Clinical manifestations

Presentation and course

Table 1 lists the sequelae of whiplash injuries, which include neck and back injuries, headaches, dizziness, paresthesias, weakness, cognitive, somatic, and psychological sequelae, as well as visual symptoms and rare sequelae (52; 53).

Table 1. Sequelae of Whiplash Injuries

Neck and back injuries
	• Myofascial • Fractures and dislocations • Disc herniation • Spinal cord compression • Spondylosis • Radiculopathy • Facet joint syndrome • Increased development of spondylosis
Headaches
	• Muscle contraction headache • Greater occipital neuralgia • Temporomandibular joint injury • Migraine • Third occipital headache
Dizziness
	• Vestibular dysfunction • Brainstem dysfunction • Cervical origin • Barre syndrome • Hyperventilation syndrome
Paresthesias
	• Trigger points • Thoracic outlet syndrome • Brachial plexus injury • Cervical radiculopathy • Facet joint syndrome • Carpal tunnel syndrome • Ulnar neuropathy at the elbow
Weakness
	• Radiculopathy • Brachial plexopathy • Entrapment neuropathy • Reflex inhibition of muscle contraction by painful cutaneous stimulation
Cognitive, somatic, and psychological sequelae
	• Memory, attention, and concentration impairment • Nervousness and irritability • Sleep disturbances • Fatigability • Depression • Personality change • Compensation neurosis
Visual symptoms
	• Convergence insufficiency • Oculomotor palsies • Abnormalities of smooth pursuit and saccades • Horner syndrome • Vitreous detachment
Rare sequelae
	• Torticollis • Tremor • Transient global amnesia • Esophageal perforation and descending mediastinitis • Hypoglossal nerve palsy • Superior laryngeal nerve paralysis • Long thoracic neuropathy • Spinal accessory neuropathy • Cervical epidural hematoma • Internal carotid and vertebral artery dissection • Symptomatic Chiari malformation • Musical hallucination

Sixty-two percent of patients presenting to the emergency room after a motor vehicle accident complain of neck pain (41). The onset of neck pain occurs within 6 hours in 65% of patients, within 24 hours in 28% of patients, and within 72 hours in the remaining 7% of patients (40). Most neck pain is due to cervical sprain, a myofascial injury (20). Cervical disc herniations, cervical spine fractures, and dislocations are uncommon. Facet (zygapophyseal) joint injury at different levels can produce characteristic patterns of referred pain over various parts of the occipital, posterior cervical, shoulder girdle, and scapular regions (46). Neck pain may arise from at least one facet joint in 54% of patients with chronic pain from whiplash injuries (14). Injury of the soft tissues of the upper cervical spine may also be responsible for pain complaints. Kaale and colleagues performed cervical spine MRI studies on 92 subjects with chronic neck pain following whiplash injuries (whiplash-associated disorder, grade 2 using the Quebec classification) and 30 random controls (69). Lesions of the alar ligaments showed the most pronounced association with the severity of neck pain and functional disability. There was a weaker association with lesions of the posterior atlanto-occipital membrane and transverse ligament.

In a prospective study of 180 patients seen within 4 weeks of the whiplash injury, 82% complained of headaches, which were occipitally located in 46%, generalized in 34%, and in other locations in 20% (10). The pain was present more than half the time in 50% of the patients.

Headaches following whiplash injuries are usually of the muscle contraction type and are often associated with greater occipital neuralgia (96; 168). In a scoping review, whiplash-associated headache is of mild to moderate intensity with a mean duration of about 7 hours and present in the occipital region but could also be in other regions, unilateral or bilateral (04). Greater occipital neuralgia or referred pain from trigger points from suboccipital muscles can produce a pattern of radiating pain variably over the occipital, temporal, frontal, and retro-orbital distribution. Whiplash trauma might also injure the temporomandibular joint and cause jaw pain often associated with headache (48; 01). Headache may be referred from the C2-3 facet joint that is innervated by the third occipital nerve and is appropriately called a "third occipital headache" (19). C2-3 facet joint injury can result in pain complaints in the upper cervical region, extending at least onto the occiput and, at times, toward the ear, vertex, forehead, or eye. Using third occipital nerve blocks to diagnose the condition, the prevalence of this type of headache among patients with persistent headaches after whiplash injury has been reported as ranging from 38% to 50% (90; 91). Occasionally, whiplash injuries can precipitate recurring common, classic, and basilar migraines de novo (173). Trigeminal sensory impairment of uncertain etiology has also been reported (153). In a study of patients with chronic posttraumatic headaches, 37% had tension-type headaches, 27% had migraine, 18% had cervicogenic headache, and 18% did not fulfill criteria of a particular category (128).

