QuestionYour reponse to Jessica in her 04/07 question regarding her car crash was very informative. In her case, I believe, Jessica's car was rear-ended. I was wondering if you could comment on the physics involved if you are in the car that rear-ends another car. I don't remember enough physics myself.
I ask this question because I was involved in an accident in 2004 which has left me on disability with Post Concussion Syndrome. Now I'm suffering from cervical spine problems in the C5-6 and C6-7 areas. I've lost 3/4 inch since the accident which the doctor says is osteoarthritis.
The brakes in my Chevy Suburban failed catastrophically (right front rotor braking surface separated from the hub) and I rear ended a tractor trailer. The tractor trailer was stopped. The estimated speed on impact was 15-20mph. The airbag in my vehicle did not deploy (the ambulance crew that got me out expressed surprise at that).
The trailer did not have the traditional underride guard. Rather it had a solid re-inforced metal shield that extended to 1-1.5 feet above the ground. It was the front portion of a double. The entire nose of my car was pushed in 6 inches or more. I kind of feel that the weight differential was significant.
All I remember is my body lifting out of the seat on impact and my back and head hitting the seat and headrest. The ER said they looked for a concussion, but I don't remember it. Actually, I don't remember much detail of my trip to the ER, being in ER, etc. All I knew was my neck and back hurt and my chest really hurt from the shoulder harness. I did tear my right rotator cuff as a result.
Thanks,
John
AnswerDear John,
First, you may want to print this out...it is lengthy and somewhat complicated in places. However, I think you will get the big picture which is what really matters.
While the physics is important, the anatomical responses are the most important aspect to discuss. The kinematic response of the occupant (driver/passenger) of a car that is the striking vehicle is different than in a rear impact. First of all at impact, your body is decelerated in the forward direction rather than accelerated. This is due to your body's inertial movements (Newton's first law of motion)...as the truck you were driving almost immediately stops, your body continues forward at the same speed until it is halted by the restraint system or you hit the vehicle interior.
When you make contact with the restraint system it acts to allow a small stretch which does permit your body to slow somewhat, and this helps to actually reduce injury. But, then the restraint system will lock to prevent you from ejecting through the windshield. At this point, your torso is halted as your neck continues in the forward direction (a force movement called shear..joint damage can occur as well as ligament damage)until it reaches the anatomical limitations of the tissue and begins to flex forward. As the head pitched forward, the spine will be elongated which is called axial tension (ligaments and muscle will limit this tension). This abruptly changes to axial compression and this is where the joint spaces can be jammed together for a second time. Now...this is a simplistic explanation of the how the body reacts.
As far as post concussion syndrome is concerned, yeah, I see this often with car crash patients. This is much more common that you think, and you can have a concussion without losing consciousness at the scene of the crash. Often the effects are more pronounced a day or two afterward and can be missed in the hospital ER or by EMS. I actually help lecture to the EMS class at our local college, and have been informed that EMS rarely check for concussion at the scene of a crash, and the ER commonly does what is called the Glasgow Coma scale which will also frequently miss concussion. The fact that you have difficulty remembering it all corroborates mild traumatic brain injury, and by the way, rotator cuff injury is also common in auto crashes.
Below I am going to copy my office explanation and protocols for mild traumatic brain injury/post concussion syndrome for you to read...please realize that some of the information is complicated and may be difficult to understand as it is written for health care professionals.
Hope this helps John.
Respectfully,
Dr. J. Shawn Leatherman
www.suncoasthealthcare.net
Traumatic Brain Injury/Mild Traumatic Brain Injury/Concussion
Motor vehicle trauma is the single most important factor in both fatal and mild brain injuries. Early reports ranged from 40% to 60% caused by motor vehicle crash (MVC) with concussion being the most common diagnosis given. (15,27,57) More recent accounts report MVC as the origin of 60% to 67% of all occurrences. (1,21) Many of these MVC-related injuries are the result of blunt head injury, which describes contact with some object without penetration of the skull, such as striking the steering wheel, dash board or the B pillar of the doorframe. However, it has been shown that non-contact concussion is a common result of acceleration type injuries. The term of choice today is traumatic brain injury (TBI) or mild traumatic brain injury (MTBI). (15)
Mechanism of Injury: Previously thought to be a direct shearing of axons, the actual mechanism is from abrupt acceleration and deceleration of brain tissue. (39) The initial shear effect creates the activation of a degenerative cascade. During a low speed whiplash injury, (7 mph) the head may be accelerated at 9-18g. (58) Since the brain is a soft structure, shear strains are created as the outer part of the brain moves at a different pace than the inner part of the brain. This is intensified as the momentum of the head changes rapidly in a sagittal direction during a whiplash trauma, and when head impact occurs inside the vehicle. The most important factors in whiplash-induced concussion are angular acceleration, flexion/extension of the neck, and increased intracranial pressure gradients. (40,41,52)
Animal studies confirm the real issue of induced concussion from acceleration/deceleration even though animals did not lose consciousness. (32,33) Portnoy et al. reported that significant increases in intracranial pressure were measured in baboons exposed to whiplash. Examination discoveries included suprascapular intramuscular hemorrhages. (47) Hemorrhages were not from contact. Acceleration, deceleration, and shear were mechanisms of injury. Non-centroidal motion in the coronal plane was found to be the most injurious and non-centroidal acceleration in the sagital plane to be least injurious concerning brain injury. (22,38,56) Although this infers that lateral whiplash motions of the head are more likely to produce concussion or diffuse axonal injury (DAI) than frontal or rear impacts, MTBI and DAI have been found in both types of collisions.
