CONCUSSION/CTE PRESCRIPTION


READERS SUMMARY:

WHAT REALLY IS A CONCUSSION?
HOW DO I TREAT A CONCUSSION IF IT HAPPENS?
WHAT THE MILITARY,NFL, NHL,MLB, NBA and NCAA SHOULD DO NOW?
WHAT EVERY PARENT NEEDS TO KNOW NOW?

Today marks the fourth blog in this series. Today also marked another early death in the NFL community. This time Orlando “Zeus” Brown was found dead in Baltimore. He was a mammoth offensive tackle who played in the NFL from 1994 to 2005. After hearing about it today I decided to post this blog tonight. I think this information is critical and needs to be considered by everyone at risk right now.

Concussion is a trauma-induced alteration in mental status that may or may not involve loss of consciousness. Headache, confusion and amnesia are the hallmarks of concussion. The confusional episode and amnesia may occur immediately after the blow to the head or several minutes later. I have also seen symptoms appear several days later from concussions especially in the younger patient and in the multiply concussed patient.

Sources of Concussion:

Blasts
Vehicle crashes
Projectiles
Falls
Sports injuries

Symptoms of concussion:

· Headaches or neck pain that do not go away;
· Slowness in thinking, speaking, acting, or reading;
· Getting lost or easily confused;
· Feeling tired all of the time, having no energy or motivation;
· Mood changes (feeling sad or angry for no reason);
· Changes in sleep patterns (sleeping a lot more or having a hard time sleeping);
· Difficulty remembering, concentrating, or making decisions;· Light-headedness, dizziness, or loss of balance;· Urge to vomit (nausea);· Increased sensitivity to lights, sounds, or distractions;
· Blurred vision or eyes that tire easily;· Loss of sense of smell or taste and or ringing in the ears.

Many use descriptive language in trying to relay information about what a concussion is. Many call it a “brain bruise” This is very inaccurate. There are no findings on imaging studies in most concussions. The best way to understand concussion biologically is that it is an energy disturbance caused by the abruptness of the trauma inflicted to the brain. Many studies of a concussed brain show blood flow changes on functional MRI’s and on PET scans. If EEG’s are also done on patients often times there is low voltage findings on the study signifying decreased energy efficiency that leads to acute changes in the neurocircuitry of the surrounding neurons. This injury depletes neurons of energy and this puts the area of injury under much higher risk to future damage because of the accumulation of the release of excitotoxic neuro chemicals released by the cells injured. When these chemicals are released by the damage neurons there is a simultaneous release of magnesium and intracellular zinc and calcium. The calcium release can result in cell death if the injury response is not contained by the brain’s endogenous immune response and by the microglia and surrounding astrocytes. These cells re-uptake the toxic chemicals released and try to contain the release of the the metal ions locally to limit damage. Concussion severity seems to correlate quite well to the release of these substances and the resulting decrease in cerebral blood flow to these areas.

According to a recent statement by Dr. Robert Stern, co-director of CSTE, new evidence shows” that 85% of concussions require about three weeks of recovery” (Abel, D., 2010). This is a longer time period than anything currently in the literature for return to play guidelines. I personally believe this statement does not come close to going far enough for those with severe concussions or those who are multiply concussed.

You also must realize that currently in 2011 there is no “level one data” on concussion risk, or treatment. Therefore there are no uniform agreed treatments. With that as a background one must entirely focus on the known biochemistry and pathophysiology to make best “guesstimates” on how one should proceed once the concussion has occurred.

HOW DO YOU PREVENT A CONCUSSION?

1. Avoidance of activities where there is risk for head trauma.
2. Avoiding situations where there are many angular momentum forces
3. Avoid severe flexion or extenuation of the neck and head.
4. If you are involved in a high risk activity you should consider limiting all glucose consumption for 6 hours prior to the activity.
5. You should maintain a ketogenic diet, loaded with medium chain triglycerides 6 hours before the at risk behavior to create a protective terroir for the brain if injury were to occur.
6. A properly fitted mouthguard should be worn at all times to avoid traumatic impact of the mandibular condyles into the base of the temporal lobes. Many concussed patient have tongue lacerations because they are not wearing mouth guards and their concussion can be quite severe because the hippocampus is often severely impacted by this type of impact. For athletes or soldiers who need to verbalize to act a voice controlled system should be developed using nanotechnology so they can wear the mouthguard. This should not be compromised due to the severe risks of what hippocampal damage can lead too.
7. All head gear should be mandatory and contain motion and impact detectors to help doctors understand injury vectors to predict injury and severity. ( IMPACT evaluation, Miltary Anam evaluation; Parallel biomarker study; Helmets with helmet blast sensors and cooling.) All helmets should have a cooling system built within the helmet to keep the head temperature cooler than normal for the neuro-protective effects of cold temperatures as biomarkers
8. Cooling shirts should be designed and worn to protect the posterior and lateral neck. This allows for a constantly controlled temperature across the vertebral and carotid arteries to mitigate risk before concussion occurs. If this is not worn, Ice packs should be immediately placed and secured to this area for any traumatic risk. Body and head cooling techniques should be used on the sideline, bench or in military theaters.
9. Prior to onset of high risk behavior one should consider supplementing with 25 mgs of zinc, 400 mgs of Magnesium. Ingestion of coconut oil in packet form should be considered as soon as help arrives to improve the neuronal energy deficit and limit neuronal damage. All patents at risk should have baseline neuro-cognitve batteries made mandatory. The younger the patient the more the testing will need to be enforced.
10. All at risk patients should avoid all MSG, artificial sweeteners, and excito-toxins to limit risk of neuronal damage pre and post injury occurrence.

