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.

Self-Driving Cars: The End Of Auto Injuries?

The era of the automobile began about 100 years ago in the US, and currently there are approximately 250 million passenger vehicles in the country. While there have been many changes in terms of safety and efficiency in cars during that 100 years, the next change is going to dramatically change the landscape of our highways and cities.

This disruptive technology is the rapid development of the self-driving car. The current leader in this technology is Google, and here’s an interesting video that describes this fascinating technology:

Removing the driver from the driving equation creates a new world of freedom and changes to how we move ourselves from place to place. For instance, a self-driving car now opens up mobility options to those who are unable to drive now: the blind, the elderly, and the young. It may even revolutionize the concept of car ownership, as we may see fleets of self-driving cars that you can order online, show up at your doorstep, and drive you to your destination automatically.

A New Era of Safety

One of the most exciting aspects of self-driving cars is the enhanced safety of automated transport. Currently in the US, we spend about $870 billion a year on automobile collisions.

According the NHTSA, each year we see about 33,000 highway fatalities, 3.9 million injuries, and 24 damaged vehicles.

The vast majority of these crashes are due to human error that involve excessive speed, poor attention, poor reaction times, distraction, or drunken driving. According to Stanford Law School, 90% of auto collisions are due to human error. Self-driving cars offer a future with far fewer crashes, as we take humans out of the equation.

The question now is: how soon will the shift from human-driven to self-driving cars happen. Whenever you disrupt an industry (and especially one as entrenched as the American automobile), there’s going to be resistance. There are a huge number of issues that need to be resolved:

  • Liability. If we’ve removed human error from the driver’s seat…who is responsible when there is a crash? No system is completely safe, of course, and we’re going to see crashes that are due to software and/or hardware problems. When these inevitably occur, how do we assess responsibility?
  • The loss of control. The shift to self-driving cars is going to face a lot of resistance from some people. Many people like the feeling of control they have behind the wheel, and that’s going to be a powerful resistance to change.
  • Economics. Not every person is able (or willing) to go out and buy a new car. Currently, the average age of a car on the road is 11 years, so it’s going to be a while before we reach a critical mass of self-driving cars on our daily commute.
  • Federal regulations. The federal government isn’t known for being nimble, and so before we see self-driving cars at our local dealership, there’s going to be a lot study and research.
  • Privacy. Some people are going to be hesitant to own a car that will track their every move and destination.
  • Insurance. In 2012, State Farm Automobile Insurance reported $3.2 billion in profit. On one hand, insurance claims rates should drop precipitously with safer vehicles. It seems unlikely that the major insurance companies are going to excited about losing the cash cow of auto insurance!

Self-driving cars seem to be the future, but we’ll have to see what types of roadblocks and resistance we face during the transition.

Injuries from Side Impact Collisions

Since 1996, dozens of studies have been conducted on the biomechanics of rear end collisions, but only a few have been done on side impact crashes. Side impact injuries, however, remain a serious problem:

“The estimated annual incidence of automotive side impacts is 3.18 million in the United States. Between 10% and 18% of occupants involved in side impacts sustain soft-tissue neck injury.”

This new study is from the Yale researchers who have brought us much of the scientific literature on rear-end impacts, and they focus their expertise on side impacts in this report. Their goal was to quantify the risks of side impact collisions and compare them to frontal and rear-end crashes.

The authors subjected six human cadaver spines to side impact forces of 3.5, 5, 6.5, and 8g. These are forces that we would expect to see during low speed crashes of less than 8 mph. The normal anatomical motion of the individual vertebral segments was carefully measured before testing, and the injury motion was recorded during the side impact tests. The movement of the spine was analyzed after the tests to determine the motion of each vertebral segment.

The study determined Injury Potential for each joint, which was the increase in mobility of the joint after the test. For instance, an Injury Potentialof 100% means that the joint experienced twice the mobility after the test impact, indicating a severe stretching of the spinal ligaments.

The graph to the right illustrates the Injury Potential of the C6-C7 joint segment at the four different test accelerations.

As the graph shows, the C6-C7 segment shows a 25% increase in joint laxity at the small 3.5g acceleration. The Injury Potential rises rapidly to the 8g acceleration, where it reaches 107%.

The researchers found that at the 6.5g impact, injuries occurred from C4-C5 through C7-T1. The 8g impact found even more severe injuries to the joints in the same spinal segments, indicating that, as in rear-end impacts, the brunt of the trauma is found in the lower cervical spine.