According to the work of Hinoki, the integrity of the brainstem reticular formation is largely responsible for maintaining levels of consciousness. A study by Jane et al. proved conclusively that non-centroidal accelerations of the head (without contact) could produce damage to axons in the inferior colliculus, pons, and dorsolateral medulla, which are in close proximity to the reticular formation. (25) The authors discussed the previous work of Povlishock et al., who presented the pathogenesis of DAI. Their proposed mechanism of trauma is not necessarily an immediate shearing of axons, but rather a reactive degeneration secondary to trauma. (48,49) Others have corroborated this concept of continuing degeneration, such as Gennerelli, in statements that MTBI should be considered a process rather than an event. (21). In addition we know that the spinal cord becomes stiffer as rates of strain increase, therefore creating a higher susceptibility to injury. (5)
Pathophysiology: The precise nature of DAI is thought to be a reactive swelling of damaged axons and capillaries throughout the brain (29,48,49) 揇irect brain trauma results in intra-axonal changes in the 68-kd neurofilament subunit which then loses its alignment and interferes with axoplasmic transport. This causes axonal swelling and eventual disconnection. The neurofilament change may be the result of either direct damage to the cytoskeleton or a biomechanical event that results in neurofilament disassembly. The temporal progression of those events is related to the severity of the injury? (16,42)
At time of injury, the brain is subjected to massive depolarization from acceleration/deceleration, and tissues are damaged due to shear currents/forces that increase intracranial pressure and mechanically deform axons. It is postulated that such events terminate with neuronal death involving the production of free radicals, and tissue acidosis. (6,7,53) In 1997, Connor and Connor showed in the American Journal of Clinical Nutrition that free radicals amplify inflammation by up regulation of genes that encode for pro-inflammatory cytokines and adhesion molecules. It is known that free radicals damage lipids, proteins, membranes and DNA. (2,8,13,18,19,28)
Micro hemorrhages develop between 12 and 96 hours post injury, arachadonic acid is released, CSF lactic acidosis is present, and lipid peroxidation occurs from membrane disruption and squalor. Free radical scavengers such as large doses of antioxidants and iron chelators have been proposed as therapeutic devices. (59) Antioxidant supplementation as well as Omega III fatty acid supplementation, (DHA-docosahexanoic acid & EPA-eicosapentanoic acid), inhibit the degradation of tissue by the reduction of oxidative stress. Oxidative stress is due to free radical damage, arachadonic acid production, lipid peroxidation/degradation, prostaglandins (pge2), and leukotrienes. (9,10,11,20,24,31,34,46,51,54) In particular, bioflavonoids play a significant role as they have been proven to act as intracellular and extra cellular antioxidants, reduce platelet aggregation, repair damage in vessel walls and have anti-inflammatory action. (12,14,17,30,35,36,44,45,50)
Even in relatively mild brain injuries, an excessive release of excitatory neurotransmitters such as acetylcholine and glutamate, contribute to the pathologic neuronal apoptosis (cell death) in the brain. The results are permanent deficits! MTBI can produce diffuse reactions in cerebral metabolic activity and can disrupt the blood brain barrier allowing an increase of excitotoxic effects. (6,7,23) Recent research affirms that brain injury leads to increased glutamate release, which in turn activates the NMDA (N-methyl d-aspartate) receptor in cortical neurons allowing an increased calcium influx. (26) This channel complex contributes to excitatory synaptic transmission at sites throughout the brain and the spinal cord, and is responsible for neuronal plasticity. When continually activated neuronal death and chronic pain may result. Specific areas known to be vulnerable to injury include the parieto-occipital lobe, the temporal lobe, amygdala, anterior frontal lobe, and para-sagital sinuses. (43) Antioxidants, magnesium and omega III fatty acid supplementation all inhibit circulating Excitotoxins and down-regulate the NMDA receptor.
Post concussion syndrome (PCS) can develop after MTBI. Posttraumatic headaches are exceedingly common residuals, and may last for years. (55) First headaches begin with a concussion and can continue for weeks or months. The head usually hurts where the head is struck if blunt force trauma was the mechanism of injury. Etiological factors in posttraumatic headaches are blunt head trauma, 57.3%, whiplash, 43.6%, Object hit head, 13.7%, other, 13.7%, and body shaken, 9.4%. (3) It has been suggested by one of the preeminent experts in this area that patients suffering from recurrent post-traumatic headaches or other elements of the PCS should be treated for migraine. (37) Other symptoms of PCS are as follows: Dizziness: Light headedness, vertigo and nausea, which is caused by injury to the semicircular canals, changes in endolymph or perilymph pressure, or direct damage to the vestibular cochlear nerve. Serious symptoms of hearing loss such as hyperacusis may occur as the result of damage to the actual hearing mechanism. Cranial nerve and brain dysfunction: Disruption of smell and taste, information speed and processing, attention, articulation, memory, new information acquisition, reaction time and sleep disturbances such as lethargy, drowsiness, and fatigue are common sequelae. (4)
**In relation to the research above, Suncoast Healthcare Professionals uses nutritional supplementation to decrease the cyto-toxic attack on neuronal tissue after resultant concussive episodes. Due to the fragile nature of brain tissue as well as the physiological makeup, it is evident that nutritional supplementation is paramount in the treatment of mild traumatic brain injury post motor vehicle trauma. The application of ant-inflammatory and antioxidant agents should be utilized initially and sequentially for a minimum period of 6 months post injury. Our office procedures and this supplementation is in line and adapted from protocols used in hospitals for the preservation of brain tissue after concussion, coma, transient ishemic attack and strokes, as well as brain surgery.**
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