Neck Pain Facts

Neck Pain Facts

Neck pain is a very common problem and the chances that it is caused by serious disease are very rare. Health practitioners can help suggest possible ways to control your pain and advise you of ways to deal with the pain and get on with your life. It is normal to worry about the cause of your pain and the impact it may have on your life. Talking with your healthcare provider about these worries and concerns can be helpful. You will usually find there is no serious cause of the pain and that there are ways to relieve the symptoms and get you back to your normal activities.

Often neck pain episodes will get better on their own as nature takes its course. It’s important to stay as active as possible as the old adage of bed rest and trying to completely avoid pain is not the best advice. Most people do just fine by staying active, coping the best they can, and modifying daily activities as to not re-agitate the tender tissues.

Back and neck pain are the most common chronic pain conditions. Back and neck pain can arise from soft tissues, bony parts of the back and neck, and joints holding the spine in alignment. It can arise directly or indirectly from the discs in the back or neck, and it can occur when nervous tissue, normally protected by the bones of the vertebral spine, is compressed by those bony elements.

The most common symptoms of neck pain are pain, stiffness, muscle spasm, clicking and grating, numbness or tingling, dizziness and/or blackouts.

Neck pain can also come from conditions directly affecting the muscles of the neck, such as fibromyalgia and polymyalgia rheumatic. Neck pain is also referred to as cervical pain.

THE ECONOMIC BURDEN OF WAD

THE ECONOMIC BURDEN OF WAD

Little is known about the individual and societal economic burden of WAD. For instance, little is known about the prevalence of long-lasting work disability due to WAD, which probably the most costly part. This burden is probably largely dependent on the legislation in different countries. In 2002, an independent and temporary Commission on whiplash-related injuries was informed in Sweden, initiated by the four largest motor vehicle insurers. The mandate of the 3-year commission was an examination of the problems of WAD from road safety, medical care, insurance and societal aspects. One of the conclusions of the final report was that the yearly cost for society and for the insurance industry was approximately SEK 1.5 billion (US$201 million), while projected costs (i.e. what new cases of WAD arising in a particular year will cost society and insurers by the time the person reaches retirement age) amounted to SEK 4.6 billion (US$648 million). These calculations were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002. Since the report’s publication, the number of WAD cases have decreased dramatically to about 16,000 claims in 2008 (173 per 100,000 inhabitants), which, of course, has an impact on the overall costs.

Comparable data has not been found, but there is some evidence from a study that addressed the incidence of WAD in 10 European countries. The administrative data suggests that the total claims cost in Switzerland was 500 million Swiss francs (US$467 million). Switzerland’s population is 80% that of Sweden. Expenditures in addition to the claims cost was not reported in that study.

SUMMARY

In summary, as in almost all other diseases and injuries, factors that are involved in the risk or prognosis of WAD are multifactorial and constitute a web of biological, psychological and social components.

REFERENCES

1.      Crowe H. A new diagnostic sign in neck injuries. Calif Med 1964; 100:12-13.

2.      Gay J. Abbott K. Common whiplash injuries of the neck. JAMA 1953; 152:1698-704.

3.      Benson BW, Mohtadi NG, Rose MS, Meeuwisse WH. Head and neck injuries among ice hockey players wearing full face shields vs half face shields. JAMA 1999; 282(24):2328-32.

4.      Versteegen GJ, Kingma J, Meijler WJ, ten Duis HJ. Neck sprain not arising from car accidents: a retrospective study covering 25 years. Eur Spine J 1998;7(3):201-5.

5.      Lorish TR, Rizzo TD, Jr., Ilstrup DM, Scott SG. Injuries in adolescent and preadolescent boys at two larger wrestling tournaments. Am J Sports Med 1992;20(2):199-202.

6.      Spitzer WO, Skovron ML, Salmi LR, et al. Scientific Monograph of the Quebec Task Force on whiplash-associated disorders: redefining “whiplash” and its management. Spine 1995;20(8 Suppl):1S-73S.

7.      Holm LW, Carroll LJ, Cassidy JD, Ahlbom A. Factors influencing neck pain intensity in whiplash-associated disorders in Sweden. Clin J Pain 2007;23(7):591-7.

8.      Ferrari R, Russell AS, Carroll LJ, Cassidy JD. A re-examination of the whiplash-associated disorders (WAD) as a systematic illness. Ann Rheum Dis 2005:1337-42.

9.      Berglund A, Alfredsson L, Jensen I, et al. Occupant- and crash-related factors associated with the risk of whiplash injury. Ann Epidemiol 2003;13(1):66-72.

10.   Bylund P-O, Bjornstig U. Sick leave and disability pension among passenger car occupants injured in urban traffic. Spine 1998;23(9):1023-8.

11.   Versteegen GJ,Kingma J, Meijler WJ, ten Duis HJ. Neck sprain in patients injured in car accidents: a retrospective study covering the period 1970-1994. Eur Spine J 1998;7(3):195-200.

Special Diagnostic Considerations

Special Diagnostic Considerations

Disc Pain Distribution

               Theannulus fibrosis has nociceptive nerve endings in it, and therefore an annular tear can cause pain referral of purely discogenic origin into the low back, buttock, and sacroiliac region, and lower extremity even in the absence of neural compression.

Facet Joint Pain Distribution

               The zygapophysial joints are well innervated, and facet naturopathy can cause lowback pain and referred pain into the buttocks and lower extremities. Classic facet syndrome pain is in the hip and buttock, with cramping leg pain primarily above the knee, low back stiffness (especially in the morning with inactivity), and the absence of paresthesia. Classic signs are local paravertebral tenderness, hyperextension back pain, and no neurologic or root tension signs with hip, buttock, or back pain on straight leg raising.

Differentiating Disc from Facet Pain Distribution

               Differential diagnosis of lower-extremity pain of disc versus facet includes the facet that facet pain rarely extends beyond the calf, usually only into the thigh, and not into the foot. Radicular disc pain is potentially worse than back pain. In facet pain, the back pain is worse than the leg pain. Radicular pain is usually accompanied by neurologic signs in disc legions but not in facet problems.

