WHIPLASH INJURY WITH NEUROLOGICAL SIGNS AND SYMPTOMS OF TBI or MTBI?
A STEP-WISE PROCESS FOR GETTING YOUR LIFE BACK!
Hello, I’m sorry this is a really long read. I had a rear-end collision a little over a year ago, my head had been turned to the left looking at the driver from the passengers seat. We were at a complete stop and this truck rammed our small car going the speed limit from behind. I had my seat belt on, but my head swung really far forward as I slammed into the seat belt, and then slammed right back. I was crying and in pain, though my boyfriend was fine. I went to the emergency room and they ran some x-rays and said I was fine, that it was a “low-impact” collision and I’d be sore for a few days.
They gave me some muscle relaxants for two days and said I’d be ready to go to work after that. I had been laying down those two days so I didn’t feel too bad, then I went to work and it was excruciating. I had to leave work and call out for the week. I went back to work and worked REALLY slow, sitting down a lot and not bending my neck. It was painful but I figured I was still sore. Then the pain in my neck and head continued for the next year but I figured it was tension headaches from stress since they said it was low impact and I’d be fine.
But after almost a year it got so bad, I’d constantly find excuses to go to the bathroom or stand in a dark place to lean on stuff. Light and sound became so overwhelming I’d feel like I was having a panic attack. I ended up quitting my job and went into the hospital for a mental breakdown, again thinking this was all just stress. The pain has progressively got worse, and over a month ago it got so bad when I went shopping that my vision was blurry, I was dizzy and disoriented and in so much pain in my neck and head that I couldn’t walk straight or see.
I ended up going to the chiropractor figuring I was just really out of alignment and needed adjusted. It helped somewhat though I was extremely dizzy and nauseous and in pain after the adjustment, they told me I’d just be a bit sore the next few days. And it did seem to be somewhat better, the huge knots in my neck lessened, but it got bad again real quick. After my third visit he took some x-rays to see what was up and he said… something was torn (he motions at a tendon/ligament or something that went across my neck at the base of my skull) The curvature in my spine/neck was completely gone, though nothing was deteriorated since I am still young. He also told me I’ve had two “pseudo seizures”, after the pain in my neck and head got so excruciating.
My body and mind can’t focus on anything else (it feels like blades from my neck to the front of my head, and like a hydraulic presser is squeezing the front part of my brain). I went to the ER again and again they said it was stress induced and I just needed to “relax and calm down”, and that it wasn’t a medical emergency, ignoring my indication that my head and neck hurt so bad. I’ve been hopping around clinics and hospitals ever since trying to find who I need to go to about fixing this this.
Do I need physical therapy? Is there some specialist I need to see? I’m so lost and everywhere I go seems to send me somewhere else. I’m on muscle relaxers and take a friends Fiorinal (to try to keep the headaches at bay), I’ve resorted to rubbing in cannabis oil in my neck/back, I’m using lidocaine roll on from the drugstore, and have a $50 neck/back heating pad, but all I’m doing is scrambling to treat the symptoms and want to fix the root of it. What should I do?
You certainly hit the nail on the proverbial head when you said that all you are currently doing is treating symptoms. Recognizing this is the first part of actually getting better — getting to the root of your problem. Be aware that what you’ve been through is typical — tests, x-rays, SCANS / MRI, etc…. And then the drugs — lots of drugs, usually from the family I call THE BIG FIVE.
There are several factors that make this impact worse for you. Firstly, I am not sure how hard the impact was, but the fact that you were stopped and they were doing the “speed limit” suggests that they were going between 35-45 mph, give or take, if the accident occurred in town. Everyone knows that high speed rear-enders cause severe problems — it’s not news. However, the internet is replete with studies on these “low speed impacts” as yours was described — many of which pertain to impacts of 10 mph or less; the sort of thing that occurs in a parking lot. Just remember that it’s not just about the speed differential between your vehicles, it’s about the mass differential as well. In other words, a big pickup truck hitting a Toyota Prius is likely to cause much more injury than the other way around, even if the accidents occurred at identical speeds.
