep in mind, I can reproduce the same outcome as you about to read at any time. To study this 15-25 minute protocol is the simpler than studying many other simple step-by-step hands-on medical massage protocols.
Professor Zabludovsly (1913) was the first one who explained the reflex effect on arterial circulation in non-massaged extremity. The phenomenon was confirmed later by many experimental and clinical studies (Guthberson, 1933; Ebel and
The Beverly laboratory of Vascular Studies in California examined the effect of medical massage therapy on arterial blood circulation in lower extremities of healthy adults by using Pulse Volume Recording (PVR), Photoplethysmology (PPG) and Thermography (TMG). All these tests measured blood circulation on the opposite lower extremity, i.e. practitioners worked on the left extremity while circulation was measured on the right extremity. Peripheral circulation was measured before the experiment and after application of medical massage.
Major changes were registered in PVR, which is a pulsate volume of perfusion through the extremity.
Let’s briefly review the results of this study. Initial PVR registered on the right lower extremity was 0.81. After this parameter was registered, a medical massage practitioner applied the treatment of the lower extremity for 15 minutes. After 15 minutes of medical massage, PVR increased to 1.22 and continued to climb during the next 2 hours after the medical massage was over. At the end of the second hour, PVR value was 1.63, i.e. blood perfusion through the contralateral lower extremity showed a double increase even after the medical massage was over.
This study is a great example of the valuable effect of medical massage on the peripheral blood circulation (Prilutsky, 2003). This is why patients with arterial circulation disturbances respond so well to medical massage.
I hope you would agree that it is impossible to overestimate the importance of contralateral extremities massage, in cases of fractures, surgeries, and significant other types of injuries when we cannot apply massage directly to the injured area. More than that, at the time of the experiment we’re described above, my models agreed to wait only two hours in order, to allow us to perform PVR measurements. As you could see after me stopping the treatment, two hours after the treatment, it continued to increase PVR.
Back in the Soviet Union, we have repeated described protocols many times, and reflex
Another researcher- Elizabeth Dickle contributed significantly to massage therapy fields by researching and proposing hands-on protocols that were clinically proven to be a very powerful methodology for treatment since 1929. Below is my extended explanation why I made this claim.
First, a short historical review: Initially, the importance of tension build-up in the connective tissue/fascia and its impact on chronic somatic and visceral abnormalities was made known to the medical community through the work of Austrian physical therapist Elizabeth Dickle in 1929. As with many important discoveries, Dickle’s discovery was an accidental find. For several years, she suffered a failure of arterial circulation in her lower extremities as a result of Thromboangiitis Obliterans. The disease had progressed to the stage that amputation was a real possibility. Dickle also experienced chronic, lower-back pain caused by her limping. While rubbing her lower back in trying to relieve tension, she noticed sensations of warmth and weak pulsations in her feet. Intrigued by her finding, she started using various techniques on her lower back. She noticed that the most intense warm sensations in her feet were triggered when she pulled the skin on her lower back. After several months of self-therapy, she was able to restore circulation through her lower extremities and prevented double amputation. Powerful stuff.
E. Dickle shared her findings with Prof. W. Kohlrausch. Their combined efforts, as well as the later works of Prof. N. Veil and Dr. Luebe in Austrian and German clinics, shaped a major method of somatic rehabilitation they called Bidegewebsmassage or connective tissue massage/fascia release and mobilization techniques as it is known by the rest of the world.
During the extensive research, they developed connective tissue massage/fascia release and mobilization hands-on protocols, including the stipulation regarding the direction of movement. This was presented in a straightforward way so that thousands of massage therapists could learn these techniques and successfully implement them on patients. Thousands were replicating outcomes when treating back and limp disorders, internal organ diseases, etc. for more information just Google Bidegewebsmassage.
The work of Prof. Sherback, which is an absolutely fundamental plateau for medical massage, is also a fundamental plateau for any massage therapy. Today, the concepts that lay the foundation of his works were tested and massively utilized for many years, and thus proved their clinical viability.
After analyzing all the available data, and experiences of other scientists and clinicians, Prof. Sherback started checking somatic components of chronically unhealthy patients.
The aforementioned changes produce pain when compressed and, in many cases, spawn localizations that are painful regardless of compression. Then a revelation come to him – “a simple revelation” as he put it that made massage a very powerful therapeutic tool.
All diseases of internal organs project pathological impulses on somatic parts that share the same level of innervations with a particular somatic part and trigger changes such as higher density of skin, tension within muscles, fascia, etc. forming reflex zones abnormalities/ somatovisceral reflex. The aforementioned changes in soft tissue can be painful and especially sensitive to touch or pressure.
The most important achievement of his and his students was that, by providing massage and eliminating these reflex zones abnormal changes, they improved the health of thousands of patients.
The huge plateau was established by Drs. Glaser and Delixo after the tremendous work. In 1955, they published segments reflex massage text, including more than 30 maps of reflex zones abnormalities, for individual internal organs diseases, as well as skeletal muscular diseases.
The contribution that prof. Sherback and Drs. Glezer and Delixo made to the development of massage science was indisputable and their influence is hard to overestimate. Similarly, it is impossible to overestimate the contribution of Dr. Sarkisov Serazini, who proposed comprehensive physiological effect of massage approach in 1938 and have established the concept of the physiological effect of massage as we know it today. This foundation allowed further generations of researchers to develop over 60 medical and sports massage hands-on protocols. Thus, the methodical research was done, and optimal step-by-step hands-on techniques where developed, all of which were standing on the foundation of the physiological effect of massage. Here is the link to a short description of the physiological effect of massage. Physiological effect of massage on the human body
During his experimental clinical researches Dr.Sarkisov Serazini said:
”…if you would like to assess the professional capability of a massage therapist, you must assess his capability to perform high-quality kneading techniques. Many different components are necessary in order to achieve rapid and sustainable results, and the quality of kneading techniques is one of this important components.”
Medical massage contains technical disciplines such as connective tissue massage/fascia release and mobilization, muscular mobilizations, trigger point therapy, circulatory massage, and more. This was my fundamental training in theoretical concepts as well as very intensive hands-on practice. As you can see no secrets what so ever.
Surely Drs. Glezer and Delixo’s segment reflex massage text, have never been translated into English. Here comes a million dollar question. If hasn’t been translated into English, can it still be scientific? Incidentally, it has been translated into Russian, German, Polish, and Hungarian.
By the way, Dr. Ross Turchaninov’s textbooks in English, covers the works of all the scientists I have mentioned above, including interpretation of science of massage. I believe this book presents more than 600 references.
In Part 3. I will discuss the secrecy of medical and sports massage developments during the Soviet Era.
Out of scope of practice or just politics?
by Boris Prilutsky
|As you may know, some time ago due to complaints Massage Magazine requested, to remove my article Specially designed medical massage protocol is the most powerful methodology for management of concussions symptoms and much more
The main complaints were:
Regrettably, Massage Magazine decided to give up. “Regrettably”, because if we would discuss the issues stated in this complaint, I am positive that everyone would be able to learn even more about our scope of practice and about other aspects of massage practice that could have arisen in a professional discussion.
Again, regrettably, and despite my promise to provide references, Massage Magazine didn’t allow me to respond to these complaints and removed my article. As far as references are concerned, I always had them. Only, in this case, I elected not to include them.
I have a friend, who is an MD, neurologist, and sports medicine expert, as well as Ph.D., and a great hands-on massage therapist. He was a student as well as the right hand of Prof. Dembo. Much older than me, during the 1970s, he was my mentor and then took me to work in his group. Almost 10 years later, he proposed me a partnership in private practice. We still are very close friends.
When I shared my frustration with him, he asked me whether within the editorial board of massage Magazine there were any professionals in our field, and if so, why didn’t they allow me to answer to the allegations? I had no answer for him at the moment. However, later, contemplating on the issue, I surmised that the magazine was subjected to so much pressure that the editorial board chose this way of handling the situation.
In my view, the magazine’s refusal to publish my rebuttal is a detrimental practice, not worthy of democratic society standards. I remember publishing a short article in “Massage Today.” It included the proposal to address trigger points. One lady disagreed with my approach. “Massage Today” published her disagreement and published my rebuttal a well. It so happened that my opponent agreed with me, but our personal agreement or disagreement was of little significance. More importantly, the readers of this professional massage magazine could learn from our discussion.