Elevated Cerebrospinal Fluid Proteins

               The protein concentration in the cerebrospinal fluid (CSF) is often increased in patients with sciatica, probably because of plasma proteins leaking through the blood-nerve root barrier into the cerebrospinal fluid. Significantly higher values of the CSF/ serum albumin ratio and the CSF/ serum immunoglobulin G ratio were found in patients with positive SLR test results and paresis compared with patients with no clinical findings. Elevated CSF proteins seem to be an important indicator of the functional status of the nerve root and a measure of the degree of seriousness of sciatica.

               Nerve root injury, as suggested by a positive straight leg raising test, appears to be neurochemically linked to altered CSF vocative intestinal peptide levels in patients with radicular pain symptoms caused by disc herniation and lumbar stenosis.

Differentiating Recurrent Disc Herniation from Scar Formation

               Gradually increasing symptoms beginning a year or more after discectomy are considered more likely caused by scar formation, whereas a more abrupt onset at any interval after surgery is more likely cause by a recurrent herniated disc.

               Symptoms and signs that best distinguish between recurrent herniation and fibrosis are pain on coughing, a severly reduced walking capacity, and a SLR test positive at less than 30 degrees; the presence of two or more of these parameters was found in 16 of 22 patients with recurrent herniation, compared with 5 of 18 patients with fibrosis.

Pathologic Change in Sciatica Foramen as Cause of Sciatica

               Longstanding sciatica symptoms and signs should include pathologic changed in the sacral foramen by benign and malignant neoplasms as well as infection. CT scanning should include the sciatic foramen in longstanding, undiagnosed sciatica.

Dorsal Root Ganglion Compression Symptoms

               Dorsal room ganglion compression can result in myalgia and tendonitis symptoms into the lower extremities, as well as intermittent claudicating, sciatica, and groin pain.

Clinical Instability Defined

               White and Panjabi states that a narrowed disc space without spondylosis is a sign of instability. Clinical instability is defined as the loss of the spine’s ability, under physiologic loads, to maintain normal relationships between vertebrae so that no damage and no subsequent limitation to the spinal cord or nerve roots occurs and no incapacitating deformity or pain develops from structural change.

Differentiating Contained from Noncontained Disc

               When a disc lesion is present, a differential diagnosis between protrusion and prolapse is necessary. The sudden onset of leg pain and absence of low back pain indicates protrusion.

Sciatic Scoliosis Defines Disc Lesion Type

               Relief of pain on lateral flexion may indicate whether the disc protrusion is lateral or medical to the nerve root.

Cervical Disc as Cause of Myofascitis and Leg Pain

               Cervical disc herniations have been reported to cause Myofascial pain and altered deep reflexes in the lower extremities; the Myofascial pain caused by this irritation ceased once the mechanical cervical disc rubbing of the cord was surgically relieved.

Leg Length Effect on Low Back Pain

               Leg length inequality alters gait efficiency and predisposes to low back pain and hip arthrosis.

What Is the Best Lifting Posture?

Back Muscle Forces in Flexion Similar to Upright Posture

               Compression forces and moments exerted by the back muscles in full flexion are not significantly different from those produced in the upright posture.

Turyn’s Sign Lumbar Disc Disease Classification

Turyn’s Sign

Lumbar Disc Disease Classification

Variation of the lumbar disc disease classification model is as follows:

1.      Disc protrusion:

a.      Type I: Peripheral annular bulge

b.      Type II: Localized annular bulge

2.      Disc herniation:

a.      Type I: Prolapsed intervertebral disc

b.      Type II: Extruded intervertebral disc

c.      Type III: Sequestered intervertebral disc

Categories of Low Back Pain

The following are five categories of low back pain:

1.      Viscerogenic pain: Pain that originates from the kidneys, sacroiliac, pelvic lesions, and retroperitoneal tumors. This type of pain is neither aggravated by activity nor relieved by rest.

2.      Neurogenic pain: Pain commonly caused by neurofibromas, cysts, and tumors of the nerve roots in the lumbar spine.

3.      Vascular pain: Pain characterized by intermittent claudication from aneurysms and peripheral vascular disease.

4.      Spondylogenic pain: Pain directly related to the pain originating from soft tissues of the spine and sacroiliac joint.

5.      Psychogenic pain: Pain that is quite uncommon and ascribed to nonorganic causes.

Sciatica

The origin of sciatica includes the following:

1.      Prolapsed intervertebral disc pressure, infection, and traumatic sciatic neuritis, perineural fibrositis, infections and tumors of the spinal cord.

2.      Lumbosacral and sacroiliac sprain and strain, degenerating intervertebral discs, fibrositis, osteomyelitis, hip joint disease, and secondary carcinomatous deposits in bone.

3.      Nephrolithiasis, prostatic, renal, and anal disease.

4.      Toxic and metabolic disorders, conversion hysteria, and arterial insufficiency.

Procedure:

1.      When the patient is in the supine position with both lower limbs resting straight out on the table, dorsiflexion of the great tor elicits pain in the gluteal region.

2.      The sign is significant for sciatic radiculopathy.

Clinical Pearl

A straight-leg-raising test this is positive under 30 degrees reveals a large disc protrusion. The nerve root is stretched long before it would normally be. The straight-leg-raising test is most useful for identifying L5-S1 disc lesions because the pressures on the nerve root are highest at this level. During straight leg raising, L4-L5 is not as apt to give as much pain as L5-S1 because the pressure between the disc and the nerve root at L4-L5 is half that at L5-S1. Therefore the L5-S1 disc lesion gives more pain in the lower back and leg than does the L4-L5 disc lesion. No movement on the nerve root occurs until straight leg raising reaches 30 degrees. No movement on L4 occurs during a straight leg raising test. From this, the presence of Turyn’s sign indicates a large disc protrusion at the level of the L5-S1 nerve root.

Multiple-Vehicle Collisions

                                                      Multiple-Vehicle Collisions

               

Multiple collisions, in which a vehicle is submitted to one or more successive collisions after the initial collision, are of special significance as far as the types of occupant injuries and the injury severity are concerned. One of the primary concerns for multiple impacts is the risk of the first impact resulting in the occupant being out-of-position (OOP) for the second crash. In addition, having injuries from a second impact superimposed upon injuries from the first impact may significantly alter the nature and extent of injuries, depending upon the circumstances. In some instances, the doctor will be confronted with a patient who has been involved in a multi-vehicle collision and has been requested to determine if the first or second crash was responsible for the injuries or the respective percentage of causation. The doctor’s opinion may be needed to determine apportionment for each collision. If two insurance carriers are involved, they may want to pass the blame for injuries to the other carrier. From a biomechanical perspective, multiple collisions are very challenging. Several issues that need to be considered:

               A) delta-V for first impact and the subsequent crash(s)

               B) mass ratios of the vehicles involved for each impact

               C) vehicle rotation for each crash, if occurring, and if so, how severe

               D) types of vehicles involved (i.e., SUV vs. a passenger car in a side impact). Height issues between the two vehicles and aggressive designs can result in differing injury patterns.

