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(Stroke. 1995;26:2194-2196.)
© 1995 American Heart Association, Inc.

Articles

Delayed Onset of Fatal Basilar Thrombotic Embolus After Whiplash Injury

L. Viktrup, MD; G.M. Knudsen, MD S.H. Hansen, MD

From the Department of Neurology (L.V., G.M.K.), Hillerød Hospital, and the Department of Forensic Medicine (S.H.H.), University of Copenhagen (Denmark).

Correspondence to Gitte Moos Knudsen, Department of Neurology N2082, Rigshospitalet University of Copenhagen, Blegdamsvej 9, DK-2100 Copenhagen, Denmark.

	Abstract

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Background Whiplash injuries are generally seen after rear-end rather than frontal car collisions. Previous reports have documented death up to 8 days after serious whiplash injury. We report a case of lethal basilar thrombotic embolus that occurred 2 months after the patient's injury in a collision.

Case Description After whiplash trauma in a car accident, a 50-year-old taxi driver suffered from headache and episodic visual disturbances. Two months after the accident he suddenly lost consciousness and was admitted to the hospital. A CT scan performed at that time was indicative of basilar thrombosis. The patient died 3 days later. The autopsy revealed a thrombosis in the right vertebral artery and a thrombotic embolus in the basilar artery. Microscopically, a lesion of the right vertebral artery was found at the level of the atlantoaxial joint.

Conclusions We conclude that the whiplash injury caused a lesion of the right vertebral artery, leading to repeated transient ischemic attacks and finally to a fatal basilar thrombotic embolus. We suggest that in patients with disturbances of the vertebrobasilar circulation, attention should be paid to occurrence of neck trauma in the preceding 3 months. Further, anticoagulant therapy should particularly be considered in patients who after suffering neck injuries develop signs of transient ischemic attacks with origin from the posterior cerebral circulation.

Key Words: cerebral ischemia, transient • trauma • vertebral artery • whiplash injuries

	Introduction

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Serious whiplash injuries are usually seen after rear-end car collisions. Trauma in which the victim's head swings backward, followed by a forward flexion, more frequently causes injuries to the cervical spine than after frontal collision due to the relative weakness of the anterior longitudinal ligament.¹ Frequently experienced symptoms include occipitonuchal pain due to local damage of ligaments and muscles² ; severe headache, neck stiffness, and anxiety or irritability may subside for several months,³ or even become chronic.^{4 5 6 7}

Postmortem studies⁸ have shown that vertebral artery lesions are found in about one third of fatally injured road traffic accident victims with vertebral atlas injury. In previous reports, neurological deficits or death have followed posterior neck injuries by up to 8 days after the accident.^{8 9 10 11} Due to the short time interval between trauma and morbidity, the relationship was quite evident in these cases.

We report a case of lethal basilar thrombotic embolus occurring as late as 2 months after a serious whiplash injury. In the time interval between the accident and death, the victim complained of episodic visual disturbances.

	Case Report

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A 50-year-old taxi driver developed sudden unconsciousness and was admitted to the emergency room. Two months earlier he had been involved in a traffic accident and had since complained of headache, concentration difficulties, and decreased vision. One month after the accident he was examined by an ophthalmologist. Surprisingly, a corrected visual acuity of only 0.2 was found in each eye (with no increase by pinhole), but was 0.7 when tested binocularly. Accordingly, centrocoecal scotomas were looked for by tangent screen (white and red objects 3/1000), but no field defects were disclosed. Eye movements and fundus examination were normal.

One morning he complained of severe headache and some hours later notified the taxi center that he was not feeling well. He was shortly thereafter found unconscious in his car. Initial neurological findings were unresponsiveness, anisocoria (left pupil larger than right), and increased tonus in the left arm. Repeated generalized seizures and later decerebrate rigidity were treated with intravenous phenytoin. He was ventilated in a respirator and slightly sedated with 10 mg diazepam. Electroencephalography showed a 1- to 3-Hz focus at the right frontotemporal region and a minor amplitude decrease over the right hemisphere. The initial CT scan was normal, but a second scan 2 days later revealed hypodense areas without enhancement in the pons, the right part of the hypothalamus, and both anterior parts of the cerebellum, suggestive of basilar infarction (Fig 1). Electrocardiography showed sinus rhythm.

View larger version (126K): [in this window] [in a new window]   Figure 1. CT scan shows hypodense areas without enhancement in the pons, the right part of the hypothalamus, and both anterior parts of the cerebellum. Border zone of the infarct shows enhancement.

The patient did not regain consciousness and died 3 days later of untreatable hyperthermia, probably caused by hypothalamic destruction. At autopsy, no cardiac or aortic source of embolism was found. In the vertebral arteries there was a minor degree of atherosclerosis. In the right vertebral artery a 1-cm-long adherent, nonocclusive thrombus was found at the level of the transverse foramen of C1 (Fig 2).

