Whiplash Injury Including Cerebral Manifestations

by

Bernard M. Abrams, M.D.
Clinical Professor of Neurology
University of Missouri School of Medicine at Kansas City
Kansas City, Missouri, U.S.A.

originally published in

Pain Digest (1997) 7:151-153
© Springer-Verlag New York Inc. 1997

Publiceras av WhiplashInfo med författarens godkännande.

Introduction

No topic in medicine appears to polarize physicians or attorneys faster than the subject of the so-called whiplash injury. Even the titles of numerous articles reflect this enigma [1-4]. In each the question is raised, is whiplash injury fact or fiction?

Although acute pain following the injury is widely accepted, chronic symptoms are often doubted.

Whiplash describes the typical mechanism of hyperextension followed by flexion of the neck which occurs when an occupant of a motor vehicle is hit from behind by another vehicle [5]. Other mechanisms of injury from other types of collisions are also recorded. These seem, statistically, to have much less chance of persisting neurological defects. An interesting facet is the definition of whiplash injury in Webster's New Universal Unabridged Dictionary: "Injury of the cervical spine and cerebral concussion occurring in an automobile collision which causes forceful flexion or extension of the neck in violent oscillation of the head forward and back, or back and forward" [6]. Synonyms include cervical sprain, acceleration/deceleration injuries, hyperextension injury, and the French term le coup du lapin.

The epidemiology of whiplash injury is quite frightening. A rough estimate is more than one million injuries per year. Rear-end collisions are responsible for about 85% of all whiplash injuries and, interestingly enough, the incidence of whiplash injury decreases as crash severity increases; so that 82% of whiplash injuries occur in collisions in which an automobile is not towed, versus 66% in which the automobile is towed. Another facet is that 73% of patients wearing a seatbelt develop neck pain, as compared with 53% not wearing seatbelts.

Head restraints for front seats have been in use since 1969 and it is said that the proper use of headrests can reduce the incidence of neck pain in rear-end collisions by 24%. Unfortunately, unless the headrest is close to the head (2.5 cm being a suitable distance) [7], the headrest may do more harm than good, especially if it is too low and forms a fulcrum for the neck to be hyperextended.

Historically the whiplash mechanism of injury may first have been recognized in US Navy pilots undergoing the launching of planes by the catapult method from decks of battleships and cruisers following World War I. These patients would often blackout for a few seconds and accidents occurred that were due to the whiplash effect. This was quickly recognized and a protective headrest devised for the pilot with adequate shoulder harness. Fifty years more would elapse before the routine use of headrests and shoulder harnesses in the civilian automotive sector. In 1919 Marshall reported on causes of mild neck injuries, including automobile accident.

The first use of the term whiplash is not entirely known. In 1968 Crow stated that, in 1928, presenting a report on eight cases of neck injury resulting from traffic accidents, he used the "unfortunate term whiplash." This expression was intended to be a description of motion; but it has been accepted by physicians, patients, and attorneys as the name of a disease; and the misunderstanding has led to its misapplication by many physicians and others over the years.

The term whiplash first appears in the medical literature in a 1945 article by Davis [8]. After that there was an explosion of use of the term in the literature.

Myofascial Pain

The vast majority of patients with whiplash injuries have injuries only to muscles, ligaments, and connective tissues and the history of myofascial injury should be considered. This is a concept which has evolved over the past 150 yrs. The foremost proponent of this has been Travell, but others in the pantheon of myofascial pain syndromes include Steindler and Cyriax [5].

Pathology

Structural damage from whiplash-type injuries has been demonstrated both in animal studies and in humans in a magnetic resonance imaging study of selected patients within 4 mos of whiplash injuries. This has demonstrated ruptures of the anterior longitudinal ligament, horizontal evulsion of the vertebral endplates, separation of the discs from the vertebral endplate, occult fractures of the anterior vertebral endplates, acute posterolateral cervical disc herniations, focal muscle injuries of the longus colli muscles, posterior infraspinous ligament injury, and prevertebral fluid collections [5]. Perforation of the esophagus and descending mediastinitis has also been described.

Signs and Symptoms

Neck pain is the most common result of whiplash injuries. Sixty-two percent of the patients presenting to the emergency room after motor vehicular accidents complain of neck pain. The onset of neck pain occurs in 65% of patients within 6 h, in 28% within 24 h, and within 72 h in the remaining 7%. Other sequelae include neck and back injuries; headaches, usually of the muscle-contraction type but occasionally greater occipital neuralgia; temporomandibular joint injury; and, rarely, de novo onset of migraine headaches. Dizziness, which has been objectified numerous times [5], is also known. Paresthesias from trigger points, cervical radiculopathy, carpal tunnel syndrome, and ulnar neuropathy at the elbow (each one of which would take the patient out of the pure whiplash category) have been reported. Trigger points are probably the major cause of paresthesias.