               E) intrusion extent into the occupant compartment for each vehicle, if any.

               F) contact point on the vehicle relative to the seating position of the occupant and proximity to the contact area, and whether the point of impact (POI) was rigid or soft. Rigid pillars and smaller structures will cause much higher acceleration levels than softer impacts or by larger objects capable of distributing loading over a larger area of the body.

               G) times of occupant acceleration. Longer impacts are better for occupants

               H) OOP issues for occupant at the time of each impact. Both impacts may have OOP issues.

               I) Second injury superimposed on first injury. Doctor needs to consider each impact with its own characteristics. For example, did each impact involve a head strike or did one impact cause inertial loading only? Need to consider the surface size and energy absorbing quality for each impact as well.

               J) Type and severity of first injury can make second impact more or less likely to cause other injuries.

               K) Patterns of injury related to vector of each crash.

               L) other human and vehicle factors.

              

               Temming and Zobel used a Volkswagen database of 1,620 occupants who suffered cervical spine injuries, concluding that about 23.5% of occupants in passenger cars were involved in at least one additional collision and 5.6% of occupants had a third impact following the initial crash. Another study found that multi-vehicle collisions occur in about 15% of total crashed, and the second collision speed has been found to be just as high as or higher than the first crash 43.2% of the time. An example is the rear-end collision in which one car is pushed into a vehicle ahead, and is struck on the side of the vehicle in the intersection, starting a chain reaction of traumatic events. Otte et al. concluded that injuries may be caused by almost all parts of the interior, due to actual impact situation and the consequent relative motion of the occupants.

               Fat et al. analyzed CCIS-UK data of 1,295 crashes looking for multiple impacts. Their study found that a secondary impact with another vehicle occurred in 22.6% of crashes and an additional 6.1% were involved in a third impact. The study concluded that there was a higher risk of occupants being seriously injured in multiple impacts, with the head having the highest frequency. The most common double impact events happened in frontal crashed followed by side impacts or side impacts followed by another side impact.

Distraction Test

Distraction Test

The complaints of patients with chronic or degenerative conditions of the cervical disc are quite different from those of patients with acute conditions. Patients with chronic conditions experience intermittent episodes of pain, discomfort, and muscle spasm. Exacerbations come from exertion. Pain and stiffness may result from weather changes or unexplained causes. Radiculopathy is not always present. Hyporeflexia, motor weakness, and sensory disturbance (especially paresthesia) are common.

1.  Delay in the onset of symptoms.  If the symptoms are not written down and documented within a few hours or days after the crash, then it is very difficult for the patient to say he/she had pain when there is no written evidence.  This can be a critical issue in a case, for example, the first doctor to note that the patient had a traumatic brain injury was made 8 to 10 months after the collision.

2.  Delay in seeing the first doctor.  Any significant delays between the date of the crash and seeing the doctor may create credibility issues for the case.  The patient needs to have a good explanation for waiting for several days to weeks for the first appointment.  There may be legitimate issues such as, some doctors have very busy schedules and may not have appointments available for several days.  The reasons for delays should be noted in the file.  The doctor or patient may have a vacation or work trip scheduled, be out of town for a medical emergency, may have an unrelated surgery that made it impossible to make an appointment, or may simply have not transportation available.

3.  There were conflicts in the history given by the patient in the records.  For example, patient stated in his deposition that he had never been involved in a crash before.  Records from 1989 indicate that the patient was involved in a rear-end crash.  The ER doctor notes that the patient did not use a seatbelt and the orthopedist noted that the patient did use a seatbelt.

4.  Little-to-no damage to vehicle.  The defense will advocate that the damage to the vehicle equals the injury potential (see Chapter 15 for crash speed thresholds for injuries).  There are generally few photographs taken of the vehicles that adequately show the extent of the damage.  Most jurors are going to see poor quality blow-ups of the vehicles or as the parts are removed for repairs.

5.  Impact forces not sufficient to cause any injury or was sufficient enough to have caused only mild muscular strain that would have healed without treatment within a few days may have occurred.  No mechanism of injury was possible in this collision.

6.  No objective findings to prove injuries.  No bruises, bleeding, lacerations, fractures, or photographic evidence of the injury to show the jury.

7.  The treatment that was provided was passive and has not been proven to work.  Patient’s condition would have been the same with or without treatment.  Exercise is the only thing that works.  Patient had only palliative benefits from the treatment.  No long-term benefits noted in file.  May look at deposition.  If patient states in the deposition that the treatment only helped for one to two weeks but the patient continued to have treatment for an additional four months. The case may have challenges.

8.  The duration of treatment was too long, was excessive, or was duplicative, and therefore is not justified from doctor’s experience.  The treatment costs were thus unreasonable for the mild nature of the injuries.  The osteopath, chiropractor, and physical therapist were doing similar things, and therefore the treatments were unnecessary.

9.  Gaps in treatment indicate that the patient did not have any pain.  That a reasonable person in pain would see a doctor is a common attack.

10.  Healing and full recovery takes two to four weeks.  This opinion is simply a hoax for most cases (see Chapter 7 for more about soft tissue healing).

11.  Every person will have full recovery following whiplash injuries.  Doctors and attorneys are to blame.  This is another hoax (see Chapter 13 for a review of prognostic studies).

12.  Patient saw too many providers, consistently self-referred himself or herself, and had a history of psychological problems.

13.  Documentation was poor.  The doctors did not note symptoms, or there are inconsistent statements made by the doctors.

14.  New injuries, including MVCs, falls, etc., or simply flared-up bending over are responsible for the problems.

15.  Prior injuries resulted in all of the problems.  The defense may attack the case by telling the jury that the injuries sustained 8 to 15 years earlier were responsible for the current pain, although there is not evidence of the patient being seen by any health providers for the past five to six years for any musculoskeletal pain.

