This is perhaps the most common cerebral vascular malformation, estimated to occur in almost 3 percent of large autopsy series. As with cavernous angiomas, these lesions are frequently detected as asymptomatic problems in brain imaging. The defining characteristics are of a caput medusa draining into a small collecting vein. The draining vein itself is often visualized most easily and fills with contrast concurrently with normal cerebral (Fig. 33-33). As mentioned earlier, up to 40 percent of cavernous malformations (probably fewer) have an associated deep venous anomaly. Although the risks of stroke in relation to one of these anomalies is low, less than 1 percent per year, small hemorrhage or infarction surrounding a deep venous anomaly may result from acute thrombosis in a collecting vein. A summary of the clinical and imaging features of venous anomalies is given by Ruiz and colleagues. They reviewed the interesting cases reported in the literature in which the anomaly has thrombosed, and discuss the possible pathophysiologic relationship between the vein and the development of a cavernous malformation.
The management of developmental venous anomalies has not been clarified although numerous forms of surgery, embolization, or focused radiation, have been used depending on the nature of an associated lesion such as cavernous malformation, and the occurrence of repeated bleeding. In general, incidentally discovered lesions are simply followed with imaging at reasonable intervals.
Other Causes of Intracranial Bleeding and Multiple Cerebral Hemorrhages
Next in frequency to hypertension, anticoagulant therapy is currently the most common cause of cerebral hemorrhage. The hemorrhages that develop, although sometimes situated in the sites of predilection of hypertensive hemorrhage, are more likely to occur elsewhere, mainly in the lobes of the brain. The reversal of anticoagulant or antiplatelet agents is discussed in an earlier section on “Treatment of Cerebral Hemorrhage.” When bleeding is associated with aspirin therapy or other agents that affect platelet function, fresh platelet infusion, often in massive amounts, may be used to control the hemorrhage; however, their effectiveness in management of cerebral hemorrhage has been questioned.
In the elderly, amyloid angiopathy appears to be a major cause of lobar bleeding, but more characteristic are small, multiple, and successive areas of bleeding. Several of our patients who later proved to have amyloid angiopathy had minor head injuries in the weeks before hemorrhage. The subject is discussed in a later section and the characteristic multiple spot hemorrhages are shown in Fig. 33-34.
Several primary hematologic disorders are also complicated by hemorrhage into the brain. The most frequent of these are leukemia, aplastic anemia, and thrombocytopenia of various causes. Often they give rise to multiple intracranial hemorrhages, some in the subdural and subarachnoid spaces. As a rule, this complication signals a fatal outcome. Other, less-common causes of intracerebral bleeding are advanced liver disease, uremia that is being treated with dialysis, and lymphoma. Usually several factors are operative in these hematologic cases: reduction in prothrombin or other clotting elements (fibrinogen, factor V), bone marrow suppression by antineoplastic drugs, and disseminated intravascular coagulation. Any part of the brain may be involved, and the hemorrhagic lesions are usually multiple. Frequently there is also evidence of abnormal bleeding elsewhere (skin, mucous membranes, kidneys) by the time cerebral hemorrhage occurs. Plasma exchange, used in the treatment of myasthenia gravis and Guillain-Barré disease, lowers the serum fibrinogen to a marked degree, but we have not observed a single instance of intracerebral hemorrhage in more than 500 patients treated in this way.