Category Archives: Auto Collision Injury

Objective Signs of Spinal Cord Injury After Rear-End Collisions

Nerve damage from auto injuriesOne of the challenges of understanding auto injuries is showing the jury proof that the clients injuries are real. Any objective proof that whiplash is a real phenomena is critical in getting your clients the care they need and the compensation they deserve.

A new study1 from Northwestern University adds some important new information in our understanding of the anatomy and physiology of auto injuries. In this report by Elliott et al, the researchers performed MRI of the cervical spine and legs, with particular focus on the muscle fat of the neck and calves, and the motor pathways of the spinal cord. The patients also had the strength of their plantar flexors tested as a measure of their central nervous system function.

In previous studies, researchers2,3 have found that patients with automotive-related neck injuries showed signs of fatty infiltration of the muscles of the. Other research4 by the same authors has found that patients with neck pain but with no trauma did not have signs of fatty infiltration, indicating that nerve injury is the cause of the phenomena.

The authors of this paper sought to corroborate that research and to see if there was a correlation between MRI findings, pain, and nerve function in the rest of the body.

The study was small: only three patients with auto injury pain were examined and one control patient who had been in a 10 mph auto collision, but who had fully recovered three months after the crash. The patients who were in pain had reported symptoms lasting between 3.5 months and 3 years; these patients had significant disability from their injuries.

The authors found the following when comparing the patients to the recovered subject:

  1. The subjects in pain had a significantly higher amount of muscle fat in the cervical spine: 30% for the injured subjects vs. 10.5% for the pain-free subject.
  2. The patients in pain had a dramatically higher percentage of fatty infiltration in the legs compared to the recovered subject: 15.6% muscle fat vs. 7.6% muscle fat.
  3. The patients suffering from pain had significantly reduced plantar flexor strength: a reduction of about 40% compared to the healthy subject.
  4. All three patients with chronic pain showed signs of decreased myelin in the spinal cord that were consistent with spinal cord injuries.
  5. “In all three chronic cases we found that the expression of lower leg muscle fat infiltration corresponded to altered cervical spinal cord pathway integrity and reductions in the ability to maximally generate plantar flexion torques and muscle fatigue.”

The authors conclude:

“These findings provide preliminary evidence to suggest that the expression of neck and lower extremity muscle fatty infiltrates and reduced central activation in this small sample of patients with chronic WAD could very-well be the result of an initial mild injury involving the spinal cord…”

While this is a small study and needs to be replicated with a larger group of test subjects, this article confirms a number of important findings:

  1. Auto injury patients with chronic pain show objective indications of nerve damage in the cervical spine.
  2. The effects of this nerve damage can alter muscles and nerve function in the lower extremities, in this case affecting plantar flexion strength.
  3. MRI of the muscles of the cervical spine can be effective at documenting fatty infiltration.

Again, this study had a very small number of test subjects, but it does provide more evidence that there are real, physiological changes associated with chronic pain in auto injury patients.

  1. Elliott JM, Dewald JP, Hornby TJ, et al. Mechanisms Underlying Chronic Whiplash: Contributions from an Incomplete Spinal Cord Injury? Pain Medicine 2014;Aug 19.
  2. Elliott J, Pedler A, Kenardy J, et al. The temporal development of fatty infiltrates in the neck muscles following whiplash injury: An association with pain and posttraumatic stress. PLoS ONE 2011;6:e21194.
  3. Elliott J, Sterling M, Noteboom JT, et al. The clinical presentation of chronic whiplash and the relationship to findings of MRI fatty infiltrates in the cervical extensor musculature: a preliminary investigation. European Spine Journal 2009;18(9):1371-8.
  4. Elliott J, Sterling M, Noteboom JT, et al. Fatty infiltrate in the cervical extensor muscles is not a feature of chronic, insidious-onset neck pain. Clinical Radiology 2008;63(6):681-7.

Ligament Damage After an Auto Injury

Our understanding of whiplash injuries has grown impressively over the last 10 years, when the first detailed analysis of spinal mechanics was done. From countless studies, we’ve seen that the human neck experiences an abnormal motion during a rear end collision, and that the facet joints of the spine can be sprained during such collisions.