In a study of 262 patients with persistent neck pain and headaches for 4 months or longer after the injury, symptoms were reported as follows: vertigo, 50%; floating sensations, 35%; tinnitus, 14%; and hearing impairment, 5% (114). Posttraumatic vertebral insufficiency and dysfunction of the vestibular apparatus, brainstem, cervical sympathetics (Barre syndrome), and cervical proprioceptive system have all been postulated as causing dizziness. Hyperventilation syndrome can also occur in patients who are anxious and in pain, producing dizziness and paresthesias periorally or of the extremities, either bilaterally or unilaterally.

In a study, 33% of patients with symptoms but no objective findings complained of paresthesias acutely, and 37% reported paresthesias after a mean follow-up of 19.7 months (108). Paresthesias can be referred from trigger points, brachial plexopathy, facet joint syndrome, entrapment neuropathies, cervical radiculopathy, and spinal cord compression. Thoracic outlet syndrome is commonly caused by whiplash injuries, occurring four times more often in women than in men (30). Thoracic outlet syndrome has been controversial, as at least 85% of cases are of the nonspecific neurogenic or so-called "disputed type" that is a diagnosis of exclusion. This nonspecific type may actually be a myofascial pain syndrome with referred pain from the anterior neck muscles, such as the anterior scalene, or from the shoulder area from the pectoralis minor and not due to neural or vascular compression. Entrapment neuropathies can occur from several mechanisms. Carpal tunnel syndrome can be caused by acute wrist hyperextension on the steering wheel (84). If the patient has a cervical radiculopathy or neurogenic thoracic outlet syndrome from the injury, a double crush syndrome resulting in carpal tunnel syndrome or cubital tunnel syndrome may ensue.

Complaints of upper extremity weakness, heaviness, or fatigue are common after whiplash injuries, even when no evidence is present of cervical radiculopathy, myelopathy, brachial plexopathy, or entrapment neuropathy. The nonspecific type of thoracic outlet syndrome can produce these complaints. Alternatively, patients may have a sensation of weakness or heaviness because of reflex inhibition of muscle due to pain that can be overcome by more central effort (07).

In a study of patients with chronic symptoms after a whiplash injury, cognitive, psychological, and somatic symptoms occurred in the following percentages: nervousness and irritability, 67%; cognitive disturbances, 50%; sleep disturbances, 44%; fatigability, 40%; disturbances of vision, 38%; symptoms of depression, 37%; headache, 85%; neck pain, 100%; vertigo, 72%; and brachialgia, 60% (77). These symptoms are nonspecific and are also common in patients with postconcussion syndrome, chronic pain syndrome, depression, and anxiety neurosis. Psychological factors (ie, premorbid neurosis) are commonly cited as the cause of persistent complaints; however, psychosocial factors, negative affectivity, and personality traits are not significant in predicting the duration of symptoms (129). Instead, cognitive and psychological symptoms may be due to somatic symptoms (131; 170). Although a 2-year prospective study did find that symptomatic subjects were impaired on tasks of divided attention but not on memory tests (44), another prospective study of 39 patients found no evidence of cognitive deficits (72). It is controversial whether persistent neuropsychological deficits following whiplash injury are evidence for mild traumatic brain injury (155).

A variety of other problems may follow whiplash injuries. About one third of patients complain of interscapular and low back pain after whiplash injuries. In one large survey, 95% of claimants reported some pain within 30 days of injury of the posterior neck, shoulder, mid-back, lumbar, and buttock areas; 86% reported posterior neck pain, 72% head pain, and 60% lumbar back pain. Just 0.4% reported neck pain only (65). Patients often report visual symptoms, especially blurred vision, usually due to convergence insufficiency (23), although oculomotor palsies can occasionally occur (25). Rare sequelae are listed in Table 1.

Prognosis and complications

Studies on the prognosis of whiplash injuries are difficult to compare because of multiple methodological differences, including selection criteria of patients, prospective and retrospective designs, patient attrition rates, duration of follow-up, and treatments used (51; 52; 36; 71; 13). Although most patients may have only soft tissue injuries, imaging studies other than plain spine films have not been routinely performed.