Why is this? The vertebral segments below C7 have a more limited range of motion than those in the neck. When the torso is accelerated with the car seat, it tends to move more as a whole unit. This creates a tremendous amount of strain on those segments directly above T1—the exact area this study (and many others) have found to be the most likely to be injured.

The authors compared their findings in this study to other studies they have done on frontal impacts and rear-end crashes. They found that the human spine is most vulnerable in rear-end crashes, side impacts are the next in injury potential, and that frontal impacts require more force to cause injury. This correlates with a study that found, “of 3,014 occupants involved in automobile collisions…31% sustained neck injuries in rear impacts, 19% in side impacts, and 15% in frontal impacts.”

This study shows that the ligaments of the cervical spine can be stretched beyond their physiological range of motion after a low speed, side impact automobile collision. When patients have been exposed to this type of crash, it is important to obtain lateral flexion x-rays, which can help identify the injured spinal segments. Excessive laxity in the joints may indicate permanent disability in some patients.

Maak TG, Ivancic PC, Tominaga Y, Panjabi MM. Side impact causes multiplanar cervical spine injuries. The Journal of Trauma: Injury, Infection, and Critical Care 2007;63:1296-1307.

Faking Mild Traumatic Brain Injury

In the October, 1996, we reported on a study1 that found that college students could not convincingly mimic the symptom profile for whiplash injuries. A new study2 examined the ability of another group of college students to malinger either multiple sclerosis (MS) or mild traumatic brain injury (MTBI).

The authors effectively summarize the problem of malingering in their introduction:

“In recent years, researchers have been examining the ability of neuropsychologists to detect malingering. The detection of malingering is of obvious importance in the context of the limited resources available for those in need of medical and rehabilitative services. Its significance also is evident in the growing number of legal claims that follow injuries in the workplace, moving vehicle accidents, and other compensable circumstances. Clinicians are increasingly being called upon to make judgments regarding the effort and performance of litigating clients.” 2

In this current study, 69 college students were divided into three groups: a group that was to malinger MS; a group that was to fake MTBI; and a control group that was asked to simply take the tests without faking any condition.

The malingering students were in turn divided into two more groups: one set of students were given an informational packet about their “condition,” and another group given no information. All of the subjects were given five minutes to plan their strategy for faking their condition.

All of the students were then run through a battery of neuropsychological tests used to measure MS and MTBI in legitimate patients.

Upon studying the resulting data, the researchers reported some interesting findings:

  • There was no significant difference between the students who were informed or uninformed about the condition they were to fake. Being informed about the condition did not assist them in malingering.
  • There was no significant difference between the MS and MTBI group of students—they all faked their conditions in the same manner, with no distinction for condition. For instance, both MS and MTBI have particular patterns of neuropsychological findings: “On measures of conceptual reasoning, the literature predicts significant MS population deficits but little or no deficits in the mild TBI population…On measures of span memory/attention, the literature predicts difficulties in the mild TBI groups yet no impairments observed in the MS groups…” None of these distinctions or patterns were found in the students asked to malinger these conditions.
  • The students consistently exaggerated the possible dysfunction and number of symptoms, as compared to what a group of physicians considered appropriate for the particular condition.
  1. Wallis BJ, Bogduk N. Faking a profile: can na�ve subjects simulate whiplash responses? Pain 1996;66:223-227.
  2. Klimczak NJ, Donovick PJ, Burright R. The malingering of multiple sclerosis and mild traumatic brain injury. Brain Injury 1997;11(5):343-352.

Auto Injury: The Neck and the Brain

There is a wide range of whiplash symptoms. The most common, of course, are neck pain and headache, but a substantial percentage of patients report other, more difficult to understand problems as well. Some of these symptoms include dizziness; problems with balance; difficulties with attention and concentration; and sleep disturbances.

Brain injury and whiplash

A number of theories have been put forth to explain these myriad symptoms. Some researchers have suggested that brain injury is responsible, while the insurance industry insists that these symptoms are fabricated.

A recent study1 from Sweden attempts to answer some of these questions by examining the functions of the brain in whiplash patients.

The study started with 40 patients with grades II and III whiplash injuries. The patients were given neuro-otological tests within two months of the injury and again two years later. These tests included auditory brainstem response tests (ABR) and oculomotor function tests, including evaluation of saccades (the rapid, step-like voluntary motion of the eyes used when reading or scanning an image).

