Soft Tissue Injuries Following Whiplash

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CHAPTER 55 Soft Tissue Injuries Following Whiplash

Paul H. Lento, William Sullivan

INTRODUCTION

Cervical soft tissue injuries resulting from whiplash are often considered controversial. These injuries are presumed to be caused by an acceleration/deceleration injury that commonly occurs during many motor vehicle collisions.¹ Although several structures may cause pain following a whiplash injury, patients with whiplash associated disorders (WAD) are often diagnosed as having an acute musculoligamentous injury referred to as a cervical sprain or strain.¹^–³ The tissues involved in this diagnosis are postulated to be the large, multisegmental muscles, the smaller one- or two-segment muscles, the fascia or connective tissue, and the spinal ligaments. Fortunately, the majority of these whiplash patients improve over time.⁴^–⁶ However, a subset of patients with whiplash injuries continue to have pain complaints despite a lack of objective diagnostic evidence confirming the presence of an injury.⁷^–⁹ Although pain generators such as the cervical disc and facet have been described elsewhere,¹⁰^–¹⁴ and may contribute to referred or radicular pain and even cervicogenic headache, many of these patients with WAD have overlying muscular or soft tissue pain that may radiate into the shoulders and upper limb in a nonradicular pattern.^8,¹⁵^–¹⁷ Since soft tissue symptoms persist despite what would seem an adequate period of healing and, since abnormal pathology cannot be identified with advanced radiologic or electrophysiological testing, these patients may be diagnosed as malingerers or felt to be seeking financial compensation for their injuries. Yet, some studies have demonstrated that litigation may not be a clear risk factor for the continuance of symptoms.^18,¹⁹ Therefore, patients are often diagnosed with myofascial pain, the etiology of which also continues to remain elusive and controversial.^15,²⁰ Recently, however, there have been theories that may better explain the persistence of these symptoms following whiplash injury.

The purpose of this chapter is to describe the cervical soft tissue injuries incurred from an acute whiplash. In addition, mechanisms that produce these injuries will be discussed, including the evidence that proves the existence of soft tissue injury following whiplash. Finally, the possible theories that may explain the etiology of chronic persistent soft tissue cervical pain following whiplash will be presented.

ACUTE INJURY

Overview

Although there are accepted pain generators of the cervical spine, it is commonly observed following whiplash that the cervical musculoligamentous tissues may contribute to WAD of the cervical spine.^1,^2,^7,^8,^21,²² The precise biomechanics of cervical whiplash have been discussed elsewhere and are more complex than a simple cantilever mechanism.^23,²⁴ However, the cervical acceleration and deceleration that occur during whiplash may help explain injury that is incurred by the supportive tissues. Although the full range of cervical motion is not exceeded during low–moderate cervical whiplash,²⁵^–²⁷ it is implied that acceleration of the torso produces relatively forceful head extension. As this occurs, the anterior cervical muscles are lengthened when the acceleration force of the impact overpowers their tone.²⁸ This eccentric force would theoretically create muscle fiber tearing and damage to surrounding vasculature, lymphatics, and even neural tissues.^2,²⁸ The brunt of the remaining force may then be taken up by passive structures such as the anterior longitudinal ligament (ALL).²⁸ Following this acceleration phase, the head flexes as the torso decelerates. Flexion of the head may be potentiated by contraction of the neck flexors stimulated by the stretch reflex from the preceding acceleration phase.²⁸ This combination may excessively load the posterior cervical structures. Studies in animal models²⁹ have implicated that, during this deceleration phase, the upper cervical spine, serving as a pivot point, sustains the greatest injury as supportive structures serve to decelerate the head. By this mechanism the ligamentous structures such as the alar and transverse ligaments as well as the tectorial membrane, suboccipital, and upper cervical muscles may be traumatized.^21,³⁰^–³³ Other authors have reported that acceleration and deceleration force may also be associated with a significant amount of cervical axial loading and distraction.^22,³⁴ These forces may create irritation of more central nervous structures such as the spinal cord, brainstem, and nerve roots.³⁵ This direct impact on neural structures, as well as the supportive musculoligamentous structures have been implicated in the development of acute pain and also the perpetuation of chronic pain following cervical whiplash, including the presence of adverse neural tension (Fig. 55.1) and central sensitization.^35,³⁶

Fig. 55.1 A physical examination maneuver to elicit adverse neural tension in the upper limb and cervical spine. The examiner depresses, abducts, and externally rotates the shoulder while extending and supinating the wrist. The elbow then can be extended slowly to see if any of the patient’s symptoms are recreated. If they are, the cervical spine can be laterally flexed side to side to lessen or worsen the symptoms.

MUSCULOLIGAMENTOUS INJURY

Despite this theoretical overview, there is a relative paucity of strong in vivo evidence that supporting structures such as the cervical muscles and ligaments are damaged during whiplash injury. Although injury to these musculoligamentous structures is often implied when clinicians use the diagnosis of cervical strain or sprain following whiplash, most of the information regarding injury to these structures comes from animal research, cadaveric and radiologic studies, electromyographic data, and some reported clinical experiences.

