Chronic Post-Traumatic Neck and Head Pain

Seymour Solomon, MD
Headache. 2005; 45 (1): 53-67. ©2005 Blackwell Publishing

Abstract and Introduction

Abstract

Objective: This is a review of current concepts of chronic post-traumatic neck and head pain. In this
article, I will emphasize the physiological and sociological aspects of these disorders.
Background: The pathophysiology of chronic post-traumatic neck and head pain has not been well
understood. Some have emphasized the organic factors and others the psychogenic aspects of these
conditions. Only in recent years have this dichotomy been integrated with sociocultural concepts.
Methods: The history of chronic post-traumatic head and neck pain is reviewed. Paradoxes are
discussed, ie, the great differences in prevalence around the world, the inconsistent relationship of
symptoms to degree of trauma, the curious phenomena of structural disease without symptoms, and
symptoms without structural disease. The organic and pathophysiologic factors are reviewed, then
those factors that modulate pain in these conditions are discussed.
Conclusion: Chronic post-traumatic neck and head pain is rarely either organic or psychogenic.
Rather physiological, social, and cultural factors play major roles in modulating pain and either
perpetuate or ameliorate these chronic pain conditions.

Introduction

This review summarizes the evidence supporting the multidimensional mechanisms of chronic neck
and head pain following trauma. The essential psychological, cognitive, social, and cultural aspects
will be emphasized. The mechanisms of chronic post-traumatic head and neck pain have not been
well understood. When injury is severe and neurological examination or imaging studies reveal serious
defects, the organic cause of pain is evident. But in many cases pain persists without objective signs,
and it is this phenomenon that will be discussed. Psychogenicity is often evoked or organicity is based
upon nonspecific changes in sophisticated tests or response to treatment. In recent decades, many of
the complex mechanisms of pain have been revealed and the dichotomy of psychogenic versus
organic has given way to the integration of sociocultural concepts with organic and
psychologic/cognitive factors.[1–3] Understanding and applying these concepts will help to decrease the
intensity and prevalence of chronic post-traumatic pain.

The concept of cerebral concussion has evolved since ancient times.[3] Modern concepts began in the
1700s.[4] In 1705, a man committed suicide by hurling himself head first against a wall.[2] The autopsy
did not reveal brain damage. In the 1800s, physicians began recording persistent symptoms after
head injury without residual signs and by the end of that century, the term postconcussion syndrome
was coined for the triad of headache, dizziness, and alcoholic intolerance with headache as the
cardinal symptom.[4] Additional features were added in the twentieth century.

With the advent of the automobile, motor vehicle accidents (MVAs) grew to be the most common
cause of head and neck injuries. The term, "whiplash" injury was first used at an orthopedic meeting in
1928 describing the effect on the head and neck of rear-end MVAs.[5] The first report was published in
1945;[6] subsequent reports in the literature of whiplash injuries have grown exponentially. Similarly, the
number of people reporting whiplash injuries has progressively and markedly increased.[7,8] Evidence of
the social and cultural factors associated with this condition has been developed only in the past
decade.

Paradoxes

There are several paradoxes associated with chronic post-traumatic head and neck pain. The
prevalence is high in some countries and low in others. The occurrence of headaches is often
inversely related to the severity of the injury. Symptoms of the postconcussion syndrome are not
usually associated with structural disease, while structural disease of the neck often occurs without
associated symptoms. Soft tissue injuries (muscle, tendon, or ligament strain, sprain, or tear) heal
quickly without residual pain in most parts of the body but these injuries to the neck and head are often
an exception.

Epidemiology

Acute

There were 13.8 million MVAs in the United States in 1997 and 3.9 million were rear-end collisions.[9] It
is estimated that well over 1 million acute whiplash injuries occur per year.[10] In another estimate, half
of the people injured in MVAs in the United States have acute whiplash injuries, while in Australia
about one-third of those involved in a rear-end collisions experienced acute whiplash symptoms.[11,12]

Of course, the brain may be injured during whiplash activity as well as with direct head trauma. The
incidence of head injury from all causes is difficult to assess. Most head injuries are mild and not
reported to physicians or authorities and those reported are from heterogeneous populations. The
estimates of incidence of mild head injury derived from in-patient or emergency room records of
hospitals in the United States range from 200 to almost 400 per 100 000 persons.[13,14]

