Have you been in a car crash? Are you suffering from chronic pain because of your injury?
You don’t need to suffer. Learn how chiropractic can help you recover from auto injuries.
Auto injuries are a common source of chronic pain. Getting the proper treatment early after your crash can be very important in recovering quickly.
Most auto injury pain originates in the spine, and that’s why chiropractic can be beneficial: we get to the underlying trauma that you experienced and help your body heal.
Watch the videos in the playlist below, or read some of our articles to learn more about how chiropractic can help you recover from an auto injury.

Brain Injury articles:

Brain injuries are common after an automobile collision, and they can occur even when there is no direct head impact. Unfortunately, many cases of brain injury are undiagnosed and unrecognized.
The key to recovery from a brain injury is to realize that injury has occurred. Some of the most common symptoms of mild brain injury are headache, dizziness, confusion, loss of concentration, and problems with memory.
Watch our videos in the playlist below, or browse our articles for some of the newest information we have on brain injury as it relates to automobile collisions.

Whiplash, Brain Injury, Concussion, Auto Injury

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. 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.

Results

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.

Traumatic Brain Injury and Chronic Pain Syndrome

There has been a reported overlap, or dual-diagnosis, of both traumatic brain injury (TBI) and chronic pain (CP) syndrome in many patients. This study set out to compare qualities and treatments of patients with both TBI/CP to patients with just chronic pain to gain a broader understanding of the relationship.

The most common cause of TBI was a motor vehicle accident. TBI/CP patients complained consistently of headaches, neck pain, and arm pain. TBI/CP patients also reported, “cognitive problems, impaired memory and concentration, and confusion about the etiology of their medical problems.” Interestingly, there was an absence of memory and concentration problems in those patients with only chronic pain. The researchers feel the differences in concentration and memory symptoms are indicative of the general patient population, and not limited to their study.
The researchers conclude:
“We propose that the CP patients who endorse or complain of memory or concentration problems, who express confusion about their diagnosis, complain of pain in head, neck, and arms, and/or were injured in motor vehicle accident should be further questioned about the possibility of concurrent TBI.”
Treatment outcome of patients with dual diagnosis is similar to patients with CP alone, although treatment length tends to be longer.
One important finding of this study was that dual diagnosis is apparently more common than previously thought. When the researchers were looking for the chronic pain patients without a history of TBI to use as a comparison group, 17% had to be disqualified because of a history of head injury. None of these patients had been evaluated or treated for TBI.
Andary MT, Crewe N, Ganzel SK, et al. Traumatic brain injury/chronic pain syndrome: a case comparison study. The Clinical Journal of Pain 1997;13:244-250.

Whiplash, Brain Injury, Concussion, Auto Injury

The biggest challenge with treating auto injuries is getting a proper diagnosis. Countless studies show that whiplash patients have objective, organic injuries; unfortunately, many of these injuries are difficult to pinpoint with conventional diagnostic imaging techniques, such as CT or MRI.
Further complicating diagnosis is the fact that the focal point of the injury in most patients is the neck. Due to the complexity of the cervical spine, many different structures can be injured and the symptoms of different types of injuries can overlap with other kinds of injuries.
Common Symptoms of Mild Traumatic Brain Injury

  • Headache
  • Dizziness
  • Tinnitus (ringing in the ears)
  • Difficult concentrating
  • Visual Symptoms
  • Memory Loss
  • Feeling dazed
  • Nausea

A current study looks at this problem; specifically, it examines the diagnostic challenge of differentiating whiplash associated disorder (WAD) from concussion in patients with neck injuries.
For many years, researchers have realized that many patients with whiplash present with symptoms similar to patients with brain injury. The chart shows the most common symptoms of brain injury. Over the last ten years, dozens of studies have been published showing that many whiplash patients complain of the same problems. The challenge is to determine which patients have TBI and which have spinal injuries.
The authors decided to study the issue by looking at hockey players. They followed 20 teams (183 players) for a single season. During that time, 13 players received either a whiplash injury or a concussion. Each of the injured players was given a thorough examination. This is what the study found:

  • All of the patients with whiplash injury (6 players) reported concussion symptoms, even if the patient had the least severe type of whiplash injury.
  • “Full resolution of concussion symptoms at the 7-10 day follow-up evaluation was reported by five of the 13 subjects. Of these five subjects, two were still experiencing WAD symptoms.”
  • 12 of the 13 injured players reported headache; 10 of the 13 reported dizziness.

At the 7-10 day follow-up:

  • 6 of the 13 injured players reported a complete resolution of whiplash symptoms, but three of the six were still experiencing the symptoms of concussion.
  • “Full resolution of concussion symptoms at the 7–10 day follow-up evaluation was reported by five of the 13 subjects. Of these five subjects, two were still experiencing WAD symptoms.”
  • “Overall, only three of the 13 subjects or 23% experienced full resolution of both their WAD and concussion symptoms at the follow-up evaluation.”

The authors have this to say about their findings:

“The athletes studied in this investigation experienced symptoms of both WAD and concussion after a head and/or neck complex acceleration/deceleration injury. However, the number of concussion symptoms they experienced did not associate with an increased severity of WAD grading. Symptom resolution during the 7–10 day follow-up period differed between athletes and injury mechanisms. Based on the observed prevalence of symptoms of both WAD and concussion irrespective of the mechanism of injury, it is important for the clinician treating a patient or athlete for WAD to evaluate for symptoms of concussion and for the team therapist/clinician to be cognizant of conducting a thorough cervical evaluation when dealing with concussed players.”
The same holds true for non-athlete patients in motor vehicle collisions. Because symptoms of traumatic brain injury can overlap with those of cervical spine injury, patients with symptoms of brain injury should be carefully examined for the presence of concussion.
Of particular concern are those patients who don’t seem to be recovering from the current treatment, or for those patients who experience personality changes after the collision. Undiagnosed brain injury can result in unemployment, divorce, depression, and other serious social and medical problems.
Hynes LM, Dickey JP. Is there a relationship between whiplash-associated disorders and concussion in hockey? Brain Injury 2006;20(2):179-188.

Cognitive Complaints After Whiplash

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 (STR Volume 3, #3), 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.