WHAT SHOULD BE DONE ONCE A CONCUSSION OCCURS?

A. All people at risk should undergo fMRI pre and post injury/deployment as well as in game/theater scanning. Functional MRI/PET scanning should be required in all front line military and sports venues.
B. Resting fMRI/PET scanning should be able to distinguish mTBI, PTSD as it has with 80-90% accuracy distinguished from neurodegenerative disorders. All fMRI scanners should have minimum 3.0 tesla MR scan capability. All scanning needs to be done during waking hours (sleep deprivation causes negative scan effects).
C. Ketogenic packets, supplements available at all at risk events. Strict avoidance of all glucose and fructose drinks or foods during at risk activities to limit risk.
D. All patients should be removed from all activities and assessed by a neurosurgeon/neurologist with correct skill set. No exceptions should be made.
E. Avoid excessive bright light in the eyes due to thalamic sensitivity/ lateral geniculate nucleus

WHAT IS THE IDEAL STUDY FOR CONCUSSION AND CTE RISK?

A. The ideal study of at risk patients: Combine/Preseason/Pre Deployment scans for baseline with formal neuro-cognitve battery.

B. Organ donor status made mandatory to allow postmortem exam of at risk patients. Allow for concussion history; Thorough neuropsychology evaluation; Genetic Testing for ApoE 4 allele

C. Scanning in dedicated scanner before at risk activity begins (3T fixed scanner)

D. Parallel biomarker study modeling the VA’s program for the military. (Banyan Biomarkers)

E. Deployment/In Game injury: Scanned in theater/ City post concussion (3T fixed scanner) with Anam evaluation Parallel biomarker study, review of Helmet sensor and vehicle blast sensor data to assess risk.

F. Post Deployment/Post Game management: Repeat scanning post deployment in exact same scanner as pre-deployment/game assessment. Complete neuropsychology evaluation with sequential brain examination using neurocognitive testing parameters like IMPACT/KIA Continued surveillance in civilian status through Veteran’s Administration Parallel biomarker Study

WHAT ARE THE SYMPTOMS OF IMPENDING CTE FOR THOSE AT RISK TO BE AWARE OF?

The clinical symptoms associated with CTE vary in severity depending on which clinical stage the individual is in (McKee, A.C., et. al., 2009). Initial early symptoms include the following:

- Deterioration in attention, concentration, memory, poor decision making
- Disorientation to person, place or time.
- Confusion that waxes and wanes. This is dramatic when the patient is intoxicated.
- Dizziness by spatial of visual cues.
- Headaches become very common. Cervical pain is also a common feature.
- Lack of insight, lack of empathy, and a personality change is apparent to everyone who knows them
- Poor judgment involves use of drugs, alcohol, risky behavior,
- Overt dementia becomes obvious to friends and family.
- Slowed muscular movements with increased activity.
- Staggered gait and loss of balance is common.
- Impeded speech: Word finding difficulty is the first sign one usually reports.
- Tremors and fibrillations in major muscle groups
- Vertigo at rest or during motion
- Deafness that can come one abruptly

The individual may progress through three stages of the disease beginning in the first stage with affective disturbances and psychotic symptoms. The emotional lability and change in personality are standouts of this stage. As the disease progresses to stage two, the individual may suffer from social instability, erratic behavior, severe memory loss, and the initial symptoms of Parkinson’s disease (McKee, A.C., et.al., 2009) . Many functional movement disorders can be seen at this stage of the disease progression. Family members should look for them to alert the doctors of the progression. Alcoholism and drug abuse are particularly common in people developing CTE from their concussions. Generally, the more pathways of inflammation that the patient sustains at this time the quicker the symptoms tend to progress. This can be from obesity, drugs, alcohol, or environmental toxins. Sometimes, the symptoms progress rapidly when their are acute spikes in cortisol, insulin, or in ingestion of excitotoxins. A new trauma or life stress can also precipitate a serious neurological decline.

The 3rd and final stage consists of a progressive deterioration to dementia and may have other symptoms including the signs associated with Alzheimer’s disease or Parkinson’s disease, speech difficulties, gait abnormalities, dysarthria (speech disorder characterized by neuromuscular weakness or lack of control of facial muscles), dysphagia (difficulty swallowing), and ptosis (drooping eyelid) (McKee, A.C., et.al., 2009).