Chronic

Reports of chronic post-traumatic neck and head pain have increased greatly during the past half-
century but there are no definitive epidemiologic studies of the prevalence of chronic whiplash
syndrome or chronic post-traumatic headache in the United States.[10,11]

Chronic Post-Traumatic Headache

The number of people who develop chronic post-traumatic headache after mild head injury ranges
from 30% to 90%; the percentages vary from one country to another.[15] In most countries, about one-
third of head-injured people report headaches after 6 months and approximately one-fourth after 4
years.[15] But in Lithuania, 2 to 3 years after a cerebral concussion and 1 to 3 years after a whiplash
injury headache is uncommon and no different in prevalence than in control groups.[16,17]

Chronic Whiplash Injury

When discussing "chronic whiplash injury" (CWI), I will be using this term as synonymous with the
term "whiplash associated disorder" (WAD) I and II as defined by the Quebec Task Force.[18] WAD I:
neck pain, stiffness, and tenderness; II: the features of I plus musculoskeletal signs of decreased
range of motion and point tenderness. The studies to be cited will not include neurological signs (WAD
III) or fractures or dislocations (WAD IV). It has been estimated that one-third of injured Americans
experience chronic whiplash symptoms 33 months after injury and about 6% of the population have
symptoms of CWI.[11] Estimates based on data from other countries are more conservative, reporting a
prevalence of as low as 1% with chronic pain as a result of whiplash injury.[19]

There are hundreds of reports of CWI. Most studies are not of sufficient scientific quality to permit
conclusions with regard to prognosis. A recent evaluation of 356 studies of CWI from 1982 to 2002
found 50 papers of 29 cohorts that furnish scientific data.[20] All were prospective studies reporting
prognostic factors. Twelve reviews were considered of high quality (containing at least 8 of 16
attributes; 8 studies had 6 or 7 attributes, 9 had 5 or less attributes). To demonstrate the extreme
variability of prognosis from one report to another, the Table summarizes the long-term outcome of the
first 20 cohorts in descending order of quality.[21–42] The authors of this summary judged functional
recovery in terms of symptoms and disability.[20] Although the outcome criteria varied from one report to
another, it is obvious that there are tremendous differences in prognosis from one cohort to another;
from one country to another. Reports from Lithuania and Greece show none or few patients with CWI,
6 months and 1 month, respectively, after injury.[33,41] In Japan and Denmark, 11% to 8% had symptoms
after 6 months and 1 year, respectively.[21,37] A recent report from Germany also noted good prognosis.
[43]
At the other extreme are persistent symptoms of CWI as high as 82% of Swedes followed for 6
years, 57% of Canadians at 1 year (before tort reform), and 49% of Britains at 1 year.[22,26,38] The
statistics for CWI may vary greatly in the same geographic area: high in Sweden, modest in Denmark,
high in Australia, low in New Zealand.[21,28,38,44] Because of these extreme ranges the data from one
country or cohort cannot be generalized to others.

Statistics with regard to symptoms after neck injury may also vary greatly within the same country.
Insurance claims for whiplash injury accounted for 20% of all traffic injury claims in Quebec compared
to 68% in British Columbia and 85% in Saskatchewan.[18] In 1987, the incidence of compensated
whiplash injuries was 70 per 100 000 inhabitants in Quebec and 700 per 100 000 in Saskatchewan.[18]
A change from tort compensation to a no-fault insurance system in Saskatchewan was followed by a
reduction in claims by 43% in men and 15% in women.[22] Neck injury claims following MVAs in
Michigan were half of those in most other states (13% versus 26%).[45] Michigan's no-fault law (unlike
most other no-fault states) required drivers to collect vehicular and personal damages from their own
insurance carrier.