Having said all of the above, I actually want to compliment Karen on her courage in allowing me to clarify the situation by posting my reply on Massage Magazine FB page. Even though most likely, the amount of subscribers to a printed magazine is much greater than Facebook membership, it is some reconciliation after all. Therefore, I will use this opportunity to present my position regarding allegations stated above.
1. All the information I’m presenting in my article is out of massage therapy scope of practice.
The concussion-rehabilitation protocol is nothing more than a massage protocol – a sequence of massage manipulations – effleurage, friction, petrissage, tractions, massage techniques to accelerate lymph as well as cerebral spinal fluid drainage etc. that I like any other massage therapist use in massage therapy procedures. Those of you, who rented my instructional videos know that I perform all stated above techniques. If massage technique that I am proposing as a part of this protocol is out of massage therapy scope of practice then we all practice out of the scope of practice.
As for the protocol itself –it was developed by Professor Dembo and his research group in 1964 for a use of massage therapists just like any other massage protocol of Medical Massage.
The concepts presented in my article I learned in 1973 from the internal informative leaflet of Soviet Ministry of Health, the department number 4. In addition, I was trained in to perform hands-on massage protocol in the classroom.
2. Massage therapists cannot treat psychiatric disorders and certainly can’t promote themselves as mental health professionals.
I never presented or/and promoted myself as a mental health professionals.
The following is an excerpt from my blog:
”The hands-on protocol starts from combining massage techniques for acceleration of cerebral spinal fluid drainage, lymph drainage massage techniques. It is followed by the lateral neck compression massage techniques, acupressure techniques for tension headaches and the full body medical stress management massage. To understand why this protocol is utilized with repeated success, I am referring you to how the biomarker was established, and summarize that the concussion biomarker is irregularities of the autonomic nervous system. After accelerating drainage of an excessive amount of cerebral spinal fluid, we immediately increase much-needed blood supply to the brain. However in order to sustain the normal cerebral circulation, normalization of autonomic activities is a must. No other methodology but massage therapy possesses this significant power/effect to balance sympathetic and parasympathetic activities. Again, the post-concussion conditions developing vicious cycle, such as secretions of excessive amounts of CSF, following by Insufficient blood supply along with dysfunctional mitochondria – intracellular source of reactive oxygen species, Programmed cell death and more, immediately reflecting in autonomic irregularity. In order to achieve sustainable results, a therapist must perform all techniques I mentioned above in order to restore blood supply and at the same time, stimulate autonomic activities to achieve the maximum possible balance.”
Thus accusing me of presenting myself as an expert for psychiatric disorders, is just as groundless as to blame me in proclaiming myself an expert in support and movement disorders, etc. I am a massage therapist, who possesses skills and knowledge in performing therapy by means of massage, which is the capability to address causes that produce pain and dysfunction. As human body has a potential to heal itself, by performing massage we stimulate this healing process.
3. Only healthcare providers can address concussions, massage therapists have no business in this cases.
The answer to this questions has to do with the distribution of tasks. Certainly, medical doctors have to diagnose the problem and prescribe the treatment plan. However, it is the obligation of a massage therapist to execute the treatment. The misunderstanding perhaps happen because the post-concussion rehabilitation protocol, so widely known and implemented for a long time in the Eastern Europe, is not very well known in the US. So the permission to use the protocol comes down to the factor of its legitimacy.
I said earlier, it was developed by scientists and it has been tested by many years of implementation in the field. Professor Dembo’s research established that the nature post-concussion biomarker was irregular autonomic activities. It was a challenge to find references to support his research written in or translated into English. The best support for his research (in English) is this video that I discovered it accidentally, and very timely. Please watch the following video:
Random picked, 21 post-concussion patients demonstrated irregular autonomic activities. This is a very solid evidence. I would recommend reading the information scientifically based and clinically proven information on physiological effect of massage on human body.
Irregular autonomic activities are very sensitive phenomena. When an individual suffers from a post-concussion encephalopathy, including irregular autonomic activities, he or she cannot control himself even under regular circumstances, which otherwise could be controlled by a healthy person. Under these circumstances just an insignificant emotional or mental irritation can escalate into absolutely irrational behavior; to, what we would call, psychiatric behavioral disorder.
In a case of successful application of massage protocol, directed to address post-concussion phenomenon, including an approximate balancing or sympathetic and parasympathetic activities, in most cases, the development of brain dysfunction could be prevented, including movement disorders, dementia, as well as psychiatric behavioral disorder.
4. I didn’t include references, supporting my statements.
Prior to answering the question of references I would like to post my own question to the complainers: Will the list of references help a patient suffering from post-concussion encephalopathies?
The friend I mentioned earlier, told to me, that the first time Professor Dembo’s research paper was published in 1965 at “Physical Culture and Sports publications” and suggested that I could have given references to this publications. However, I wasn’t sure that searching in old Soviet magazines was the right approach in this case. At the time when Professor Dembo proposed the Post-Concussion Rehabilitative Medical Massage Protocol, the prevailing opinion in the contemporary scientific community was that the terms such as a stunned brain, hibernating brain cells, apoptosis or programmed cell death meant the same thing – a non-reversible cell death. That means that a reversible apoptosis as well as the post-concussion inflammatory response, weren’t possible because the brain was incapable of marshaling a post-concussion inflammatory response due to the selective permeability of the blood–brain barrier (BBB).
Today, 40+ years later many researchers support all that Prof. Dembo hypothesized and clinically proved. The outcomes were reproduced thousands of times.
However, my point still stands; will the list of those references help a patient suffering from post-concussion encephalopathies?
When Prof. Dembo proposed this concept and massage protocol, he was a maverick in this research and, therefore, couldn’t offer any references because, as it was mentioned above, it was contrary to the prevailing opinion of the contemporary scientific community on the issue. Yet has his method been less effective because of this?
In the interim, the friend I mentioned above, Dr. Ross Turchaninov, my kids, and my current partner convinced me to always present references, in order to avoid unnecessary “misunderstandings”. Ok, from now on I will always present references. At the same time, I find this attempt to pretend, making a terrible disservice to our communities, including professional publications. Many times, following the given references within published articles, I discovered that they had nothing to do with presented subject relying on the fact that editorial board is not checking, or not capable of check them. How about the readers? Do most of them ever follow or read references that come with each article?
When massage Magazine removed my article, without allowing me to reply to those complaints my partner wrote Karen Manahan editor in chief an emotional personal e-mail. To his and later to my surprise Karen decided to publish his letter. To me, her decision seemed odd; to refuse me to publish a reply to complainers, and, suddenly, to agree to publish my partner’s letter? The readers might remember these sentences from his letter: ”Again, this information was classified. You actually might find some publications in some old Soviet scientific magazines, but it has never been published in English?” and, as a result, be left with the partial or wrong impression.
In my next post, I will include the text of his letter – the same text as it was printed in the editorial section of “Massage Magazine.” My partner is not massage therapists or in any way connected to our field. Therefore, in the next blog will offer my additional explanations and clarifications regarding the information he included into his letter.
A contemplation about “Concussion”
By Michael Gaft
I would like to start by saying that I am not a massage therapist or a medical professional and my interest in this matter is rather philosophical than medical.
Recently, I watch “Concussion” movie and was impressed with it in a couple of different respects, least of which was a great job by Will Smith imitating Nigerian accent.
It was very touching how Will Smith portrayed Dr. Omalu. He’s shown a person of unusual courage, resolve, and perseverance, and, at the same time, someone very humble, without preemptive sassiness and tantamount of drama. “The true American” as they put it in the movie. I might add “the true citizen of the World” since it’s not only in America that the big business is throwing its weight around. Maybe that belief in the exclusivity of the US as a beacon of justice and opportunity actually kept him going through the entire ordeal and the success, he has eventually enjoyed in the US, couldn’t have been possible somewhere else. That and the pretty partner that Hollywood has furnished Will Smith in the movie. Surely, behind every great man, there’s got to be a great woman. “Serse la fam” so to speak. Not sure whether this is how this reality happen in the life of real Dr. Omalu as he is not as tall and handsome as Will, but let’s give this plot line the benefit of a doubt.
