Diverticulitis and lower back pain
Prior to getting familiar with the case I am about to describe, I highly recommend to read this article. https://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 10.1517/135437220.127.116.111 [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.
Is massage therapy, remedy to all diseases?
I was inspired to write this when I came across the article Blood Pressure Reactivity to Psychological Stress Predicts Hypertension in the CARDIA Study conducted research.
Here is the fragment from the abstract for this article:
Absolutely. Young people who are under psychological stress are at risk of developing essential hypertension. An increase in sympathetic tone produces arteriolar vasoconstriction with a subsequent increase in the peripheral vascular resistance. At the onset, these changes exhibit a transient character and the body uses self-regulatory mechanisms to restore the proper relationship between sympathetic and parasympathetic tones. This is why in earlier stages there are episodes of increased arterial blood pressure, without symptoms of hypertension. With time and repeated episodes of hypertension attacks, the body resets baroreceptors, in the arterial circulation to the new level, and the elevation of arterial blood pressure becomes sustained.
The correctly established protocol of medical massage therapy may play a critical role in controlling arterial blood pressure in some patients with EH. More details on the subject is in my article link below: Medical Massage and Control of Arterial Hypertension
In addition please take a look at the link below, where I am presenting well-documented case of repeated hypertonic crisis. Massage therapy was the only methodology that could save this precious life. The power of massage
Of course, if massage can be helpful and effective when we treat established hypertension, then it must be a great preventive effort as well. It should be noted that hypertension should not be segregated from other stress related illnesses. It is fair to say that nowadays, humanity facing epidemics of stress related illnesses, including but not limited to essential hypertension, anxieties, sleep disorders, clinical depression, diabetes type II, tension headaches, muscular aches and pains. In most cases stress leading to combinations of illnesses I have mentioned above. For a better understanding please view the video below, where I am explaining the chain reaction of the emotional stress mechanism that debilitates the human body.
At the risk of repeating myself I’d like to emphasize that it is very difficult to find person who are suffering from essential hypertension, and not experiencing anxieties attacks, and /or muscular aches and pains, sleep disorders, stress related over eating , pre-diabetes or diabetes type II, etc.
The method section of the study Blood Pressure Reactivity to Psychological Stress Predicts Hypertension in the CARDIA Study proposes the following artificial stressors: cold pressor, star tracing, and video game tasks.
In fact, many surveys suggest that on average 80% of doctor visits are stress related casing such diseases as essential hypertension , anxieties attack , tension headaches , sleep disorders ,TMJ disorders , spinal disorders and more. Not to consider this information while talking about healthcare is wrong by all means.
Let me point out though that these 3 stressors where not the only the ones that effected the stress group. Outside the research experiment, participants were exposed to additional stressors. Even the modern technologically advanced life is applying am additional tremendous amount of stress. The link below is to a four minute video presentation where, under different angles, I propose a view at a stress exposure. Workplace conditions that worsen stress
It is clinically and scientifically proven that massage therapy is the most powerful methodology in stress management. Of course, scientific fundamental base of massage therapy that explains the power of massage is the physiological effect of medical massage on human body. Here is the link to brief explanation. Physiological effect of massage on the human body
In my blog Concerned about stress related illnesses I am offering extended view on role of massage in stress management.
So, is massage therapy, a remedy to all diseases? I wouldn’t say so. However, I know that this is a very powerful preventive medicine methodology, as well as the great treatment tool that must be integrated with the conventional medical treatments. In this case the statistics of stress related illnesses will change for the better Increasing unwillingness to bear even small pains and general public will be not blamed for suffering.