Degree of Trauma

If organic factors were the predominant mechanism of post-traumatic neck and head pain, one would
expect that the degree of trauma would commensurate with the incidence and prevalence of the pain
syndromes. But there is no consistent pattern. In some studies, poor recovery from acute whiplash
injury was related to the severity of initial trauma.[46,47] But in other studies, there was no correlation or
the incidence of whiplash injuries decreased as crash-severity increased.[48,49] In one study, poor
prognosis was associated with increasing age, but in another report older drivers made less neck-
injury claims than younger drivers.[45,50]

In several studies, the incidence of headache and other features of the postconcussion syndrome was
not influenced by the severity of the head injury.[51–53] Others noted an inverse relationship between
severity of injury and headache.[54–56] Headaches occurred in more patients with concussion than those
with traumatic brain damage. Headaches were less often reported when computerized tomograms of
the head were abnormal after trauma and when periods of post-traumatic amnesia were long.[55]

Structural Lesions Without Symptoms

Imaging studies of the cervical spine may reveal prominent abnormality but without relationship to
neck pain or other symptoms.[57,58] Cervical spine disease occurs with increasing frequency as people
age.[59] Spondylosis occurs in 13% of men during the third decade of life, 66% in the fourth decade,
and 98% after the age of 70. These figures are not influenced by prior injury. Asymptomatic
degenerative disc disease is noted in 25% during the fifth decade of life and 75% in the seventh
decade.[60] Asymptomatic incidental cervical disk protrusions were noted in MRIs of the larynx in 20%
of patients 45 to 54 years of age and in 57% of patients older than 64 years.[61] Cord impingement was
found in 16% and 26% and cord compression in 1% and 6% of these groups, respectively. In another
study of asymptomatic subjects, MRI of the cervical spine revealed disc degeneration, or narrowing in
25% of subjects less than 40% and 60% of those older than 40.[62] Herniated discs were noted in 10%
and 5%, respectively.

Symptoms Without Structural Disease

The lifetime prevalence of headache is more than 90%; a small fraction may have suffered head
injury.[63] One-third of the population has neck pain unrelated to injury.[49] The postconcussion syndrome
is a prime example of a symptom-complex without associated structural disease.[64] The many
symptoms of this syndrome may be categorized as somatic, psychological, and cognitive. Of the
somatic symptoms, headache and dizziness are most common. The psychological symptoms are
often manifested as depression or change in personality. Cognitive impairment is usually attributable
to disturbances in attention and concentration. This symptom-complex need not be related to head
trauma. Similar symptoms have been noted in people making personal injury claims unrelated to head
or neck injury.[65] Moreover, cognitive, physical, and psychological symptoms following head injury are
similar to the base rates of these symptoms in uninjured subjects.[66]
Whiplash injury can cause brain damage without associated direct head trauma.[67] Whiplash injured
patients have impairment of memory and concentration more than the healthy population but no more
than patients with similar somatic symptoms without trauma.[19]

Organic and Pathophysiologic Factors

Histological Changes

Histological evidence of cerebral injury includes microscopic axonal injury, manifested by axon
retraction bulbs and microglial clusters.[68] These changes are presumably due to the shearing effects
or to metabolic consequences of trauma.[68–70] In most reports, axonal injury noted in the brains of
experimental animals and humans was observed in injuries of at least moderate degree and the
degree of brain damage was commensurate with the degree of injury.[68,69,71] However, retraction bulbs
were noted in some people with relatively mild concussion who died of other injuries.[68,69] A more
recent study of five patients who sustained mild head injuries and died of other causes showed
multifocal axonal injury 2 to 99 days after trauma; but all were older than 59 years.[72] The degree and
extent of damage in these cases is considered too small to explain all of the symptoms of the
postconcussion syndrome.[73]

Physiological Factors

A number of physiological changes in the brain have been reported in people with chronic post-
traumatic neck or head pain; however these changes are not specific. Single photon emission
computed tomography (SPECT), positron emission tomography (PET), and regional cerebral blood
flow (rCBF) studies have shown reduction in glucose consumption and in blood perfusion of some
areas in people with chronic whiplash and postconcussion syndromes. These changes were found in
open studies, as well as when compared to control groups, but the numbers were small.[74–77]
Interhemispheric cerebral blood flow differences were seen in a higher percentage of people with
chronic post-traumatic headache than in those with migraine or a control group.[76] Changes in SPECT,
PET, and rCBF have been noted in migraineurs and in people who are depressed or seeking
psychological help.[75,79,80] In patients with post-traumatic headache, there may be alterations in event-
related potentials (eg, increased latency of P300).[75,81] But alterations in these potentials are also noted
in people with depression and anxiety. Complaints of visual disturbances and dizziness may persist
into the chronic phase of whiplash injury.[82] The visual symptoms have been attributed to defects in
visual pursuit.[83] Dizziness has been associated with abnormal electronystagmography. In a poorly
controlled study, abnormal electronystagmography was found to be greater in patients with whiplash
injuries than in normal subjects, but another study found no difference between the two groups.[84,85]