Also, it is important to realize that the two biggest injury-magnifiers are being female (especially a tiny female) and not being aware of the impending impact. This is widely reported throughout the peer-reviewed literature, and has been for at least twenty five years. And while seat belts can certainly save your life, they can actually make the whiplash worse by holding your body in place while your neck and head whip violently. In other words, the biggest part of the impact is forced through your neck instead of being dissipated by the rest of your body.
Let’s not forget about still another of big injury-magnifiers taking place in this accident — L’s head was turned at impact. The head is designed to be put into a great deal of flexion and extension (forwards and backwards movements) as well as rotation (the ability to turn both right and left). However, it is not nearly as adept at lateral flexion (the ability to tip your ear toward your shoulder). To see why this is a big deal, first tip your head backwards. Now turn your head as far as you can either right or left and then tip it backwards. Bottom line, everything else being equal, a rear-end impact when the head is turned is going to potentially tear lots more tissue than if the occupants are looking straight ahead.
Speaking of tearing tissue; part of the problem is that in most cases the damage (“tearing”) done is subclinical. What do I mean by this? Only that because there is often times no overt damage seen in imaging studies it is assumed (at least by many doctors and all insurance companies) that you are malingering — faking to garner a settlement. When you tear connective tissues such as LIGAMENTS, TENDONS, and especially FASCIA, (or for that matter, MUSCLES), the tearing is not usually “tearing” as we think of the word being used. What I mean is that the tissue is not typically torn in half; it’s torn microscopically — at the cellular level. The medical community actually has a name for the process that occurs after the tear. FIBROSIS. If you want to actually see what this looks like, HERE is a short video.
Fibrotic tissue (I usually refer to this as SCAR TISSUE rather than fibrosis) is bad news because despite the fact it cannot be imaged with MRI (HERE), it’s potentially more than 1,000 times more pain sensitive than normal tissue — this from a tissue that when healthy is widely touted as the most potentially pain-sensitive in your body. And from here it gets even more interesting. If you look at my COLLAGEN SUPER PAGE you’ll see that I have included the various phases of healing. Even though insurance companies will tell you that the healing process takes place in 6-8 weeks, you can see for yourself that this is absolutely false. The final stage of healing — the remodeling phase, where the tissue is made more elastic and stronger — lasts as long as two years or more.
Beyond the obvious tissue damage, L has obvious neurological damage as well. The tipoff? Language like blurry vision, dizziness, disoriented, couldn’t see, couldn’t walk straight, can’t focus, seizures, light sensitivity, sound sensitivity, headaches, panic attacks, and nervous breakdown that she uses to describe her problem. Just for the heck of it, I plugged these terms into Google as is, and after articles about temporal lobe epilepsy, Valium withdrawal, and brain cancer, I came to a page called Facts About Concussion and Brain Injury. Needless to say, her list encompasses many of the classic symptoms of TBI (TRAUMATIC BRAIN INJURY), sometimes referred to as MTBI (Mild Traumatic Brain Injury).
As far as where to go from here, I must start by saying that post-adjustment extreme dizziness and nausea are both red flags. There are probably certain kinds of adjustments you could tolerate very well (Atlas Orthogonal, Activator, various soft tissue techniques, etc, etc, etc), but any kind of adjustment that heightens the symptoms of your head injury more than very briefly should be discarded for something else. As to the whole “something is torn at the base of the skull” thing; not really sure what your chiro is talking about there (if it were the Transverse Ligament of the posterior odontiod there is no way he would consider adjusting you). Let me just tell you what I would do clinically if a similar scenario had happened to one of my THREE DAUGHTERS.
The first thing to remember is that after an accident like this, you are working against a clock. What I mean by that is that numerous studies show that if you are not “well” or at least significantly improving at 30 days, 60 days, and 90 days, your odds of becoming chronic increase dramatically. Bottom line, THE MOST CURRENT RESEARCH on whiplash is saying that as many as 1 in 2 people injured in an MVA, progress to chronic. Do whatever it takes not to become a statistic.
