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[Cerebral bypass surgery]
1Neurochirugische Klinik, Universitätsspital Zürich.
When an obstruction of a cerebral vessel is hemodynamically relevant and insufficiently collateralized--and when the mechanisms of compensation are exhausted--it can lead to ischemia. The second and more common way a vascular obstructive lesion can become symptomatic is the shedding of emboli to the periphery. The extra-/intracranial arterial bypass (EIAB), most often constructed as an anastomosis between the superficial temporal artery (STA) and a cortical branch of the middle cerebral artery (MCA), increases cerebral blood flow when all the mechanisms of compensation are exhausted. When not, it augments the cerebral perfusion reserve. If cerebral ischemia is due to embolism, the therapy of choice is elimination of the embolic source. When using the EIAB in hemodynamically caused ischemia, there are two indications: a therapeutic and a prophylactic one. Differentiation between functional and structural damage of neurons is difficult. Because reversible longlasting functional loss is rare, we reject it as a therapeutic indication. The prophylactic EIAB has to overcome the hemodynamic consequences of an intentional or spontaneous obstruction of extra- or intracranial cerebral vessels. Currently, neither the asymmetry of cerebral perfusion nor a decrease of the the cerebral perfusion reserve are established as risk factors for future ischemic cerebral events. If the MCA is to be occluded, a prophylactic EIAB is indicated: When the intention is to occlude the ICA with its extensive collateral system, the necessity for a bypass has to be evaluated. Most often, spontaneous occlusion of cerebral vessels is of atherosclerotic origin. Because no reliable method exists to differentiate between embolic (arterio-arterial) and hemodynamic ischemia; and since the spontaneous course of atherosclerosis is not predictable, the prophylactic indications for EIAB are unresolved. Nevertheless, many uncontrolled studies have shown a good prophylactic effect after the EIAB. The randomized international EC/IC Bypass Study, which is not accepted without reservation, denies any advantage of the EIAB in treating atherosclerotic vessel lesions when compared to medication with aspirin. Our experience leads us to believe that a prophylactic effect of the EIAB, even with atherosclerotic vessel obstruction, cannot be denied point blank. On the other hand, our experience also confirms that the EIAB should not be the standard treatment for atherosclerotic vessel obstruction. Considering the broad differences in the individual architecture of the cerebral vascular system and its varied amounts of acquired vascular lesions and through the spontaneous development of collaterals, the indications for EIAB, which in some circumstances is very effective, must be assessed for each individual patient.
When an obstruction of a cerebral vessel is hemodynamically relevant and insufficiently collateralized--and when the mechanisms of compensation are exhausted--it can lead to ischemia. The second and more common way a vascular obstructive lesion can become symptomatic is the shedding of emboli to the periphery. The extra-/intracranial arterial bypass (EIAB), most often constructed as an anastomosis between the superficial temporal artery (STA) and a cortical branch of the middle cerebral artery (MCA), increases cerebral blood flow when all the mechanisms of compensation are exhausted. When not, it augments the cerebral perfusion reserve. If cerebral ischemia is due to embolism, the therapy of choice is elimination of the embolic source. When using the EIAB in hemodynamically caused ischemia, there are two indications: a therapeutic and a prophylactic one. Differentiation between functional and structural damage of neurons is difficult. Because reversible longlasting functional loss is rare, we reject it as a therapeutic indication. The prophylactic EIAB has to overcome the hemodynamic consequences of an intentional or spontaneous obstruction of extra- or intracranial cerebral vessels. Currently, neither the asymmetry of cerebral perfusion nor a decrease of the the cerebral perfusion reserve are established as risk factors for future ischemic cerebral events. If the MCA is to be occluded, a prophylactic EIAB is indicated: When the intention is to occlude the ICA with its extensive collateral system, the necessity for a bypass has to be evaluated. Most often, spontaneous occlusion of cerebral vessels is of atherosclerotic origin. Because no reliable method exists to differentiate between embolic (arterio-arterial) and hemodynamic ischemia; and since the spontaneous course of atherosclerosis is not predictable, the prophylactic indications for EIAB are unresolved. Nevertheless, many uncontrolled studies have shown a good prophylactic effect after the EIAB. The randomized international EC/IC Bypass Study, which is not accepted without reservation, denies any advantage of the EIAB in treating atherosclerotic vessel lesions when compared to medication with aspirin. Our experience leads us to believe that a prophylactic effect of the EIAB, even with atherosclerotic vessel obstruction, cannot be denied point blank. On the other hand, our experience also confirms that the EIAB should not be the standard treatment for atherosclerotic vessel obstruction. Considering the broad differences in the individual architecture of the cerebral vascular system and its varied amounts of acquired vascular lesions and through the spontaneous development of collaterals, the indications for EIAB, which in some circumstances is very effective, must be assessed for each individual patient.