Carotid artery dissection begins as a tear in one of the carotid arteries of the neck, which allows blood under arterial pressure to enter the wall of the artery and split its layers. The result is either an intramural hematoma or an aneurysmal dilatation, either of which can be a source of microemboli, with the latter also causing a mass effect on surrounding structures.
Carotid artery dissection is a significant cause of ischemic stroke in all age groups, but it occurs most frequently in the fifth decade of life and accounts for a much larger percentage of strokes in young patients.  Dissection of the internal carotid artery can occur intracranially or extracranially, with the latter being more frequent. Internal carotid artery dissection can be caused by major or minor trauma, or it can be spontaneous, in which case, genetic, familial, or heritable disorders are likely etiologies.
Although in practice, dissections are labeled spontaneous in the absence of major blunt or penetrating trauma,  when they are associated with minor mechanism trauma they may be caused or influenced by an underlying arteriopathy.  Patients can present in a variety of settings, such as a trauma bay with multiple traumatic injuries; a physician’s office with nonspecific head, neck, or face pain; or an emergency department (ED) with a partial Horner syndrome.
Sophisticated imaging techniques, which have improved over the past two decades, are required to confirm the presence of dissection. Most ischemic cerebral symptoms arise from thromboembolic events; therefore, early institution of antithrombotic treatment provides the best outcome. 
Once diagnosed and treated, patients with carotid artery dissection require regular follow-up and imaging studies of both carotid arteries. Healing usually takes 3-6 months, and the incidence of contralateral dissection is higher in these patients than in the general population. When the condition is diagnosed early, the prognosis is usually good. A high index of suspicion is required to make this difficult diagnosis.
Patients with internal carotid artery dissection can present with nonspecific complaints and in all settings. Maintaining a high index of suspicion for carotid dissection is critical whenever a patient presents with unusual focal neurologic complaints, particularly if the cranial nerves are involved and of the patient has sustained major mechanism trauma, minor mechanism stress, or a direct impact on the neck. Failure to consider the diagnosis in young patients presenting with neurologic symptoms is a potential medicolegal pitfall.
In cases of high-impact trauma, a history of cervical hyperextension, flexion, or rotation should alert the physician to the possibility of dissection. In patients with multiple traumatic injuries, the appearance of these nonspecific symptoms may be delayed for 1-5 days after the injury.
Even patients with seemingly minor trauma can develop dissection of the internal carotid artery. Symptoms may range from headache to hemiparesis. Precipitating events should be sought and may include chiropractic manipulation, yoga, gymnastics, sports injuries (including direct impact of high-velocity ball or other direct impact to the neck), overhead painting, coughing, or sneezing.
Typical presenting symptoms are as follows:
- Headache, including neck and facial pain – This can be constant, instantaneous, gradual, throbbing, or sharp
- Transient episodic blindness (amaurosis fugax) – This is caused by decreased blood flow to the retina
- Ptosis with miosis (partial Horner syndrome) – This is usually painful when caused by internal carotid artery dissections
- Neck swelling
- Pulsatile tinnitus – This can occur in as many as 25% of patients with dissection of the internal carotid artery
- Decreased taste sensation (hypogeusia)
- Focal weakness
- Migrainelike symptoms (eg, a scintillating scotoma, which is loosely defined as a transient visual field disturbance in the form of shimmering or arcs of light)
Pain is the initial symptom of a spontaneous internal carotid artery dissection presenting to a physician. Headache (including neck and facial pain) is usually described as constant and severe and is commonly ipsilateral to the dissected artery. It usually precedes a cerebral ischemic event, unlike headache associated with stroke, which usually follows or accompanies the ischemic event. Recurrence of neck pain suggests extension or recurrence of the dissection.
Unilateral facial or orbital pain is also common, and 25% of patients have isolated ipsilateral neck pain. Cluster-like headache with pain centered in or around the eye has been described in a case of spontaneous internal carotid artery dissection. 