How is CTE distinguished from other neurodegenerative tauopathies, (i.e. Alzheimer’s Disease)

A. CTE usually Involves superficial cortical layers, specifically neocortical layers 1 and 2.
B. Patchy distribution in frontal and temporal cortices is the rule in CTE and not in AD or PD.
C. Propensity for injury in sulcal depths as opposed to surface gyri – Deposition of β-amyloid occurs in <50% of cases - Marked accumulation of tau immunoreactive astrocytes (concentrated around glutamate receptors of the neocortex)
D. Superficial cortical laminae: layers II and III Perivascular Patchy, irregular Prominent glial tangles
E. Key MRI findings: Often greatest at sulcal depths, Dot like tangles, spindle-shaped neuritis, subcortical white matter defects on STIR or T2 imaging. Dilated ventricles due to cerebral atrophy, fenestrated septum pellucidum is extremely common in this group, atrophic mammillary bodies (due to memory loss), loss of thalamic volume, loss of neocortex volume, Loss of medial temp lobe structures resulting in profound memory changes.
F. Decreased Apo E and Aβ spinal fluid concentrations in acute injury settings. Most patients do not have CSF examined but this should be considered by neurosurgeon/neurologists rendering independent assessments in severe persistent concussion symptoms. Regular MRI/CT is worthless in initial assessments. Functional MRI, connectome mapping and Diffusion tensor imaging should be considered gold standard imaging testing for this group of patients. (tractographic imaging)
G. Auto antibodies can show up 5-7 days post injury and can persist for years in at risk patients. This should be mandatory testing for all at risk patients post injury for their lifetime. (4 biomarkers in clinical testing)

Conclusions:

fMRI, through connectome mapping, will detect organic changes in functional neural architecture after significant mTBI. These can all be made available in most cities supporting professional athletics of in the military theater. For younger patients parents should assess whether these treatment options exist in their areas before consenting to allowing participation in at risk activities.

The presence of these changes should serve as a warning that repeated exposure to concussive forces may lead to the development of chronic traumatic encephalopathy as the patient ages. This tool should be used in all cases in my opinion. Cost is steep but the cost of CTE is steeper to the patient and to their family due to its debilitating and possibly lethal results.

The pairing of RfMRI with other biomarker studies will provide cross validation of methods and the development of less complex methods of detection of significant mTBI, i.e., easily obtained serum biomarkers. (Banyan Biomarkers)
Dietary and supplement regimens should be instituted at the time of injury. Neurosurgical or neurology consultation should be mandatory in all cases and decision tree analysis should be uncoupled from the employment/deployment situation in all cases.
Everyday more data is released causing me to update this Rx.

CITES:

http://journals.lww.com/neurosurgery/Abstract/2011/07000/Emerging_Histomorphologic_Phenotypes_of_Chronic.20.aspx

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2945234/

Thalamus Damage and Persisting Concussion Symptoms Radiology. Tang L, Ge Y, Sodickson DK, Miles L, Zhou Y, Reaume J, Grossman RI.

http://www.cdc.gov/Concussion/

Comments

  1. Great series Jack! I wish ALL parents, coaches and athletes as well as MD's would read this and follow your guidelines. So many lives can be saved or improved!

  2. Are you including whiplash injuries in this category? It seems to me that they would be closely related. Even if the brain does not directly receive a blow there could still be shearing, certainly the spinal cord must have some sort of shearing injury. Thanks for the great blog.

  3. So, in the grand scheme of things, how bad is MSG for the average person who isn't involved in contact sports or employed where a concussion is likely? I eat a pretty good paleo diet, so I thought, but MSG seems to be in everything! It's in the canned beef stock I use, in my bacon, in my whey powder.

    Great series! I hope this is getting out to doctors who can use it in practice.

    • @Tim In the grand scale of things I think it should be pretty obvious. For years no one has been able to find any experimental causes of ALS, AD and PD etc…….now along comes this data from athletics due to chronic trauma and we have perfect correlation of what we see in cases that have no trauma. The link to both is the use of excitotoxins. The concussed athlete gets these disease much earlier and sooner because their pre existing brain injury concentrates the glutmate and aspartate at the injury site. The damaged neurons cant clear the collected excitotoxins so they are able to inflict the damage to the neurons mitochondria right there. Science has always had a difficult time understanding how ALS, HD, PD seem to affect certain fiber tracts and not others. Now we know…….this is where glutamate and aspartate receptors are found biologically in high amounts.

      The take home if this series was not clear………if you eat this stuff and have a concussion your are toast in your fourth and fifth decades. This is precisely what we are seeing in many professional athletes. The third post in this series shows you the ages they got these diseases. Belak was not even 35 years old! Moroever, for people like you without a brain injury……my belief is you're toast too but it may not get you until your older because you did not face the concentration effects of the injury. The disease pathology and pathophysiology is the same. You need to avoid this crap like the plague in my view. If your a diabetic and you use a lot of low carb foods with artificial sweeteners and MSG compounds you are throwing gasoline on the fire of Alzheimer's. We already know that T2D carries a very high risk of developing AD…….I think this is part of the reason why the numbers are so daunting.