16.  Prior pain and / or treatment for this pain within the past couple years clearly indicates that the patient’s pain was long-term and would have been present despite the crash.

17.  No justification for the amount of time off work.  May state that the typical patient is back to work within one week (see Chapter 12 for more information).

18.  The MRI scan results showing a bulging or herniated disc are also seen in the general population and are not related to the accident.  Typically, if any degeneration or spurring is noted in the radiology report, the defense medical and biomechanics expert will use that as his/her basis for that opinion using a “Natural Progression” theory.

19.  Future treatment is not needed.  The defense attorney may tell the jury in the opening statement that “Everyone knows that once the case settles the plaintiff’s pain will go away.”

20.  Conservative jurors who have a “Hollywood mentality” can make a case extremely difficult even with the best documentation, proof of bulging discs, and great doctors.  The jury may perceive the plaintiff as looking healthy and there are no photographs of blood and guts.  Some court districts are known as being very conservative, thus making it difficult to get any significant awards.  Some jurors may see that there is monetary motivation for the plaintiff.

The Cervical Spine

 The Cervical Spine

Axioms of Cervical Spine Assessment

1.      Cervical spine syndromes are extremely common and are probably the fourth most common cause of pain.

2.      At any given time, 9% of men and 12% of women have neck pain with or without arm and hand pain, and 35% of the population can remember having had neck pain at some time.

3.      The cervical spine is the origin of a large proportion of shoulder, elbow, hand, and wrist disorders.

4.      Most people who develop pain in the neck do not seek medical attention because they regard such pain as a part of life, so they simply wait for it to disappear.

Disability and Handicap

Disability and Handicap

Disability is a present when a tissue, organ, or system cannot function adequately. A handicap exists when disability interferes with a patient’s daily activities or social/occupational performance. A marked disability does not necessarily cause a handicap. Conversely, minor disability may produce a major handicap. Both conditions require separate assessment. Patients’ perception of their problems will be molded by their adaptation to the depreciated tissue as well as their aspirations for recovery.

Assessing Disability

An aid in assessing the more important aspects of disability is the PILS mnemonic, which considers four issues:

1.       P Preventable causes of disability (e.g., falls, direct trauma)

2.      I Independence (e.g., self-care)

3.      L Lifestyle (roles, goals)

4.      S Social factors (e.g., family, friends, shelter)

Functional Assessment

A complete functional assessment includes evaluation of the following:

1.      Self-care: ability to wash, bath, attend to toilet needs, dress, cook, and feed oneself

2.      Mobility: ability to stand, transfer, walk, negotiate stairs, drive, and use public transportation

3.      Lifestyle: nature of occupation, work capacity, and Social Security benefits

CRASH-RELATED FACTORS

CRASH-RELATED FACTORS

Numerous crash-related factors have been investigated for their predictive capacity. Some of these include the vehicle being stationary when hit, a frontal collision, a rear-end collision, side or other collision, being unprepared for the collision, no seat belt use and no head restraint. However, few of these factors have demonstrated significant predictive power. The exceptions to this are not wearing a seat belt, which was reported to nearly double the risk of developing persistent pain or disability. This is an interesting finding as, in certain jurisdictions where compulsory seat belt use is legislated, the voluntary admission of not wearing a seat belt would not be expected to be common, particularly in jurisdictions operating under a fault-based system. Thus, it is possible that the risk of developing a chronic condition associated with not wearing a seat belt may be even higher than that reported by Walton and colleagues. Scholten-Peeters et al. reported some limited prognostic value for accidents that occur on a highway, but also reported that there was strong evidence that rear-end collisions have no predictive value for poor functional recovery.

Thus, the weight of evidence indicates that crash-related factors are of limited value in attempting to predict poor recovery following whiplash injury.

SOCIODEMOGRAPHIC FACTORS

The predictive capacity of sociodemographic factors has been studied extensively in musculoskeletal pain conditions, and whiplash is no exception. Older age (>50 years), while showing predictive 

Use of the Guides in the Workers’ Compensation and Other Disability Systems

Use of the Guides in the Workers’ Compensation and Other Disability Systems

Workers’ Compensation

There is increased use of the Guides to translate objective clinical findings into a percentage of the whole person. Typically this number is used to measure the residual deficit, a loss--a number that is then converted to a monetary award to the injured party. The scheme is most commonly used in various workers’ compensation systems in the United States and abroad.

In the United States, 44 states, 2 commonwealths, and federal employee compensation systems (in about 90+% of US jurisdictions) either mandate or recommend using the Guides to measure impairment in workers’ compensation cases, the Guides is often used to assess damages in personal injury claims under federal statutes and state common law.

Fundamental Principles of the Guides

1. Concepts and philosophy in this chapter are the fundamental rules of the Guides; they shall preempt anything in subsequent chapters that conflicts with or compromises these principles.

2. No impairment may exceed 100% whole person impairment. No impairment arising from a member or organ of the body may exceed the amputation value of that member.

3. All regional impairments in the same organ or body system shall be combined as prescribed by the rule, at the same level first and further combined with the other regional impairments at the whole person level.

4. Impairments must be rated in accordance with the chapter relevant to the organ or system where the injury primarily arose or where the greatest dysfunction consistent with objectively documented pathology remains.

5. Only permanent impairment may be rated according to the Guides, and only after Maximum Medical Improvement (MMI) status is certified.

6. A licensed physician must perform impairment evaluations. Chiropractic doctors, if authorized by the appropriate jurisdictional authority to perform rating under the Guides, should restrict rating to the spine.

7. A valid impairment evaluation report based on the Guides must contain the 3-step approach

8. The evaluating physician must use knowledge, skill, and ability generally accepted by the medical scientific community when evaluating an individual, to arrive at the correct impairment rating according to the Guides.

9. The Guides is based on objective criteria. The physician must use all clinical knowledge, skill, and abilities in determining whether the measurements, test results, or written historical information are consistent and concordant with the pathology being evaluated. If such findings, or an impairment estimate based on these findings, conflict with established medical principles, they cannot be used to justify an impairment rating.

10. Range of motion and strength measurement techniques should be assessed carefully in the presence of apparent self-inhibition secondary to pain or fear.

11. The Guides does not permit the rating of future impairment.

12. If the Guides provides more than one method to rate a particular impairment or condition, the method producing the higher rating must be used.