ABR tests involve measuring the patient’s neurological response to a repetitive sound stimulus:

“A brief sound causes a series of electrical waves, in the nanovolt range, that can be recorded from the surface of the head. The signals are so small that they are normally buried in background electrical noise, but when the same brief stimulus is presented many times and the responses are averaged, the waves can be measured reproducibly. Early peaks in the waveform represent electrical activity in the eighth nerve arriving at the cochlear nuclei, and later peaks represent combined activity at successive sites in the auditory pathway.” 2

By analyzing the waveform, it is possible to identify dysfunction along the neurological pathway.


At the two-year follow-up, 16 of the patients (40%) had no symptoms from the original injury. Ten patients (25%) complained of intermittent neck pain, headache, and radiating pain in one or both arms. Four patients (10%) also reported memory impairment, concentration problems, and showed neurological deficits. Another 4 patients (10%) were still on sick leave.

In the smooth pursuit tests, 5 patients showed abnormalities in the first test. Three of these patients improved, but two showed worse results at the two-year follow-up. These two patients who worsened over time also showed problems with their ABR tests.

Ten patients showed a worsened score on saccade velocity at the two-year follow-up.

What is at the root of the chronic pain and the neuro-otological signs? The authors suggest two possible explanations: altered neurological responses of the brainstem, and direct trauma to the brainstem.

The first explanation would describe the symptoms of most chronic whiplash patients and works as follows: The cervical spine plays a key role in how the brain maintains balance, and signals from the injured cervical spine travel through the spinal core to the brainstem—specifically the vestibular and oculomotor nuclei. This is the same part of the brain that receives the signals from the inner ear, via the eighth cervical nerve. A painful neck can cause overexcitation of the nerve pathways, resulting in altered functioning of the brainstem. These alterations in the brainstem can in turn cause dysfunction in eye motility and balance, since these different systems all work together as the Posture Control System.

Most patients with chronic whiplash pain and ocular and auditory signs would fit in this category. However, this mechanism may not account for those patients with the most severe symptoms: “In the present study, we found two patients with pronounced pursuit abnormalities compatible with organic brain/brainstem lesions.”

So, according to this small study, about 2% of whiplash patients have signs of brainstem damage. This may seem like an insignificant number, but when we consider that there are approximately 1 million whiplash injuries in the US each year, there may be 20,000 cases of brainstem injury from auto collisions annually.

This study provides two important pieces of information about chronic whiplash: the first is that ABR and saccade tests are an objective way to measure altered neurology in these patients; the second is that some patients may have actual brain injury from these collisions.

For patients with more severe symptoms, it may be advisable to have them evaluated for saccade movements and ABR by an audiologist.

  1. Wenngren BI, Pettersson K, Lowenhielm G, Hildingsson C. Eye motility and auditory brainstem response dysfunction after whiplash injury. Acta Otolaryngologica 2002;122:276-283.
  2. Nolte J. The Human Brain: An Introduction to Its Functional Anatomy. 2002, Mosby, p. 355.

Tinnitus and Cervical Spine Injury

Tinnitus is an auditory disorder in which the patient hears a noise that is not actually present. “Tinnitus is common; estimates of its prevalence range up to 80% of all adults. About 10% of people complain of chronic tinnitus, whereas 0.5% of adults describe it as interfering with their ability to lead a normal life.”

Many patients who have a whiplash injury or temporomandibular pain report tinnitus as one of their symptoms. The problem with these patients is that seldom are there the objective signs of nerve dysfunction commonly associated with tinnitus.

The reason for this is that there are two different types of tinnitus: “otic” and “nonotic.” “Otic” tinnitus can be directly associated to disorders of the inner ear or auditory nerve through testing. “However, there are many other patients who have either no detectable ear/nerve disorders or there is no close temporal relationship between such a disorder and tinnitus, so that the initiating event of the “nonotic” tinnitus is obscure.”

The author of this study uses a review of the literature and case reports to describe the phenomenon of “somatic” tinnitus, or tinnitus that originates in the lower head or the cervical spine.