  4. @Deb……been getting lots of emails about this series. It seems that many of my friends and current patients who are athletes who have this risk are sending this link to the them. Many dont want to publish their comments and I can understand why. But this information is critical for the younger athletes and parent of these kids. They need to know how they can help their kids when most of the answers are it "just needs time to resolve" I dont accept OK…….I want optimal.

  5. Wow! making even more sense. I took a bad fall in 2002. I am 5'10" and was on roller skates and fell straight down on my tail bone. I started having major problems from head, neck and shoulder pain to sleep problems, dizzyness, eye problems, trouble hearing, etc. No doctor could find anything wrong. I started the LR 11 weeks ago, but I still fell neurological problems. I really never thought it was that. I kind of pushed it off as not getting enough sleep and my body just not making the energy it needs. Where do I start from such an old injury?

  6. Great blog Dr. K! My 29 year old son has had a couple of head traumas over the years (fell on his head snowboarding at about 12; swimming under water and hit the edge of the pool at about 20; he and his girlfriend violently bumped heads recently; and he was in a minor fender bender this year and his neck hurt afterwards). He has seen MD's and went to a concussion clinic in LA (where he lives) and they aren't taking it very seriously. He is doing acupuncture for the pain in his neck. His neck often hurts. His maternal grandmother has AD. Any suggestions for how he should proceed with this? Any recommendations for a good neurologist in LA?

  7. Dr. Kruse,

    I'm a little confused why glutamate from MSG is dangerous while the glutamate found in meat is not. It seems like, in almost any diet, meat would be a much bigger source of glutamate than MSG. I have no sciece background, so I'm guessing I've misunderstood some basic biochemistry or your posts, but, regardless, clarification would really be useful to me.

    Thank you.

  8. I found this on: http://www.truthinlabeling.org/FoodForThought_Lis

    Please delete this post if you think it's too long…

    - It is only amino acids that are free (outside of protein) when you ingest them that cause MSG-type adverse reactions.

    - Amino acids in protein (bound in protein) will not cause MSG-type adverse reactions.

    - MSG in organic products is just as toxic as any other source of MSG. There are a number of MSG-containing ingredients that have been given "organic" status by the National Organic Program. Organic or not, the MSG in all products is neurotoxic.

    - Protein powders are a prime source of MSG. They don't contain intact protein. They contain amino acids that have been freed from protein through a manufacturing process. They invariably contain neurotoxic (brain damaging), endocrine disrupting processed free glutamic acid (MSG) and neurotoxic, endocrine disrupting aspartic acid. Some, if not all, also contain neurotoxic L-cysteine.

    - Umami is the taste of monosodium glutamate that MSG sensitive people can't taste. If MSG has a taste of its own (umami), why aren't highly motivated MSG-sensitive people able to taste it?

    - MSG kills brain cells and causes a variety of adverse reactions. It doesn't matter if you call it "umami" or not.

    - The glutamate industry has a lock on the media. Not since the "60 Minutes" segment on MSG aired in 1990 has there been mention in any national media that MSG might be toxic.

    - Mercury in combination with MSG increases the adverse affects of MSG.

    - Obesity begins in the womb if mother is passing neurotoxic MSG to her fetus.

    MSG is more a political issue than a medical issue.

  9. Might-o'chondri says:

    Brain glutamate insult (among other factors) can cause endothelial reticulum (ER) stress &, in experimental rodents, alters the hippocampal neuron ER membrane. Glutamate hyper-excitation induces the release of ER calcium 2+ (Ca++) for nearby mitochondria to bring in through their Ca++ uniporter. The result is an altered mitochondria membrane potential from the ER stress (free Ca++ inside that cell is not the culprit in this dynamic). So the degree of ER stress shunting over it's specific level of ER Ca++ ( ER normally always need Ca++ inside the ER & have ways hold Ca++) is going to make that cellular outcome vary.

    Extreme mitochondrial membrane alteration can be pro-apoptosis (cell suicide) if cytochrome c is released from the mitochondria into that cell's cytosol and the cell doesn't abort the process. Excess glutamate increases that cell's risk because glutamate up-regulates the pro-apoptosis transcriptor CHOP (CEBP homologous protein). A less than fatal outcome for the cell could be mitochondrial membrane "leaking" out normally contained reactive metal ions to interact with cell cytosol ROS (ER also generate ROS because their oxidative protein folding needs electrons transferred to oxygen molecules) to form dangerous hydroxyl molecules that foster degenerative processes.

    Even if the ER stress is not drastic the resultant mitochondrial membrane deformation still impairs cell energy production. The loss of curvature in the mitochondrial inner membrane affects the mitochondrial proton trapping cristae. This electrical field normally has a higher potential gradient & micro-environment of extra +/- 0.5pH at the "tip" of an apex shaped cristae ; so any elongation of the membrane that a cristae snugs up to flattens the conformation, which means less efficiency. The loss in proton motive force from weaker electro-potential gradient is +/- 3.5 times less once get away from the ideal cristae apex curvature; that's a lot of less ATP energy being made to maintain that neuron's function.

