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Vascular malformations composed mainly of clusters of thinwalled veins without important arterial feeders and with little or no intervening nervous tissue make up a signi cant group, some 7 to 8 percent of our series of AVMs Conventional subdivisions of this group into cavernous, venous, and telangiectatic types have not proven useful We have, therefore, roughly designated them all as cavernous They have several attributes that set them apart Their tendency to bleed is probably no less than that of the more common AVMs, but far more often the hemorrhages are small and clinically silent The exact incidence of bleeding is uncertain but is estimated to be less than 1 percent per year per lesion Often there are multiple lesions They are generally not seen in arteriograms The diagnosis is based on their clinical manifestations and MRI, which discloses a cluster of vessels surrounded by a zone of hypodense ferritin in the T1-weighted images (Fig 34-28), the product of previous small episodes of bleeding A small but uncertain number are associated with adjacent venous malformations, visualized by imaging studies The lack of formation of a mass over a long period of time separates this lesion from a malignant tumor that has bled About one-half of all cavernous angiomas lie in the brainstem, and in the past (before the availability of MRI), many of them were misdiagnosed as multiple sclerosis because of a stepwise accumulation of neurologic de cits with each hemorrhage About 10 percent of these lesions are multiple and 5 percent are familial In one of the families we have followed of ItalianAmerican origin, there were 29 affected members in three generations The inheritance followed an autosomal dominant pattern; Marchuk and coworkers have localized the abnormal gene in other kindreds to the long arm of chromosome 7 One interesting characteristic of this group, as pointed out by Labauge and colleagues, is the appearance over time of new lesions in one-third of patients The follow-up of some of our patients has documented this Treatment Cavernous angiomas on the surface of the brain, within reach of the neurosurgeon, even those in the brainstem, can be plucked out, like clusters of grapes, with low morbidity and mortality Kjellberg and colleagues have treated 89 deeply situated cavernous angiomas with low-dose proton radiation Our impression is that these vascular malformations, like the hemangioblastoma, respond poorly to radiation and are not amenable to treatment by endovascular techniques Lesions that cause recurrent bleeding and are surgically accessible with little risk are often removed, but incidentally discovered angiomas and those that are inaccessible may be left alone Although this is the approach usually taken, there is not adequate data on the rate and risk of bleeding to determine the proper approach.

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Figure 34-28 Large cavernous vascular malformation MRI in the sagittal (above) and axial (below) planes demonstrates a medial left frontal lesion with a prominent rim of hemosiderin-laden macrophages and no associated edema Most cavernous angiomas are much smaller and sometimes mulitple but have the same signal characteristics

Next to hypertension, anticoagulant therapy is currently the most common cause of cerebral hemorrhage The hemorrhages that develop, though sometimes situated in the sites of predilection of

hypertensive hemorrhage, are more likely to occur elsewhere, mainly in the lobes of the brain When the bleeding is precipitated by warfarin therapy, treatment with fresh-frozen plasma and vitamin K is recommended; when bleeding is associated with aspirin therapy or other agents that affect platelet function, fresh platelet infusion, often in massive amounts, is required to control the hemorrhage The use of thrombolytics in the treatment of stroke is complicated by intracranial hemorrhage in 6 to 20 percent of cases, depending on the dose and timing of drug administration after the onset of symptoms, as discussed on page 694 In the elderly, amyloid angiopathy appears to be a major cause of lobar hemorrhages, especially if they appear in succession or are multiple Several of our patients have had minor head injuries in

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the weeks before hemorrhage In our own material, only severe impregnation of vessels with amyloid and brinoid change in the vessel wall were associated with hemorrhage (Vonsattel et al) Greenberg and colleagues have found that apolipoprotein E4, the same marker that is overrepresented in Alzheimer disease, is associated with severe amyloid angiopathy and intracerebral hemorrhage, but others have found an association with the E2 allele Contrary to previous notions, there is probably no greater risk in evacuating these clots surgically than in the case of other cerebral hemorrhages, but most of them are of a size that allows conservative management Several primary hematologic disorders are also complicated by hemorrhage into the brain The most frequent of these are leukemia, aplastic anemia, and thrombocytopenic purpura Often they give rise to multiple intracranial hemorrhages, some in the subdural and subarachnoid spaces As a rule, this complication signals a fatal issue Other, less common causes of intracerebral bleeding are advanced liver disease, uremia being treated with dialysis, and lymphoma Usually several factors are operative in these hematologic cases: reduction in prothrombin or other clotting elements ( brinogen, 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, kidney) by the time cerebral hemorrhage occurs Plasma exchange, used in the treatment of myasthenia gravis and Guillain-Barre disease, also lowers the serum brin ogen to a marked degree, but we have not observed a single instance of intracerebral hemorrhage in more than 500 patients treated in this way Acute extradural and subdural hemorrhage, typically traumatic in origin, must also be considered in the patient who, under unknown circumstances, has rather abruptly developed a neurologic de cit such as hemiparesis or confusion, with or without bloody CSF The use of anticoagulant drugs and intrinsic coagulopathies of all types are risks for these extracerebral hemorrhages In chronic subdural hemorrhage, which can occur without remembered trauma, the inde nite picture of drowsiness, headache, confusion, and mild hemiparesis may erroneously be attributed to a stroke, especially in elderly persons There should be no hesitation in subjecting patients to CT scanning whenever the diagnosis of subdural hemorrhage cannot readily be excluded on clinical grounds In the patient who falls and strikes his head at the onset of a stroke, it may be dif cult or impossible to decide whether blood in the CSF is due to the stroke or to cerebral contusion These disorders are discussed more fully in the next chapter Occasionally the origin of intracranial hemorrhage cannot be determined clinically or pathologically In some postmortem cases, a careful search under the dissecting microscope discloses a small arteriovenous malformation; this is the basis for suspecting that an overlooked lesion of this type may be the cause of cerebral hemorrhage in other cases Primary intraventricular hemorrhage, a rare event in adults, can sometimes be traced to a vascular malformation or neoplasm of the choroid plexus; more often, such a hemorrhage is the result of periventricular bleeding, in which blood enters the ventricle without producing a visible parenchymal clot Hemorrhage into primary and secondary brain tumors is not rare; when this is the rst clinical manifestation of the neoplasm, diagnosis may be dif cult Choriocarcinoma, melanoma, renal cell and bronchogenic carcinoma, pituitary adenoma, thyroid cancer, glioblastoma multiforme, intravascular lymphoma, and medullo-.

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