Because the first few days of the process constitute the “INFLAMMATORY” portion of the healing process, this would be a good time to use cold therapy. And because addressing diminished RANGES OF MOTION is so critical to the long-term prognosis, as long as they can be tolerated, massage, GENTLE ADJUSTMENTS, and simple range of motion exercises need to be added as well. If you can tolerate these things, you can move on to the NORMAL PROTOCOL. If you cannot, there are a couple of things you must do.
Firstly, you need to treat your problem as though it were systemic because as I am going to show you, it likely is. Violent impacts and head injuries are big deals for many reasons. However, one of the biggest — a reason that seems to not be talked about much in the mainstream medical community even though there are mountains of peer-review backing this assertion — is that head injuries lead to autoimmunity. Let me take a moment to show you the mechanism as well as some of the other issues that can occur along the way.
- CAN WHIPLASH CAUSE TBI / MTBI PART I? An article in Harvard Magazine called The Traumatized Brain began by talking about an individual who had been in a rear-ender accident, going on to describe the millions of Americans with similar problems as having symptoms that, “extend well beyond the physical injury and can unfold over long periods of time. Unlike the damage resulting from a stroke, which is often localized to one part of the brain, traumatic injuries often affect many areas of the brain in sometimes unpredictable ways.” Neurosurgeon dot com says in an article called Whiplash that, “Whiplash injury is the most common injury resulting from car accidents. Whiplash injury symptoms are often chronic problems that persist for years. Microscopic research has shown that irreversible nerve damage can occur even when the head does not strike an object, but instead is only shaken violently as in a whiplash incident. Even in a low speed rear impact collision of 8 mph, your head moves roughly 18 inches, at a force as great as 7 G’s in less than a quarter of a second. The Discovery space shuttle is only built to withstand a maximum of 3 G’s. The force that an accident victim is exposed to is generally two and a half times greater than that which the vehicle is struck. Rapid change in the spinal fluid result in pressure damage to nerve fibers because the forces that occur during a rear impact happen too fast to allow normal fluid exchange.” And in case this was not clear enough…..
- CAN WHIPLASH CAUSE TBI / MTBI PART II? An incredible study from a 2012 issue of Rehabilitation Research and Practice (Postconcussion Symptoms in Patients with Injury-Related Chronic Pain) showed that the most common injury — by at least two and a half times — that resulted in MTBI was whiplash from a car crash. It’s a great (free) study that has a bibliography with many similar studies, some from the early 1990’s. Another interesting study, this one from the July 2002 copy of the British Columbia Medical Journal (Purports of Brain Damage Following Presumed Whiplash Injury) went on to say that, “Mild traumatic head injury, with or without direct impact to the head, is a possible consequence of an acceleration-deceleration mechanism of injury (whiplash). Patients may present without a history of significant loss of consciousness and may not demonstrate any short-duration superficial loss of consciousness. Although there may be numerous short-lasting (days) somatic, psychological, or cognitive symptoms following mild whiplash trauma, a tissue damage cause, and a basis on which these symptoms may be demonstrated over a prolonged period of time (months), is a matter of controversy. Patients making claims of brain damage but without the prerequisite unconsciousness and peritraumatic amnesia should not be considered bogus…..” In other words, even though there are no great tests for showing soft tissue and related nurological damage, the damage is nonetheless there.
- DO MEDICAL FACILITIES ADEQUATELY DIAGNOSE, DOCUMENT, AND ADDRESS THESE INJURIES? I think we just answered this (there are only about a million studies on this topic), but I found a study I thought was interesting and helpful. At least two weeks post-accident, the September 2012 issue of The Journal of Emergency Nursing (Mild Traumatic Brain Injury: Are ED Providers Identifying Which Patients are at Risk?) looked at over fifty individuals who were diagnosed with whiplash or some sort of MTBI. “Between 1 and 23 MTBI symptoms were reported by 84.6% of the participants. Headache and fatigue were the most common; female patients had almost twice as many symptoms on average as male patients. Of MVC (motor vehicle crash) patients, 83.3% reported moderate severity scores for all 4 Post Concussion Symptom Scale categories, and these represented the highest overall severity scores. Emergency nurses need to be aware patients may have an MTBI regardless of their presenting symptoms or injury severity.” Bottom line, this is extremely common and is not being reported nearly as often as it should be. Many of the patients I see complain about essentially being “blown off” when the tests come back negative, which invariably they will.