  10. Dr K – I think it follows from this post that the so-called Mixed Martial Arts are all but DESIGNED to create CONCUSSIONS, as is boxing. This might explain the behavior of so many of the participants in MMA, and why they keep doing it – their brains are scrambled.

    • @Terrence I think it depends upon perspective. From your optic your post is spot on. I bet Randy Couture tries his best to avoid concussion with a great defense and a lethal offense. Those who are successful win the spoils of victory and those who lose get Alzheimer's disease. To me that seems like a big risk to benefit ratio but people seem to like to bet their nerves for cash I guess.

  11. Doctor Kruse: Coconut Oil seems to be something you feel should be taken in abundance from what i can tell from most of your posts. Perhaps a post on it along with recommendations as to daily consumption of it in recommended amounts for those with disease, LR, and once LS. Could also discuss MCT oil intake and coco manna etc.

    Thanks

  12. Hi Jack, thanks for your great blog!

    Please help me figure out the MSG in soya sauce issue. I have looked a lot online, but can't find anything :(

    I know that soya sauce has MSG, but if it is brewed naturally, is it still bad for you as synthetic MSG? Should we not eat soya sauce?

    Also, I'm not sure, but I think that home made bone broth can have MSG in it as well, is it also bad?

    Thanks for Jack and everybody else for reply.

    • @Anna K anything soy is no good. Home brewed bone broth is fine as long as you dont use any produced stock. Make your own.

  13. Excellent series of posts on craniocerebral injuries. I hope the medical community becomes aware of this information and uses it, especially in high school, college and professional sports. One of my colleagues, Dr. Mary Case, who is a neuropathologist and forensic pathologist, lectures on 2nd impact syndrome. This sydrome occurs when the brain is impacted while still recovering from a concussion. It usually results in fatal cerebral edema. Concussions are serious injuries.

    • @Bob I have personally seen two cases of second impact syndrome and both patients died of subdural hematoma. It is real and it can kill.

  14. Might-o'chondri says:

    Tissue trans-glutaminase enzymes are found in almost every cell, all over the human body; which indicates to me that we are designed to function with glutamine (and glutamate) in moderation. Humans have Ruthia bacteria in our oral cavity with glutamin edo-peptidase enzymes that help us degrade glutamine; and glutamine can be processed for ATP, with glutamino-lysis in various tricarboxylic acid cycle steps.

    A commentator's link refered to how fermentation and hydrolysis of many foods makes glutamine more biologically available, and implicitly thus more problematic. Hydro-lysates of some foods afford us increased action of angiotensin converting enzyme inhibition (ACE inhibitor); this is neurologically beneficial since high blood pressure increases cognitive impairment .

    (Al i had to edit this here for completeness…….in most neurodegenerative diseases there is an impairment of CPP so these patients require high MAP to perfuse their brains. Your comment is directed at normal brains. This series is about the abnormal ones! Dr. Kruse)

    Select Aspergillus variety (mycellial) fermented soy in Japan called "Touchi" and in China "Douchi" undergoes hydrolysis and is considered to act as an ACE inhibitor. Asian researchers also cultured soy with Monascus purpureus finding the byproduct had ACE inhibition properties.

  15. More troops mild brain trauma diagnosed – USATODAY.com:

    http://tinyurl.com/64nkpdc

  16. Here's another link in regards to msg in MREs as well as aspartame use. The ALS connection seems pretty convincing.

  17. Link didn't post first time.

    http://www.msgtruth.org/al

  18. Might-o'chondri says:

    2009 details ALS "Amyotrophic Lateral Sclerosis" in full article online http//www.ncbi.nlm.nih.gov/pmc/articles/PMC2656493/?tool=pubmed

  19. Might-o'chondri says:

    edit, link above needs colon after http to work; use http://www.ncbi.nlm.nih.gov/pmc/articles/PMC26564

  20. @Al. The data grows daily……Steve Gleason of the Saints just got diagnosed with ALS. Another victim.

  21. Might-o'chondri says:

    Non-neuronal involvement in ALS (as opposed to the motor neuron dynamics) merits mention for the role of glia cells (astrocytes and microglia) in the pain; there seems to be a re-organization distinct from the non-pathological pain dynamic. The astrocyte factor in pathological pain may (?) also be applicable to Gulf War Syndrome's wide range of pain patterns (ex: diabetic neuropathy) and other chronic neuro-inflammation conditions.

    Astrocytes, when "insulted" (traumaticly &/or inflammatory) will express too much iNOS (inducible nitric oxide synthase) that activates pro-inflammatory cytokines (like IL-1beta, IL-6, & TNFalpha); these types of cytokines' phosphorylation of the NMDA receptor accentuates any pain transmission. The end result is "sensitization", whereby the pain experience rewires to the chronic neuropathic state of hyper-algesia; and to be precise IL-1 & 6 are not the cause of pain in non-pathological pain experiences.