Hypogeusia, or decreased taste sensation, may also be a presenting symptom.
In fewer than half of patients presenting with a carotid artery dissection, unilateral oculosympathetic palsy (partial Horner syndrome), may develop, and these patients will experience miosis, visual disturbance, and mild ptosis that may not be detected clinically. Isolated transient vision loss may also be a presenting complaint. Irreversible blindness from an ischemic optic nerve injury is rare. As many as 20% of patients may present with an ischemic stroke without any warning signs.
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If a diagnosis of spontaneous internal carotid artery dissection is under consideration, laboratory studies are largely irrelevant for diagnostic purposes. However, if contrast-enhanced computed tomography (CT) or arteriography is planned, it is appropriate to obtain a baseline creatinine concentration. If surgery is planned, the patient’s blood type, a complete blood count (CBC), and a coagulation profile (including prothrombin time [PT] and activated partial thromboplastin time [aPTT]) should be obtained.
Baseline coagulation studies may be appropriate in certain settings before the initiation of anticoagulation therapy or in cases where a patient is already taking an anticoagulant at the time that dissection is identified.
Cervical spine immobilization, which is usually appropriate, should be performed in the setting of any significant traumatic injury that could involve the neck.
Patients with internal carotid artery dissection may present to the emergency department (ED) in various ways and with various nonspecific complaints, but in all cases, the emergency physician should maintain a high index of suspicion. If internal carotid artery dissection is included in the differential diagnosis, the possibility should be pursued until it is clinically ruled out.
Depending on the likelihood of dissection, patient characteristics, neurologic status, and hemodynamic stability, medical management may occur during the diagnostic process or after the diagnosis is made. As in all medical care decisions, the benefits of treatment must be carefully weighed against the risks. Input from endovascular and surgical consultants should facilitate management decisions.
Initial computed tomography (CT) of the head is usually warranted, depending on the patient’s presentation. If the scan yields negative results or the findings do not correlate with the patient’s symptoms and signs, it should be followed up by a more definitive imaging modality, such as magnetic resonance angiography (MRA), CT angiography (CTA), or conventional angiography (depending on institutional preferences; see Workup).
In a prospective study that used repeated MRI over 6 months to investigate spatial and temporal dynamic changes of intramural hematomas in 10 patients with acute spontaneous internal carotid artery dissection, Heldner et al found an early postdissection volume increase with progression of the internal carotid artery stenosis in five patients.  Overall, spontaneous internal carotid artery dissection had a good prognosis with spontaneous hematoma resorption in all of the investigators’ patients, but early follow-up imaging may be considered, particularly in the case of new clinical symptoms
Pharmacologic, Endovascular, and Surgical Therapy
There is no general consensus regarding optimal management of internal carotid artery dissection, but the choice among medical, endovascular,  and surgical options may depend on the type of injury, the anatomic location, the mechanism of injury, coexisting injuries, and comorbid conditions. Therefore, after the diagnosis is made, the risk-to-benefit ratio of antithrombotic therapy should be determined, especially in cases of high-impact trauma, and vascular surgery or interventional radiology consultations should be obtained.
Anticoagulant therapy should be initiated when a thrombus is detected. Anticoagulation with intravenous (IV) heparin followed by warfarin has generally been accepted as adequate medical management for preventing thromboembolic complications. Do not initiate anticoagulation in trauma patients without first ruling out intracranial hemorrhage (ICH) and extracranial sources of hemorrhage.
Antiplatelet therapy has also been used alone, especially when systemic anticoagulation is contraindicated. Do not initiate either anticoagulation or antiplatelet therapy in pregnant patients without consulting an obstetrician.
Candidates for angioplasty and stent placement include patients with persistent ischemic symptoms despite adequate anticoagulation, patients with a contraindication to anticoagulant therapy, patients with an iatrogenic dissection developing during an intravascular procedure, and patients with significantly compromised cerebral blood flow