13. Subjective complaints alone are generally not ratable under the Guides.

14. Round all fractional impairment ratings, whether intermediate or final, to the nearest whole number.

PROGNOSTIC FACTORS FOR NON-RECOVERY

PROGNOSTIC FACTORS FOR NON-RECOVERY

            The capacity to predict outcome following whiplash injury is important for several reasons. Predictive factors may be modifiable or non-modifiable, and treatments directed at the former factors may improve outcomes for those identified as at risk of poor recovery. This, in turn, may assist in the curtailment of both personal and financial costs associated with the condition. The identification of those who show good potential for recovery is also important so that both injured people and clinicians can have greater confidence in a good outcome. An understanding of prognostic indicators for both outcomes will allow the appropriate allocation of resources by policy-makers.

Fifteen years ago, the Quebec Task Force identified predictive studies as an area requiring urgent investigation in whiplash research. Since that time the number of cohort studies has substantially increased and now several systematic reviews of prognosis are available. However, these have not been undertaken without difficulty owing to shortcomings in some of the primary cohort studies, including inconsistencies between studies in time from injury until baseline data collection, time to follow-up and use of various and sometimes un-validated outcome measures. There is also variation between the systematic reviews, with some performing meta-analysis, others indicating that due to heterogeneity data pooling could not be undertaken, and others comprising task force findings that were not peer reviewed. Nevertheless, the findings of the various reviews have generally been in agreement that the factors of higher initial predictors of poor functional recovery.

It is not the aim of this chapter to conduct another systematic review of currently available cohort studies. Rather, it is to present an overview of systematic potential findings, discuss emerging factors that show potential for prognostic capacity of both recovery and non-recovery, and outline the clinical implications for the recognition of prognostic indicators.

PRESENTING SIGNS AND SYMPTOMS

Clearly, the most consistent predictor of poor functional recovery is the intensity of neck pain at the initial or baseline assessment point. Walton et al. synthesized the data from eight cohorts and established a cut-off point of 55 out of 100 or 5 out of 10 on a visual analogue pain scale. These authors report that a pain intensity of greater than 55 out of 100 demonstrated a nearly six-fold (OR, 5.77; 95% CI: 2.89-11.52) increase in the risk of persistent pain or disability at follow-up. This factor was slightly more robust at predicting an outcome of disability when compared to pain outcomes. Initially, moderate-to-high levels of pain-related disability have also shown predictive capacity.

Some reviews pointed to other symptoms, such as the presence of headache, or neurological symptoms, such as arm pain or paresthesia, as also showing predictive capacity. The Quebec Task Force classification (see Chapter 1 for description), a predominantly symptom-based system, was evaluated in two reviews, with the authors concluding that increasing grades of whiplash associated disorders (WAD) predicted increasingly higher pain intensities and disability two years later. Walton et al. reported that the size of effect was significant when WAD grades II and III were compared against grades I and 0, and this effect was consistent at various follow-up times points.

Other symptoms, such as dizziness, reported sleep disturbances and cognitive difficulties, have not emerged from the systematic reviews as showing any predictive capacity.

THE ECONOMIC BURDEN OF WAD

THE ECONOMIC BURDEN OF WAD

Little is known about the individual and societal economic burden of WAD. For instance, little is known about the prevalence of long-lasting work disability due to WAD, which probably the most costly part. This burden is probably largely dependent on the legislation in different countries. In 2002, an independent and temporary Commission on whiplash-related injuries was informed in Sweden, initiated by the four largest motor vehicle insurers. The mandate of the 3-year commission was an examination of the problems of WAD from road safety, medical care, insurance and societal aspects. One of the conclusions of the final report was that the yearly cost for society and for the insurance industry was approximately SEK 1.5 billion (US$201 million), while projected costs (i.e. what new cases of WAD arising in a particular year will cost society and insurers by the time the person reaches retirement age) amounted to SEK 4.6 billion (US$648 million). These calculations were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002. Since the report’s publication, the number of WAD cases have decreased dramatically to about 16,000 claims in 2008 (173 per 100,000 inhabitants), which, of course, has an impact on the overall costs.

Comparable data has not been found, but there is some evidence from a study that addressed the incidence of WAD in 10 European countries. The administrative data suggests that the total claims cost in Switzerland was 500 million Swiss francs (US$467 million). Switzerland’s population is 80% that of Sweden. Expenditures in addition to the claims cost was not reported in that study. 

COURSE AND PROGNOSIS OF WAD AFTER A MOTOR VEHICLE CRASH

COURSE AND PROGNOSIS OF WAD AFTER A MOTOR VEHICLE CRASH

Course of Recovery

Understanding the course and prognosis in WAS is critical. Will people recover from this common injury? Is so, when? If the injury is transient and self-limiting, there would be no need for major prevention and intervention strategies. The natural course and prognosis of WAD has been a controversial matter. Some claim that the prognosis is solely determined by the physical injury and its severity, and that pre- and post-psychosocial factors are not relevant in recovery. Others claim that persistent WAD is mainly a ‘psycho-cultural’ illness, and refer to studies from Lithuania and Greece where there is no or little awareness or reporting of WAD resulting from a whiplash mechanism. Studies from these countries report that 2% or less of study participants report long-lasting symptoms after car collisions. However, drawing firm conclusions based on the findings of these studies is inappropriate, since ‘psychocultural’ factors were not studied per se. Nevertheless, when persons who do not experience neck pain following a car collision have been asked to report on which symptoms they would expect after neck injury or minor head injury, those from Lithuania and Greece do not expect to have as many symptoms or do not have as long-lasting symptoms compared to persons in Canada.

In the majority of studies, the recovery rate is substantially lower than recovery rates reported in Greece and Lithuania. Some report a 66-68% recovery rate at one year after the injury, whereas others report a less than 40% recovery rate at a similar time point. Differences in recovery rates are at least partially due to selection bias. For instance, in the study by Miettinen et al., only 58% of the invited study population was followed up 12 months post injury, so it was unknown what the recovery rate was for the 42% of participants who could not be contacted at follow-up.