Other changes noted soon after mild brain injury may have implications for chronic symptoms.
Localized increased activation was seen in functional MRIs after high memory load.[86] Polymorphism
of the APOE gene was associated with a poor prognosis after head injuries in patients admitted to a
neurosurgical unit; only one-third of these patients had mild head injury.[87] Biochemical evidence of
brain perturbation following experimental head injury includes the release of excitatory amino acids
(eg, glutamate and aspartate) and modulation of inhibitory agents (eg, magnesium and endogenous
opioids).[88–93] Again, these phenomena were usually noted when trauma was acute or moderate or
severe in intensity.

Response to Therapy

Pain relief after anesthetic blocks of atlantoaxial joints and zygapophysial joints have been presented
as evidence of unrecognized sites of neck and head pain.[94,95] Some experts believe that traumatic
lesions of zygapophysial joints cause chronic neck pain in spite of the absence of objective signs on
clinical examination or imaging studies.[95,96] Traumatic lesions of the zygapophyseal joints may not be
seen on routine roentgenograms or magnetic resonance imaging. But technetium 99m isotope
scanning also failed to detect abnormality, such as periosteal irritation, that might occur with ligament
injury in patients with whiplash injury.[97] Using different anesthetic blocks having short and long lasting
effects, neurotomies at zygapophysial joints and controlled sham procedures resulted in prolonged
pain relief in a majority of patients who underwent neurotomy or an appropriate block.[95,96] However, in
a recent study radiofrequency neurotomy of cervical facet joints when compared to sham treatment in
a double blind protocol failed to reveal differences in outcome between the two groups.[98]

Nerve blocks or ablative procedures are not as diagnostically specific as they appear. Anesthetic
nerve blocks have a low sensitivity and low specificity.[99] The placebo response and the false positive
rate of uncontrolled diagnostic blocks are high.[100,101] Moreover, pain may be relieved by anesthetic
blocks in zones of pain radiation distal to the nerve root site of pain production and even in areas of
perceived pain or pain projected from the central nervous system.[99] In short, interruption of peripheral
afferent neurons may evoke nonspecific pain relief. As a general rule, it is not wise to diagnose an
illness based on amelioration of symptoms following therapy.

An increasingly popular mode of therapy is injections of botulinum toxin. This was found to greatly
diminish pain, tenderness, and disability in patients with chronic neck pain but the same degree of
improvement was noted in patients who received placebo injections.[102]

Cognitive Factors

Neuropsychological symptoms are common features of the post-concussion syndrome and are often
present after whiplash injury. Neuropsychological testing is often helpful in documenting the degree of
cognitive impairment. In one study, the degree of neuropsychological deficits 1 month after injury
appeared to be related to the severity of injury.[103] But in two neuropsychological studies of patients
after mild head injuries the cognitive changes were similar to control groups.[104,105] The validity of
cognitive changes depends on the patient's attentiveness, concentration, and motivation.[106] The
testing also can be adversely affected by depression, anxiety, fatigue, pain, and medication.[107–109]
Certain memory deficits in patients with chronic pain are also related to fear of pain and
catastrophizing beliefs.[110] Cognitive defects in the chronic postconcussion syndrome and chronic
whiplash syndrome are considered, for the most part, to be due to one or several of the above factors.
[19,64]

Pain Modulation

Pain, particularly chronic pain, may be modified by many factors especially psychological and
cognitive.[111] Expectation of and attention to pain can prolong and amplify pain. The lack of expectation
and distraction can have the opposite effect. In addition, chronic pain is often incorrectly attributed to a
past traumatic event. These factors may be greatly influenced by different societies and cultures.[112] All
of the above are interrelated but will be discussed individually.

