Patients with stenoses of the intracranial arteries frequently show cerebral ischemic events while being traditionally treated with an antiplatelet agent or oral anticoagulant and general management of vascular risk factors . Despite the dynamic course, prognosis is poor with significant morbidity and death rates. These limitations and the high current stroke rates require a more aggressive treatment regimen in patients with symptomatic intracranial artery stenosis. The treatment of these patients is still controversial and several questions have to be answered. For example, whether only antiplatelet/anti-coagulation therapy or angioplasty/stenting is the best first-line therapy , or what is the best or maximal medical therapy? Furthermore, what is the risk of stroke with medical therapy or with interven-tional therapy or, what is the risk of complications from interventional therapy? Is stenting necessary or is angioplasty alone sufficient? Do the interventio-nalists have sufficient experience and routine clinical use. Are there any contraindications against a sufficient peri- and postprocedural anticoagulation/anti-platelet therapy? . All of these questions have not yet been clearly answered and must be considered for each patient on an individual basis.
The so-called best medical treatment plan is based on the control of vascular risk factors and the application of antiplatelet/anticoagulation drugs, statins (HMG-CoA reductase inhibitors) and an-giotensin-converting enzyme inhibitors. Maximal medical treatment can be defined as receiving daily doses of >81 mg acetylsalicylic acid, 500 mg ticlopi-dine, 75 mg clopidogrel, or comparable doses of marcumar/warfarin or heparin . A more aggressive treatment regimen like angioplasty should be considered in cases where maximal medical therapy fails to prevent massive ischemic stroke. Medical therapy failure is not clearly defined, but should be assumed when recurrent cerebral symptoms occur under maximal medical treatment .
Despite unsatisfactory experiences during the 1980s involving high rates of stroke or death, advances in micro-guidewires, microcatheters, balloon technology and stent technology have been made as a result of positive in coronary angioplasty and stenting. Angioplasty or stenting methods have emerged as a potential therapeutic option over the last decade. Stent placement has proven to be as technically feasible as for angioplasty or stenting of the extracranial carotid artery .
Angioplasty or stent treatment can be performed using the typical transfemoral access. Some physicians perform the interventional procedure without general anesthetic or sedative, in order to recognize slight changes in clinical neurological status such as motor activity or speech. But for quiet examination conditions and reduced patient movement, a general anesthetic is recommended. During all examinations, the continuous measurement of blood pressure, electrocardiogram and transcuta-neous oximetry is mandatory during the entire in-terventional procedure. Despite preexisting imaging modalities, like a MRA of the circle of Willis or the carotid arteries, a four-vessel cerebral DSA must be performed to verify the stenosis and to provide a description of the existing collateral circulation. Three-dimensional rotational angiography can be a very helpful method for the imaging and evaluation of the stenosis. The diameter of the stenosis, referring to the next normal sized vessel part and the stenosis length have to be measured based on the standardized criteria . The choice of the appropriate micro-guidewire to be used for probing the stenosis is also of considerable importance. Intracranial vessels are located in the subarachnoid space surrounded by the cerebrospinal fluid and follow quite a convoluted course. Additional, small penetrating vessels extend from the major intracranial arteries supplying the brain tissue with blood. These small penetrating vessel are invisible in neuroimaging. Particular care must be taken with the lateral lenti-culostriate arteries arising from the Ml-segment of the middle cerebral artery. The use of stiff micro-guidewires, involves the risk of injuring (e.g., dissection) or penetrating the vessel and tearing off the small penetrating vessels. Subsequent severe intracranial bleeding or infarction may occur. Occlusion caused by a stent or a dissection or microtrauma to the vessel wall as a result of angioplasty may lead to subsequent ischemic stroke. Hydrophilic micro-guidewires (usually 0.010-0.014 inches) with a soft or floppy tip should thus be used. These wires must be placed more peripherally, so that the system can be well stabilized , . In case of an Ml medial cerebral artery stenosis, this requires the positioning of the tip in the M2 insular branches. All manipulations with the micro-guidewire - microca-theter-system have to be performed very carefully since each step runs the risk of vessel rupture, vaso-spasm or dissection. After positioning a 6 French guiding catheter in the upper cervical part of the internal carotid artery and crossing of the intracranial lesion by the micro-guidewire or micro-guidewire -microcatheter-system, a predilation of a high-grade stenosis is often necessary, since the stent delivery system might not cross the lesion or can cause a dissection or shearing off of atherosclerotic plaques. Otherwise, primary stenting is normally preferred. Some authors are of the opinion that a predilation should always be performed if the diameter of the stent delivery system is smaller than that of the lesion , . Small-profile balloon-catheter-systems should be given preference and, in order to reduce the risk of rupture or dissection, a balloon diameter size smaller than the normal adjacent vessel diameter should be used. Balloon-dilation should be performed very slowly lasting several seconds or even minutes . As mentioned above, intracranial vessels follow a quite tortuous course, thus the matched stent and the stent delivery catheter system have to be soft, flexible and must offer a low profile with excellent trackability and pushability. Balloon-expandable stents derived from coronary angioplasty are very suitable stents and, based on experience in this area, special stents for intracranial angioplasty were developed . In general, the stent size should be matched to the vessel diameter proximal or distal to the stenosis or slightly undersized, and in case of a less than optimally deployed stent, a further expansion with a balloon catheter can be performed .