Clinical experience

Janes and Hooshmand ² in 1965 was one of the first to clinically report on the etiology of soft tissue pain following cervical flexion–extension injuries. They referred to these injuries as cervical sprains and inferred that in a rear-end collision, the patient is in a relaxed position, deprived of the protection usually achieved by contraction of the cervical paraspinal musculature. In Janes’s experience, these ‘sprains’ were caused by injury to the cervical ligaments such as the interspinous ligaments, ligamentum nuchae, and ALL. They provided evidence for this statement by reporting on the surgical findings of 32 patients with cervical pain following cervical trauma. Twenty-three had experienced whiplash injuries. Upon surgical exploration, eight of these patients had definite rupture of the interspinous ligament at C6 or C7 with scar formation, while 13 had hypermobility of one or two spinous processes of the cervical vertebrae. Additionally, the ligamentum nuchae and interspinous ligaments had developed calcifications indicative of degenerative changes and scarring. Approximately 90% of patients in this case series had good to excellent outcomes with 1–7 year follow-up after posterior cervical fixation. Unfortunately, Janes and Hooshmand did not report on disc or zygapophyseal injuries in this case series but this report provided clear evidence that ligamentous damage may serve as a potential pain generator following a cervical whiplash.

Hohl ^8,²¹ and later Hirsch et al.²² reported on clinical findings associated with soft tissue injury following whiplash based upon clinical observations. They concluded that acute cervical pain following whiplash was partly from soft tissue injury, namely musculoligamentous damage, but provided no new substantial clinical proof to support this theory. Like most, they postulated that rear-end collisions resulted in the most disability and that injury to the anterior or posterior musculature occurred during cervical acceleration and deceleration^33,³⁷ Front-end collisions, creating forward cervical flexion, it was felt, would result in injury mainly to the posterior musculature and ligaments.^8,^21,²² Interestingly, these authors were among the first to report that patients often had pain radiating into the upper limb that did not follow a radicular pattern and suggested that these unexplainable symptoms may be due to irritation of injured musculoligamentous structures. It is known that stimulation of these supportive structures with hypertonic saline produces somatic pain patterns.³⁸^–⁴¹ More recent clinical observations suggest that these nonradicular referral patterns may also be attributable to central neural irritation, as evidenced by adverse neural tension.³⁶

Animal studies

Despite these case series and clinical experiences, the majority of evidence suggesting damage to the musculoligamentous structures following cervical whiplash is found predominantly from animal studies. Macnab,¹⁹ utilizing a monkey model, simulated significant acceleration injuries to the cervical spine. His studies produced cervical muscular injuries that ranged from minor tears in the sternocleidomastoid to tears of the longus colli muscle and hemorrhage within the esophagus. In addition, damage to the longus colli resulted in associated retropharyngeal hemorrhage and damage to the cervical sympathetic nervous system. These findings may explain the clinical complaints of dysphagia, dizziness, and vertigo in patients following whiplash. These acceleration injuries also resulted in avulsion of the anterior longitudinal ligament and separation of the disc from the cervical vertebrae²⁸ but these injuries never occurred without concomitant injury to the anterior cervical musculature. Although Macnab admitted that less severe injuries would not result in such significant soft tissue trauma, he was among the first to provide pathological evidence that the cervical muscle and ligaments could contribute to pain and cervical dysfunction following a whiplash injury.

Wickstrom et al.,⁴² also utilizing a primate model, produced acceleration and deceleration injuries to the cervical spine. With this more accurate simulation of the whiplash injury, there was a high proportion of damage to the posterior ligamentous complex and cervical nerve roots. Inflammation and hemorrhage within the trapezius and splenius capitis muscles was detected in approximately 25% of the specimens. Additionally, Wickstrom et al.⁴³ confirmed Macnab’s findings, demonstrating that the ALL may indeed be damaged during the acceleration phase of whiplash, separating from the anterior cervical disc and vertebral body. Understandably, these injuries were not identified by utilizing plain radiographs, suggesting that patients, even with significant soft tissue injury, will have negative radiographic examination.

Unterharnscheidt ²⁹ was among the first to separate what damage would be created by the acceleration phase versus the deceleration phase of the whiplash. He remarked that the deceleration phase of whiplash produced hemorrhage and tearing to the origin of cervical musculature as well as damage to the posterior longitudinal ligament, tectorial membrane, transverse, and alar ligaments. Ironically, he failed to reveal any major alterations in the ligamentous structures during the acceleration phase but did confirm the presence of bleeding within the sternocleidomastoid. Liu et al.,⁴⁴ as well as Bocci and Orso,³⁰ have shown in experimental animal models that during the acceleration phase of whiplash, the cervical ALL, alar ligament, transverse ligament, and even PLL may be injured. This is noteworthy, as previous authors have implicated the role of deceleration as the cause of injury to these posterior structures.