Now a new study has looked more closely at what happens to the neck, but this time by studying the anterior ligaments of the spine. Previous studies have shown that some patients experience injuries to the anterior longitudinal ligament after whiplash. This new report by leading whiplash researchers used a sophisticated mathematical analysis (based upon experimental anatomical and crash data) to see what happens to the ALL during a crash.

Anterior longitudinal ligament
The anterior longitudinal ligament runs along the front of the human neck, providing stability for the vertebrae of the spine. During a rear end collision, this ligament can become sprained, resulting in pain and even chronic degeneration of the spine.

The human spine model was subjected to three different collision speeds: 5.3, 6.7, and 8 mph. The amount of distraction, or displacement at each vertebral segment was analyzed.

The researchers found that as the speed increased, the amount of strain increased and the time of the peak distraction also occurred earlier in the motion.

The authors report a number of findings that are relevant to those who work with whiplash cases:

  • The ALL reached stretches that were near the failure rate of the ligament, at collision speeds of just 8 mph.
  • Injuries that don’t result in failure may be even more difficult to diagnose, since they will be virtually undetectable on plain film radiographs.
  • The anterior ligaments of the spine have been shown to have pain receptors. Sprains or tears of the ALL can cause referred pain that can affect adjacent areas of the spine.

The authors summarize some of the potential serious, chronic problems that can result from these types of injury:

“A possible clinical implication associated with ALL injury is cervical instability. Catastrophic injury of the ALL can result in acute disability while sub-catastrophic injury may lead to chronic pathology. Injuries to the ALL had the highest correlation to extension instability. However, that study also indicated high correlation of ALL injury to axial rotation instability and anterior column injury to lateral bending instability. Injuries produced experimentally in that study were similar to clinically observed injuries. Anterior cervical injuries sustained in whiplash are typically distractive extension stage 1 injuries resulting in an absence of neurologic abnormalities. These injuries are not visible using conventional radiographyand result in cervical instability. The ALL is intimately connected to the annular fibers of the intervertebral disc. Presuming all sub-components of the intervertebral motion segment are normal prior to injury, subcatastrophic failure of the ALL (stretch) will likely result in chronic changes within the disc as a result of decreased extension stability. The added hypermobility may lead to spinal disorders such as early degeneration of the connected intervertebral disc or vertebrae. In addition, segmental hypermobility leads to long-term instability. Catastrophic failure of the ALL in a whiplash injury will almost inevitably result in simultaneous injury to the intervertebral disc, and is likely to require surgical intervention.”

This study shows that the anterior ligaments of the spine undergo potentially injurious motion and that this motion may lead to long-term disability. For patients who have experienced a rear-end collision, it is advisable to get a thorough diagnosis to determine cervical instability and the potential for spinal degeneration years later.

Stemper BD, Yoganandan N, Pintar FA, Rao RD. Anterior longitudinal ligament injuries in whiplash may lead to cervical instability. Medical Engineering & Physics 2006;28:515-524.

TMJ Disorders Cause Teeth Grinding and Headache, Study Finds

TMJ Disorders Cause Teeth Grinding and Headache, Study FindsDamage to the temporomandibular joint is known to cause a long list of problems and medical complications in patients with temporomandibular disorders, or TMD. Former research has linked TMD with fibromyalgia, and studies have also demonstrated that TMD patients are at risk of chronic headache, just to name a few associations.

To further our understanding of pain and complications related to TMD, researchers recently analyzed the association between TMD, sleep bruxism, and primary headaches in patients with injuries in the jaw and pain in this crucial joint. Sleep bruxism, which is excessive grinding of the teeth and clenching the jaw while sleeping, as well as certain types of primary headache, were found to be mutually associated with TMD.

The study included 301 TMD patients aged 18 to 76. Researchers examined each patient, classifying their TMD using the Research Diagnostic Criteria for Temporomandibular Disorders, diagnosing possible bruxism using clinical criteria from the American Academy of Sleep Medicine, and diagnosing headaches according to the International Classification of Headache Disorders-II.

Patients with painful TMD were found to be at risk of migraine and tension-type headaches. The highest association was between TMD and chronic migraine. Participants also were diagnosed with episodic migraine and episodic tension-type headache, associated with pain in the temporomandibular joint.