Multiple studies have documented that neck pain and headaches can persist in significant numbers of patients. A well-designed prospective study reported the following percentages of patients with complaints of neck pain and headaches, respectively, at various times after the injury: 92% and 57%, 1 week; 38% and 35%, 3 months; 25% and 26%, 6 months; 19% and 21%, 1 year; and 16% and 15%, 2 years (133; 132). Symptoms present 2 years after injury are still present 10 years after the injury (59). In an 11-year follow-up study, 31.6% reported persistent symptoms, which were more prevalent in females (106). In a 17-year follow-up study of patients first seen in the emergency room, 55% reported persistent neck pain with no gender difference as compared to 29% of control subjects (24).

In a 15-year prospective follow-up study using MRI findings and symptoms as compared to controls in 60 consecutive subjects enrolled after whiplash injury, temporomandibular joint symptoms were higher in patients compared with controls at inception (44% vs. 20%) and remained significantly higher throughout the study period (138). The prevalence of disc displacement did not differ significantly between groups at study inception or at 15-year follow-up.

In a 20-year follow-up study comparing subjects with acute whiplash injuries and asymptomatic controls, the prevalence of shoulder stiffness, headaches, and arm pain was significantly greater in injured subjects than in controls (172). All MRI findings were similar at the 20-year follow-up.

The following risk factors have been reported for persistent symptoms (124; 132; 45; 72; 73; 74; 31; 106).

Table 2. Risk Factors for Chronic Symptoms

Accident mechanisms
	• Inclined or rotated head position • Unpreparedness for impact • Car stationery when hit
Occupant's characteristics
	• Older age • Female gender • Pretraumatic headache for injury-related headache • Significant life events unrelated to the accident • Depression • Early expectations of prolonged recovery • Poor self-rated health
Symptoms
	• Intensity of initial neck pain or headache • Occipital headache • Interscapular or upper back pain • Multiple symptoms or paresthesias at presentation
Signs
	• Reduced range of movement of the cervical spine • Objective neurologic deficit
Radiographic findings
	• Preexisting degenerative osteoarthritic changes • Abnormal cervical spine curves • Narrow diameter of cervical spinal canal

In a meta-review of 12 systemic reviews, the following were associated with continuation of pain and disability: post-injury pain and disability, whiplash grades, cold hyperalgesia, post-injury anxiety, catastrophizing, compensation and legal factors, and early healthcare use (140). Post-injury magnetic resonance imaging or radiographic findings, motor dysfunctions, or factors related to the collision were not associated with continuation of pain and disability in patients with whiplash injury.

In a prospective study of 37 acutely injured subjects enrolled in the emergency department, the neck disability index did not correlate with objective collision data, repair invoices, and characteristics of the crash (47). There was a significant positive association between self-reported neck disability at 3 months post-accident and posttraumatic distress, negative affect, and uncontrolled pain.

Although psychological factors such as neurosis are commonly cited as the cause of persistent symptoms, a prospective study of 78 consecutive patients with whiplash injuries demonstrated that psychosocial factors, negative affectivity, and personality traits were not significant in predicting the duration of symptoms (129). An additional study found that psychosocial factors and vocation were not predictive of persistent symptoms during a 1-year follow-up (133). In another prospective study, successful radiofrequency neurotomy resolved psychological distress in those with chronic neck pain due to a single painful facet joint following whiplash injuries (171).

Some evidence exists for a role for psychological factors. In a prospective study comparing the results of the Structured Clinical Interview for DSM-IV for patients with chronic pain from whiplash injuries after 1 year to those who had recovered, a history of psychiatric disease (most commonly depression) was more common in patients with chronic symptoms both before and after the accident (78). Richter and colleagues performed a 6-month prospective study of 43 consecutive patients with grade 1 or 2 whiplash-associated disorders with a 74% follow-up rate (135). Psychological factors were more relevant than collision severity in predicting the duration and severity of symptoms. Atherton and colleagues also found that a high level of general psychological distress and a pre-collision history of widespread body pain predicted the persistence of symptoms (09). In a systemic review of psychological risk factors for chronic whiplash-associated disorder, the most consistent prognostic factors of chronic neck pain or disability were poor expectations of recovery, posttraumatic stress symptoms, and passive coping (29).

Radanov and colleagues performed a prospective study to assess psychological risk factors for disability (130). At 6 months, 7% of the patients had partial or complete disability. The disabled and nondisabled patients still symptomatic at 6 months did not differ with respect to psychosocial stress, negative affectivity, and personality traits as initially assessed at baseline. Nygren reported that permanent medical disability occurred in 9.6% of patients involved in rear-end collisions and in 3.8% of patients involved in front- or side-impact accidents (109). Mayou and Bryant found no special psychiatry of whiplash neck injury (98).