    IL-10 is intriguing since it is experimentally shown to alleviate neuropathic pain and I think (?, can't readily cite it) in ALS ; it is should be noted that there are receptors for IL-10 only on the glia cells and not on neurons. Which makes me wonder if the ability of certain bacterial peptidase enzymes to hydrolize dietary proteins into bio-active peptides that stimulate T regulatory cells to produce IL-10 can be incorporated into our diet. (A Lactobacillus paracasei strain peptidase hydrolizes the main milk allergen Beta-lactoglobulin into peptides that stimulate IL-10 output. Has anyone heard sufferers report that simple Kefir quark makes them feel less pain ?)

  22. Might-o'chondri says:

    ALS stem cell trials imminent at Mass. General Hosp./U. Mass. Med. Sch. for BrainStorm Cell Therapeutics' "NurOwn"; developed over 10 years, takes patients bone marrow stem cells to differentiate into astrocyte-like cells that release neurotrophic factors. (Research published in Stem Cell Review & Reports.)

    • @ Might-0-chondrial I am aware of these trials. I still think the clearance of excitotoxins at the footplate of the astrocytes is most critical. Replacing just the stem cells will do nothing if we dont figure out how to increase excitotoxin clearance from the newly developing neurons. The best way we know of now is to avoid excessive excitotoxin use.

  23. majkinetor says:

    M-Al dude, where are you. Why did you remove all your posts from WHS ?

    Anyway, there seems to be some patent describing use of soy kefir for pain (see google scholar). Its also reported to be beneficial with stomach pain. One of the reasons might be that its effective helicobacter antibiotic (See Kefir Improves the Efficacy and Tolerability of Triple Therapy in Eradicating Helicobacter pylori [by 30%]).

  24. Paul Adams says:

    Dr. Kruse,

    I wish I had read this about 40 years ago. I am 61 now and have had several serious head injuries.One at 20 that was combat related and another when I was hit by a drunk driver while crossing the street while in graduate school. Both injuries required extensive tissue debridement. On top of these two, I have suffered approximately 6 other concussions due to sports injuries. The combat injury left me with a seizure disorder that is controlled by phenobarbital. All attempts to change to other AEDs were unsuccessful. So to use your terminolgy, I guess I am "toast."

    • @Paul Do not ever give up. You need to make sure your progesterone and DHEA level are rockstarish with that history. Eat an excitotoxin free ketogenic paleo diet and optimize your hormones and I bet you come back in one yr and thank me. You can have more than you got now. I also would tell you phenobarb can cause osteoporosis so see if they can change off to keppra or something else…..if not take high dose Vitamin K2 and D3. Read my current osteoporosis blog on this area……

  25. Paul Adams says:

    Dr. Kruse,

    Thanks. I won’t give up (haven’t yet) but it gets frustrating. I do have osteoporosis. Found out after a minor fall about 4 years ago left me with a fractured pelvis and broken arm. Had to do all my own research to find the cause. I have several vertebral wedge fractures and a crush fracture.I have been on HRT since I found out about the osteoporosis but it’s been a challenge. Phenobarbital catablizes T, raises SHBG and aromatase. Even taking 200 mg. of test cyp IM weekly and .5 Arimidex 3 x weekly, my T levels are subpar and my estrogen stays high. I tried Keppra, Zonegran and Lamictal. Lots of seizures. The last time I was tested my progesterone was high normal but it varies. I take no progesterone supplements. My physician says DHEA can raise estrogen levels so I stopped supplementation.

    I did read your osteo blog and it is great! I’ve been taking high dose D2 (50,000 IU 3 x weekly) for a while per my physician’s directions and K2 on my own (but only 100 mcg. per day). After reading your blog, I plan to increase to 5 mg. per day. Been eating Paleo for a while but not ketogenic. Do you have any further advice? I really appreciate it.

  26. The Cost of Concussions

    By Jean Rickerson of http://www.sportsconcussions.org

    Nicholas Harris, 17, was allegedly sent back into a junior varsity football game last year in Medford, Oregon, after telling his coaches he had sustained a concussion.  That could cost the Medford School District $585,000, according to a lawsuit filed by his mother on Oct. 17.

    In Pittsburgh, Pennsylvania, Megan Alt says her son's cognitive disabilities are the result of him being forced to play while concussed, by Highlands School District football coaches.  Her lawsuit, filed in federal court in April 2011, cannot specify a dollar amount but is in excess of $75,000, says her attorney.

    Concussion-related lawsuits, particularly at the high school level, get a bad rap.  In an unrelated case involving a high school player who required brain surgery, I watched the media coverage, talked to community members, and perused the comments in their local newspaper after this student's lawsuit was announced.  Overall, the public's view was quite negative, many believing that the boy's family should be held solely responsible because they had allowed their son to play football, an inherently dangerous sport. Most felt that the school district and coaches were not to blame.

    Right now, with the adoption of new concussion laws pertaining primarily to youth athletes, no one really knows what the legal ramifications will be.  But what I do know is that the impairment can be very real.  I know too many teenagers who have participated in a variety of sports -not just football – who have dropped out or postponed college, dropped out of high school, or are just looking for some relief after years of suffering from post-concussion syndrome.  They need help, and in some cases, compensation. 

