Discussion
In cases of direct (blunt) or indirect cervical trauma, CAD should be considered, as it carries a risk of potentially debilitating ischemic stroke in otherwise healthy young patients. Fortunately, CAD is rare; its annual incidence is 1 in 100,000, occurring in 0.08% to 1.2% of blunt trauma cases.9
As symptoms of ICA dissection can vary depending on stenosis severity, diagnosis can be challenging. The classically associated triad of symptoms includes unilateral head, facial, or neck pain accompanied by partial Horner syndrome with progression to cerebral or retinal ischemia. However, these symptoms occur in less than a third of patients with ICA dissection.2 Neck pain may occur secondary to blunt cervical trauma, consistent with a cervical soft-tissue contusion; however, it may have more severe implications and should be carefully monitored, particularly if accompanied by additional symptoms, such as headache. Headaches, which are present in 44% to 69% of patients, are often unilateral and constant. Either headache or neck pain in isolation is relatively uncommon, occurring in <10% of cases,2 though retrospective reviews of delayed-onset ICA dissection found atypical headache or neck pain in 100% of patients,11 indicating that persistent symptoms should be further evaluated.
More commonly, patients present with neurologic symptoms, particularly Horner syndrome, which is caused by the disruption of the sympathetic nerve fibers adjacent to the ICA, resulting in ipsilateral ptosis and miosis. In addition, patients may present with cranial nerve palsies, most commonly involving cranial nerve XII (the hypoglossal nerve), resulting in tongue weakness and abnormal taste. These and other neurologic findings associated with retinal or cerebral ischemia should raise clinical suspicion for the injury and prompt computed tomography or MRA evaluation.
MRA has largely replaced conventional angiography for the diagnosis of CAD. As MRA is noninvasive, it allows for improved visualization of luminal narrowing and for evaluation of the arterial wall and intramural hematoma.2 Because of the potential for devastating sequelae with missed or delayed diagnosis, several authors have become proponents of early aggressive screening for detection of these injuries.9 Postdiagnostic treatment depends on the presence of neurologic symptoms. Management is directed toward limiting neurologic deficits; anticoagulant or antiplatelet agents are used to prevent thromboembolic events. A randomized controlled trial and other studies have failed to find any appreciable difference in subsequent rates of stroke or associated complications with use of either class of medication.8,12 Conventionally, treatment is continued for 3 to 6 months, depending on clinical resolution. Endovascular or surgical intervention typically is reserved for extreme luminal narrowing, conditions that are preventing anticoagulation, an expanding area of dissection with a persistent pseudoaneurysm, and cases of failed medical management with subsequent ischemic stroke.2The literature includes several case reports involving indirect trauma in recreational athletes. First, a 31-year-old woman sustained an ICA dissection secondary to a head injury that occurred during a soccer match; she presented with headache, altered sense of taste, and objective findings of ptosis and miosis consistent with Horner syndrome.13 Second, a 39-year-old man had an ICA dissection after a snowboarding fall that caused neck hyperextension; he presented with periocular headache, ptosis, and miosis.6 Third, 3 people who participated in CrossFit training sustained ICA dissection.7 They presented with varying degrees of neurologic symptoms: ptosis and miosis; right-side upper extremity ataxia; and visual distortion and receptive aphasia. Our patient’s ICA dissection resulted from indirect trauma that caused sudden hyperextension and lateral flexion in response to contact from a hockey puck. However, his case is unique in that symptoms onset was delayed, and there were no associated neurologic findings on clinical presentation. His case should raise awareness of this potential diagnosis, even in the absence of overt neurologic findings. In addition, the patient’s return to sport at 8 weeks was facilitated by full clinical resolution of symptoms and thorough radiographic documentation of improved intramural narrowing. Finally, to our knowledge this is the first report of this injury in a professional athlete.