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D.L., a 34-year-old white male, presented to the emergency room of a community hospital complaining of vomiting, dizziness, double vision, finger numbness, and a severe frontal and occipital headache. He was treated for acute labyrinthitis with intravenous Valium [R] and Compazine [R], and released after an overnight stay. Three days later he presented to the emergency department of the medical center complaining of severe occipital headache, slurred speech, ataxic gait, left drift, and lack of coordination. The admission CT was significant, with multiple bilateral cerebellar infarctions in the distribution of the anterior inferior cerebellar artery (AICA), and possibly the posterior inferior cerebellar arteries (PICA). Embolization from vertebral artery dissection secondary to cervical manipulation was considered the likely causative factor. Magnetic resonance angiography (MRA) and arteriogram supported the diagnosis. The arteriogram revealed total occlusion of the proximal two-thirds of the right vertebral artery. The patient had been seen by a chiropractor approximately 1 week prior to admission for a “neck adjustment.”

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The patient was admitted to the neuro unit with the diagnosis of cerebellar infarction. Other possible diagnoses included vasculitis, coagulopathy, cardiac sources of stroke, primary diseases of the basilar artery, and antiphospholipid antibody syndrome, all of which were ruled out. The patient was treated with heparin and Coumadin [R], and received physical and occupational therapy. After 3 days he was transferred to a regular medical-surgical unit. A transcranial Doppler study was conducted on hospital day 5, which showed good collateral cerebellar circulation. Seven days after admission, D.L. was discharged home. At this time he was able to ambulate independently, his speech was clear, and he had no complaints of headache. Physical and occupational therapy were arranged to re-evaluate his progress once at home. He continued on Coumadin, and planned to followup with the neurologist.
Overview
Stroke is the third leading cause of death in the United States, claiming about 145,000 lives per year (American Heart Association, 1994), and a major contributing factor to disability. Cerebral artery dissections are an important etiology of ischemic stroke, especially in the younger stroke patient. Dissections may be spontaneous or occur following trauma; location may be intracranial or extracranial. Spontaneous carotid artery dissection has been diagnosed in approximately 10% to 20% of young adults with stroke (Schievink, Mokri, & O’Fallon, 1994). The most common site of dissection is the internal carotid artery (ICA). The vertebral artery (VA) has also been frequently reported as a site, and de Rocondo, Rougemont, and Guichard (1995) describe dissections of the common carotid artery.
Incidence
While blunt trauma to the neck arteries is uncommon, it is seen increasingly clinically (Fukuda et al., 1989). Actual incidence of cerebral artery dissection is unknown, because the condition frequently produces mild, transient signs. Heightened awareness of the condition has led to an increased rate of diagnosis. Injury of the unilateral vertebral artery has been reported in approximately 1% to 2% of the major blunt thoracic injuries (Fukuda et al., 1989). Sixty percent of these injuries occur in people between the ages of 14 and 45, but injuries from minor head and neck trauma have also been described in children (Palmer, Emery, & Paterson, 1995).
Vertebral artery dissection is less common than carotid dissection. Post-traumatic dissection has been reported following neck manipulation. This includes chiropractic procedures, automobile accidents, sports injuries, strangulation, sudden head turning, and direct blows to the back of the neck (Greenberg, 1994). There is a clear difference in the course and outcome between spontaneous dissection resulting from definitive severe trauma, and dissection or that caused by minor trauma (Schievink et al., 1994). However, it is important to keep in mind that unrecognized or forgotten trauma, or sudden head motion, may have occurred in some cases reported as spontaneous (Greenberg, 1994).
Pathophysiology
Dissections may be seen in conjunction with a variety of conditions (see Table 1). Damage to the artery can occur either directly or by a rotational-stretch injury. Disruption of the media or intima occurs, resulting in hemorrhage into the medial layer, platelet aggregation, and thrombosis with or without actual vessel dissection. Embolic occlusion of distal vessels is a common result of such disruption (Palmer et al., 1995). The end result is cerebral ischemia.
Table 1.
Conditions Associated with Cerebral Artery Dissections
* Fibromuscular Dysplasia (FMD)
* Oral Contraceptive Use
* Cystic Medial Necrosis
* Marfan’s Syndrome
* Migraine
* Atherosclerosis
* Takayasu’s Disease
* Medial Degeneration
* Syphilitic Arteritis
* Variant Periarteritis Nodosa