The use of Doppler insonation of the middle cerebral arteries is being studied to detect transient signals called HITs (high-intensity transients) as a manifestation of small emboli during surgery but, as for the transients frequently noted during cerebral arteriography, the clinical importance of these emboli is not known. In an attempt to avoid neurologic complication related to extracorporeal circulation, off-pump coronary artery bypass has been popularized in many centers. Unfortunately, most studies have found no fewer cognitive complications as compared to conventional coronary artery bypass surgery (e.g., see Shroyer et al). This is contrary to the notion that the extracorporeal apparatus is the cause of the problem. The issue of the neurologic complications of cardiac surgery may be summarized by noting that strokes originating from the aorta are the main cause of cognitive failure. The clinical syndromes seem to fall on a continuum; a few strokes (less than 3 percent) are recognizable as obvious deficits (e.g., hemiplegia), instead, many have multiple small emboli that are evident with imaging and these are manifest as an acute encephalopathy. When the burden of emboli is lower, no deficit is recognized in the acute period. It is likely that in patients with premorbid presymptomatic Alzheimer disease, confusion and dementia are made manifest by the stress of cardiac surgery and the surgery is then blamed for the emergence of an ostensibly new problem (see Samuels).
The other special stroke problems relating to prosthetic heart valves—mainly infective endocarditis causing embolic strokes and anticoagulant-related cerebral hemorrhage—are described in later sections of this chapter.
This is the third most frequent cause of stroke, following cerebral embolism and thrombotic disease. Although more than a dozen causes of nontraumatic intracranial hemorrhage are listed in Table 33-8, hypertensive primary (“spontaneous”) intracerebral hemorrhage, ruptured saccular aneurysm and vascular malformation, and hemorrhage associated with the use of anticoagulants account for the majority. Cerebrovascular amyloidosis and acquired or congenital bleeding disorders account for a smaller number. The small brainstem hemorrhages secondary to temporal lobe herniation and brainstem compression (Duret hemorrhages), hypertensive encephalopathy, and brain purpura might be included in this group, but they do not simulate a stroke.
This is the often devastating “spontaneous” brain hemorrhage. It is still predominantly a result of chronic hypertension and degenerative changes in cerebral arteries. In recent decades, with increased awareness of the need to control blood pressure, the proportion of hemorrhages attributable to causes other than hypertension, mainly anticoagulation, has greatly increased so that more than half such hemorrhages on our services now occur in normotensive individuals, and the hemorrhages more often arise in locations that are not typical for hypertension. Nevertheless, the hypertensive cerebral hemorrhage serves as a model for understanding and managing other cerebral hemorrhages.