Researchers also discovered that sleep bruxism was prevalent in patients with both painful TMD and chronic migraine. They found that patients with both painful TMD and sleep bruxism were significantly more likely to suffer chronic migraine, episodic migraine, or episodic tension-type headaches.

Jaw symptoms are common among patients with whiplash injuries. However, jaw pain often does not appear immediately after a crash. The long-term effects may not be immediately realized for victims of auto injuries who are affected not only by jaw pain, but also debilitating headache and tooth-damaging grinding. This is why research that demonstrates the connection between TMD and damage to the cervical spine is so important. Patients who sustain whiplash injuries have the potential for a whole host of health problems down the road, and this should be considered when assessing the damage caused by a collision.


Fernandes G, Franco AL, et al. Temporomandibular disorders, sleep bruxism, and primary headaches are mutually associated. Journal of Orofacial Pain 2013; 27(1): 14-20. doi: 10.11607/jop.921.

Mechanisms That Cause Chronic Whiplash Pain

Mechanisms That Cause Chronic Whiplash PainWhiplash is a multi-faceted type of injury and the subject of a great deal of scientific research and discussion. There are dozens of ways that whiplash can manifest depending on the type and location of the injury, the victim subjected to the injury, and the specific factors and severity of the crash, in addition to other variables.

A recent research review, published in The Journal of Forensic and Legal Medicine, attempted to analyze a wide array of current data to provide some insights about the mechanisms that underlie whiplash injury developing into chronic pain.

The author of the study, Dr. Charles Davis, referred to whiplash-associated disorders (WAD) as “a wide variety of clinical manifestations.” Indeed, because whiplash injury can damage bones as well as soft tissue, victims of whiplash can suffer a great variety of different symptoms.

Researchers have traditionally distinguished acute from chronic whiplash pain by using an interval of time of pain symptoms, usually either three months or six months since the collision. But what happens biologically to whiplash victims that develops into a chronic condition?

Dr. Davis looked at what happens when the whiplash injury activates pain receptors in peripheral nerve endings called nocicpetors. These neurons can send pain signals throughout a person’s body through the spinal cord, and tissue injuries can release chemical reactions that exacerbate the sensitivity to pain stimuli even further.

Other factors identified in the study as possible causes of chronic WAD involved central sensitization. Dr. Davis cited that whiplash has been shown to damage the facet joint and the intervertebral disc, which can result in an overall pain sensitivity in the nervous system and spinal cord.

This sensitization creates an abnormal perception of pain in some whiplash patients. But even this is manifested in different ways. Some experience a spontaneous, continuous pain (described as “burning” or “aching”); some experience spontaneous, intermittent pain (described as “stinging”); others suffer from abnormally evoked pain from touch or movement, meaning either an overreaction to normally painful stimuli or pain produced by normally non-painful stimulation.

Whiplash can also result in inflammation in the soft tissue, which produces its own type of pain. To help the injured area heal and repair, the patient’s sensory nervous system can go into overdrive responsiveness, making pain feel exaggerated or prolonged.

Other types of pain are even more difficult to pinpoint and may be present without any inflammation or structural damage to the nervous system. The study cited cases of neuropathic pain, sensory hypoesthesia, mechanical allodynia, and chronic cervical radiculopathy. Among these, there is evidence that different pain-processing mechanisms are underlying causes.

In addition, muscle fatty infiltrates that develop after a whiplash injury may contribute to the vulnerability of a subsequent injury and the risk of posttraumatic stress disorder in whiplash patients.

In the study’s conclusion, Dr. Davis highlighted the usefulness of animal experiments for additional data about whiplash-injury mechanisms. He also urged that patients with whiplash injuries be assessed with proper imaging and quantitative sensory testing. He wrote that if injury to the discs, facets, or upper cervical ligaments are found, it is unlikely the patient will recover spontaneously and will likely develop chronic symptoms. He also said that patients with a nociceptive type of pain may be difficult to treat, and that neuropathic pain is likely to cause hypersensitivity and a higher rate of pain and disability.