Psychological Factors

Patients with chronic pain demonstrate more psychopathology than pain-free controls and subjects
with chronic post-traumatic headache have the highest degrees of psychopathology.[113] Although
psychological distress is often part of the postconcussion syndrome and chronic whiplash syndrome
these symptoms are more likely a consequence of chronic pain than of preexisting traits.[114–117] The
psychological consequences of chronic whiplash pain (somatization, depression, obsessive-
compulsive qualities) are similar to those of people who have chronic pain from other musculoskeletal
injuries.[118] Stressful life events are more likely to be related to poor outcome after whiplash injuries
than clinical signs.[19] In humans pain is always accompanied by an affective response. Anxiety and
depression augment pain intensity.[119,120] They enhance attention to pain and pain in turn generates
anxiety and depression leading to a vicious cycle.

Behavioral Factors

The response to pain may vary from confrontation to avoidance.[121] Some people view pain as an
annoyance and are strongly motivated to return to normal activity. At the other extreme are those who
avoid activities that are anticipated to increase pain. The fear of pain leads to reduction in physical and
social activities and prolonged disability with attendant physical and psychological consequences.[122,123]
This fear-avoidance model may account for exaggerated pain perception and hypervigilance to pain.
The fear of pain and associated behavior may be more disabling than the pain itself.[124] Fear
avoidance beliefs about work were predictors of disability at 4 weeks after onset of low back pain and
may be an important factor in the transition of acute to chronic pain.[125] Conversely, higher pain self
sufficiency belief is associated with reduction of avoidance behaviors.[126] In compassionate societies,
victims of injury or the assumption of a victim's sick status exempts people from the usual standards of
behavior. Withdrawal from interpersonal relationships at home or at work is tacitly sanctioned.[127]
Perception of control reduces stress and associated symptoms while perception of the loss of control
may have demotivational effects.[128]

Expectation

Just as expectation of a favorable outcome may evoke a placebo effect, expectation of a poor
prognosis may result in a self-fulfilling nocebo response.[112] Both verbal and nonverbal
communications of expectations play roles in etiology and prognosis.

Expectation as a major etiologic factor in the postconcussion syndrome was studied in 100
consecutive patients referred for neuropsychological examination because of chronic postconcussion
complaints.[129] The symptoms of patients were compared to 223 volunteers who had not experienced
head injury. Both groups were given a list of 30 symptoms including affective, somatic, and memory
items. The volunteers were to note the symptoms they presently experienced and then imagine the
symptoms that would be present 6 months after an MVA that caused transient loss of consciousness.
The patients referred for examination were asked to check off the symptoms they experienced before
the accident, soon after the accident and at the time of the present evaluation (an average of 1.7 years
after injury). Of the 30 symptoms, 22 were anticipated by the volunteer control group. Their responses
did not significantly differ from those of patients following an MVA. There was a common expectation
of the following symptoms listed in order of decreasing frequency: headache, anxiety, depression,
difficulty concentrating, dizziness, visual impairment, trouble thinking, irritability, fatigue, sensitivity to
light, and memory impairment. Headache and visual symptoms were expected more often in
volunteers than their occurrence in patients.

Expectation as a major factor in chronic post-traumatic pain was studied by comparing the responses
to queries in different countries.[130] One hundred and seventy-nine Canadians and 171 Lithuanians
who had not been involved in MVAs were given a 56 symptom check list and asked to imagine
symptoms that might occur after an MVA with brief loss of consciousness. The acute symptoms
anticipated by the Canadians and Lithuanians were similar. Canadians anticipated chronic symptoms
much more often then Lithuanians. Forty-five percent of Canadians expected headache for months or
years after MVA while only 23% of Lithuanians had this expectation. Similarly, 44% of Canadians
thought they would have neck pain months or years after such an MVA, but only 1% of Lithuanians
anticipated this symptom. The differences were similar when subjects were asked to imagine the
effects of MVA causing neck sprain.[131] Headache months or years later was anticipated in 32%
Canadians and 1% Lithuanians; neck pain in 50% Canadians and 20% Lithuanians. A similar study
compared the expectations of Greeks (n = 200) and Canadians (n = 179) following minor head injury.
[132]
Again, both groups anticipated similar acute symptoms commonly reported by accident victims but,
in contrast to Canadians, very few Greeks selected symptoms likely to present a chronic problem. Five
percent of Greeks and 45% of Canadians expected headache or neck or shoulder pain lasting months
or years.[132] Most recently, the same methodologic study was carried out in Germany.[133] Again,
anticipation of acute head injury symptoms were similar in Germans and Canadians but strikingly
different in expectation of chronic symptoms. Thirty-two percent of Canadians expected headache,
and 50% anticipated neck pain as chronic symptoms, while the expectations of these symptoms in
Germans was 5% and 6%, respectively. (The expectation of chronic disability due to rheumatoid
arthritis was similar in Canadians and Germans.)[133] In a smaller study, patients who were symptomatic
2 years after whiplash injury had shown more concern for long-term suffering and disability at the time
of injury than those who did not have chronic pain.[50]