It’s actually amazing that the real Dr. Omalu was able to persevere through that struggle. Even being truly righteous and courageous, he was also very lucky. I am thinking of many doctors who on the brink of such discoveries were shut down, intimidated, were stripped of their licenses, lost their jobs or, perhaps, careers.
However, to me, the most striking inference of the movie was in the fact that Mr. Omalu had to make the discovery of chronic traumatic encephalopathy (CTE) in 2002, while this phenomenon was discovered many years earlier, before he was even born, in the Soviet Union. Only this condition was detected in connection with boxing rather than with Football. However, as I can recollect, Joe Luis had the 750 lb punch, as was the case with many other knock-out artists, which is quite enough to create a concussion and leave a person with CTE.
As I was saying, this phenomenon was discovered in the Soviet Union in 1963 in connection with a very famous, at the time, boxer Valery Popenchenko, who was called “Mr. Mystery Knock Out.” Rather than describing the history here I’d like to offer you the link, where Boris discusses it at length.
Interestingly, not only that in the Russian doctors discovered these encephalopathies, but they also developed the massage protocols to handle this condition. Among many bad things that a police state might enforce, this came out good as all the boxers and athletes of other sports susceptible to the possibility of concussion were obligated to go through the appropriate treatment and only then were allowed to return to training.
If instead of pushing the players to the field after sustaining the concussion, NFL would employ these very safe and cheap treatment protocol, there would be no brain damage and consequent deaths of so many icon players. I remember this sentiment coming many times from Boris when visiting him in the past, I saw huge burly fellows leaving his office after receiving this protocol. So I actually very glad that the movie like this has finally arrived.
The whole situation with Dr. Omalu discovery reminded me the case of the father of genetics Gregor Johann Mendel who made his discoveries in 1865 and 1866, and which had been forgotten to be rediscovered in 1900’s.
As I am contemplating about the movie and the real case that this movie is about, I have a bitter taste in my mouth – “what a waste” of a talent! Why can’t we, as the only Homo sapiens on this planet, communicate the knowledge and be helpful to one another?
The opening scene in the movie, where Dr. Omalu is subjected to inquest regarding his credentials, is very indicative of the overall US approach to an “alien” source of knowledge. It wasn’t enough to say that he was a pathology anatomist and established the cause of death on a daily basis. He had to mention that he had degrees from the several accredited American schools, before his testimonial been given any weight. It sort of blows my mind. Here it is this protocol that prevents long-lasting brain damage, just take it.
Surely, there is some justifiable safety precaution here for who knows what people came from other countries can claim? Thank god the US has enough of its own quacks. However, if someone offers methods of treatments that has been proven safe and effective over many years, why not give them the benefit of the doubt enough to test them?
Another unsettling moment in the movie was when NFL finally started listening to Dr. Omalu’s reasoning only because one of their own upper-level managers, ex-football player, also committed a suicide. Do we have to wait for another fifty years until someone like Dr. Omalu would develop the protocol in the US?
Diverticulitis and lower back pain
Prior to getting familiar with the case I am about to describe, I highly recommend to read this article. http://medicalmassage-edu.com/critical-vs-clinical-thinking/
I called this article “Critical vs. Clinical Thinking.” I hope we all agree that critical thinking is involved in most situations of our life, including and not limited to intellectual dynamics of clinical thinking. But if critical thinking will compel you to a search for scientific data, it will lead you astray from the specific clinical picture thus becoming useless and having nothing to do with clinical thinking process and the outcome of it.
Last Monday, September 7th, 2015, a 47-year-old lady, a nurse practitioner came to me, complaining about an intensive lower back pain; more toward the left side. According to her report, the last three days it was getting worse. Painkillers and anti-inflammatory drugs did not really help.
Palpation is the part of a massage therapy examination procedures where we try to discover trigger points, tension within the fascia, muscles, etc. I didn’t discover many trigger points that would support skeleton-muscular disorder in the lower back. The description of symptoms she offered, and what I have felt with my fingers didn’t match. However, when I examined abdominal, even a light touch produced an unusually sharp pain, and mostly on the left site. I told her that this was not the case for a massage therapist, and highly recommended her to go to an emergency room. She asked me to explain her my suspicions.
As usual in such cases, my responses that I am not a medical doctor and cannot diagnose, but from my experiences it didn’t look good. I also explained to her that if the trip to an emergency room would not entail any real concerns it also would also not pose any threat – better be safe than sorry. However, if this is a life-threatening condition, not going to ER, at the very least, is irresponsible.
She told me that she was a nurse practitioner and she could diagnose and that she wanted to hear my opinion. I said that her condition looks like diverticulitis, and, possibly, her condition was progressing. I felt with my hands an unusual stuff. Luckily I examined her at a hospital research laboratory, a few yards from ER where I volunteered to walk to.
Three days later, when I was back in the laboratory, I asked about her and the guys who knew the story praised me, claiming that my actions saved her life. I answered what saved her life was simply my refusal to treat at that moment.
What it turned out to be was a difficult case of peritonitis, including infected pouch ruptures, spilling intestinal contents into the abdominal cavity. The client’s condition required emergency surgery, IV and significant amount of Antibiotics. She was in a life-threatening condition. The confusing part of the diagnostic process was the fact that she didn’t experience abdominal pain, but the pain in the lower back.
There are cases when people complain about pain in certain body parts, which isn’t an indication of orthopedic disorders. We, as massage therapists, should be careful prior to starting a treatment if we cannot palpate obvious trigger points that can explain the symptoms. I advise forming questions in a specific manner. They should clarify if a client feels pain in places where trigger points, related to the described symptoms, usually reside. Unless this is done, it is easy to misinterpret the complaint and come to the wrong conclusion. It could be a coincidence. A person can develop trigger points, but similar to what happened in this case, it wouldn’t be related to diverticulitis.
In the aforementioned case, I asked the questions in the manner I recommend. The client’s recognized the presence of trigger points, but they were not related to her lower back pain. She just described what she felt, and this helped me to make the right decision, after careful investigation of abdominals. Three days later, I went to visit her at the hospital. She presented me to nurses and doctors as a hero. I responded that all my heroism was in the fact that I decided not to provide a treatment.
Sometimes even doctors can make mistakes and refer us patients with a similar clinical picture. In the above case, it was very easy to miss diverticulitis without complaints on the abdominal pain, high fever, and much nausea. Just a light touch was enough to determine that this is not the case for a massage therapist, and to come to a conclusion that this was diverticulitis. We are not only the first door-keepers but sometimes, also frontiers in recommending the urgent medical attention.
You’re welcome to post any questions, comments.
Specially designed medical massage protocol is the most powerful methodology for management of concussions symptoms and much more.
The mainstream position on concussion treatment states that “rest and time” will provide a sufficient cure.
Partially this is true – with time and rest the immediate concussion symptoms go away. The symptoms like disorientation, dizziness, nausea, sleep disorders, headaches will disappear during the first ten to fifteen days after a concussion. But would the development of post-traumatic brain degenerative diseases stop? Would brain dysfunction symptoms go away?
Many athletes in all contact sports suffer from post-concussion encephalopathies such as movement disorders, dementia, chronic headaches, psychiatric behavioral disorders, etc. (of course, the most violent sports like football and boxing suffer more) These are terrible and, sometimes, irreversible pathologies. Lately, many young promising football players are giving up million dollar contracts, their entire athletic careers, because they are afraid of side effects of concussions. They don’t want to live their lives with chronic headaches, psychiatric behavioral disorders, tremors, dementia, etc. Again all this mentioned above dysfunctions can and must be prevented.
Athletes who get concussions repeatedly develop these brain dysfunctions after or even during their careers. The good example is “the domestic violence” cases exhibited by football players. We all probably have seen the video I mentioned earlier. The video where a strong athletic fellow is punching his girlfriend in the face, the Ray Rice video.