    In Harris' case, the lawsuit states that he was struck in the first quarter of the game and then again in the second.  He told his coaches after the second hit that he thought he had a concussion, but was allegedly told to keep playing and was returned to the game.  Shortly afterward, he was struck for a third time, suffered a seizure, and lost consciousness.  Taken by ambulance to the hospital, Harris was placed in a medically induced coma and admitted to the intensive care unit. According to the lawsuit, he suffered brain damage, along with post-concussive seizures and other symptoms.

    Zachary Alt, now 19, is unable to work a full day due to numerous concussions he suffered as a varsity fullback in 2007 when he was a 15-year-old sophomore, according to the complaint. That season he suffered at least three concussions within the span of a few weeks, the last one when he was put back in the game after wandering "aimlessly" on the field from a previous hit.  He has no recollection of his last block.  Taken to the hospital, he was diagnosed with a significant concussion.  Even though he missed much of the following semester and struggled with his schoolwork he was given straight-A's and graduated on time. The case is being heard in federal court on grounds that Alt was denied the right to an education. Alt's suit names the school principal, assistant principal, football coach, and athletic trainer as defendants.

    My own son's non-catastrophic injury cost nearly $25,000, and we did nothing over and above the accepted standard of care.  Several ambulance transports, three ER visits including an evaluation at a regional trauma center, imaging, and post-concussion care lasting several months, all added up.

    For those athletes that require overnight hospitalization or surgery, the financial burden on the families is tremendous.  Shoring up medical coverage on insurance policies or spending a few extra dollars on secondary coverage is a wise move.  As our trauma care bills started rolling in, I was glad we were "over-prepared," realizing now, there is no such thing, particularly if you have a child involved in contact sports.

  27. Dr. Kruse,

    I am dealing with serious effects of excitotoxic damage to the hypothalamus. I strictly avoid MSG, etc. and find that I am even sensitive to homemade bone broth.

    You wrote on another blog that L-glutamine is fine, but the couple of times I tried it (for gut repair), it messed me up. Does this make any sense to you?

    What I am really confused about is whether I should be wary of NAC. I started taking it a couple of days ago with vitamin C in order to increase glutathione, but if it can also cause excitotoxicity I will stay far away.

    Thanks so much for your time.

  28. Dr. Kruse,

    Thank you for all of your help so far.

    Beyond what you have written in this article, if one is having an excitotoxic episode, is there anything that can be done or taken to stop it in its tracks?

    Again, I have discovered that excitotoxicity is deeply involved in my disease and may even be the primary factor. By being extremely careful about what I eat I have kept things mostly under control, but occasionally I will eat something — and I am not talking about food additives, only whole paleo food or sometimes a supplement — that sets my brain on fire and causes further damage. Excess calcium and glutamate seem to be the main problems, but I still have a lot to learn, and yesterday I made another mistake.

    This is a disaster when it happens. It does not just set me back a few months — it damages me worse than before and leads to serious new pathologies. I consider it a true emergency and would head to the ER if I thought that they would be able to help.

    I have learned a lot on the internet, primarily from the autism community, about things that supposedly reduce glutamate toxicity or protect from excess calcium, but I have not yet found anything that works reliably.

    I know that you cannot diagnose over the internet. I simply want to ask, have you found anything to be effective?

    • @MM I think my CTE RX is pretty clear. Lots of coconut oil is what I would do as a preventative method. MAke sure the brain has a ton of DHA/EPA and no PUFA and lower insulin levels and higher levels of dietary D3 and K2 and Vitamin A

  29. Dr. Kruse,

    First, Thanks a lot for this information it is really enhancing my research for a paper I am doing on sports Concussions in my College writing course.

    Second, I am a sophomore in college and I was just reading the comments regarding MSG and I was just curious what your advice is for a college student trying to eat healthy? I realize I might not be able to eat super healthy for these next few years I am relying on a cafeteria to feed me, but what should I try the hardest to stay away from? I do make some Mcdonalds trips with my roommates when we are desperate and not financially equipped to eat healthy and I realize that probably is not the best, but when it comes to trying to stay away from the worst while I am in College, I was just wondering what your thoughts were?

    Thanks,

    Shane

    • @shane avoid grains a PUFA like the plague…….and MSG and artificial sweeteners. If you must eat grain fed beef try offsetting it with supplementing fish oil and Vitamin D

  30. What would be prognosis for 65 year old lady (not over weight;on statins 2 or 3 years – a sigh) who has had skiing accidents in last 3 years (injured back), fractured arm) and now two weeks ago she had a concussion with loss of consciousness… (she has also survived breast cancer)?

  31. Dr. Kruse,

    My son (now age 16) had a series of 3 concussions, seems that one of them was quite rough, but healed up for six months after concussion dr visits. Then he started having liver pain and major symptoms like concussion that no dr could put together. We found multiple bacteria (bartonellas, babesia, lyme) and parasites finally, but the treatment with pharma of these made him more violent and sick. We have been working with a naturopath for 9 mo now who has gotten his body less toxic, but still has many symptoms.

