Introduction

Approximately 8 to 10% of ischemic strokes in the United States are thought to be due to intracranial atherosclerotic disease (ICAD), accounting for nearly 60,000 to 90,000 new strokes annually. Intracranial atherosclerosis accounts for nearly 26% of strokes in ethnic populations, including Asians and African Americans. The annual ipsilateral stroke risk based on the natural history of the disease is 3.1 to 8.1% for the internal carotid artery (ICA) and 0 to 7.8% for the middle cerebral artery (MCA). The most common intracranial locations for stenosis in decreasing order are MCA, 33.9%; ICA, 20.3%; basilar artery (BA), 20.3%; vertebral artery (VA), 19.6%; and a combination of these arteries, 5.9%. Although anterior circulation strokes do not have as high mortality as posterior circulation strokes due to the area they supply, they account for a large number of strokes and significant morbidity ( 1 , 2 in algorithm ).

Major controversies in decision making addressed in this chapter include:

1. 
   

   Whether (or not) treatment is indicated.

   
   
2. 
   

   Timing for intervention.

   
   
3. 
   

   Open vascular versus endovascular treatment.

   
   
4. 
   

   Different modalities of endovascular treatment (submaximal angioplasty and/or stenting).

Whether to Treat

Asymptomatic intracranial stenosis is thought to be a benign entity. Nearly one-third of the patients enrolled in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) were found to have a moderate degree of intracranial stenosis in addition to extracranial carotid artery stenosis. The most definitive evaluation of symptomatic intracranial stenosis was the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial in which the investigators found an 11 to 12% first year risk of stroke in the same area of stenosis. Nearly 73% of strokes were in the territory of the stenotic vessel distribution. Patients with 50 to 69% stenosis had a 1-year stroke risk of 6% and patients with more than 70% stenosis had a 1-year stroke risk of 19% in the distribution of the stenotic vessel ( 1 , 2 in algorithm ). In addition, a review of the angiographic progression of untreated stenosis has shown that 40% of lesions remain stable, 20% regress, and 40% progress. Defining whether a lesion causes symptoms and is progressive suggests better outcomes with intervention. Asymptomatic patients and those with regression tend to do better with lifestyle modifications ( 1 , 2 in algorithm ).

Anatomical Considerations

ICAD affects primarily the ICA and MCA vessels. The ICA is conventionally divided into seven segments, with segments from the petrous bone into the cavernous sinus being extradural but within the confines of bone and the cavernous sinus and the last three segments being intradural. The supraclinoid ICA has many tortuosities that pose challenges for easy repair, access, and endovascular therapy. The normal luminal diameter of the supraclinoid ICA tends to be 3 to 4 mm in diameter. The MCA is conventionally divided into four segments. The normal luminal diameters of the proximal MCA segments are between 2 and 3 mm and tend to show marked stenosis with diameters less than 1 mm. The lenticulostriate arteries are clinically significant branches that arise from the M1 segment.

Each VA usually arises from the first portion of the subclavian artery or the aortic arch. The artery is divided into four portions, with the last portion being intradural, and the confluence of the VAs forming the BA. The normal luminal diameter of the VA is 3 to 5 mm and 2 to 3 mm for the BA. Diameters less than 2 mm suggest significant stenosis and the presence of atherosclerosis. The posterior inferior cerebellar artery (PICA) arises from the intracranial portion of the VA and is one of the largest branches, with 1 to 25% of VAs ending in a PICA.

Pathophysiology/Classification

Ischemic symptoms due to ICAD arise from (1) hypoperfusion; (2) thrombosis at the site of stenosis secondary to plaque rupture, plaque hemorrhage, or progressive occlusive plaque growth; (3) thromboembolism distal to the stenosis; and (4) occlusion and ischemia of small perforating arteries and branch vessels at the site of the plaque. Chronic hemodynamic insufficiency has been classified into three stages: stage 0, normal hemodynamics; stage 1, reflex vasodilation in response to poor collateral flow and falling perfusion pressures with increased time to peak, preserved cerebral blood flow (CBF), and elevated cerebral blood volume (CBV); and stage 2, poor perfusion in response to cerebral perfusion pressure being outside the autoregulatory range. Stage 2 can best be noted with acetazolamide (Diamox, Teva Pharmaceuticals, North Wales, PA) perfusion studies (referred to as acetazolamide challenge testing) and will be discussed later.

Intracranial stenosis can be classified as described by Mori and colleagues according to lesion type as follows: type A, ≤5 mm in length and concentric lesions; type B, 5 to 10 mm in length with eccentric plaque or completely occluded vessel for less than 3 months of follow-up; and type C, more than 10 mm length and angulated with substantial tortuosity. This classification system plays a role in stroke risk and restenosis rates on follow-up.

Workup

Imaging

The initial diagnostic workup for symptomatic intracranial stenosis should include noncontrast computed tomography (CT) of the head to exclude a completed ischemic event and hemorrhage. Diffusion-weighted magnetic resonance imaging (MRI) with and without magnetic resonance angiography (MRA) and CT perfusion studies give more information regarding vascular patency and hemodynamic status (▶ Fig. 5.1 ). Transcranial Doppler imaging has been shown to be predictive in terms of showing elevated velocities in stenotic vessels but has not been validated as a good screening technique. However, in lesions affecting the ICA and MCA, a transcranial Doppler breath-holding test can serve as a hemodynamic marker with normal elevations of velocities (Stage 1) and pathologic depressions of velocities (Stage 2) with insufficiency.

Vessel patency and vessel caliber are best seen on MRA and CT angiography (CTA), although MRA may overestimate the degree of stenosis. Cone beam CT and MRA are also helpful in determining plaque morphology. Chronic versus acute hemorrhagic plaque may be seen on these dedicated studies more clearly. Quantitative flow MRA (Noninvasive Optimal Vessel Analysis [NOVA], VasSol, River Forest, IL) can be a very useful measure to assess for collateralization and flow dynamics at the level of the circle of Willis. Even with good screening techniques, their specificity is not reliable enough to replace cerebral diagnostic subtraction angiography (DSA). Intra-arterial ultrasound and optical coherence tomography are two newer techniques that are still being evaluated for how effectively they can determine plaque morphology and treatment paradigms. Their current main limitation is the size and navigability of current probes to deliver into the intracranial circulation.

CT perfusion studies can be used to quantify cerebral perfusion and flow-related changes within neural parenchyma. These studies permit an understanding of metabolic use, oxygen extraction, CBF, and CBV (▶ Fig. 5.1 ). These studies, as well as positron emission tomography (PET) and single-photon emission computed tomography (SPECT), are excellent tools for monitoring patients in follow-up and were used as a predictive measure in the Japanese Extracranial-Intracranial Bypass Trial (JET) to determine whether patients would benefit from bypass surgery. Eighty-eight percent of these patients benefited from surgery performed after these studies showed changes in flow and volume relations in areas of tissue that had stenotic feeding vessels.

Related posts:

Section I Ischemic Stroke and Vascular Insufficiency Section I Ischemic Stroke and Vascular Insufficiency 9 Vertebral Artery Ostium Stenosis 13 Traumatic and Iatrogenic Vertebral Artery Injury 15 Spontaneous Vertebral Arterial Dissection 12 Traumatic and Iatrogenic Carotid Artery Injury

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