I don’t think Ray is a wicked or a violent person. If not for his brain trauma, most likely… he’d be able to control his urges. Even a violent person, knowing about the surveillance and the repercussions following the domestic violence case, would have restrained themselves in a similar from being exposed like her was in that situation. Should Ray Rice have no brain trauma, he’d realize that his power unleashed to a woman could kill her. A very strong violent man, in most cases, are rational, and should he happen to hit the loved one, he would restrain his power.
Yes, specially designed protocol of massage therapy is the most powerful methodology, to prevent post-concussions brain dysfunctions, as well as to treat this type of encephalopathies.
From the neurological perspective, a concussion is a head injury that causes head trauma. When it happens to brain cells are in the mode that is called “stunned brain” or “hibernating brain cells”, apoptosis or “programmed cell death.” All these terms describe the state when some brain cells go into hibernation in order to allow other neighboring cells to survive. The main reason for apoptosis is an immediate decrease in blood supply to the brain, due to an abrupt increase of cerebral spinal fluid secretions and an increase in intracranial pressure. The purpose of hibernation is a decrease in cellular function to the point when fewer resources of blood supply, such as oxygen, glucose are required for some cell function thus allowing the neighboring cells a chance to survive.
It is crucial to understand that during Programmed cell death (PCD) process, brain cells don’t die immediately. Moreover, in many cases, hibernation is a reversible process. In some cases, cells can resurrect and brain function will be normalized during nine months without treatments, with some minor functional disabilities such as the lack of concentration, headaches, etc. However, in many concussion cases and especially in cases of repeated concussions, if left without treatment, these resurrections never happens and people who suffered concussions develop movement disorders, psychiatric behavioral disorders, chronic headaches, dementia etc.
As stated above, the hibernation is an initiation of a degenerative change that can be reversed. However, the only way to reliably prevent neurons from going into permanent hibernation is to increase cerebral circulation. The massage protocol proposed by the former Soviet sports medicine expert, neurologist Prof. Dembo, was directed toward stimulation of blood supply to the brain, which in turn is the prevention of irreversible apoptosis.
It is very hard to predict which concussion case would lead to dead cells/brain dysfunction. Therefore, it is crucially important to apply the entire concussion rehabilitation medical massage protocol immediately after concussion. Of course, doctors have to exclude hemorrhage, but the moment doctors give “okay” the program have to be implemented immediately. The sooner it will be applied after a concussion has taken place, the higher is the probability that PCD process will be contained and a person wouldn’t be subjected to organic brain dysfunction, detrimental consequences of concussion.
Although “treating” concussions industry is booming, none of them established a biomarker to diagnose a post-concussions brain dysfunction, as well to assess an improvement of brain function. What is the goal of this therapy?? You can read about it by following this link
In order to successfully treat post-concussion brain dysfunctions, it is extremely important to understand the mechanism of concussions. For a detailed description of the issue please follow the link below The mechanism of concussions and its consequences
The hands-on protocol starts from combining cerebral spinal fluid drainage techniques and lymph drainage techniques. It is followed by the lateral neck compression techniques, acupressure techniques for tension headaches and the full body medical stress management massage. To understand why this protocol is utilized with repeated success, I am referring you to how the biomarker was established, and summarize that the concussion biomarker is irregularities of the autonomic nervous system.
After accelerating drainage of an excessive amount of cerebral spinal fluid, we immediately increase much-needed blood supply to the brain. However in order to sustain the normal cerebral circulation, normalization of autonomic activities is a must. No other methodology but massage therapy possesses the power to balance sympathetic and parasympathetic activities. Again, the post-concussion conditions develop vicious cycle, such as secretions of excessive amounts of CSF, insufficient blood supply along with dysfunctional mitochondria – intracellular source of reactive oxygen species, Programmed cell death and more, immediately reflecting in autonomic irregularity. In order to achieve sustainable results, a therapist must perform all techniques I mentioned above in order to restore blood supply and at the same time, stimulate autonomic activities to achieve the maximum possible balance.
American football is a huge part of American life. Is it impossible to imagine America without the Super Bowl? Even people like me, who have no clue about the game, never miss the Super Bowl, because this is the nationwide event. It is a good cause for families and friends to come together, to have beer and food, to enjoy watching the opening, to be moved by listening to the U.S. National Anthem, watching marching bands and cheerleaders. Always at the half time some famous singer performs and, of course, let’s not to forget the great advertisings brought here to the level of art. Not less important to note that that NFL is a multi-billion industry and will likely to stay forever.
I don’t have the statistics, but I’m suspicious that throughout their careers in high school, college and NFL players receive concussions multiple times. In many cases, even without experiencing the real symptoms, so-called asymptomatic concussions, these traumas accumulatively fuel encephalopathies developments.
My biggest concern is about the high school football. Again, I don’t have the exact statistics, but I am suspicious that many high school students, because of an adverse effect of encephalopathies developments, are diagnosed with attention deficit disorders, or tagged as “dumb” or “academically incapable.” Our programs can prevent many personal tragedies.
I almost finished working on the educational video, where during almost two hours, considering the inclusion of the full stress management protocol, I am explaining and demonstrating a step-by-step massage protocol for concussion symptoms management, and prevention of encephalopathies developments. This video will be available for rent, at a very affordable price. If you have an interest and would like to be notified on day of release, please e-mail us at
The more I get familiar with the pandemic proportions of concussions incidents in the United States, the more it becomes obvious that there is a huge market, where our treatment is needed, and where, as massage therapists, we are capable of making the difference in the life of many.
Below is the link to my video presentation. A new movie “Concussion” is scheduled to release on December 25, 2015, which certainly will bring much attention to this serious issue. I highly recommend everyone in our fields to learn this protocols and to start treating people in order to prevent movement disorders, dementia, chronic headaches, psychiatric behavioral disorders, etc. Together, we can make a big difference in people’s lives.
Prior to the 1965 publication of Professor Dembo in the “Physical Culture and Sports” publication on a post-concussion inflammatory response, it was believed that the brain was incapable of marshaling a post-concussion inflammatory response due to the selective permeability of the blood–brain barrier (BBB).
However, in the 1960s, Prof. Dembo hypothesized and clinically proved that this was possible and now it is a well-established fact that neuroinflammation can occur independently of changes in BBB permeability and is commonly seen in response to almost all neurological disorders, including concussions.