Children, athletes, drivers in demolition derby, human volunteers rarely develop chronic pain at least in
part because they don't expect to.[134–137] Other factors may also be operative. Children are more
malleable, athletes have stronger musculature, people anticipating trauma can brace themselves.
Conversely, acute whiplash symptoms may be evoked by exposure to a placebo rear-end collision.[138]

Attention and Amplification

Lack of attention (distraction) may suppress pain (eg, the soldier wounded in battle), focusing attention
on pain reinforces and amplifies pain.[139] Attention to pain is a primary factor in its intensity and
duration.[111] This is in part innate but it also derives from experience and culture.[140] Attention to the
pain experience may evoke fear of pain and catastrophizing beliefs.[110] Attention to chronic pain is
dependent on pain-related fear and creates a state of hypervigilance to pain.[141] Chronic post-traumatic
headache is unrelated or inversely related to the severity of trauma perhaps because people with
obvious structural lesions are paying attention to their defects (eg, paresis, visual loss) rather than to
headache. In volunteers, nociceptive-evoked potentials were modulated by attention to the pain stimuli
applied to one hand in contrast to unattended stimuli applied to the other hand.[142]

These phenomena have practical implications. Labeling a condition may focus attention to and
increase concern of pain. The labels of "cervicalgia" and "cephalalgia" are more threatening and imply
a more serious condition than "neck pain" and "headache." Others have noted that applying the
diagnosis of "whiplash" may be more disabling than the injury.[143] There are important therapeutic
implications. Treatment by medication, physical therapy, or chiropracty may re-enforce pain behavior.
[144]
Of 200 patients who experienced whiplash neck injuries, those who were encouraged to engage in
normal activities had less symptoms after 2 years than the patients who were given time off from work
and prescribed a cervical collar.[24] (Moreover prolonged use of a cervical collar impedes the early
mobilization that is an effective method of management.)[145] People with chronic back pain who were
working had lower pain scores than a matched group who were not working.[146]

Amplification of pain may be associated with central pain sensitization which accounts for
hypersensitivity beyond the area of primary pain.[147] Generalized muscular hyperalgesia has been
demonstrated in people with the chronic whiplash syndrome.[148]

In summary, the trauma and initial pain activate symptom expectancies. The more attention paid to the
symptoms (prompted by the therapeutic and legal communities) the more they are augmented in
intensity and duration. Anxiety is generated about their significance reinforcing or amplifying
expectations of chronic pain attributed to trauma, completing the cycle.[149]

Attribution

It is natural to attribute pain to a past injury. Conversely, symptoms in the past are often forgotten.[150]
Symptoms attributed to trauma occur frequently in the population as a whole and at an incidence
similar to that following injury.[66,151–153] People who have had a history of headache before an MVA are
more likely than others to experience headache after the accident.[50] If patients overestimate chronic
symptoms attributed to injury, they would be expected to underestimate these symptoms prior to
injury. In one study, a control group was asked to imagine being involved in an MVA with brief loss of
consciousness and to note the symptoms they had prior to the imagined trauma.[129] Patients with
chronic post-traumatic symptoms reported fewer premorbid symptoms than the controls. For example,
prior to the injury 7% of patients reported headache while this symptom was noted in 12.5% of
controls. In another study, only 16% of subjects admitted neck symptoms prior to neck injury while
34% of their noninjured peers experienced these symptoms.[154] However these results were modified
in another study.[155]