Prognostic Factors

A prognostic factor is a factor that is independently associated with the prognosis, and which can contribute to or work against recovery from a condition. Some factors known to contribute to a poor prognosis in WAD are similar to those for other forms of persistent neck pain. These factors include, among others, passive coping strategies, poor mental health, high level of stress, high pain intensity and more ‘associated’ symptoms, such as arm pain, headache and nausea. Similar to the literature on neck pain in the general population, gender does not seem to be a clear prognostic factor in WAD, after adjustments have been made for psychosocial factors. This suggests that the observed poor prognosis in females in some studies might be explained in terms of the psychosocial factors rather than the biological factors of gender. Furthermore, societal factors, such as insurance systems with possibilities to claim for pain and suffering, and extensive healthcare utilization in the early stage of the injury, have been suggested to be associated with delayed recovery in WAD.

Surprisingly, the bulk of evidence suggests that crash-related factors (e.g. impact direction, awareness of collision, head position) are not associated with the prognosis.

There is evidence that people’s lowered expectations of recovery and return to work, assessed early in the process of recovery, are an important predictor for long-lasting WAD, even after controlling for other factors, such as prior health, pain areas and acute post-traumatic stress symptoms. An expectation is defined as a degree of belief that some as being tied to an outcome, such as a recovery state or return to work, rather than the individual behaviors required to achieve that outcome (self-efficacy expectations). It is believed to be influenced by personal and psychological features, such as anxiety, self-efficacy, coping abilities and fear, and recent studies have demonstrated that in those with WAD, initial pain, depressive symptomatology, and some crash and demographic factors were associated with recovery and return-to-work expectation.

Health expectations are postulated to be primarily learned from the cultural environment, and based on ‘prior knowledge’. The mechanism by which expectations influence emotional and physical reactions may also actually affect the autonomic nervous system, involving biochemical processes, which may explain some of the power observed in studies of the placebo and nocebo effect. These mechanisms help to explain why persons who strongly anticipate they will recover really do, and why strong expectations about bad health actually lead to bad health. A concept that is closely related to expectations is a person’s belief—the lens through which a person views the world—which is shaped by the environment. In a study where injured persons were asked about their belief of the origin of their neck pain (casual belief), those who believed that something serious had happened to their neck had greater perceived disability during follow-up compared to those who did not have such beliefs.

WAD and Widespread Pain

One important aspect about the course of recovery from WAD is whether the neck injury is a trigger for subsequent widespread body pain. This has been suggested from cross-sectional studies, but knowing whether widespread pain came before the neck injury remains unclear from this type of study design. A potential aetiological explanation is a neurophysiological disturbance in the peripheral and central nervous system, which, in some stances, leads to an increased sensitivity to pain in other ‘uninjured’ areas. Another possible explanation for widespread pain is that new tissue damage may result from an altered pattern of movement in the body due to the neck pain. The exact aetiology of widespread pain is that new tissue damage may result from an altered pattern of movement in the body due to the neck pain. The exact aetiology of widespread pain is probably complex and multifactorial, but there are no indications that it would be specific to WAD. It can also occur after surgical intervention or any tissue damage. In addition, large prospective studies on pain of other aetiology have demonstrated that psychosocial factors at work, repetitive strains or other physical strains at work, awareness of symptoms and illness behavior may increase the risk of development of widespread pain. Thus, it seems that biological as well as psychological and social factors contribute to the development of widespread pain.

Prospective studies on WAD and its association with widespread pain are sparse and the evidence is not clear. The results from one study suggest a relationship between the onset of neck pain or other associated symptoms as well as self-perceived injury severity, after an MVC, and subsequent widespread pain. However, age, gender, health behavior and somatic symptoms prior to collision were at least as important. Another study investigated the incidence of onset of more extensive pain during 12 months of follow- up of WAD claimants, and associated factors with such an outcome. In that study, a less conservative definition of widespread pain was used and probably have resulted in higher incidences. The main conclusions were that widespread pain was common over a 12-month period (21%), but most improved over the follow- up period. Female gender, poor prior health, greater initial symptomatology (including pain intensity) and more depressive symptoms were associated with the development of extensive pain. The authors also found that local neck/ back pain, raising the question of the potential cause of widespread pain in other studies.

Work absenteeism and work disability

Many persons with acute WAD also have some absence from work, and no clear difference occurs between ‘blue’ and ‘white’ collar workers. In one population- based study, 46% persons had been off work due to the injury. A similar figure (49%) was seen in a Dutch study. The majority of people returned to work within a few days and only 4-9% were reported to be off work at six months past injury. In a study form the Netherlands, factors associated with not returning to work were older age and concentration problems. There was no association between degrees of manual labor, (‘blue’ or ‘white’ collar work). 

CUMULATIVE INCIDENCE OF AND RISK FACTORS FOR WAD

CUMULATIVE INCIDENCE OF AND RISK FACTORS FOR WAD

The cumulative incidence is the number of new cases of an event or outcome occurring in a population over a certain time period. Some evidence from the literature indicates that the incidence of WAD differs between countries. There is also some evidence that the incidence of WAD has increased from the beginning of the 1990s to after the year 2000, with the annual incidence for the latter period being about 300 per 100,000 inhabitants in the studies where emergency setting visits are used. In some instances, the increase is between three and tenfold. It is not known if this increase is partly due to a change in care-seeking behavior.

There are also some indications from administrative insurance claims database in different European countries (e.g. Norway, the Netherlands and Sweden) of a reduction in the number of WAD claims, whereas such decreases have not been seen in Denmark or the United Kingdom. Sweden, for instance, has seen a 33% decrease in personal motor vehicle crash (MVC) injuryclaims between 2002 and 2008. The relative decrease is similar between the incidence of WAD and other types of injuries, with WAD constituting about 50% of all MVC injury claims. This decrease is not due to reduction in the number of MVCs, and nor has the insurance system in Sweden changed. Instead, this decrease is likely to be due to a combination of reasons. For example, some care manufacturers have developed whiplash-protection devices for new car models, which presumably will result in fewer cases of WAS as a result of rear-end collisions. Secondly, during the second half of the 1990s, police personnel in Sweden showed an increased awareness that there is no need to advise car occupants to seek healthcare if no symptoms are present. Thirdly, the mass media focus in Sweden on whiplash has decreased substantially from over 800 articles in the beginning of the 2000s to only about 200 articles in 2008.

Incidence calculation through insurance claims may be prone to other forms of bias. For instance, insurance systems where there are no benefits for the person responsible for a collision may underestimate the frequency of injuries, since fewer claims would be reported. This would also happen with insurance systems where insurance claim access us limited, or where payments for compensation result in a significant increase in the insurance premium. On the other hand, healthcare data may also be prone to bias, since such data only captures those who seek the type of healthcare utilization in question (e.g. emergency care).