Cognitive, somatic, and psychological sequelae are troublesome and controversial. There are claims of memory, attention, and concentration impairments; nervousness and irritability; sleep disturbances; fatigability; depression; personality changes; and "compensation neurosis" ("railway spine") [5].

Cerebral symptoms occurred in the following percentages: (1) 67%, nervousness and irritability; (2) 50%, cognitive disturbances; (3) 44%, sleep disturbances; (4) 40%, fatigability; (5) 38%, disturbances of vision; (6) 37%, symptoms of depression; (7) 85%, headache; (8) 100%, neck pain; (9) 72%, vertigo; and (10) 60%, arm pain. The concept that a cerebral whiplash injury without direct head trauma can result in a cerebral concussion has been controversial [9].

Various types of data have been reported to support the cerebral concussion hypothesis, including studies using monkeys [10] as well as anecdotal evidence such as that of Ommaya and Yarnell [ I I ] who reported two people with subdural hematomas after whiplash injury. Neuro-otologic studies have suggested central pathology in some patients with complaints of vertigo. Abnormal EEGs in moderately impaired patients with whiplash injury, no direct trauma, and brief or no loss of consciousness have been reported, with 46% abnormal records in one study [5]. But a more recent study has demonstrated minimal EEG abnormalities in a small percentage of patients [5].

Three recent studies [12-14] demonstrated cognitive impairment in a small minority of patients sustaining whiplash injury, although another study found equivocal abnormalities. Deficits were noted in tests of attention, concentration, cognitive flexibility, and memory [5]. Psychological factors such as neurosis are commonly cited as the cause of persistent symptoms. However, recent studies have demonstrated that psychosocial factors, negative affectivity, and personality traits were not significant in predicting the duration of symptoms. Older age of patients, initial neck pain intensity, and injury-related cognitive impairments were significant factors predicting illness behavior. It is of interest to note that, in patients who have whiplash injuries plus other abnormalities, the other abnormalities such as fractures will clear up in a given period of time, which is usually expected; while whiplash will continue with pain for a much longer period of time than expected.

Finally, rare sequelae of whiplash include torticollis, transient global amnesia, esophageal perforation, and descending mediastinitis.

Return to Work and Long-Term Disability

In a series of consecutive medical-legal cases, 79% of patients returned to work by 1 mo, 86% by 3 mos, 91% by 6 mos, and 94% by 1 yr [5]. There is a report that permanent medical disability occurred in 9.6% of patients involved in rear-end collisions and 3.8% involved in front or side collisions. In a retrospective study of more than 5000 cases of whiplash, 26% of patients were not able to return to normal activities at 6 mos. Risk factors for persistent symptoms include older age of the patient, intrascapular or upper back pain, occipital headaches, multiple symptoms, or paresthesias at presentation, reduced range of movement of the cervical spine, objective neurological deficit, preexisting degenerative osteoarthritic changes, cervical stenosis for the development of myelopathy, upper middle occupational category, and abnormal cervical spine curves.

The result of litigation on symptoms is a matter of dispute rivaling that of religion and politics. Sympathetic accounts [7] claim almost no effect on litigation, while more hostile accounts [1] claim almost total responsibility for the resulting symptoms. The most even-handed account would seem to be Evans' [5]. Secondary gain, exaggeration, and malingering should be considered in all patients seen with whiplash injury, although the evidence suggests that these psychological factors are responsible for only a minority of patients with persistent complaints. A number of studies have examined the effect of settlement of litigation on symptoms. These studies have assorted flaws [5]. A significant factor is the length of time from injury until settlement of litigation. The summary statement in Evans [5] is probably fair:

The evidence indicates that most patients who are still symptomatic when litigation is completed are not cured by a verdict. The end of litigation does not signal the end of symptoms for many patients. The patients who exaggerate or malinger are a distinct minority.

The final word on whiplash for the present was written by Gowers in 1904 [15]:

At present we are without any direct evidence of the real nature of the affections, such as can only be furnished by the microscope and modern methods of discerning that which it reveals. We cannot wonder at our ignorance, still less complain of it, for it is only quite recently that the minute structure of the sensory elements of muscle and tendon has been clearly perceived, and much of the normal structure still seems obscure. It is one of the departments of pathology in which the recognition of the changes that attend disease has to come long after the full discernment of the normal structure. We must therefore be content to wait, and content also meanwhile to rely on the apparent meaning of symptoms of disease, as far as that meaning can be made out.

References