The concepts presented in my article I learned in 1973. In addition, I was trained in a classroom environment to perform the corresponding hands-on massage protocol. As you can see from viewing supplied references, to this day, many researchers provide a solid support to all the concept introduced by Prof. Dembo
Allan S. M., Rothwell N. J. (2001). Cytokines and acute neurodegeneration. Nat. Rev. Neurosci. 2, 734–744 10.1038/35094583 [PubMed] [Cross Ref]
Andersen B. J., Marmarou A. (1992). Post-traumatic selective stimulation of glycolysis. Brain Res. 585, 184–189 10.1016/0006-8993(92)91205-S [PubMed] [Cross Ref]
Arnett H. A., Mason J., Marino M., Suzuki K., Matsushima G. K., Ting J. P. (2001). TNF alpha promotes proliferation of oligodendrocyte progenitors and remyelination. Nat. Neurosci. 4, 1116–1122 10.1038/nn738 [PubMed] [Cross Ref]
Aubry M., Cantu R., Dvorak J., Graf-Baumann T., Johnston K., Kelly J., et al. (2002). Summary and agreement statement of the First International Conference on Concussion in Sport, Vienna 2001. Recommendations for the improvement of safety and health of athletes who may suffer concussive injuries. Br. J. Sports Med. 36, 6–10 10.1136/bjsm.36.1.6 [PMC free article] [PubMed] [Cross Ref]
Babikian T., Difiori J., Giza C. C. (2012). Chapter 5: Pathophysiological Outcomes. New York, NY: The Guilford Press
Barkhoudarian G., Hovda D. A., Giza C. C. (2011). The molecular pathophysiology of concussive brain injury. Clin. Sports Med. 30, 33–48, vii–iii. 10.1016/j.csm.2010.09.001 [PubMed] [Cross Ref]
Barone F. C., Parsons A. A. (2000). Therapeutic potential of anti-inflammatory drugs in focal stroke. Expert Opin. Investig. Drugs 9, 2281–2306 10.1517/13543722.214.171.1241 [PubMed] [Cross Ref]
Bazarian J. J., McClung J., Shah M. N., Cheng Y. T., Flesher W., Kraus J. (2005). Mild traumatic brain injury in the United States, 1998–2000. Brain Inj. 19, 85–91 [PubMed]
Bazarian J. J., Zhong J., Blyth B., Zhu T., Kavcic V., Peterson D. (2007). Diffusion tensor imaging detects clinically important axonal damage after mild traumatic brain injury: a pilot study. J. Neurotrauma 24, 1447–1459 10.1089/neu.2007.0241 [PubMed] [Cross Ref]
Benveniste E. N., Tang L. P., Law R. M. (1995). Differential regulation of astrocyte TNF-alpha expression by the cytokines TGF-beta, IL-6 and IL-10. Int. J. Dev. Neurosci. 13, 341–349 10.1016/0736-5748(94)00061-7 [PubMed] [Cross Ref]
Bermpohl D., You Z., Lo E. H., Kim H. H., Whalen M. J. (2007). TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. J. Cereb. Blood Flow Metab. 27, 1806–1818 10.1038/sj.jcbfm.9600487 [PubMed] [Cross Ref]
Biegon A., Joseph A. B. (1995). Development of HU-211 as a neuroprotectant for ischemic brain damage. Neurol. Res. 17, 275–280 [PubMed]
Bonnet M. S., Pecchi E., Trouslard J., Jean A., Dallaporta M., Troadec J. D. (2009). Central nesfatin-1-expressing neurons are sensitive to peripheral inflammatory stimulus. J. Neuroinflammation 6, 27 10.1186/1742-2094-6-27 [PMC free article] [PubMed] [Cross Ref]
Browne K. D., Iwata A., Putt M. E., Smith D. H. (2006). Chronic ibuprofen administration worsens cognitive outcome following traumatic brain injury in rats. Exp. Neurol. 201, 301–307 10.1016/j.expneurol.2006.04.008 [PubMed] [Cross Ref]
Campbell I. L., Abraham C. R., Masliah E., Kemper P., Inglis J. D., Oldstone M. B., et al. (1993). Neurologic disease induced in transgenic mice by cerebral overexpression of interleukin 6. Proc. Natl. Acad. Sci. U.S.A. 90, 10061–10065 [PMC free article] [PubMed]
Cantu R. C., Aubry M., Dvorak J., Graf-Baumann T., Johnston K., Kelly J., et al. (2006). Overview of concussion consensus statements since 2000. Neurosurg. Focus 21, E3 [PubMed]
Cantu R. C., Register-Mihalik J. K. (2011). Considerations for return-to-play and retirement decisions after concussion. PM R 3, S440–S444 10.1016/j.pmrj.2011.07.013 [PubMed] [Cross Ref]
Chao C. C., Hu S., Ehrlich L., Peterson P. K. (1995a). Interleukin-1 and tumor necrosis factor-alpha synergistically mediate neurotoxicity: involvement of nitric oxide and of N-methyl-D-aspartate receptors. Brain Behav. Immun. 9, 355–365 10.1006/brbi.1995.1033 [PubMed] [Cross Ref]
Chao C. C., Hu S., Sheng W. S., Tsang M., Peterson P. K. (1995b). Tumor necrosis factor-alpha mediates the release of bioactive transforming growth factor-beta in murine microglial cell cultures. Clin. Immunol. Immunopathol. 77, 358–365 10.1006/clin.1995.1163 [PubMed] [Cross Ref]
Clausen F., Hanell A., Bjork M., Hillered L., Mir A. K., Gram H., et al. (2009). Neutralization of interleukin-1beta modifies the inflammatory response and improves histological and cognitive outcome following traumatic brain injury in mice. Eur. J. Neurosci. 30, 385–396 10.1111/j.1460-9568.2009.06820.x [PubMed] [Cross Ref]
Clausen F., Hanell A., Israelsson C., Hedin J., Ebendal T., Mir A. K., et al. (2011). Neutralization of interleukin-1beta reduces cerebral edema and tissue loss and improves late cognitive outcome following traumatic brain injury in mice. Eur. J. Neurosci. 34, 110–123 10.1111/j.1460-9568.2011.07723.x [PubMed] [Cross Ref]
Comper P., Bisschop S. M., Carnide N., Tricco A. (2005). A systematic review of treatments for mild traumatic brain injury. Brain Inj. 19, 863–880 [PubMed]
Cortez S. C., McIntosh T. K., Noble L. J. (1989). Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations. Brain Res. 482, 271–282 10.1016/0006-8993(89)91190-6 [PubMed] [Cross Ref]
Csuka E., Hans V. H., Ammann E., Trentz O., Kossmann T., Morganti-Kossmann M. C. (2000). Cell activation and inflammatory response following traumatic axonal injury in the rat. Neuroreport 11, 2587–2590 [PubMed]
Csuka E., Morganti-Kossmann M. C., Lenzlinger P. M., Joller H., Trentz O., Kossmann T. (1999). IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury: relationship to IL-6, TNF-alpha, TGF-beta1 and blood-brain barrier function. J. Neuroimmunol. 101, 211–221 [PubMed]
Dalgard C. L., Cole J. T., Kean W. S., Lucky J. J., Sukumar G., McMullen D. C., et al. (2012). The cytokine temporal profile in rat cortex after controlled cortical impact. Front. Mol. Neurosci. 5:6 10.3389/fnmol.2012.00006 [PMC free article] [PubMed] [Cross Ref]
Davalos D., Grutzendler J., Yang G., Kim J. V., Zuo Y., Jung S., et al. (2005). ATP mediates rapid microglial response to local brain injury in vivo. Nat. Neurosci. 8, 752–758 10.1038/nn1472 [PubMed] [Cross Ref]
Davis G. A., Iverson G. L., Guskiewicz K. M., Ptito A., Johnston K. M. (2009). Contributions of neuroimaging, balance testing, electrophysiology and blood markers to the assessment of sport-related concussion. Br. J. Sports Med. 43Suppl. 1, i36–i45 10.1136/bjsm.2009.058123 [PubMed] [Cross Ref]
Deford S. M., Wilson M. S., Rice A. C., Clausen T., Rice L. K., Barabnova A., et al. (2002). Repeated mild brain injuries result in cognitive impairment in B6C3F1 mice. J. Neurotrauma 19, 427–438 10.1089/08977150252932389 [PubMed] [Cross Ref]
Dekosky S. T., Styren S. D., O’Malley M. E., Goss J. R., Kochanek P., Marion D., et al. (1996). Interleukin-1 receptor antagonist suppresses neurotrophin response in injured rat brain. Ann. Neurol. 39, 123–127 10.1002/ana.410390118 [PubMed] [Cross Ref]