Collision Variables That A Doctor Or Biomechanist Should Consider

Collision Variables That A Doctor Or Biomechanist Should Consider

               

               A) Never assume that all vehicles have the same crash worthiness or safety ratings

               B) Weight of the occupant’s vehicle relative to striking vehicle

               C) Aggressive nature each vehicle (e.g., a F-250 PU strikes a passenger car)

               D) Primary Direction of Force (PDOF) or impact angles

               E) Point of impact

               F) Relative heights of each variable

               G) Intrusion amount relative to sitting position of occupant and occupant motion during impact

               H) Driver versus front passenger and vehicle structures in front of each position

               I) Secondary impacts

               J) Vehicle rotation during and after impact

               K) Type of seatback

               L) Crash pulse characteristics and timing

               M) Seatbelt’s interaction

               N) Airbag deployment interaction

Disc injuries in Frontal Impacts

Disc injuries in Frontal Impacts

              

  Wismans et al performed twelve postmortem human subjects (PMHS) autopsies in a frontal impact testing at 15 and 23 gs. These PMHS had died from non-traumatic causes, such as poisoning or suffocation. All cadavers were restrained in three-point belt systems. After the sled impacts, each PMHS was autopsied. In seven tests cervical disc injuries were noted, including hemorrhage, tears, protrusions in the C3-C4-C5-C6-C7 levels. Disc protrusions were noted under the posterior longitudinal ligament. Lacerations to the ligamentum flavum were also observed. The detailed autopsy found no evidence of any fractures to the cervical spine, although two cadavers had anterior T2 fractures. Kallieris et al conducted cadaver testing in 23 frontal impact tests with delta-Vs of 30-60 km/h into a barrier. The most common injury noted in the cervical spine was intervertebral disc hemorrhages (20%), followed by ligamentum flavum injuries at C6-T1 levels, and fractures at T2 level.

Disc Injuries in Frontal, Side, and Rear-end Crashes

Disc Injuries in Frontal, Side, and Rear-end Crashes

               

         In a trail, two of the biomechanical and surgical opinions that defense experts often testify about are disc bulges and herniations after MVCs, proposing that all are preexisting phenomena and that single-event MVCs cannot cause herniations of the disc until after the spine fractures to some massive degree. One study often quoted by these experts as the basis for this opinion concluded, “With regard to the relationship between disc rupture and impact loading on the spine, it can be safely said that disc ruptures do not occur as the result of a single loading event, unless there are associated massive bony injuries to the spine.” Although controlled laboratory studies have shown that vertical compression of a spine are associated with bony fractures and disc injuries, this is not representative of real-world frontal, side, or rear impacts. It is deceptive to imply that vertical loading studies from pilots rejecting from airplanes, or two cadaver vertebrae (muscles removed) that are mounted on a testing device and then compressed until fracture/disc bulging occurs can be compared to horizontal loading in MVCs. In most collisions where rollovers do not occur, most of the forces are in the horizontal axis and the vertical components are significantly less. The sources that King cites used axial loading for their opinion or used cadaver spines that were not allowed all six-degrees of motion (flexion, extension, rotation in both directions, and lateral flexion in both directions).

               Post-traumatic disc injuries, including annular rears, disc fissures, disc bulging, and herniations are commonly seen in clinical practice. Many of these cases have a recent or prior history of being involved in a MVC. Invertebral disc injuries are routinely seen in occupants involved in rear-end and side collisions, and are seen less often and at higher delta-Vs in frontal impacts in my experience. Circumstances of the collision, occupant age, proneness to injury, out-of-position (OOP) issues, and other factors can change the delta-V threshold for any collision type. These disc injuries are seen in low-speed impacts as well as higher velocity crashes. Although some defense biomechanists and DMEs contend that it is impossible to herniated a human disc without previously fracturing vertebrae, this is not supported in cadaver tests that replicate real-world collisions using entire cadavers, which allow for typical human kinematic motion experienced in a MVC. Some defense experts who opine that the fracture of the vertebrae is a requirement for a traumatic disc herniation to occur may rely on airplane ejection studies that subjected the cadaver to rapid, high force vertical loading or used cadaver spines mounted on plates and forced into various motions. The majority of these tests did not allow the spine to move in all sex-degrees of freedom in same manner as seen in a MVC. For example, the spine may be compressed and analyzed for damage and then flexed in a separate test. Unfortunately, there has been little research of disc injuries following frontal, side, or rear-end crashes.

               I have seen several cases in my office where an MRI was taken of a person’s spine before and after an MVC, confirming a disc bulge. These pre-crash MRIs were usually taken to rule out the cause of a prior episode of neck or back pain with out without radiculopathy, and were found normal. In some instances there was a confirmed contained minimal disc bulge with post-collision MRI showing significantly larger disc protrusion with spinal cord impingement. The majority of disc injuries occur without concomitant fractures of the spine. However, there are many cases where the MRI will detect some degenerative changes in the disc or surrounding joint.

               It is common for a defense biomechanist or defense doctor to opine that the x-rays do not show any abnormalities, thus providing that there is no objective evidence of any injuries and all post-traumatic complaints were not due to the crash event. The assumption used by some of those defense experts is that if the x-ray looks normal, then the injury doesn’t exist. However, this premise has little scientific merit after a close examination of the available cadeveric research and the clinical literature.

               In fact, contrary to some defense theories, several real-world studies using cadaver spines that were allowed to move in all six degrees of motion showed that disc tears/hemorrhage and bulging often occur without any fractures of the spine. Taylor and Taylor performed autopsies of 109 humans who died following blunt trauma, where MVCs accounted for 72 of the fatalities, 34 from blows/falls, and 3 from sporting activities. The study noted that, “Most injuries involved the joints rather than the vertebrae; e.g., injuries to the discs were four times more frequent than fractures to the vertebrae.” The study also found that severe disc avulsions, disruptions, and traumatic herniations were located primarily at the C5-C6-C7 regions. There were almost equal numbers of disc injuries and facet injuries in the autopsy analysis. When determining the type of force vector from the police reports, 54% were from extension or extension-compression injuries and 27% from flexion or lateral-flexion injuries. The C2 and C6 vertebrae were the most common sites for fractures. In the upper cervical spine, bruising of the posterior synovial folds was the most common injury noted with hematoma around the C2 nerve. The study also compared radiologists’ diagnosis of 58 sets of x-rays with the findings at autopsy, concluding that the radiologist failed to detect 199 of the 309 lesions noted in autopsy.