Claimants of personal injury of all types, when compared to controls, report higher rates of
neuropsychological symptoms.[65] In one study, 170 patients filed personal injury claims for industrial
stress, for example, back pain or emotional distress, for example, harassment.[65] Excluded from this
group were claimants who had a history of neuropsychological impairment or head injury. The
following symptoms were recorded by patients on average of 2 years after injury or event and
compared to controls (in parenthesis) somatic: headache 88% (62%), dizziness 44% (26%);
psychological: anxiety 93% (54%), depression 89% (32%); cognitive: impaired memory 53% (20%),
impaired concentration 78% (26%). Other features of the postconcussion syndrome were also
affirmed.

Litigation

"If you have to prove you are ill, you can't get well" and claimants are not "cured by a verdict."[156,157]
After attributing chronic pain to a past injury, settlement of litigation or compensation may not alter the
pain syndrome.[32,158–161] Indeed some believe that financial settlement confirms the diagnosis and may
reinforce illness behavior.[162] Litigants with chronic back pain had higher pain scores than a
comparable group who were not litigating.[146] Poor outcomes after low back surgery were associated
with worker's compensation coverage and consultation with an attorney before surgery.[163] In
Saskatchewan, delay in recovery was strongly associated with retention of a lawyer and the type of
insurance or compensation system.[22] In one study in the United Kingdom of the patients with the
postconcussion syndrome who were admitted to a hospital, the duration of work absence was very
much longer in those who claimed compensation than those who did not.[52] This fact was not
influenced by the age or gender of the patient or the severity of the head injury. But in another study in
the United Kingdom, persistence of whiplash symptoms was not associated with compensation
proceedings.[26] Work-related litigation for chronic pain was associated with the highest levels of
disability even after accounting for other factors associated with poor outcomes.[164] In any case,
litigation is only one of many pain reinforcing components. Removing or diminishing litigation from the
start is associated with a marked decrease in claims for whiplash injury and may be one of the factors
associated with the low prevalence of chronic symptoms in Lithuania and other countries.[33,41]

Most patients complaining of chronic post-traumatic head and neck pain are not malingering. But in
one study of people with late postwhiplash symptoms there was a high prevalence of cognitive
underperformance as a manifestation of malingering in a short-term memory malingering test.[165] The
results were highest in those involved in litigation. The insurance industry estimates that post-
traumatic symptoms are fabricated from 20% to 47% of claimants, especially in big cities.[166]

Social and Cultural Factors

The great disparities in the prevalence of chronic post-traumatic head and neck pain cannot be
explained by organic disease. Social, cultural, and ethnic factors may influence ones appraisal of pain
and the emotional and behavioral response to pain.[167] The small prevalence of post-traumatic pain in
Kaumas, Lithuania, and Patras, Greece was attributed to the facts that the population had little or no
preconceived notion or expectation of chronic whiplash pain and no fear of long-term disability.[33,41]
Those injured in Lithuania and Greece return to work in a few days after the MVA and have little or no
involvement in ongoing therapy, insurance companies, or litigation. Cultural and social expectations
and other concepts of chronic post-traumatic symptoms appear to account for the striking differences
in the prevalence of these symptoms from one country and one society to another. This concept was
supported by a recent extensive review of WADs.[168] The best prognosis was associated with societies
that have little litigation, no compensation for pain and suffering, and least disability payments.
Accident victims who initially consulted physicians, physical therapists, chiropractors, or lawyers took
longer to recover and these factors were unrelated to the severity of injury.

Summary

The biopsychosocial model of chronic symptoms after whiplash injury has been emphasized in recent
years.[1–3,169] Structural and pathophysiological factors undoubtedly play a part in the etiology of some
patients with chronic post-traumatic head and neck pain. But psychological and cognitive factors,
effect expectation, amplification, and attribution of symptoms. These are influenced by cultural and
social concepts of chronic post-traumatic pain and appear to be the predominant mechanisms.

The need to integrate scientific and social concepts of disease has been noted in the past but has
been emphasized only in recent years.[1,3,151] One should not revert to the old dichotomy of organic
versus psychological. Rather altered physiology and psychological factors molded by society and
cultures are inextricably interwoven.

Table 1. Prognosis of WADs