    I figure that this diet would help, but what else can we do? He doesn't want to see any more drs, and has lost hope. Please advise. Thx.

    • @Cathy you tell him for me he has no choice……if he does not get this fixed now his life is going to be one nightmare after another………now is the time to take action. You are the parent……..his participation is directly under your control. He has no options unless you give him some. Stop being a friend and lay the law down. He is too young and immature to make this life decision. And what ever caused the concussions he better avoid until his brain is fully mature at 25 years old. If he has Lyme etc on top the concussions treatment should make him sicker……its called a Herxheimer reaction and the doctor treating him should have told you all that.

  32. Thx for the quick response–but we would make him go to a dr if we felt we could find one that would put the picture together for us. We have been to drs in PA, NJ, & FL who all said they could help (gave hope) and then threw their hands in the air after a few months. Yes- the concussion chiro (cranio-sac) did make him more ill, so we had to stop going there too as we work against the bacteria to minimize the herx. Do you think that the diet will change his outlook enough to get back to a good dr–and how do I find one that understands the hell we are going thru without adding to it? He simply can't tolerate any pharma drugs, as he feels like they make him crazy…

    Thx SO much!

    • @Cathy to me the diet is his best Rx. HE also needs to avoid all trauma and all excitotoxins like artificial sweeteners.

  33. THX SO MUCH!

  34. Dr. Kruse – I have been following your Leptin Resistance Rx for five days. Three days ago I fell and hit my head on the corner of a low shelf and got a mild concussion. I went to the ER yesterday and they said no need for C-T, and that I would be having the nausea/dizziness/ear-ringing for the next week. They said to come back if anything gets worse. I am continuing to eat and follow the LR Rx, is there anything else I should be doing? I am getting the impression that the concussion discussed here is bigger, and athletic-based? I am wondering though if I should insist on a C-T, or what your suggestions are. Thank you so much in advance!

    • @chasmyn. I dont think you need a CT but you better not eat any wheat or artificial sweetners after this incident! Any concussion is very serious.

  35. Dr. Kruse,

    This is Cathy, mom of the 16 yr old boy from a few posts back–We started the keto diet 3 days ago and he feels awful! His head is spinning, he feels very agitated and angry, and he always feels hungry. Help!

    • @Cathy it will take time for him to adjust…..but he should not be hungry. You need to up the protein content of his meals with bacon or some other meats. We generally cook two packages of bacon an AM and eat it like jerky additions to any meal. He could do the same with deviled eggs too.

  36. He is allergic to eggs and dairy. He has had lots of protein with each meal-mainly that is the meal- for instance 2 turkey burgers and a small side salad, or bacon with a small salad, etc. Including MCT oil on salads, cooking in coconut oil. Drinking only water. I have done Atkins before so I can''t believe he was still hungry after all that protein! What could be happening?

    • @Cathy……turkey is not what I call high quality protein. Too many omega 6's Grass fed meat, offal, fish…..lots of fish. If he is allergic to dairy can he tolerate whey? With his history the reason he maybe hungry is because he cant assimilate the protein. The proof would be low B12, folate, and betaine with constipation. If that happens you need to consider starting him on betaine HCL tabs before he eats. And then re evaluate.

  37. Thank you, Dr. Kruse. No worries about my eating wheat or artificial sweeteners – I'm a Paleo girl from here on out. I read "Wheat Belly" recently after a 3 month fling with wheat and sugar (after eating GF/no grains/sugar for 2 ears) and there is no way I am ever eating wheat again. My mother has cerebellar ataxia and the chapter in that book on CA alone was enough to scare me straight (and I was reading it for he science behind my weight gain!)

  38. Souldanzer says:

    I think I’m in pretty good shape… no carbs in 24hrs when accident happened, 600mg mag several hours before and after, unfortunately didn’t know about taking CO right after injury. Exposed my head to 26 degree air temp/snow until ski patrol got me. Ice pack in my neck for most of the time since I managed to get one in the ER.

    Took some CO this AM, more mag, CTed, more ice on my head, and am heading for cryotherapy session in a bit. I’m in a constant state of shivering… anything to save my brain cells.

    Thx for getting this info out into the world. I got lucky b/c of leptin rx… this would have been much worse if I had been dosed up on sugar and mag depleted, I’m guessing.

  39. Dr. Kruse,

    I attended a presentation last night given by a local Neurosurgeon & ND’s team doctor on the subject of concussions. Not one word on nutrition & when I asked that question they looked at me like I was from Mars. Is not rest, proper “brain food”, and CT the best way to really heal from a concussion? Thanks for any thoughts.

    Larry

Speak Your Mind

*

Please Note: The author of this site is not engaged in rendering professional advice or services to the individual reader. The ideas, procedures, and suggestions contained within this work are not intended as a substitute for consulting with your physician. All matters regarding your health require medical supervision. I shall not be liable or responsible for any loss or damage allegedly arising from any information or suggestions within this blog. You, as a reader of this website, are totally and completely responsible for your own health and healthcare.
x
Are you a doctor or Health Care practitioner? Join our Platinum Klub SIGN UP NOW