Clearly, postprocedural angiograms have to be carried out immediately in order to evaluate cerebral blood flow. The main risks of intracranial intervention remain the possibility of vessel rupture, vaso-spasm, dissection, stroke, severe intracranial bleeding or even death. These risks can be reduced by increased experience and the use of novel, improved materials, as described above. Crossing and dilating the lesion carry the greatest risks in intracranial intervention. Careless pushing of the stent delivery system leads to the danger of a shear stress to these small vessels with associated disruption or dissection. It is well known from coronary or peripheral angioplasty, that abrupt inflation of the balloon produces severe stress on the vessel wall causing the vessel to dissect. Slow inflation and deflation of the balloon is mandatory and can reduce the dissection rate for angioplasty from 75% to 14% . After predilation, the stent should be positioned and deployed quickly but carefully in order to diminish the vessel recoil.
Initial positive experiences with undersized stents have been reported in the literature , . These studies showed a good balance between efficacy and safe procedure, where the risk of vessel rupture could be reduced, without affecting the clinical outcome. If the predilated lesion can not be easily reached with the stent delivery catheter, prolonged attempts should be abandoned to reduce procedural risks. In such cases, angioplasty alone can sometimes be safer than stent placement . The aim being to just slightly stretch the vessel, since a small increase in vessel diameter results in a large increase in perfusion .
After the recanalization of a major intracranial artery, intracerebral reperfusion hemorrhage within a preexistent hemodynamic stroke can occur. In case of acute thrombosis, the application of urokinase or tissue plasminogen activator during intervention is necessary. It should be clear that this thrombolytic treatment increases the risk of intracerebal hemorrhage. Intraarterial papaverine or nitrogylcerin may sometimes be necessary in case of arterial spasm during the procedure.
To reduce the risk of acute vessel occlusion due to acute thrombosis, a rigorous periinterventional anticoagulation/antiplatelet therapy is mandatory. As mentioned above, the best medical treatment in patients with intracranial atherosclerotic lesions is still unknown. Similarly, the best periinterventional medical treatment is also not known , , , . Despite the increased risk of intracerebral hemorrhage, the risk of thrombembolic events during and after intervention has to be reduced. The anticoagulation and antiplatelet regimen should be performed as known from interventions for the extracranial internal carotid artery. Before intervention, 75 mg clopidogrel daily or 250 mg ticlopidine daily should be administered for three to five days. Additionally, 100-300 mg acetylsalicylic acid daily should be administered three to five days prior to the procedure. During the interventional procedure, heparinization with up to 10,000 IU (acquired coagulation time ACT about 200-300 sec) is recommended. In addition to heparin, glycoprotein IIb/IIIa inhibitors can be used as well with similar results , but with a possibly higher risk of intra-cerebral hemorrhage. A burst suppression-inducing dose of etomidate may help to protect the brain from ischemic events, especially while the treatment device transverses the stenosis . The intervention should be followed by a daily dose of clopido-
Table 1. Classification of intracranial stenotic lesions modified from a scheme for coronary arteries for intracranial angioplasty alone 
Lesion Type A
Lesion Type B
Lesion Type C
Concentric or moderate eccentric
Angulation < 45°
No prominent calcifications
No thrombus present
No major branch involvement
Lesion length < 5mm
Angulation 45°-90° Irregular contours Heavy calcifications Ostial
Total occlusion < 3 months old Some thrombus present Major branch involvement possible Lesion length 5-10mm
Eccentric Severe tortuosity
Total Occlusion > 3 months old
Lesion length > 10 mm grel or ticlopidine and acetylsalicylic acid for up to six months and acetylsalicylic acid monotherapy (or clopidogrel/ticlopidine monotherapy if necessary) should be continued for life.
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