Davis CG. Mechanisms of chronic pain from whiplash injury. Journal of Forensic and Legal Medicine 2013; 20: 74-85.

Evidence of Whiplash Hyperexcitability to Pain

Evidence of Whiplash Hyperexcitability to PainIt has long been noted that whiplash seems to cause widespread sensitivity to pain in some chronic patients. About half of people who suffer from whiplash-associated disorder (WAD) continue to report pain and disability one year after their injury. Many experts believe that these long-term effects are due to lasting damage to the spine and central nervous system as a result of a whiplash injury. A growing body of research supports these claims, including a recent study confirming a link between whiplash and pain hypersensitivity and another study that demonstrated a possible relationship between whiplash and emotional sensitivity to trauma.

Researchers at the Center of National Research on Disability and Rehabilitation Medicine in Australia conducted a systematic research review to make determinations about sensory hyperexcitability to pain stimuli, lowering the pain threshold and increasing “excitability” of the reflexes in chronic WAD patients.

The study authors selected 13 research articles and conducted a full review and a meta-analysis of all the data. This data reflected results from research on 483 WAD patients and 334 health controls. The tests that study-participants had been subjected to included pain threshold data involving pressure, cold, and heat; Nociceptive Flexor Reflex threshold (which tests spinal cord excitability); Electrocuaneous Stimulation; Brachial Plexus Provocation; and cold and heat detection thresholds.

The results of the review demonstrated significantly lower pain thresholds and reflex thresholds among the whiplash patients compared to healthy controls, present both in the injured area of the body as well as in other body parts far from the injured area. They also found that WAD patients demonstrated less ability to detect heat and cold when subjected to detection testing, compared to controls. Researchers said that these results were indicative of damage to the central nervous system processes. They concluded that their results supported the involvement of central hyperexcitability in chronic WAD.

The study team also found that some of the quantitative sensory testing that had been used may not be reliable, due to the scattered and inconsistent results in this meta-analysis, especially Pressure Pain Threshold, which they suggested may not be an optimal test for future studies to use. They wrote that cold and heat, Nociceptive Flexor Reflex tests, and Electronic muscle stimulation may be stronger measures to determine pain thresholds. However, these tests, in addition to the other tests in the study that may be more reliable options, are limited because they have not be used extensively. Further investigations using these methods will be needed in independent settings to determine the most reliable clinical testing.


Stone A, Vicenzino B, Lim E, Sterling M. Measures of central hyperexcitability in chronic whiplash associated disorder- a systematic review and meta-analysis. Manual Therapy 2013; 18: 111-117.


Is the “Fight or Flight” Reponse on Overdrive in Whiplash Patients?

Is the "Fight or Flight" Reponse on Overdrive in Whiplash Patients?Up to half of all patients with whiplash develop chronic symptoms but scientists are still uncovering why. Earlier research has suggested that posttraumatic stress disorder may play role, since WAD patients with PTSD tend to have worse recovery. Despite the connection between PTSD and whiplash, few studies have analyzed the underlying biological mechanisms behind this link.

Some researchers have hypothesized that PTSD may activate the sympathetic nervous system. The sympathetic nervous system is a part of the autonomic nervous system that controls stress and the body’s “flight or fight” response. After a traumatic auto accident, it’s common for patients to develop post-traumatic stress disorder. The stress, negative emotion, and thoughts related to PTSD may activate the sympathetic nervous system into a perpetual “flight or fight” response. It is hypothesized that this activation of the sympathetic nervous system affects the descending pathways, or the nerve pathways that allow the brain to control the rest of the body, which causes additional pain and emotional distress.

To test this hypothesis, researchers from Belgium studied autonomic stress responses in 30 patients with chronic whiplash and 30 health controls in a new study. The participants agreed to rate their pain scores during two test designed to measure pain sensitivity. In one test, the participants reported their pain while having pressure applied to their backs. In another test, participants wore an inflated cuff that squeezed tightly around their arms at varying levels of pressure. During the tests, the researchers looked for signs that the sympathetic nervous system was being activated in the participants by monitoring the heart rate variability and skin conductance, or the reflex that controls sweat.