View larger version (143K): [in this window] [in a new window]   Figure 2. Photograph of the right vertebral artery shows thrombosis in the opened artery (long arrow) at the level of the transverse foramen of C1. Foramen magnum is indicated by the short arrow.

The intracranial arteries showed a minor degree of atherosclerosis, and in the distal part of the basilar artery a 2-cm-long occluding thrombotic embolus (probably originating from the thrombus in the right vertebral artery) was found. An approximately 4-day-old pontine infarction was present.

The atherosclerotic plaques in the vertebral and intracranial arteries showed no signs of ulceration or thrombosis. The cervical spine was not fractured or dislocated, and there were no signs of arthrosis or spondylosis.

Microscopically, a thrombus adhering to the intima was found in the right vertebral artery. Underneath the thrombus, a minor subintimal hemorrhage was seen. At the same level the media was thickened and the adventitia was partially split from it, while the elastic membrane was destroyed and replaced by fibroblastic proliferation and fibrosis, suggestive of a recent traumatic dissection (Figs 3 and 4). The adventitia was intact, but there was perivascular lymphocytic infiltration (Fig 5). No hemorrhage or other signs of extravasal injuries were found. A microscopic examination of the basilar artery was normal.

View larger version (153K): [in this window] [in a new window]   Figure 3. Photomicrograph of the right vertebral artery shows thrombosis adherent to the intima (long arrow), with a thickened media and a partial splitting between the media and the adventitia (short arrow).

View larger version (101K): [in this window] [in a new window]   Figure 4. Photomicrograph of the right vertebral artery shows the splitting zone between the media and the adventitia, with lymphocytes and fibroblasts (long arrows) and a destroyed elastic membrane and elastica externa (short arrows).

View larger version (148K): [in this window] [in a new window]   Figure 5. Photomicrograph of the right vertebral artery shows lymphocytic infiltration in the adventitia and a partial splitting from the media (arrow).

Although the lethal embolus in the basilar artery occurred as late as 2 months after the initial accident, the localization of a lesion in the right vertebral artery at the atlantoaxial joint, as found in this case, is suggestive of a causal relationship between the whiplash lesion and thrombosis. This is further supported by the microscopic findings in the right vertebral artery showing thickening of the media, partial splitting of the adventitia, and destruction of the elastic membrane, with replacement by fibroblastic proliferation and fibrosis, changes which are unlikely to be caused by atherosclerosis.

Intermittent ischemia of the occipital cortex due to repeated microemboli released from the injured vertebral artery may explain the patient's visual disturbances.

	Discussion

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Posterior neck injuries may lead to different affections of the vertebral arteries.^{8 9 10 11 12 13 14 15 16} In fatal traffic accidents the most frequently injured part of the spine, as evaluated in postmortem studies^{8 17} is at the upper two cervical vertebrae. Autopsies performed on 32 traffic accident victims with posterior neck injuries who died shortly after the accident showed injuries to the vertebral arteries at this location. Most arterial lesions were incomplete tears, of which a substantial number were adventitial.⁸ Eight of 10 victims with vertebral artery injuries died within 1 hour after the injury, and the remaining 2 victims within 1 week after the trauma.

Thrombotic obstruction of a vertebral artery 1 week after a lethal frontal whiplash injury has been described previously,¹⁰ while a lethal vertebral-basilar thrombosis followed a few hours after cervical manipulation.⁹ As in our case, a lesion in the vertebral artery was found after the whiplash injury; in the case involving cervical manipulation, only mild intimal hyperplasia, indicative of an early atheromatous process, was found.

Traumatic dissection of the extracranial part of the internal carotid arteries may occur after only moderate blunt trauma.¹⁶ Acute compression of the extracranial part of the vertebral arteries due to injury and swelling of the spinal cord, the discs, or the cervical column,^{8 10} or because of prevertebral hematomas,¹⁵ may lead to hypoxia of the cervical spinal cord and brain. Strangulation of the vertebral arteries, however, has been argued to occur only in victims with preexisting spondylosis or extreme arthrosis.¹⁴ Depending on the severity of the whiplash injury, other sensitive neck structures can be damaged, such as the spinal cord,¹¹ nerve roots, or areas adjacent to the transverse foramen.⁸

Retrospectively, if the episodic visual disturbances had been recognized as transient ischemic attacks, our patient might have benefited from anticoagulant therapy. We suggest that anticoagulant therapy be considered, particularly in patients who after whiplash trauma develop signs of transient ischemic attacks resulting from posterior cerebral circulation disturbances. Also, patients with signs or symptoms of disturbances in the posterior cerebral circulation should be asked about a history of neck injuries within the preceding 3 months. Apart from these considerations, we find that the demonstration of a 2-month delay between whiplash injury and death could have both legal and insurance implications.

Received April 10, 1995; revision received June 8, 1995; accepted July 5, 1995.

	References

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