The distinction between hemodynamic and embolic stroke in the setting of chronic internal carotid artery occlusion is important. Embolic symptoms are those of classic stroke or transient ischemic attack (TIA) and typically are focal. Symptoms may include a contralateral motor or sensory deficits or amaurosis. Hemodynamic symptoms may be similar to those of classic stroke or TIA, but may also be less predictable and atypical. Patients have reported symptoms such as limb shaking, retinal claudication, headache from large pulsatile external carotid artery collaterals, syncope, and generalized fatigue. One-third of all strokes are related to a cervical carotid disease. Standard risk factors for coronary and systemic atherosclerosis such as age, male sex, family history, smoking, hypertension, hyperlipidemia, sedentary lifestyle, and high dietary fat apply to this patient population. The mechanism of cervical carotid stroke is usually embolization from the carotid bifurcation plaque, but hemodynamic compromise from stenosis may also play a role. The risks of embolization and hemodynamic compromise increase with increasing carotid artery stenosis.
Carotid artery stenosis is a consequence of systemic atherosclerotic disease. Thus, any risk factor predisposing a patient to progressive atherosclerosis can potentially manifest itself as stenosis of the carotid artery with resultant ischemic stroke and or TIA like symptoms. Risks include smoking, hyperlipidemia, male gender, and age.
In a minority of patients, especially young females with stenosis of the carotid artery, fibromuscular dysplasia (FMD) plays a much more significant role. Fibromuscular dysplasia is a noninflammatory, nonatherosclerotic process that most commonly affects the carotid and renal arteries, although it can occur elsewhere in medium-sized vessels. Fibromuscular dysplasia usually occurs in the mid and distal internal carotid artery, sometimes extending into the intracranial region. Aneurysms may be a component of the disease process as well.
Symptomatic internal carotid artery occlusion has an incidence of six per 100,000, though the rate of asymptomatic chronic occlusion is unknown and may be higher.
Internal carotid artery occlusion is a known risk factor for stroke in the United States. In fact, one-third of all the strokes are related to carotid occlusive disease. Stroke ranks third among all causes of death in the United States, behind heart disease and cancer. Annually about 55,000 more women are affected compared with men, and approximately 60% of all stroke deaths occur in females. African Americans and Mexican Americans have a higher risk of stroke compared with Caucasians. Thus diagnosis, prevention, and treatment of the carotid artery stenosis play a pivotal role in stroke prevention.
Total internal carotid artery occlusion results from thrombosis in the setting of chronic stenosis. Cardiogenic embolization to a normal carotid bifurcation or carotid dissection may also cause total occlusion of the internal carotid artery occlusion. Acute occlusion may result in a carotid territory stroke. A previously asymptomatic chronic internal carotid artery occlusion may become symptomatic if related to embolic or hemodynamic issues. Embolism may occur from the ipsilateral external carotid artery via collaterals to the cerebral circulation. It may also occur when there is occult patency of the occluded internal carotid artery occlusion, which then serves as the source of embolic material. Hemodynamic insufficiency may occur when any condition that interferes with cerebral perfusions such as orthostasis, hypotension, volume depletion, or cardiac failure is superimposed on the carotid occlusion, especially when the contralateral carotid disease is significant.
Usually, patients will present with recent stroke (slurred speech, cranial nerve deficits, limb weakness, or visual disturbances) which either have resolved or should be expected to improve within 48 hours otherwise known as transient ischemic attack. Typically, history and physical are notable for a patient in their 70s and 80s because they may have a history of smoking, high lipid profile, sedentary lifestyle. It is imperative to realize that carotid artery atherosclerotic disease is not a segmental disease, rather it has the propensity to involve other arteries in the human body. Of concern are the coronary arteries. Hence, it is prudent for this patient to undergo a cardiac evaluation should surgical intervention be contemplated in treating the degree of stenosis.
Evaluation should include but not be limited to a thorough physical exam. The physical should be coupled with diagnostic imaging (CT head), followed by telemetry floor admission, as only third of ischemic strokes are due to carotid artery disease, the remaining is due to the cardiac embolic phenomenon. Thus, consultation with a stroke specialist like a neurologist, as well as a cardiologist is of paramount importance.
Regarding diagnosing carotid artery stenosis, one usually starts with a least invasive inexpensive test such as Carotid Duplex. This examination typically shows a high-resistance signal in the carotid bulb and the very proximal internal carotid artery. Distally, there are no Doppler signals audible in the carotid artery. As a confirmatory test, some form of contrast examination such as digital subtraction arteriography, magnetic resonance arteriography (MRA), or computed tomographic (CT) arteriography is required to confirm the diagnosis and plan a surgical approach.
Acute symptomatic carotid occlusion should be treated with urgent revascularization in select cases with immediate presentation. This can be accomplished with carotid endarterectomy (CEA) or interventional techniques including thrombolysis. In the setting of chronic total internal carotid artery occlusion (ICA) occlusion, medical management is preferred over revascularization. However, several special clinical indications exist for procedural intervention. Ipsilateral hemodynamic symptoms in the setting of ipsilateral ICA occlusion and contralateral ICA stenosis may benefit from contralateral ICA revascularization to ameliorate hemodynamic insufficiency. Ipsilateral embolic symptoms in the setting of ipsilateral ICA occlusion and ipsilateral external carotid occlusion (ECA) stenosis may be treated with ipsilateral ECA revascularization to eliminate the source of embolization, which occurs via enlarged ECA collaterals; ligation of the ipsilateral ICA also eliminates a source for embolization. Finally, ipsilateral hemodynamic symptoms in the setting of a patent contralateral carotid system, ipsilateral ICA occlusion, and ipsilateral ECA stenosis indicate ipsilateral ECA revascularization to improve ipsilateral hemodynamic flow.
There are no specific criteria for surveillance of patients with chronically occluded ICA, nor are there criteria to specify the degree of ECA stenosis by duplex ultrasound. A reasonable regimen is to follow the patient clinically every six months to a year, with or without duplex study. The development of symptoms indicates investigation with imaging of some kind to see if cerebrovascular revascularization is indicated.