Whiplash patients perceived pain more intensely than the controls during the tests, indicating their increased pain sensitivity. But despite this pain sensitivity and poorer disability scores, their heart rate variability and skin conductance was essentially the same. Even in the 33% of patients who did have PTSD, there were no signs of increased sympathetic activation. The authors concluded that these findings refute the hypothesis that there is a stronger sympathetic response to acute pain in chronic whiplash patients.

While more research is needed to confirm these preliminary findings, the study brings us closer to understanding the connection between chronic whiplash symptoms, hypersensitivity, and PTSD.



Koonig M, et al. Autonomic response to pain in patients with chronic whiplash associated disorders. Pain Physician 2013; 16:E277-E285.

Texting Behind the Wheel Now Biggest Killer Among Teen Drivers

Texting Behind the Wheel Now Biggest Killer Among Teen Drivers
Photo by Intel Free Press

Texting while driving has officially surpassed drinking and driving as the leading cause of death from motor vehicle collisions among teenagers.

The number of teen deaths and injuries as a result of texting and driving crashes has reached new highs as more and more young people use mobile devices.

According to researchers at Cohen Children’s Medical Center and the Centers for Disease Control and Prevention, the estimated number of teen deaths from texting and driving is 3,000 per year, compared to around 2,700 who die after driving drunk. The number of injuries is also greater among those texting compared to those drinking, with 300,000 texting-and-driving injuries and 282,000 drinking-and-driving injuries.

In addition to the increased numbers of phone users, the data is also a result of a dramatic decline in drunk driving among adolescents. Additionally, drinking is typically a behavior that most teens engage in only occasionally, while texting is a daily activity.

A team of researchers at Cohen Children’s Medical Center also found about 49% of boys and 45% of girls aged 15 to 18 admitted to texting while driving. They also discovered that older teens were more likely to engage in the risky behavior, with 58% of 18-year-olds acknowledging that they do it regularly.

Typing and engaging in texted conversation is especially dangerous compared to other distracted driving habits. The activity involves manual, visual, and mental distractions, all at the same time.

Adolescents aren’t the only drivers endangering themselves and others with mobile devices. Other research has found that up to one-third of adult drivers aged 30 to 64 admitted to sending text messages while driving.

Another recent study revealed the ineffectiveness of laws prohibiting texting and driving among adolescent drivers. Comparing states with laws to states without them, researchers found an insignificant difference in the numbers of teens taking the risk.


Ricks D. Study: Texting while driving now leading cause of death for teen drivers. Newsday May 8, 2013.

Increasing Seat Belt Use for Teen Drivers

Increasing Seat Belt Use for Teen Drivers
Photo courtesy of State Farm

Motor vehicle crashes remain the leading cause of adolescent death in the United States. Teens have higher collision rates and a decreased likelihood of using seat belts compared to older, more experienced drivers.

In a new study published in the journal Accident Analysis & Prevention, researchers tested the effectiveness of a service-learning program in teaching teens better seat belt habits. The educational intervention was conducted in eleven high schools across the U.S. in the 2011-2012 school year.

Direct observation of students wearing seat belts both before and after school was used during the fall semester to create a baseline of seat belt use. After the service-learning intervention, seat belt use was again observed in the spring semester for comparison.

After the service-learning program, seat belt use increased 12.8%, from 70.4% usage in the fall to 83.2% usage in the spring. The increase in using seat belts was noted among white, black, and Hispanic teen drivers. However, researchers found that black and Hispanic teens were still less likely to use seat belts compared to white drivers.

The study found that female teen drivers were significantly more likely to be influenced by service-learning and use seat belts than their male counterparts. It was also discovered that the teens who drove with passengers in their vehicle had an increased likelihood of seat belt use.

The authors of the study concluded that a service-learning intervention can be effective for increasing the use of seat belts. They recommended that high schools utilize curricula continuously incorporating service-learning about safety and seat belts.

Additional research has sought areas of needed improvement for teen safety in motor vehicles. One such study revealed the prevalence of risky driving behaviors among teens. Another found that almost 43% of adolescents admit to the dangerous habit of texting and driving.

Education about safe driving shouldn’t stop at drivers’ training courses. Parents can help their teens make safe choices behind the wheel by communicating and revisiting the topic often.


