Occasionally the origin of intracranial hemorrhage cannot be determined clinically or pathologically. In some postmortem cases, a careful microscopic search 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 or one of the choroidal arteries; more often, such a hemorrhage is the result of periventricular bleeding often from a medial thalamic hemorrhage, in which blood enters the ventricle without producing a large parenchymal clot.
Hemorrhage into primary and secondary brain tumors is not rare. When this is the first clinical manifestation of the neoplasm, diagnosis may be difficult. Choriocarcinoma, melanoma, renal cell and bronchogenic carcinoma, pituitary adenoma, thyroid cancer, glioblastoma multiforme, intravascular lymphoma, carcinoid, and medulloblastoma may present in this way, but bleeding is most characteristic of the first three types. Careful inquiry will usually disclose that neurologic symptoms compatible with intracranial tumor growth had preceded the onset of hemorrhage or the primary neoplasm had been revealed previously. Needless to say, a thorough search should be made in these circumstances for evidence of intracranial tumor or of secondary tumor deposits in other organs, particularly the lungs.
A number of disparate diseases may result in a multitude of simultaneous or at least temporally clustered cerebral hemorrhages. Among the most common causes are cerebrovascular amyloidosis (amyloid angiopathy) as mentioned earlier and shown in Fig. 33-34, those related to hematologic and clotting disease, particularly ones that progress rapidly, such as leukemia, but almost any coagulopathy, including those brought on by the administration of medications. The most overwhelming examples in our experience have occurred in the hours after injecting tPA for acute stroke. Serious cranial injury itself may produce a passel of scattered contusions, some of which have the appearance of ball hemorrhages, but most are recognized to be along force lines (see Chap. 34). Occlusion of cerebral veins, particularly of the superior sagittal sinus, causes several biparietal hemorrhages.
Multiple small hemorrhages, brain “microbleeds,” are most commonly considered to be the result of vascular amyloid as discussed in the next section, but may also be associated with chronic hypertension according to Cordonnier and colleagues, but we have been unable to confirm this latter view from our own material. Often, these dozens of small areas of residual blood products or acute hemorrhages do not cause symptoms and are revealed on MRI that is performed for other reasons with gradient-echo and other susceptibility sequences (Fig. 33-34). Certainly, other forms of cerebrovascular disease are found disproportionately in these patients and several series suggest that they represent a risk for future bleeding or ischemic stroke, including lacunes. Multiple cavernous angiomas, the earlier-described amyloid angiopathy, CADASIL, bacterial endocarditis, moyamoya, and mutations that affect blood vessel integrity may also be implicated but the cause in any individual case often remains uncertain.