The article describes nine patients with tinnitus and describes the various details of their cases. Here are brief descriptions of three of these cases:

  • Case 1 was a 52-year-old woman who had surgery on her right shoulder. She developed a frozen shoulder from the surgery, and immediately upon injection of the local anasthetic being administered (for treatment of the frozen shoulder) she developed tinnitus in her right ear that has persisted since 1994. Clinical examination reported spasm of the right occipital muscles.
  • Case 2 was a 39-year-old woman who had tinnitus since her teens. “Head position has always modulated her tinnitus loudness. On a 0 to 10 loudness scale, she rates her tinnitus as 3/10. When turning the head to either side or tilting to the left, loudness increases to 5/10, whereas with tilting to the right, the loudness was barely perceptible (1/10). Clenching her teeth increased the loudness only slightly (4/10). On examination, 2 regions of increased muscle tension and tenderness were noted in the right neck as compared with the corresponding regions on the left, namely the upper sternocleidomastoid and the medial suprascapular regions.”
  • Case 8 was a 50-year-old woman who developed tinnitus after neck manipulation. Her symptoms were intermittent, and, “When initially examined, she was not having tinnitus. Her left suboccipital muscles, however, were noted to be tender and under increased muscle tension compared with the corresponding muscles on her right side. Within an estimated 5 minutes of examining the cervical musculature, she reported that her left-sided tinnitus has started. On reexamination, her left suboccipital muscle tension had become much more pronounced. Within another 5 minutes, her tinnitus abated, and her suboccipital muscles were more relaxed.”

The author cites a number of whiplash and TMJ studies that refer to tinnitus, and suggests that these conditions are not related to any pathology in the auditory nerve or inner ear, but are based in the cervical spine and jaw.

The key component in this neurological model is the Dorsal Cochlear Nucleus, or DCN. Disturbance of the DCN (which resides in the brain stem) has been found in other studies to be related to tinnitus. The author’s proposed model goes something like this:

  1. The nerves in the head and neck converge as they enter the brainstem and upper cervical spine (shown at right as the “CST,” where they all meet in the medullary somatosensory nuclei (MSN).
  2. The MSN is directly connected via neural pathways to the DCN.
  3. Stimulation of the nerves in the head and neck (from injury or stress) could result in activation of the MSN and, in turn the DCN, resulting in tinnitus.

The details of this proposed model are really only useful to theorists. The importance of this study is that there is some strong evidence that neck and facial injury can result in tinnitus:

“Whether or not the proposed model for somatic (craniocervical) tinnitus is correct in all its details, it represents a focus for future systematic studies of somatic tinnitus and a framework for approaches to treatment. Moreover, we have presented a series of patients in whom the evidence argues for a craniocervical, nonotic basis for their tinnitus. As such, it seems likely that some cases of somatic tinnitus may result from interactions between the somatic and auditory pathways within the central nervous system with no involvement of the auditory periphery (cochlea or auditory nerve).”

Levine RA. Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis. American Journal of Otolaryngology 1999;20(6):351-362.

Dizziness Increases Risk of Chronic Whiplash

After pain symptoms, dizziness and unsteadiness are the most common symptoms experienced by whiplash patients. Seventy percent of patients with persistent whiplash symptoms report that they suffer from dizziness. A new review from the journal Spine suggests that dizziness may be linked to the development of chronic whiplash symptoms.

Although there are a range of etiologies, dizziness associated with auto injuries is likely a result of one of four major causes.

Injury to the cervical spine: The cervical spine plays a critical role in the body’s ability to balance because of its connection to the postural control system (PCS). This system takes information from the eyes, inner ear, and proprioceptors in the neck to help the body maintain postural stability. In an auto collision, trauma to the neck can disrupt proprioceptors, causing dizziness.

Benign paroxysmal positional vertigo: Dizziness can also be a sign of benign paroxysmal positional vertigo, or BPPV. Otoliths inside the inner ear tell the brain where the head is positioned. In an auto collision, violent movement of the head can jar otoliths from their normal position, causing confusion of the PCS and dizziness. These patients feel their symptoms worsen when they move their head and neck in certain directions like lying down or rolling over in bed.

Vascular injury: Damaged blood vessels in the neck can disrupt the blood flow to the brain causing dizziness.

Brain injury: If the occupant obtained a head injury, mild traumatic brain injuries can cause confusion, dizziness, and memory loss.

For whiplash patients, dizziness is typically the result of trauma to the cervical spine and disruption of the proprioceptors. Treleaven outlined several key studies suggesting a link between dizziness and chronicity in whiplash patients:

  • 80% of patients with normal eye movements had healed or were nearly recovered after the 8 month follow-up. This reinforces the link between the PCS and whiplash recovery.
  • Early signs of dizziness were associated with pain levels six months after the initial whiplash injury.
  • Early symptoms of dizziness were also associated with poor prognosis.