Godzweig I, Levine R, et al. Improving seat belt use among teen drivers: findings from a service-learning approach. Accident Analysis & Prevention 2013 May 21 (online only). doi: 10.1016/j.aap.2013.04.032.

Whiplash Causes Driving Difficulties After Injury

Whiplash Causes Driving Difficulties After InjuryPeople with chronic whiplash-associated disorder (WAD) often report that they have difficulty driving after the collision that left them injured. Among other problems caused by WAD, the result can be inconvenience and a decreased quality of life. Driving is one of the tasks that most adults take for granted. But WAD-victims may not have that luxury.

To explore the reasons that contribute to driving difficulty after whiplash, researchers recently analyzed the physical, cognitive, and psychological factors that may contribute to troubles with driving.

The study involved 40 patients with chronic WAD. Participants self-reported their driving difficulty, using a measurement tool to indicate the magnitude of difficulty and pinpoint the contributions associated with the trouble driving. Researchers adjusted the results to measure factors other than the obvious ones: neck pain and dizziness. Their goal was to discover if other variables came into play to keep WAD- victims from getting behind the steering wheel. Their list of possibilities included reduced speed of head rotation, gaze instability, eye-head coordination, cognitive symptoms like fatigue, and psychological problems like traumatic stress, depression, fear of neck movement, and fear of driving.

The study found that chronic WAD resulted in both physical and cognitive impairments that can possibly harm a patient’s driving ability and enjoyment. Researchers concluded that self-reported driving difficulty goes beyond neck pain and dizziness for WAD victims.

These results are consistent with other research tying psychosocial factors to whiplash symptoms and recovery. In one recent study, scientists discovered that a positive attitude could have a more favorable outcome for whiplash recovery than a negative one. Additionally, research has shown that post traumatic stress disorder often accompanies chronic whiplash-associated disorder and discovered that cognitive-behavioral therapy significantly improved symptoms of PTSD as well as whiplash neck disability.

Whether struggling to drive a car or being forced to quit working, chronic WAD can harm a person’s quality of life, all too often with long-term results.


Takasaki H, Treleaven J, Johnston V, Jull G. Contributions of physical and cognitive impairments to self-reported driving difficulty in chronic whiplash-associated disorders. Spine 2013 May 21. [Epub ahead of print].



Saving Children’s Lives with Booster Seat Laws

Saving Children's Lives with Booster Seat Laws
Photo by V Kanaya, Creative Commons

At a national conference, the American Academy of Pediatrics (AAP) presented compelling research in support of mandating booster seat use in all states. It was discovered that state laws requiring booster seats at least until age eight were associated with fewer fatalities and severe injuries in motor vehicle collisions. Presenters argued that standardizing the law throughout the country would help protect many more children.

The AAP recommends that parents use booster seats to secure their children in vehicles, optimizing the proper positioning of the seat belt. The suggestions have changed through the years, with both the size and the age of recommended use increasing. Currently, the AAP recommends a booster seat for children under four feet, nine inches tall, which is usually reached between eight and 12 years old.

Right now, it is up to each state to write booster seat law. Some have laws that reflect the AAP recommendations, but others set age allowances, only requiring a booster seat until the age of six or seven. Still other states do not have any booster seat laws in place.

The study referenced at the AAP conference was published last year in the journal Pediatrics and included data collected between 1999 and 2009, comparing fatality and serious injury rates in states before and after booster-seat litigation. There were nearly 10,000 fatalities and incapacitating injuries in children aged four to eight during the study period. The children between four and six years old were 20% more likely and children between seven and eight were 33% more likely to die or be incapacitated in an auto collision if they lived in a state without booster laws.

The children in the study who were only restrained by a seat belt had drastically increased odds of fatality or severe injury.

The study authors, in addition to the American Academy of Pediatrics, now recommend legislation to standardize booster seat regulations and to extend the current laws to older children to optimally protect them while riding in motor vehicles.


Boston Children’s Hospital. Standardized booster seat laws could save lives of children. Science Daily 5 Nov 2012.

Mannix R, Fleegler E, et al. Booster seat laws and fatalities in children 4 to 7 years of age. Pediatrics 2012; 130(6): 996-1002.