Obermann and colleagues performed a prospective study of 464 patients recruited from emergency departments, finding 15.2% complaining of headache lasting more than 42 days and 4.6% developing chronic headache according to the International Classification of Headache Disorders, 2nd edition criteria. Predictive factors were preexisting facial pain, lack of confidence to recover completely, sore throat (due to trauma from the accident), medication overuse, high Neck Disability Index, hopelessness or anxiety, and depression (112).

Posttraumatic stress disorder symptoms are common after whiplash injuries and are associated with pain-related symptoms. In a prospective study of 229 subjects of posttraumatic stress disorder less than 4 weeks after injury, 3 months, and 6 months, there were the following three trajectories: little or no posttraumatic stress disorder symptoms over time (75.1%); high initial posttraumatic stress disorder symptoms then decreasing substantially, 10%; and high initial posttraumatic stress disorder symptoms and a small increase over time (14.9%) (134).

Many clinicians and certainly the insurance industry and defense attorneys believe that pending litigation is a major cause of persistent symptoms that promptly resolve once the litigation is completed (87). In one study of litigants, 88.7% were found to have inconsistent, nongenuine abnormalities on examination (123). Schmand and colleagues performed neuropsychological studies of patients with late whiplash syndrome reporting memory or concentration problems (141). In the context of litigation, the prevalence of underperforming was 61% as defined by a positive score on the malingering test. Monaro and colleagues review the variety of techniques in the detection of malingering in forensic contexts, highlighting the lack of rigorous methodologies (104).

However, most of the literature does not support this position. Litigants and nonlitigants have similar recovery rates (122), persistent pain 6 weeks after injury (100), and similar response rates to treatment for facet joint pain (91; 139). Filing a lawsuit within 1 month of the injury does not influence recovery at 1 year (73). Most plaintiffs who have persistent symptoms at the time of settlement of their litigation are not cured by a verdict (144; 53; 148). Certainly, some patients exaggerate or lie about persisting complaints to help or make their legal case. Neurotic, histrionic, or sociopathic patients may thrive on the attention and endless treatments recommended by some physicians and encouraged by some plaintiff attorneys. The clinician should evaluate the merits of each case individually (35). The available evidence does not support bias against patients just because they have pending litigation (16).

Clinical vignette

A 45-year-old man employed as a handyman and carpenter was a passenger in a pickup truck. He was hit from behind by a sport utility vehicle while stopped on the freeway and was jarred. In the emergency room, a cervical spine series was negative, and he was diagnosed with a cervical sprain. He saw an orthopedist with complaints of neck pain with an intensity of 8 out of 10 without upper extremity sensorimotor symptoms or signs. There was no prior history of neck problems.

He was placed on nonsteroidal antiinflammatory medications and sent to physical therapy three times weekly for 20 weeks (billed at 626). A cervical spine MRI revealed a posterocentral C5-6 disc protrusion without neural compression. He underwent two cervical epidural steroid injections (billed at 00 each) without benefit. Two left superior trapezius trigger point injections resulted in 80% improvement. He was discharged from treatment 7 months after the accident with a diagnosis of a cervical sprain and given a full release to work. As part of his lawsuit against the driver of the vehicle that hit him, he gave a deposition 21 months after the accident. He reported intermittent neck pain and no plans for additional medical treatment.

Biological basis

Etiology and pathogenesis

Physicians generally attribute common whiplash symptoms within the first 3 months to soft tissue injuries; however, when symptoms persist, the etiology of the chronic or late whiplash syndrome is controversial (49). Nonorganic explanations advanced for persistent complaints include emotional problems, a culturally conditioned and legally sanctioned illness or cultural expectations (103; 137; 56), social and peer copying (87), secondary gain and malingering (141; 32), expectations for recovery (31), and demands for an explanation outside the realm of organic psychiatry and neurology (120). Evans reviews the nonorganic explanations for associated headaches (54). Harth critiques the unrealistic cultural expectations argument (64). In addition, persistent complaints of those involved in low-speed, rear-end collisions are not seen in volunteer subjects exposed to speed changes from 4 to 14 km/h (33). However, in another study, approximately 29% and 38% of the subjects exposed to 4 and 8 km/h speed changes, respectively, experienced other symptoms with cervical symptoms, with headaches predominating (22).