- CAN WHIPLASH INJURIES CAUSE NEURO-INFLAMMATION? This is sort of a no-brainer because if there is an injury to the brain (MTBI) there will be some degree of INFLAMMATION. Four months ago, the journal Nature Reviews Neurology (The Far-Reaching Scope of Neuroinflammation After Traumatic Brain Injury) concluded that, “The ‘silent epidemic’ of traumatic brain injury (TBI) has been placed in the spotlight… Neuroinflammation can cause acute secondary injury after TBI, and has been linked to chronic neurodegenerative diseases; however, anti-inflammatory agents have failed to improve TBI outcomes in clinical trials.” I’ve shown you numerous times that THE BIG FIVE (NSAIDS and Corticosteroids included) are not therapeutic but only palliative. In other words, they cover symptoms without addressing underlying pathologies. BTW, with nearly 250 citations, this study’s bib is a goldmine.
- INFLAMMATION DISRUPTS THE BODY’S BARRIER SYSTEMS, AND MOST PARTICULARLY, NEURO-NFLAMMATION DISRUPTS THE BLOOD BRAIN BARRIER: There are over 10,000 studies showing that inflammation causes something called LEAKY GUT SYNDROME. But would you have guessed that neuro-inflammation can disrupt the barrier that keeps toxicity out of the brain — the BBB or Blood Brain Barrier? How big a deal is this? Last April’s issue of the FASEB Journal (Blood-Brain Barrier Dysfunction and Microvascular Hyperpermeability Following Mild Traumatic Brain Injury) concluded that, “Brain edema, elevated intracranial pressure and reduced cerebral perfusion pressure occurring in traumatic brain injury (TBI) are attributed heavily to the hyperpermeability of the blood-brain barrier (BBB).” This “hyperpermeability of the brain is widely known as “LEAKY BRAIN SYNDROME“. Furthermore, just a few months ago on his blog, Ivy League Neurosurgeon and researcher, David Younger, wrote that, “Treatment options have generally been lacking for the early syndromes and late presentations of TBI and the associated neurobehavioral and neuropsychiatric symptoms. With increasing recognition of the contribution of neuro-inflammation as a major mediating factor in animal models and human translational studies, there is the prospect for improving the understanding of the mechanisms of TBI, and developing therapeutic strategies to improve the outcomes of the millions of people affected each year. Systemic and neuro-inflammatory mechanisms result from disruption of the blood-brain barrier (BBB) that normally delimits its immune privileged status, at the time of, or after the insult, are important mediators of neurological outcome of TBI. The motor, cognitive, emotional, and psychosocial consequences of TBI can be devastating and long-lasting leading to deterioration of one or more domains of adaptive functioning, with loss of independent function and safe performance of activities. The associated symptoms and neurobehavioral changes can mimic the psychiatric manifestation of an endogenous psychiatric disorder.” Big words one and all, but just realize that the very symptoms we talked about earlier can be caused by inflammation / neuroinflammation.
- WHIPLASH-INDUCED NEURO-INFLAMMATION AND BBB DISRUPTION LEADS TO GLIAL CELL ACTIVATION: When we think of the brain, we think of nerve cells called neurons. The thing is, there are ten times more GLIAL CELLS in the brain than neurons. Activate large numbers of them and you have problems on your hands. Two years ago last month, the World Journal of Virology (New Advances on Glial Activation in Health and Disease) revealed that, “Astrocytes are the most numerous cells in the mammalian brain. In addition to being the support cells of the central nervous system (CNS), astrocytes are now recognized as active players in the regulation of synaptic function, neural repair, and CNS immunity. Astrocytes are among the most structurally complex cells in the brain, and activation of these cells has been shown in a wide spectrum of CNS injuries and diseases. Astrocytes respond to [are activated by] CNS trauma. After traumatic injury, stroke, infection, or other severe CNS insult, areas of focal tissue damage become filled with inflammatory, fibrotic, and other cells that derive from the perivascular cells, endothelia, bone marrow, and meninges. These tissue lesions become surrounded by reactive astrocytes forming glial scars that serve to separate necrotic from healthy tissue. Evidence has demonstrated that astrocytes contribute to sustained inflammation in the CNS after trauma or infection and growing research implicates sustained glial inflammation in neurodegenerative disorders. Chronically activated microglia and astrocytes can release reactive oxygen intermediates [free radicals], nitric oxide, and inflammatory cytokines, which are toxic to neurons. One mechanism by which astrocytes may contribute to sustained inflammation in the CNS is through upregulation of inflammatory pathways…. triggering a self-sustaining inflammatory loop and long-term glial activation.” Glial cells should be activated after an injury, but too much activation creates a viscous cycle of inflammation / damage / glial activation / repeat.