Difiori J. P., Giza C. C. (2010). New techniques in concussion imaging. Curr. Sports Med. Rep. 9, 35–39 10.1249/JSR.0b013e3181caba67 [PubMed] [Cross Ref]
Fan L., Young P. R., Barone F. C., Feuerstein G. Z., Smith D. H., McIntosh T. K. (1995). Experimental brain injury induces expression of interleukin-1 beta mRNA in the rat brain. Brain Res. Mol. Brain Res. 30, 125–130 10.1016/0169-328X(94)00287-O [PubMed] [Cross Ref]
Fan L., Young P. R., Barone F. C., Feuerstein G. Z., Smith D. H., McIntosh T. K. (1996). Experimental brain injury induces differential expression of tumor necrosis factor-alpha mRNA in the CNS. Brain Res. Mol. Brain Res. 36, 287–291 10.1016/0169-328X(95)00274-V [PubMed] [Cross Ref]
Farkas O., Lifshitz J., Povlishock J. T. (2006). Mechanoporation induced by diffuse traumatic brain injury: an irreversible or reversible response to injury? J. Neurosci. 26, 3130–3140 10.1523/JNEUROSCI.5119-05.2006 [PubMed] [Cross Ref]
Fassbender K., Schneider S., Bertsch T., Schlueter D., Fatar M., Ragoschke A., et al. (2000). Temporal profile of release of interleukin-1beta in neurotrauma. Neurosci. Lett. 284, 135–138 10.1016/S0304-3940(00)00977-0 [PubMed] [Cross Ref]
Feinstein A., Rapoport M. (2000). Mild traumatic brain injury: the silent epidemic. Can. J. Public Health 91, 325–326, 332. [PubMed]
Field M., Collins M. W., Lovell M. R., Maroon J. (2003). Does age play a role in recovery from sports-related concussion? A comparison of high school and collegiate athletes. J. Pediatr. 142, 546–553 10.1067/mpd.2003.190 [PubMed] [Cross Ref]
Fineman I., Giza C. C., Nahed B. V., Lee S. M., Hovda D. A. (2000). Inhibition of neocortical plasticity during development by a moderate concussive brain injury. J. Neurotrauma 17, 739–749 [PubMed]
Fukuda K., Tanno H., Okimura Y., Nakamura M., Yamaura A. (1995). The blood-brain barrier disruption to circulating proteins in the early period after fluid percussion brain injury in rats. J. Neurotrauma 12, 315–324 [PubMed]
Gadient R. A., Cron K. C., Otten U. (1990). Interleukin-1 beta and tumor necrosis factor-alpha synergistically stimulate nerve growth factor (NGF) release from cultured rat astrocytes. Neurosci. Lett. 117, 335–340 10.1016/0304-3940(90)90687-5 [PubMed] [Cross Ref]
Galic M. A., Riazi K., Pittman Q. J. (2012). Cytokines and brain excitability. Front. Neuroendocrinol. 33:2 10.1016/j.yfrne.2011.12.002 [PMC free article] [PubMed] [Cross Ref]
Gardiner M., Smith M. L., Kagstrom E., Shohami E., Siesjo B. K. (1982). Influence of blood glucose concentration on brain lactate accumulation during severe hypoxia and subsequent recovery of brain energy metabolism. J. Cereb. Blood Flow Metab. 2, 429–438 10.1038/jcbfm.1982.49 [PubMed] [Cross Ref]
Gentleman S. M., Leclercq P. D., Moyes L., Graham D. I., Smith C., Griffin W. S., et al. (2004). Long-term intracerebral inflammatory response after traumatic brain injury. Forensic Sci. Int. 146, 97–104 10.1016/j.forsciint.2004.06.027 [PubMed] [Cross Ref]
Giza C. C., Difiori J. P. (2011). Pathophysiology of sports-related concussion: an update on basic science and translational research. Sports Health 3, 46–51 10.1177/1941738110391732 [PMC free article] [PubMed] [Cross Ref]
Giza C. C., Hovda D. A. (2001). The neurometabolic cascade of concussion. J. Athl. Train. 36, 228–235 [PMC free article] [PubMed]
Goldberg A. S., Moroz L., Smith A., Ganley T. (2007). Injury surveillance in young athletes: a clinician’s guide to sports injury literature. Sports Med. 37, 265–278 [PubMed]
Gosselin N., Saluja R. S., Chen J. K., Bottari C., Johnston K., Ptito A. (2010). Brain functions after sports-related concussion: insights from event-related potentials and functional MRI. Phys. Sportsmed. 38, 27–37 10.3810/psm.2010.10.1805 [PubMed] [Cross Ref]
Gurkoff G. G., Giza C. C., Hovda D. A. (2006). Lateral fluid percussion injury in the developing rat causes an acute, mild behavioral dysfunction in the absence of significant cell death. Brain Res. 1077, 24–36 10.1016/j.brainres.2006.01.011 [PubMed] [Cross Ref]
Habgood M. D., Bye N., Dziegielewska K. M., Ek C. J., Lane M. A., Potter A., et al. (2007). Changes in blood-brain barrier permeability to large and small molecules following traumatic brain injury in mice. Eur. J. Neurosci. 25, 231–238 10.1111/j.1460-9568.2006.05275.x [PubMed] [Cross Ref]
Herx L. M., Rivest S., Yong V. W. (2000). Central nervous system-initiated inflammation and neurotrophism in trauma: IL-1 beta is required for the production of ciliary neurotrophic factor. J. Immunol. 165, 2232–2239 [PubMed]
Holmin S., Schalling M., Hojeberg B., Nordqvist A. C., Skeftruna A. K., Mathiesen T. (1997). Delayed cytokine expression in rat brain following experimental contusion. J. Neurosurg. 86, 493–504 10.3171/jns.1997.86.3.0493 [PubMed] [Cross Ref]
Holmin S., Soderlund J., Biberfeld P., Mathiesen T. (1998). Intracerebral inflammation after human brain contusion. Neurosurgery 42, 291–298 discussion: 298–299. [PubMed]
Ibrahim N. G., Ralston J., Smith C., Margulies S. S. (2010). Physiological and pathological responses to head rotations in toddler piglets. J. Neurotrauma 27, 1021–1035 10.1089/neu.2009.1212 [PMC free article] [PubMed] [Cross Ref]
Inglese M., Makani S., Johnson G., Cohen B. A., Silver J. A., Gonen O., et al. (2005). Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study. J. Neurosurg. 103, 298–303 10.3171/jns.2005.103.2.0298 [PubMed] [Cross Ref]
Jeter C. B., Hergenroeder G. W., Hylin M. J., Redell J. B., Moore A. N., Dash P. K. (2012). Biomarkers for the diagnosis and prognosis of mild traumatic brain injury/concussion. J. Neurotrauma. [Epub ahead of print]. 10.1089/neu.2012.2439 [PubMed] [Cross Ref]
Kabadi S. V., Stoica B. A., Byrnes K. R., Hanscom M., Loane D. J., Faden A. I. (2012). Selective CDK inhibitor limits neuroinflammation and progressive neurodegeneration after brain trauma. J. Cereb. Blood Flow Metab. 32, 137–149 10.1038/jcbfm.2011.117 [PMC free article] [PubMed] [Cross Ref]
Kalimo H., Rehncrona S., Soderfeldt B. (1981). The role of lactic acidosis in the ischemic nerve cell injury. Acta Neuropathol. Suppl. 7, 20–22 [PubMed]
Katayama Y., Becker D. P., Tamura T., Hovda D. A. (1990). Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury. J. Neurosurg. 73, 889–900 10.3171/jns.1990.73.6.0889 [PubMed] [Cross Ref]
Kawamata T., Katayama Y., Hovda D. A., Yoshino A., Becker D. P. (1992). Administration of excitatory amino acid antagonists via microdialysis attenuates the increase in glucose utilization seen following concussive brain injury. J. Cereb. Blood Flow Metab. 12, 12–24 10.1038/jcbfm.1992.3 [PubMed] [Cross Ref]
Khuman J., Meehan W. P., 3rd., Zhu X., Qiu J., Hoffmann U., Zhang J., et al. (2011). Tumor necrosis factor alpha and Fas receptor contribute to cognitive deficits independent of cell death after concussive traumatic brain injury in mice. J. Cereb. Blood Flow Metab. 31, 778–789 10.1038/jcbfm.2010.172 [PMC free article] [PubMed] [Cross Ref]