What is a traumatic event?

What is a traumatic event?

A traumatic event occurs when the forces experienced during the various stages of the collision are greater than what is tolerable or is beyond the stress/strain threshold for the specified region of the body or type of tissue. These forces may cause minor (AIS 1 level) injuries, having no risk of fatality, and at the same time may present the occupant with sub catastrophic injuries, including strains, sprains, contusions, bruising and swelling and resultant symptoms and findings consistent with a WAD. Just because an injury or the cause of a patient’s subjective complaints is not objectively seen does not mean that it doesn’t exist. Unfortunately, current technology is not sensitive enough to detect some types of injuries. More severe injuries may also occur, resulting in more obvious injuries, including fractures, bleeding, organ disruption, and death.

Vascular Events

Vascular Events

            

   In addition to the vascular changes associated with the bleeding, there are also marked changes in the state of the intact vessels. There are changes in the caliber of the blood vessels, changes in the vessel wall and in the flow of blood through the vessels. Vasodilation follows an initial but brief vasoconstruction and persists for the duration of the inflammatory response. Flow increases through the main channels and additionally previously dormant capillaries are opened to increase the volume through the capillary bed. The cause of this dilation is primarily by chemical means (histamine, prostaglandins and complement cascade components C3 and C5) while the axon reflex and autonomic system exert additional influences. There is an initial increase in velocity of the blood followed by prolonged slowing of the stream. The white cells marginate, platelets adhere to the vessel walls and the endothelial cells swell. In addition to the vasodilation response, there is an increase in the vasopermeability of the local vessels (also mediated by numerous of the chemical mediators), and thus the combination of the vasodilation and vasopermeability response is that there is an increased flow through vessels which are more “leaky”, resulting in an increased exudate production.

               The flow and pressure changes in the vessels allow fluid and the smaller solutes to pass into the tissue spaces. This can occur both at the arterial and venous ends of the capillary network as the increased hydrostatic pressure is sufficient to overcome the osmotic pressure of the plasma proteins. The vessels show a marked increase in permeability to plasma proteins. There are several phases to the permeability changes but essentially, there is a separation of the endothelial cells, particularly of the venules, and an increased escape of protein rich plasma to the interstitial tissue spaces. The chemical mediators responsible for the permeability changes include histamine, serotonin (5-HT), bradykinin and leukotreines together with a potentiating effect from the prostaglandins.

               The effect of the exudate is to dilute any irritant substances in the damaged area and due to the high fibrinogen content of the fluid. A fibrin clot can also form, providing an initial union between the surrounding intact tissues and a meshwork which can trap foreign particles and debris. The meshwork also serves as an aid to phagocytic activity. Mast cells in the damaged region release hyaluronic acid and other proteoglycans which bind with the exudate fluid and create a gel which limits local fluid flow, and further traps various particles and debris. 

Tucker History

Tucker's History Predates the Civil War

In the early 1800s a tall young man from Scotland named Greenville Henderson made his way from the battles of the Indian Wars to his Georgia home. As a reward for his valiant services, the governor of Georgia gave Henderson 3,000 acres of land in what is now known as the Tucker area.

This land, valued at 50 cents an acre, roughly encompassed from east to west the area from Tucker to below Northlake Festival Shopping Center on LaVista Road and north of Henderson Mill Road south to Lawrenceville Highway (U.S. 29). Settling on this tract of land, Henderson operated large apple and peach orchards, corn fields, and a prosperous whiskey and brandy making business. He shipped finished product to Savannah by wagon train in exchange for window glass, salt, sugar, coffee and building brick brought to the Atlantic seaport by boat.

Before the Civil War, Henderson built the historic grist mill on Henderson Mill Creek at the intersection of Midvale Road and Henderson Mill Road. Near the mill was the old frame Henderson Post Office. Mail was brought by horse and buggy from Decatur for people in the Tucker area. The post office was abandoned in 1895 and the mill demolished in 1911. Henderson's home was on a sloping hillside overlooking the grist mill is now the site of St. Bedes Church.

In 1861, the Civil War swept the countryside. Seven of Henderson's sons left to fight in the Confederate Army. Two never returned.

On a hot day in 1864 word came to the Tucker area that the Union Army was advancing on the area. The army of Tennessee under the command of Gen. James McPherson decided to come to the Southeast to cut off the Georgia railroad near Stone Mountain where Atlanta would be isolated from the east. The Federals 15th Army Corps under the command of Maj. Gen. John Logan crossed the Chattahoochee River at Roswell and detoured to Browning's Courthouse in Tucker to give support to Garrard's Army in the destruction of the railroad. This courthouse was recently moved to the grounds of the Tucker Recreation Center on LaVista Road. Garrard's soldiers headed toward Stone Mountain long Fellowship Road on July 18, 1864.

Confederate soldiers under the command of Gen. Joseph Wheeler fought hard to stop the march. The Federal troops reached Stone Mountain and destroyed a two-mile section of the Georgia Railroad tracks, several culverts and the water tank. Approximately 150 of the Confederate soldiers who were killed in defending the railroad are buried in a small cemetery near the mountain.

Meanwhile, the mission at Stone Mountain accomplished, Logan's Federal troops withdrew from Browning's Courthouse in Tucker to Henderson Mill the evening of July 18 to camp near a water supply. Early the next morning Logan's troops joined Blair's Army Corps near Midway Baptist Church (the small church across from Northlake Mall on Henderson Mill Road) and marched toward Decatur to fight in the Battle of Atlanta.

In 1869, four years after the war, Greenville Henderson died. He is buried in a small cemetery off Henderson Mill Road near the intersection of Midvale Road. Buried with him are about 30 relatives including his wife, Nancy, who died in 1892 at the Age of 102.

Growth was steady in the area after 1892 when the Georgia, Carolina and Northern built the railroad through the center of what is now called Tucker. The first business in Tucker was a saloon and horse race track on Fellowship Road. The area had been known as Browning's District until 1907 when the Seaboard Line Railway acquired the railroad and surveyed the unincorporated town of Tucker and named the town after an Officer of the company, Capt. Tucker.