A study that retrospectively examined the incidence of chronic symptoms from persons reporting rear-end motor vehicle accidents to police in Lithuania, where few people are covered by insurance, also challenged the organicity of chronic complaints (142; 110). Chronic pain and headaches were no more common in 202 accident victims than in controls. The authors concluded that expectation of disability, a family history, and attribution of preexisting symptoms to the trauma may be important determinants for those who develop chronic symptoms. Although the results are intriguing, the study is probably not valid because of significant sampling bias (18; 57). Despite the faults of this study, the medico-legal setting is important. When the tort compensation system in Saskatchewan, Canada, was changed to a no-fault system without payments for pain and suffering, the number of claims decreased by about 25% (32).

Pobereskin performed a similar study in the United Kingdom of 503 adults (66% female) who reported a rear-end collision to the Devon and Cornwall police (response rate of 44%). Of the respondents, 78% had neck pain lasting for more than a week, and 52% still had pain at 1 year (the 1-year response rate was 80.5%). The most important predictors of pain at 1 year were the initial neck visual analogue scale score (1.03, 1.01 to 1.05) and the presence of a compensation claim (4.09, 1.62 to 10.32). There was no improvement in symptoms once the claim was settled. In fact, people who had settled their claim by 2 years seemed more likely to have neck pain of similar severity compared to those who had ongoing claims. Pobereskin states, “This suggests that something about the stress and anxiety of the claim itself that tends to prolong symptoms in people seeking compensation” (126). However, it is also possible that the subjects had persistent pain complaints because they were really injured and were not cured by a verdict. The low response rates and disproportionate percentage of female respondents may have biased the outcome of the study. A systemic review found no clear evidence that compensation and its related processes lead to worse health following whiplash injuries (147).

Both animal and human studies have demonstrated structural damage from whiplash-type injuries. In different species of monkeys, experimentally caused acceleration and extension injuries have revealed a variety of lesions: muscle tears, avulsions, and hemorrhages; rupture of the anterior longitudinal and other ligaments, especially between C4 and C7; avulsions of disc from vertebral bodies and disc herniations; retropharyngeal hematoma; intralaryngeal and esophageal hemorrhage; cervical sympathetic nerve damage associated with damage to the longus colli; nerve root injury; cervical spinal cord contusions and hemorrhages; cerebral concussion; and gross hemorrhages and contusions over the surface of the cerebral hemispheres, brainstem, and cerebellum (95; 113).

Human studies have similarly revealed damage of multiple structures. An MRI study done within 4 months of the whiplash-type injury revealed ruptures of the anterior longitudinal ligament, horizontal avulsion of the vertebral end plates, separation of the disc from the vertebral end plate, occult fractures of the anterior vertebral end plate, acute posterolateral cervical disc herniations, focal muscular injury of the longus colli muscle, posterior interspinous ligament injury, and prevertebral fluid collections. An MRI study of 92 patients with chronic whiplash injuries found abnormal tectorial and posterior atlanto-occipital membranes (81) and alar (80) and transverse ligaments (82) in the injured as compared to controls. Autopsy series have shown injuries similar to those in the animal studies, including injuries to intervertebral discs and soft tissue injuries of facet joints (156; 157).

Ishikawa and associates provide evidence that some patients with persistent symptoms may have a dural cerebrospinal fluid leak (68). They performed a prospective study of 124 patients with neck injuries and at least two of the following symptoms occurred for at least 3 months after the injury: headache, cervical pain, dizziness, nausea, visual impairment, auditory symptoms, and memory loss. Fifty-eight patients were excluded for a variety of reasons. The remaining 66 patients (whiplash injuries in 51) underwent radioisotope cisternograms, and 37 (28 with whiplash injuries) were found to have cerebrospinal fluid leaks, most in the thoracic or lumbar spines with a mean duration of symptoms of 33 months. Thirty-six of the patients underwent 2.2 ± 0.7 lumbar epidural blood patches with significant improvement at 6-month follow-up. MRI scans of the brain to demonstrate diffuse dural enhancement or confirmation of cerebrospinal fluid leaks by MRI of CT-myelography are not reported. Reproduction of this study would be of interest.

Central hyperexcitability or sensitization (sensitization of spinal cord neurons that results in increased responsiveness to peripheral stimuli) is a possible mechanism for increased levels of subacute pain and chronic pain. In a study of 80 subjects evaluated within 1 month of the accident, acute whiplash subjects with higher levels of pain and disability were distinguished by sensory hypersensitivity to a variety of stimuli suggestive of central nervous system sensitization (152). These responses occurred independently of psychological distress. Spinal cord hypersensitivity was also suggested in a study of 29 patients with whiplash pain as compared to controls who had significantly lower reflex thresholds of the nociceptive withdrawal reflex on stimulation of the sural nerve (12).