Kim K. S., Wass C. A., Cross A. S., Opal S. M. (1992). Modulation of blood-brain barrier permeability by tumor necrosis factor and antibody to tumor necrosis factor in the rat. Lymphokine Cytokine Res. 11, 293–298 [PubMed]
Kirchhoff C., Buhmann S., Bogner V., Stegmaier J., Leidel B. A., Braunstein V., et al. (2008). Cerebrospinal IL-10 concentration is elevated in non-survivors as compared to survivors after severe traumatic brain injury. Eur. J. Med. Res. 13, 464–468 [PubMed]
Knoblach S. M., Faden A. I. (1998). Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury. Exp. Neurol. 153, 143–151 10.1016/0006-8993(95)01501-9 [PubMed] [Cross Ref]
Knoblach S. M., Fan L., Faden A. I. (1999). Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment. J. Neuroimmunol. 95, 115–125 [PubMed]
Kolesnick R., Golde D. W. (1994). The sphingomyelin pathway in tumor necrosis factor and interleukin-1 signaling. Cell 77, 325–328 [PubMed]
Kopf M., Baumann H., Freer G., Freudenberg M., Lamers M., Kishimoto T., et al. (1994). Impaired immune and acute-phase responses in interleukin-6-deficient mice. Nature 368, 339–342 10.1038/368339a0 [PubMed] [Cross Ref]
Kossmann T., Hans V., Imhof H. G., Trentz O., Morganti-Kossmann M. C. (1996). Interleukin-6 released in human cerebrospinal fluid following traumatic brain injury may trigger nerve growth factor production in astrocytes. Brain Res. 713, 143–152 [PubMed]
Kossmann T., Hans V. H., Imhof H. G., Stocker R., Grob P., Trentz O., et al. (1995). Intrathecal and serum interleukin-6 and the acute-phase response in patients with severe traumatic brain injuries. Shock 4, 311–317 [PubMed]
Kremlev S. G., Palmer C. (2005). Interleukin-10 inhibits endotoxin-induced pro-inflammatory cytokines in microglial cell cultures. J. Neuroimmunol. 162, 71–80 10.1016/j.jneuroim.2005.01.010 [PubMed] [Cross Ref]
Kumar A., Loane D. J. (2012). Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. Brain Behav. Immun. 26, 1191–1201 10.1016/j.bbi.2012.06.008 [PubMed] [Cross Ref]
Kushima Y., Hama T., Hatanaka H. (1992). Interleukin-6 as a neurotrophic factor for promoting the survival of cultured catecholaminergic neurons in a chemically defined medium from fetal and postnatal rat midbrains. Neurosci. Res. 13, 267–280 [PubMed]
Kutcher J. S., Giza C. C., Alessi A. G. (2010). Sports concussion. Continuum (Minneap. Minn) 16, 41–54 10.1212/01.CON.0000391452.30299.67 [PubMed] [Cross Ref]
Laker S. R. (2011). Return-to-play decisions. Phys. Med. Rehabil. Clin. N. Am. 22, 619–634, viii. 10.1016/j.pmr.2011.08.004 [PubMed] [Cross Ref]
Ledic D., Sosa I., Linic I. S., Cvijanovic O., Kovacevic M., Desnica A., et al. (2012). Vomiting as a reliable sign of concussion. Med. Hypotheses 78, 23–25 10.1016/j.mehy.2011.09.032 [PubMed] [Cross Ref]
Lenzlinger P. M., Morganti-Kossmann M. C., Laurer H. L., McIntosh T. K. (2001). The duality of the inflammatory response to traumatic brain injury. Mol. Neurobiol. 24, 169–181 10.1385/MN:24:1-3:169 [PubMed] [Cross Ref]
Ley E. J., Clond M. A., Singer M. B., Shouhed D., Salim A. (2011). IL6 deficiency affects function after traumatic brain injury. J. Surg. Res. 170, 253–256 10.1016/j.jss.2011.03.006 [PubMed] [Cross Ref]
Lowrance J. H., O’Sullivan F. X., Caver T. E., Waegell W., Gresham H. D. (1994). Spontaneous elaboration of transforming growth factor beta suppresses host defense against bacterial infection in autoimmune MRL/lpr mice. J. Exp. Med. 180, 1693–1703 [PMC free article] [PubMed]
Lyng K., Munkeby B. H., Saugstad O. D., Stray-Pedersen B., Froen J. F. (2005). Effect of interleukin-10 on newborn piglet brain following hypoxia-ischemia and endotoxin-induced inflammation. Biol. Neonate 87, 207–216 10.1159/000083131 [PubMed] [Cross Ref]
Maas A. I., Murray G., Henney H., 3rd., Kassem N., Legrand V., Mangelus M., et al. (2006). Efficacy and safety of dexanabinol in severe traumatic brain injury: results of a phase III randomised, placebo-controlled, clinical trial. Lancet Neurol. 5, 38–45 10.1016/S1474-4422(05)70253-2 [PubMed] [Cross Ref]
Maier B., Laurer H. L., Rose S., Buurman W. A., Marzi I. (2005). Physiological levels of pro- and anti-inflammatory mediators in cerebrospinal fluid and plasma: a normative study. J. Neurotrauma 22, 822–835 10.1089/neu.2005.22.822 [PubMed] [Cross Ref]
Martin N. A., Patwardhan R. V., Alexander M. J., Africk C. Z., Lee J. H., Shalmon E., et al. (1997). Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. J. Neurosurg. 87, 9–19 10.3171/jns.1997.87.1.0009 [PubMed] [Cross Ref]
Maskin B., Gammella D., Solari L., Videta W., Barboza M. F., Geliz L., et al. (2001). [Early release of the antiinflammatory cytokine IL-10 in traumatic brain injury]. Medicina (B Aires) 61, 573–576 [PubMed]
McCrea M., Hammeke T., Olsen G., Leo P., Guskiewicz K. (2004). Unreported concussion in high school football players: implications for prevention. Clin. J. Sport Med. 14, 13–17 [PubMed]
McCrory P., Meeuwisse W., Johnston K., Dvorak J., Aubry M., Molloy M., et al. (2009). Consensus statement on concussion in sport: the 3rd International Conference on Concussion in Sport held in Zurich, November 2008. J. Athl. Train. 44, 434–448 10.4085/1062-6050-44.4.434 [PMC free article] [PubMed] [Cross Ref]
McCullough B. J., Jarvik J. G. (2011). Diagnosis of concussion: the role of imaging now and in the future. Phys. Med. Rehabil. Clin. N. Am. 22, 635–652, viii. 10.1016/j.pmr.2011.08.005 [PubMed] [Cross Ref]
Metting Z., Wilczak N., Rodiger L. A., Schaaf J. M., Van Der Naalt J. (2012). GFAP and S100B in the acute phase of mild traumatic brain injury. Neurology 78, 1428–1433 10.1212/WNL.0b013e318253d5c7 [PubMed] [Cross Ref]
Morganti-Kossmann M. C., Hans V. H., Lenzlinger P. M., Dubs R., Ludwig E., Trentz O., et al. (1999). TGF-beta is elevated in the CSF of patients with severe traumatic brain injuries and parallels blood-brain barrier function. J. Neurotrauma 16, 617–628 [PubMed]
Morganti-Kossmann M. C., Rancan M., Otto V. I., Stahel P. F., Kossmann T. (2001). Role of cerebral inflammation after traumatic brain injury: a revisited concept. Shock 16, 165–177 [PubMed]
Mustoe T. A., Pierce G. F., Thomason A., Gramates P., Sporn M. B., Deuel T. F. (1987). Accelerated healing of incisional wounds in rats induced by transforming growth factor-beta. Science 237, 1333–1336 10.1126/science.2442813 [PubMed] [Cross Ref]
O’Connor W. T., Smyth A., Gilchrist M. D. (2011). Animal models of traumatic brain injury: a critical evaluation. Pharmacol. Ther. 130, 106–113 10.1016/j.pharmthera.2011.01.001 [PubMed] [Cross Ref]
Penkowa M., Camats J., Hadberg H., Quintana A., Rojas S., Giralt M., et al. (2003). Astrocyte-targeted expression of interleukin-6 protects the central nervous system during neuroglial degeneration induced by 6-aminonicotinamide. J. Neurosci. Res. 73, 481–496 10.1002/jnr.10681 [PubMed] [Cross Ref]
Penkowa M., Giralt M., Carrasco J., Hadberg H., Hidalgo J. (2000). Impaired inflammatory response and increased oxidative stress and neurodegeneration after brain injury in interleukin-6-deficient mice. Glia 32, 271–285 10.1002/1098-1136(200012)32:33.0.CO;2-5 [PubMed] [Cross Ref]
Perry R. T., Collins J. S., Wiener H., Acton R., Go R. C. (2001). The role of TNF and its receptors in Alzheimer’s disease. Neurobiol. Aging 22, 873–883 [PubMed]