Dizziness, Anxiety, and Pain Symptoms

Dizziness also appears to be linked to anxiety and pain symptoms, both of which can contribute to chronicity. Treleaven argued that there is “a potential for a vicious cycle of cervical dizziness, pain, anxiety, altered sympathetic nervous system function.” Symptoms of high pain levels and dizziness may also act as combined predictors of poor prognosis. Additionally postural control deficits could exacerbate central pain centralization “via a number of mechanisms including altered somatosensory representation, altered joint mechanics, and decreased descending inhibition of pain.” Addressing dizziness and pain symptoms could allow patients to break the cycle of central sensitization.

While a number of factors lead to chronicity, early treatment of dizziness and postural deficits could help patients avoid developing chronic whiplash symptoms.

Treleaven J. Dizziness, unsteadiness, visual disturbances, and postural control: implications for the transition to chronic symptoms after a whiplash trauma. Spine 2011; 36(25S): S211-217.

Cognitive Complaints After Auto Injuries

One of the major areas of debate in the whiplash literature in 1998 has been the issue of brain injury. Cognitive and attentional deficits after whiplash injury are fairly well recognized in the medical literature. The question is, however, not whether these symptoms exist but whether they are based on organic pathology of the brain or are secondary symptoms related to whiplash pain in general.

Some researchers, such as Kessels et al1 and Schmand et al2, have reported that the psychological symptoms of whiplash arise only after the patient experiences chronic pain. Bogduk et al3 reported that when the pain was alleviated in whiplash patients, the psychological symptoms vanished.

On the other hand, researchers such as Otte et al4 have repeatedly found that whiplash patients show brain abnormalities when they are tested with sensitive PET and SPECT scans. The source of these abnormalities has been postulated as a direct trauma related to the whiplash motion, or a secondary reaction related to altered nociception in the cervical spine.

In short, this is a new area of study, and one that has not yet been—and may not ever be—proven one way or the other.

Still, a new study5 from Swiss researchers provides some more information on the role of PET and SPECT scans on the brains of whiplash patients, and what abnormalities found on such tests mean.

This study performed SPECT, PET and MRI scans on 13 patients with “late whiplash syndrome” and 16 non-whiplash control subjects. The objectives were: “First, how does the cerebral metabolism of whiplash patients differ from that of healthy subjects? Second, can potential abnormalities be reliably demonstrated for individual patients? Third, what are the implications of potentially abnormal PET or SPECT findings?”

Clinically, 7 of 13 patients (54%) scored below normal on working memory, and 6 of 13 patients (46%) scored below normal on divided attention, indicating some kind of cognitive dysfunction.

Here is a summary of what the researchers found when they reviewed the imaging scans:

“In our study, significantly decreased FDG uptake in the putamen and the frontopolar and lateral temporal cortex was found among patients with persistent symptoms resulting from whiplash injury. An important issue is whether the abnormalities are of purely functional origin or whether there might be microscopic damage. This question cannot be answered with PET or SPECT imaging. Major structural damage as a possible cause was excluded at MRI. The hypometabolism in the pathologic areas could be explained through the presence of depression as indicated by the significant correlation with BDI. Hypometabolism in the frontopolar and lateral temporal cortex and the basal ganglia has been reported among patients with depression without whiplash injury. A significant correlation between BDI scores and FDG uptake was found in the frontopolar region but not in the putamen or the lateral temporal cortex. The frontopolar and lateral temporal areas with pathologically reduced FDG uptake seen in this study correspond to the ones found to have microscopic damage in experimentally induced mild head injury. Frontopolar and laterotemporal microscopic damage in the study group is therefore not excluded. In the putamen, however, microscopic damage seems unlikely, because experimental research has demonstrated that lesions in deeper brain structures may be expected only when high acceleration forces are used. An explanation for the reduced FDG uptake in the putamen might be decreased corticoputaminal input.”

In short, the researchers found evidence of brain abnormalities—but they don’t know what they represent. From the correlation between BDI scores (the Beck Depression Inventory used to diagnose depression) and areas of cerebral hypometabolism, the abnormalities may be caused by depression. But they may also be due to microscopic damage of the brain tissue itself—a condition provable only by autopsy. Furthermore, the researchers state that even if the abnormalities are due to brain tissue damage, this information provides little help, as treatments for this type of problem “are not yet defined.” An editorial6 in the same issue of Neurology sums up the problem well: “At this moment, medical treatment of some of the psychological consequences (depression or anxiety) of whiplash or MTBI is a better developed science than the treatment of the neurologic consequences.”