In a prospective study of 76 whiplash subjects evaluated within 1 month of injury and then 2, 3, and 6 months postinjury, whiplash groups demonstrated local mechanical hyperalgesia in the cervical spine at 1-month postinjury (151). This hyperalgesia persisted in those with moderate-to-severe symptoms at 6 months but resolved by 2 months in those who had recovered or reported persistent mild symptoms. Only those with persistent moderate-to-severe symptoms at 6 months demonstrated generalized hypersensitivity to all sensory tests. These changes occurred within 1 month of injury and remained unchanged throughout the study period. These findings suggest that those with persistent moderate-to-severe symptoms at 6 months display, soon after injury, generalized hypersensitivity suggestive of changes in central pain processing mechanisms. This phenomenon did not occur in those who recover or those with persistent mild symptoms.

Compared with controls, patients with chronic whiplash had muscle hyperalgesia and large areas of referred pain after intramuscular injections of hypertonic saline both in the infraspinatus and anterior tibialis muscles, which suggests a generalized central hypersensitivity (79). Similar findings in patients with whiplash have also been reported with electrical cutaneous and intramuscular stimulation of both the neck and lower limbs (38).

Finally, in a study of brainstem-mediated antinociceptive inhibitory reflexes of the temporalis muscle of 82 patients with acute posttraumatic headache following whiplash injury, abnormal durations and latencies were present as compared to controls (75). This suggests a transient dysfunction of the brainstem-mediated reflex circuit, mainly of the late polysynaptic pathways. The reflex abnormalities are considered a neurophysiological correlate of the posttraumatic (cervico)-cephalic pain syndrome and point to an altered central pain control in acute posttraumatic headache due to whiplash injury.

Epidemiology

In the United States in 2018, there were 13,500,000 motor vehicle accidents, including 4,300,000 rear-end collisions (107). No reporting system exists; thus, the actual number of whiplash injuries per year is unknown. However, if Dolinis' finding that 35% of Australian drivers in rear-end collisions sustained whiplash injuries (45), more than 1 million persons in the United States may have whiplash injuries yearly. Although neck injuries can commonly occur after side- or front-impact collisions, rear-end collisions are responsible for about 85% of all whiplash injuries (41). In a low-velocity, rear-end collision, occupants of the vehicle struck are more likely to develop neck pain than are the occupants of the striking or rear vehicle, who sustain a flexion-type injury (143; 95). In rear-end collisions, the incidence of whiplash injuries decreases as crash severity increases (70). Neurologists frequently evaluate and treat patients with whiplash injuries. According to one survey, neurologists see an average of 10.3 patients per month with whiplash injuries (49). Women, especially in the 20- to 40-year age group, have persistent neck pain more often than men do by a ratio of 7:3 (11). The greater susceptibility of women to whiplash injuries might be due to a narrower neck with less muscle mass supporting a head of roughly the same volume or a narrower spinal canal compared with men (124). Another possible explanation is the greater early neck displacements in the average woman with less weight in the stiffer car seats used in recent years as compared to the yielding seats (165).

Prevention

General measures directed at driving safety, such as reducing the number of drunk or distracted drivers or improving the driving habits of young men, would reduce the number of whiplash injuries. Vehicle safety measures have been implemented. Proper use of head restraints can reduce the incidence of neck pain in rear-end collisions by 24% to 28.3% (105; 166); however, in one study, only 10% of drivers had headrests adjusted to the most favorable position to prevent neck extension (166). In a study of a self-aligning head restraint available designed to move upward and forward by occupant motion in a rear crash, providing earlier neck support even when the head restraint is positioned low, the incidence of whiplash injuries was reduced from 18% in a Saab with a standard restraint to 4% in a Saab with the self-aligning restraint (167). Center high-mounted stop lamps have reduced the number of rear-end collisions. Even though seat belt use should be encouraged, 73% of occupants wearing a seat belt develop neck pain as compared to 53% not wearing seat belts (40). Automatic emergency braking will become a standard feature in years to come and will help prevent or reduce the impact of rear-end collisions (66). If the promise of self-driving cars is realized, whiplash injuries may become a rarity in decades to come.