- CHANGES IN PERSONALITY ASSOCIATED WITH MTBI FROM WHIPLASH: I have included this bullet because it seems like L is already here or is headed here fast. A study from a 1996 issue of Brain Injury (The Spectrum of Emotional Distress and Personality Changes After Minor Head Injury Incurred in a Motor Vehicle Accident) started things off by letting readers know that, “This is a systematic presentation of the emotional and personality disorders of 33 patients who incurred minor traumatic brain injury (MTBI) in a vehicular accident.” What were some of these changes? I won’t go into it here, but suffice to say that almost anything you could possibly think of was on the list. Another study, this one from last September’s issue of BMJ Open (Psychological Impact of Injuries Sustained in Motor Vehicle Crashes) searched over 2,500 studies and concluded that, “Elevated psychological distress was associated with MVC-related injuries with a large summary effect size in whiplash associated disorders (WAD)… the negative psychological impact of a WAD injury is substantial.“
- WHIPLASH INJURIES LEAD TO NEURO-INFLAMMATION THAT CAN CAUSE AUTOIMMUNITY: Remember the neurosurgeon I spoke of earlier, Dr. David Younger? He said that, “the switch to a second wave of autoimmunity inherent in the adaptive immune response culminates in the infiltration by immune T-cells and B-cells across the disrupted BBB, with the production of antigen-specific antibodies. The importance of heightened cell-mediated immunity is in the possibility of immune reactivation by a subsequent injury such as another neuro-inflammatory stimulus or infectious process that subsequently reopens the BBB, exposing memory immune cells to self-antigens leading to a variety of post-traumatic syndromes.” The inflammation causes the gaps that make up the BBB to get bigger so that they let things through that should never get through (Leaky Brain). When the immune system sees various sorts of brain cells in the blood stream due to the injury, because they are not where they should be, the body recognizes these as foreign (antigens) and makes antibodies against and starts attacking. As you might imagine, this is not a good thing. By the way, Dr. Y concluded that, “Early and mild psychiatric symptoms following a TBI may be the best indicator of underlying neurophysiological, neurocognitive, and neuropsychiatric changes of altered brain pathology.” In other words, since standard medical tests don’t cut it, changes in behavior (psychiatric symptoms) offer as good a diagnostic tool as any. A great overview of this process can be found HERE or HERE.
- THE LIST OF AUTOIMMUNE DISEASES RELATED TO TBI / MTBI IS ALMOST ENDLESS: All one has to do is plug in the name of any AUTOIMMUNE DISEASE (HERE is a short list) alongside MTBI / TBI, and see what comes up. For instance, when I did that with MS, the first thing I got was a study from a 2012 issue of the Journal of Neurotrauma (Increased Risk of Multiple Sclerosis After Traumatic Brain Injury) that concluded that six years post-trauma, “patients with TBI are at higher risk for subsequent MS.” Why? Probably because studies like THIS ONE have conclusively shown that, “Impact-acceleration forces to the head cause traumatic brain injury (TBI) with damage in white matter tracts comprised of long axons traversing the brain. White matter injury after TBI involves both traumatic axonal injury and myelin pathology that evolves throughout the post-injury time course.” The axon is the long finger carrying impulses away from nerve cells and covered in myelin (an insulating material made by glial cells and known as “White Matter”) is the fatty covering of the brain and nerves.