Prins M. L., Hales A., Reger M., Giza C. C., Hovda D. A. (2010). Repeat traumatic brain injury in the juvenile rat is associated with increased axonal injury and cognitive impairments. Dev. Neurosci. 32, 510–518 10.1159/000316800 [PMC free article] [PubMed] [Cross Ref]
Pulsipher D. T., Campbell R. A., Thoma R., King J. H. (2011). A critical review of neuroimaging applications in sports concussion. Curr. Sports Med. Rep. 10, 14–20 10.1249/JSR.0b013e31820711b8 [PubMed] [Cross Ref]
Putukian M. (2011). Neuropsychological testing as it relates to recovery from sports-related concussion. PM R 3, S425–S432 10.1016/j.pmrj.2011.08.003 [PubMed] [Cross Ref]
Quintana A., Molinero A., Borup R., Nielsen F. C., Campbell I. L., Penkowa M., et al. (2008). Effect of astrocyte-targeted production of IL-6 on traumatic brain injury and its impact on the cortical transcriptome. Dev. Neurobiol. 68, 195–208 10.1002/dneu.20584 [PubMed] [Cross Ref]
Ramilo O., Saez-Llorens X., Mertsola J., Jafari H., Olsen K. D., Hansen E. J., et al. (1990). Tumor necrosis factor alpha/cachectin and interleukin 1 beta initiate meningeal inflammation. J. Exp. Med. 172, 497–507 [PMC free article] [PubMed]
Ramlackhansingh A. F., Brooks D. J., Greenwood R. J., Bose S. K., Turkheimer F. E., Kinnunen K. M., et al. (2011). Inflammation after trauma: microglial activation and traumatic brain injury. Ann. Neurol. 70, 374–383 10.1002/ana.22455 [PubMed] [Cross Ref]
Randolph C., Millis S., Barr W. B., McCrea M., Guskiewicz K. M., Hammeke T. A., et al. (2009). Concussion symptom inventory: an empirically derived scale for monitoring resolution of symptoms following sport-related concussion. Arch. Clin. Neuropsychol. 24, 219–229 10.1093/arclin/acp025 [PMC free article] [PubMed] [Cross Ref]
Scherbel U., Raghupathi R., Nakamura M., Saatman K. E., Trojanowski J. Q., Neugebauer E., et al. (1999). Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury. Proc. Natl. Acad. Sci. U.S.A. 96, 8721–8726 10.1073/pnas.96.15.8721 [PMC free article] [PubMed] [Cross Ref]
Schiff L., Hadker N., Weiser S., Rausch C. (2012). A literature review of the feasibility of glial fibrillary acidic protein as a biomarker for stroke and traumatic brain injury. Mol. Diagn. Ther. 16, 79–92 10.2165/11631580-000000000-00000 [PubMed] [Cross Ref]
Scorza K. A., Raleigh M. F., O’Connor F. G. (2012). Current concepts in concussion: evaluation and management. Am. Fam. Physician 85, 123–132 [PubMed]
Shiozaki T., Hayakata T., Tasaki O., Hosotubo H., Fuijita K., Mouri T., et al. (2005). Cerebrospinal fluid concentrations of anti-inflammatory mediators in early-phase severe traumatic brain injury. Shock 23, 406–410 [PubMed]
Shohami E., Bass R., Wallach D., Yamin A., Gallily R. (1996). Inhibition of tumor necrosis factor alpha (TNFalpha) activity in rat brain is associated with cerebroprotection after closed head injury. J. Cereb. Blood Flow Metab. 16, 378–384 10.1097/00004647-199605000-00004 [PubMed] [Cross Ref]
Shohami E., Gallily R., Mechoulam R., Bass R., Ben-Hur T. (1997). Cytokine production in the brain following closed head injury: dexanabinol (HU-211) is a novel TNF-alpha inhibitor and an effective neuroprotectant. J. Neuroimmunol. 72, 169–177 [PubMed]
Shohami E., Ginis I., Hallenbeck J. M. (1999). Dual role of tumor necrosis factor alpha in brain injury. Cytokine Growth Factor Rev. 10, 119–130 [PubMed]
Shohami E., Novikov M., Bass R., Yamin A., Gallily R. (1994). Closed head injury triggers early production of TNF alpha and IL-6 by brain tissue. J. Cereb. Blood Flow Metab. 14, 615–619 10.1038/jcbfm.1994.76 [PubMed] [Cross Ref]
Shojo H., Kaneko Y., Mabuchi T., Kibayashi K., Adachi N., Borlongan C. V. (2010). Genetic and histologic evidence implicates role of inflammation in traumatic brain injury-induced apoptosis in the rat cerebral cortex following moderate fluid percussion injury. Neuroscience 171, 1273–1282 10.1016/j.neuroscience.2010.10.018 [PubMed] [Cross Ref]
Singh S., Swarnkar S., Goswami P., Nath C. (2011). Astrocytes and microglia: responses to neuropathological conditions. Int. J. Neurosci. 121, 589–597 10.3109/00207454.2011.598981 [PubMed] [Cross Ref]
Slobounov S., Sebastianelli W., Hallett M. (2012). Residual brain dysfunction observed one year post-mild traumatic brain injury: combined EEG and balance study. Clin. Neurophysiol. 123, 1755–1761 10.1016/j.clinph.2011.12.022 [PMC free article] [PubMed] [Cross Ref]
Stirling D. P., Khodarahmi K., Liu J., McPhail L. T., McBride C. B., Steeves J. D., et al. (2004). Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury. J. Neurosci. 24, 2182–2190 10.1523/JNEUROSCI.5275-03.2004 [PubMed] [Cross Ref]
Sullivan P. G., Bruce-Keller A. J., Rabchevsky A. G., Christakos S., Clair D. K., Mattson M. P., et al. (1999). Exacerbation of damage and altered NF-kappaB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury. J. Neurosci. 19, 6248–6256 [PubMed]
Szmydynger-Chodobska J., Strazielle N., Gandy J. R., Keefe T. H., Zink B. J., Ghersi-Egea J. F., et al. (2012). Posttraumatic invasion of monocytes across the blood-cerebrospinal fluid barrier. J. Cereb. Blood Flow Metab. 32, 93–104 10.1038/jcbfm.2011.111 [PMC free article] [PubMed] [Cross Ref]
Takahashi H., Manaka S., Sano K. (1981). Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury. J. Neurosurg. 55, 708–717 10.3171/jns.1981.55.5.0708 [PubMed] [Cross Ref]
Tang C. H., Fu X. J., Xu X. L., Wei X. J., Pan H. S. (2012). The anti-inflammatory and anti-apoptotic effects of nesfatin-1 in the traumatic rat brain. Peptides 36, 39–45 10.1016/j.peptides.2012.04.014 [PubMed] [Cross Ref]
Tanno H., Nockels R. P., Pitts L. H., Noble L. J. (1992). Breakdown of the blood-brain barrier after fluid percussive brain injury in the rat. Part 1: distribution and time course of protein extravasation. J. Neurotrauma 9, 21–32 [PubMed]
Taupin V., Toulmond S., Serrano A., Benavides J., Zavala F. (1993). Increase in IL-6, IL-1 and TNF levels in rat brain following traumatic lesion. Influence of pre- and post-traumatic treatment with Ro5 4864, a peripheral-type (p site) benzodiazepine ligand. J. Neuroimmunol. 42, 177–185 [PubMed]
Tavazzi B., Vagnozzi R., Signoretti S., Amorini A. M., Belli A., Cimatti M., et al. (2007). Temporal window of metabolic brain vulnerability to concussions: oxidative and nitrosative stresses–part II. Neurosurgery 61, 390–395 discussion: 395–396. [PubMed]
Vanden Berghe W., Vermeulen L., De Wilde G., De Bosscher K., Boone E., Haegeman G. (2000). Signal transduction by tumor necrosis factor and gene regulation of the inflammatory cytokine interleukin-6. Biochem. Pharmacol. 60, 1185–1195 10.1016/S0006-2952(00)00412-3 [PubMed] [Cross Ref]
Vos P. E., Jacobs B., Andriessen T. M., Lamers K. J., Borm G. F., Beems T., et al. (2010). GFAP and S100B are biomarkers of traumatic brain injury: an observational cohort study. Neurology 75, 1786–1793 10.1212/WNL.0b013e3181fd62d2 [PubMed] [Cross Ref]
Wahl S. M. (1992). Transforming growth factor beta (TGF-beta) in inflammation: a cause and a cure. J. Clin. Immunol.