Differential diagnosis

Although most whiplash injuries result in myofascial or facet joint injuries, less common consequences include fractures, cervical disc herniations, spondylotic radiculopathy, and myelopathy. Table 1 lists the differential diagnosis for other symptoms after whiplash injuries.

Diagnostic workup

Cervical spine series are often obtained to exclude the occasional fracture (93). In patients with abnormal neurologic examinations or persistent complaints suggesting the possibility of radiculopathy or myelopathy, a cervical spine MRI study may be indicated. In patients without radicular complaints, cervical MRI studies have a low yield (169). A cervical myelogram followed by CT scan may be helpful if the MRI study cannot be done or if the study demonstrates equivocal findings. In some cases, especially for spondylotic disease, CT scan or myelography may be more sensitive than MRI for nerve root compression.

Asymptomatic radiographic findings are common; thus, it is often difficult to determine what findings are new and what findings are preexisting. Cervical spondylosis and degenerative disc disease occur with increasing frequency with older age and are often asymptomatic (58). Cervical disc protrusions are also common in the general population and are often asymptomatic. Protrusions occur in 20% of patients who are 45 to 54 years of age and in 57% of patients older than 64 years (161). A prospective 11-year follow-up study of 133 patients who suffered whiplash injuries found that Modic changes (degenerative changes of the vertebral bone adjacent to the endplates) occurred with a similar frequency in control subjects (97).

In a prospective study of 100 consecutive patients who underwent cervical MRI studies within 48 hours after sustaining a whiplash injury compared to matched controls, the following findings were significantly associated with injuries: occult fracture, bone marrow contusion of the vertebral body, muscle strain or tear, and the presence of perimuscular fluid (06).

EMG and nerve conduction studies may help demonstrate evidence of radiculopathy, brachial plexopathy, or entrapment neuropathies. Somatosensory and dermatomal evoked potential studies are not adequately sensitive or specific to justify the use for evaluating possible radiculopathy.

Cerebral hypoperfusion has been reported after whiplash injuries. In a small study of six patients compared to 12 controls, positron emission tomography and SPECT evidence of parieto-occipital hypometabolism was reported (116). One possible explanation is stimulation of pain-sensitive afferents in the cervicotrigeminal system, which could have widespread effects on local vasoactive peptides and the cranial vascular system (117; 116). In another study of 20 patients with chronic whiplash, most with cognitive complaints (88), 65% had brain perfusion abnormalities in one or more regions. Eight out of 15 patients tested had abnormal P300 event-related potential studies. There was no significant correlation between the SPECT findings or the P300 results and the scores of attention and working memory on neuropsychological testing. There was, however, close agreement between the SPECT and P300.

However, in another functional imaging study of 21 patients with late whiplash syndrome, Radanov and colleagues found no significant correlations between regional perfusion or metabolism in any brain area on SPECT or positron emission tomography studies and the scores of divided attention or working memory. There were significant relations between state anxiety and divided attention (127). In an MRI-based brain volumetry study of 21 patients with persistent concentration and memory deficits that are subjectively reported but not objectively verifiable as neuropsychological deficits, there were no abnormalities suggesting diffuse axonal injury as compared to matched controls (154).

Although HmPAO and ECD brain SPECT studies in patients with late whiplash syndrome and cognitive complaints have demonstrated parieto-occipital hypoperfusion (117; 115), similar findings have also been seen in patients with nontraumatic chronic cervical pain (117). Depression can also cause perfusion abnormalities (02) and FDG-PET does not allow reliable diagnosis of metabolic disturbances for individual patients (17); therefore, FDG-PET and HmPAO SPECT should not be used as diagnostic tools in the routine evaluation of patients with late whiplash syndrome (17).

Management

Few prospective controlled studies of treatment exist (149; 136; 164; 67; 05) with modest effects (43). Early mobilization of the neck using the Maitland technique followed by local heat and neck exercises produces more rapid improvement after acute injuries than does the use of a cervical collar and rest (101) and is as effective as physical therapy performed during the first 8 weeks after the injury (99). In a large, randomized prospective study, Vassiliou and colleagues found that physical therapy and active exercise for 10 sessions reduced pain significantly compared to a soft collar only over 7 days at 6-week and 6-month assessments (163). Another study found a significant benefit of active over passive physical therapy (42). A large prospective trial found that up to six physiotherapy sessions had a modest benefit at 4 months compared to advice, but not at 8 or 12 months (85).