- AUTOIMMUNE PITUITARY, HYPOTHALAMUS, AND OTHER ENDOCRINE ISSUES POST-TBI: A 2008 study from the European Journal of Endocrinology (Antipituitary Antibodies After Traumatic Brain Injury) stated plainly that, “This study shows for the first time the presence of the APA (anti-pituitary antibodies) in TBI patients 3 years after head trauma. Moreover, present investigation indicates preliminary evidence that APA may be associated with the development of TBI-induced pituitary dysfunction.” Another study, this one from the May 2015 issue of the Journal of Clinical Medicine (Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury) essentially said the same thing about the hypothalamus (a very important part of the brain as well). “Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI.” This is a huge deal because these two parts of your brain release the hormones that regulate the rest of the endocrine system (HERE). An article from the Feb 2016 issue of Medscape (Post Head Injury Endocrine Complications Clinical Presentation) stated, “Approximately 30-50% of patients who survive post–traumatic brain injury (post-TBI) demonstrate endocrine complications.”
- IMMUNE SYSTEM SUPPRESSION FOLLOWING HEAD INJURY: Part of the reason that people develop autoimmunity for any reason is because their TREGS (T-Regulatory Cells — the cells that keep the immune system in check and help prevent it from attacking itself) are themselves being suppressed. Thus suppressing TREGS causes autoimmunity. However, when the other part of the immune system is suppressed, you are likely to get sick as well; just in a different manner. Two years ago, Frontiers in Neurology (Traumatic Brain Injury and Peripheral Immune Suppression: Primer and Prospectus) said, “infections are a common occurrence in patients following traumatic brain injury (TBI) and are associated with an increased risk of mortality, longer length of hospital stay, and poor neurological outcome. Systemic immune suppression arising as a direct result of injury to the central nervous system (CNS) is considered to be primarily responsible for this increased incidence of infection, a view strengthened by recent studies that have reported novel changes in the composition and function of the innate and adaptive arms of the immune system post-TBI.” As an interesting side note to this point, be aware that IMMUNE SYSTEM SUPPRESSION is America’s number one form of medical treatment.
- CAN WHIPLASH LEAD TO SEIZURES? Because L was diagnosed with “Pseudo Seizures” it behooves us to answer this question. Although it is doubtful that L has developed epilepsy, the title of this study in a 2011 issue of Cardiovascular Psychiatry and Neurology (Blood-Brain Barrier Breakdown Following Traumatic Brain Injury: A Possible Role in Posttraumatic Epilepsy) makes us at least pause and think. Two months ago the journal Brain Disorders and Therapy published an abstract presented at the 3rd International Conference on Neurological Disorders and Brain Injury held in London saying that, “Abnormal EEG is 37% correlated with seizures and 20% related with memory loss. The patients who experienced seizures after the mTBI were six times more likely to have an abnormal EEG than those who did not experience any seizures.” Not sure that this proves anything, but is interesting nonetheless.
- MTBI AND ALZHEIMERS / DEMENTIA: A study from the Journal of Neuropathology and Experimental Neurology (Repetitive Mild Traumatic Brain Injury Augments Tau Pathology and Glial Activation…..) tells the story via its title. Just remember that Tau plaques are the junk that foul up the brain in ALZHEIMER’S DISEASE. Another study, this one from a 1999 issue of the American Journal of Epidemiology (Traumatic Brain Injury and Time to Onset of Alzheimer’s Disease) showed that the age that people developed Alzheimer’s Disease dropped if they had been exposed to an MTBI. In other words, they developed that disease at an earlier age.
Many of you reading this are no longer dealing with a simple whiplash injury (as if there really is such a thing). You are dealing with a TBI / MTBI that unfortunately, few people in the medical field really understand. This means that it must be dealt with as the systemic problem that it is (HERE). Which brings me to my second point. Because time is of the essence, once you see that things are not coming around but are headed south, it’s time to find a FUNCTIONAL NEUROLOGIST trained by Ted Carrick, and well-versed in the work of Dr. Datis Kharazzian.