Introduction

Chronic internal carotid artery (ICA) occlusion resulting from atherosclerotic disease causes approximately 10% of transient ischemic attacks (TIAs) and 15 to 25% of ischemic strokes in the ipsilateral carotid territory. When compared to acute ICA occlusion presenting with acute onset of severe neurological symptoms, these patients often present with a more gradual course of decline in cognitive function and have recurrent disabling TIAs, symptomatic hypoperfusion, and recurrent strokes. In addition, even in the absence of obvious neurological events, serial imaging may review progressive cerebral volume loss. The 2-year risk of ipsilateral ischemic stroke is 10 to 15% even while the patient is on best medical therapy. In 1969, Yasargil first described the direct extracranial–intracranial (EC-IC) bypass procedure, anastomosing the superficial temporal artery (STA) to a distal branch of the middle cerebral artery (MCA) to augment hemispheric perfusion. Since that time, few neurosurgical procedures have been more controversial. Two large randomized controlled trials have failed to show benefit of surgery over medical therapy, with stroke as the primary end point; however, there still exists a subset of patients who may benefit from surgical revascularization.

Major controversies in decision making addressed in this chapter include:

1. 
   

   Should chronic ICA occlusion be treated?

   
   
2. 
   

   Should chronic symptomatic ICA occlusion be treated medically, endovascularly, or by EC-IC bypass?

   
   
3. 
   

   The role of open endovascular techniques.

   
   
4. 
   

   The role of low- and high-flow EC-IC bypass.

Whether to Treat

There is an extensive body of literature available on atherosclerotic occlusive disease of the carotid artery. There is overwhelming support for carotid endarterectomy and endovascular angioplasty and stenting in the setting of symptomatic severe carotid stenosis. The management of carotid occlusion is somewhat less clear. The occurrence of symptoms with chronic carotid occlusion theoretically relates primarily to the adequacy of the circle of Willis and the cerebral autoregulatory system such that perfusion may be preserved in the face of reduced inflow from the occluded carotid artery.

It is generally accepted and supported by guidelines that all patients with severe atherosclerotic disease and carotid stenosis or occlusion, regardless of neurological symptoms, should be treated with aggressive medical management ( 1 , 3, 5 in algorithm ). This includes treatment of hypertension (goal blood pressure below 140/90 mm Hg), smoking cessation, hyperlipidemia (goal low-density lipoprotein cholesterol less than 100 mg/dL), and diabetes (goal hemoglobin A1C less than 7.0%). Antiplatelet treatment with either aspirin (ASA) or clopidogrel is also recommended in these patients.

If symptoms persist despite best medical management, surgery can be considered. Surgical options generally consist of revascularization via either direct or indirect EC-IC bypass ( 6 in algorithm ). In our practice, the patients selected for surgical treatment must have persistent symptoms that are refractory to medical therapy and objective evidence of cerebral hypoperfusion, as discussed below (▶ Fig. 16.1 ).

Anatomical Considerations

The primary anatomical considerations are the adequacy of the external carotid artery (ECA) as a donor and the specific anatomy of the circle of Willis and collateral patterns. Patients who have atherosclerotic occlusion of the proximal ICA often also have disease in the proximal ECA. In these cases, ECA endarterectomy or stenting may be necessary prior to the intracranial anastomosis. In a few patients, we have seen distal collaterals to the proximally occluded ECA indicating patency of the STA and have utilized common carotid or subclavian to ECA bypass to revascularize the ECA prior to EC-IC bypass.

Generally, for a direct EC-IC bypass to remain patent, the STA should be at least 1 mm in diameter. If the STA is either very small or nonexistent, then indirect bypass via some variation of encephaloduralmyoarterialsynangiosis (EDAMS) can be attempted. We have not been as satisfied with the outcomes of indirect bypass procedures in the adult population with carotid occlusion as in younger patients with moyamoya.

The collateral patterns are very important in consideration of EC-IC bypass ( 3, 4, 5 in algorithm ). Angiography of both internal and external carotid arteries and the vertebral arteries should be obtained (see below). In some patients, the collaterals are good enough that there is no objective evidence of hypoperfusion and the cause of ongoing symptoms should then be reevaluated. Patients who have patent anterior and posterior communicating arteries may maintain relatively normal perfusion patterns in the hemisphere. Patients who do not have a complete circle of Willis often fill part of the supraclinoid segment via ECA collaterals to the ophthalmic or middle meningeal arteries. Care should be taken not to interrupt these collaterals at the time of craniotomy.

Pathophysiology

The vital functions of the brain are directly dependent on near continuous blood flow for the delivery of metabolic substrates. The brain, unlike other organ systems, has little intrinsic energy reserves and little capacity for repair once damaged. Studies have suggested that flow rates less than 15 mL/100 g/min sustained for more than 1 hour can cause permanent cellular injury and cell death. It is also known that flow below 18 mL/100 g/min for a short time during carotid endarterectomy results in near-uniform depression of electroencephalogram (EEG) tracings, suggestive of cellular dysfunction. It is flow rates in this range in a “penumbra” of the hemisphere that may lead to progressive infarction in chronic carotid occlusion. This is directly related to the collateral pattern and adequacy of perfusion pressure. Left untreated, hypoperfusion can lead to a cascade of abnormal cellular signaling and release of inflammatory markers that can lead to apoptosis and cell death.

Workup

Related posts:

Section I Ischemic Stroke and Vascular Insufficiency Section I Ischemic Stroke and Vascular Insufficiency 9 Vertebral Artery Ostium Stenosis 10 Pediatric Moyamoya Disease 13 Traumatic and Iatrogenic Vertebral Artery Injury 15 Spontaneous Vertebral Arterial Dissection

Stay updated, free articles. Join our Telegram channel

Join