In a prospective study of 172 subjects with chronic whiplash randomized to receive either 20 exercise sessions or advice, simple advice was as effective as the exercise program (102). A meta-analysis suggested that exercise therapy may provide additional benefit for improvement in neck pain and disability (34). In a study of 216 volunteers with chronic whiplash, after 1 to 2 years, those randomized to neck-specific exercise with or without a behavioral approach were more improved than those who were prescribed general physical activity (94). In another study, the outcome was better for patients who were encouraged to continue engaging in their normal preinjury activities than it was for patients who took sick leave from work and were immobilized during the first 14 days after the injury (21). Cervical traction may be no more effective than exercises alone (122). Overall, the evidence for benefit of physical therapy compared to no treatment is limited (164).

A review of educational interventional studies did not show benefit for pain, function, global perceived effect, quality of life, or patient satisfaction (63). In one study in an insurance setting, early multidisciplinary evaluation and advice actually increased the risk for chronic neck pain when participants were followed up 3 years postinjury (118). In a study of primary care physicians, the therapeutic relationship was associated with higher odds of recovery (62).

In a small, prospective, randomized study of patients with neck pain and musculoskeletal signs (75% of study group) and others with additional neurologic signs (25% of study group), the administration of high-dose methylprednisolone within 8 hours of the injury prevented extensive sick leave as compared to the placebo controls at 6 months (125). The evidence does not support the use of cervical epidural steroid injections for neck pain without radicular symptoms and signs, and there is limited evidence of efficacy for neck pain with radicular symptoms (121).

According to uncontrolled studies, trigger point injections can be beneficial for acute and chronic myofascial injuries (60). One group reported benefit from the injection of sterile water in, or subcutaneous to, trigger points caused by whiplash injuries (26; 27). Current evidence does not confirm a clinically or statistically significant benefit from the use of botulinum toxin type A injections (86). Transcutaneous electrical nerve stimulator units might be beneficial (83). Cognitive behavior therapy may be effective for chronic symptoms (119). Exercise programs may be effective for those with chronic complaints (158; 159; 160).

Treating pain arising from facet joint injury may be effective (162). A controlled prospective study showed a lack of effect of intraarticular corticosteroid injections in the cervical facet joints for chronic pain after whiplash injuries (15). Percutaneous radiofrequency neurotomy and lower cervical medial branch neurotomy should be used cautiously to treat chronic facet joint pain documented by anesthetic blocks (89). In a small study of patients with chronic facet joint pain confirmed with double-blind, placebo-controlled local anesthesia, percutaneous radiofrequency neurotomy with multiple lesions of target nerves provided at least 50% relief for a median duration of 263 days compared to similar relief for 8 days in the control group (92).

In a study of 15 patients with cervical spondylotic radicular pain after whiplash injuries, a mean of 3.7 therapeutic selective nerve rootsblocks was not effective (146). Alpar and colleagues have proposed that chronic neck and shoulder pain in chronic whiplash syndrome is due to carpal tunnel syndrome with normal electrodiagnostic studies. In a series of 38 such patients, 90% were reported as improved (03). This study should certainly be replicated.

Routine treatment for acute injuries often consists of pain medications, nonsteroidal antiinflammatory medications, and muscle relaxants. Using a soft cervical collar may actually impede recovery (158; 159; 160). Neurologists frequently prescribe range-of-motion exercises, physical therapy with various modalities, and transcutaneous electrical nerve stimulator units, although the level of evidence is not strong (158; 159; 160). Standard treatments are provided for posttraumatic headache (111). For example, some patients with greater occipital neuralgia benefit from nerve blocks (08). The chronic, frequent use of narcotics, benzodiazepines, barbiturates, and carisoprodol should be sparingly recommended because of the potential of habituation. Medication overuse headaches can also develop.

Patients with chronic complaints seek out a multitude of unproven treatments, such as chiropractic adjustments (occasionally under general anesthesia) (145), acupuncture (28), prolotherapy, and pain clinics. Well-meaning practitioners often uncritically provide treatments without allowing for the importance of placebo effects, whereas others are more economically motivated. Some plaintiffs and their attorneys encourage excessive treatment in an attempt to magnify an alleged injury.

Clearly, adequately controlled prospective studies of current treatments and more effective treatments for chronic pain are greatly needed (149). Until then, a compassionate, sympathetic approach by the neurologist might result in greater patient satisfaction and reduce unnecessary expenditures from patients' therapeutic quests.

Special considerations

Pregnancy

Medications should be avoided or, if necessary, prescribed in cooperation with the obstetrician.