At this point, the researchers can only make one conclusion: something is happening in the brains of patients with chronic whiplash pain, but what exactly that may be is unknown. Therefore, such sophisticated imaging techniques like PET and SPECT scans are at present “of doubtful value in the routine evaluation of late whiplash syndrome.”
[Side note: At the “International Symposium, Whiplash ’98,” this study was mentioned with the statement that it found that there were no signs of brain abnormalities in whiplash patients using PET or SPECT. This is not what the study reported, as we elucidated above. Professionals should be aware, however, that this misconception is out there and is likely to appear in litigation.]

  1. Kessels RPC, Keyser A, Verhagen WIM, et al. The whiplash syndrome: a psychophysiological and neuropsychological study towards attention. Acta Neurologica Scandinavica 1998;97:188-193.
  2. Schmand B, Lindeboom J, Schagen S, et al. Cognitive complaints in patients after whiplash injury: the impact of malingering. Journal of Neurology, Neurosurgery and Psychiatry 1998;64:339-343.
  3. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomized, double-blind, placebo-controlled trial. Pain 1997;73:15-22.
  4. Otte A, Goetze M, Mueller-Brand J. Statistical parametric mapping in whiplash brain: is it only a contusion mechanism? European Journal of Nuclear Medicine [Letter] 1998;25:306-312.
  5. Bicik I, Radanov BP, Schafer N, et al. PET with 18fluorodeoxyglucose and hexamethylpropylene amine oxime SPECT in late whiplash syndrome. Neurology 1998;51:345-350.
  6. Alexander MP. In the pursuit of proof of brain damage after whiplash injury. Neurology 1998;51:336-340.

Hearing Disorders After Auto Injury

This study sought to shed some light on the problem of hearing loss or dysfunction after rear-end collisions. The researchers started with 153 auto injury patients and 33 healthy control subjects, and performed audiograms on these subjects. The audiogram tests the ability of patients to recognize a pure tone. All patients were also asked about the presence of hearing problems. Of the 153 whiplash patients, 14% were found to have a hearing impairment “exceeding the 90th percentile of the ISO standards.”

The researchers did not stop here, however. Next, they took a group of 33 patients with chronic whiplash pain with a duration of 3 years or more. These patients had no hearing loss or minor hearing impairment, as based on the audiogram. They tested these subjects and the controls using a “standardized speech-in-noise test.” This test is more useful, as, “Speech recognition is a perceptive-cognitive function, in contrast to pure-tone hearing, which is a threshold identification function.” The speech recognition test (SRN) is more sensitive, and can provide more information to the clinician.

After performing the SRN test, the authors found that “40% of this subgroup of patients with WAD [whiplash associated disorder] reported hearing problems. As many as 30% of the patients with WAD had an abnormal SRN test result, as against 5% of the controls. Significant relations were found between the SRN test and self-assessed hearing loss…”
The authors propose a number of explanations as to how whiplash injuries can cause hearing dysfunction:

  1. “The trauma might cause lesions other than the neck injury affecting the auditory system. Subliminal injury of the cochlea, which is so delicate that conventional tests cannot detect it, is quite possible. Lesions affecting the central auditory system, from the brainstem to the temporal lobe cortex, are also conceivable…” although less likely.
  2. The hearing problem may be a “auditory stress disorder.” “Most patients under stress have increased tension of the neck muscles, as have patients with WAD.”
  3. “A reflexogenic disturbance from the neck via divergent afferent proprioceptive activity to the central auditory nervous system might be an alternative explanation. Some support for this theory is the single-photon emision computed tomography (SPECT) results by Otte et al. this group found parieto-occipital hypoperfusion in a group of patients with WAD and interpreted it as caused by activation of nociceptive afferents from the upper cervical spine, sicne a group of patients with non-traumatic chronic neck pain also showed parieto-occipital hypoperfusion.”

No matter what the mechanism of injury, this study demonstrates that the SRN is more accurate at uncovering hearing problems than a simple audiogram, and that a significant percentage of whiplash patients show signs of hearing dysfunction.

Tjell C, Tenenbaum A, Rosenhall U. Auditory function in whiplash-associated disorders. Scandinavian Audiology 1999;28:203-209.