The mycotic aneurysm may appear on only one artery or several arteries, and the hemorrhage, if it has happened, may recur. A consensus regarding the treatment of mycotic aneurysm has not been reached. The underlying endocarditis or bacteremia mandates appropriate antibiotic therapy and, in at least 30 percent of cases, healing of the aneurysm can be observed in successive arteriograms with this approach alone. Antibiotic or antifungal treatment is usually continued for at least 6 weeks. Some neurosurgeons favor excising an accessible aneurysm if it is solitary and the systemic infection is under control. Many mycotic aneurysms do not bleed, and in our view medical therapy takes precedence over surgical therapy.
The finding of blood over a convexity of the cerebral hemisphere, usually discovered because of an evaluation for sudden headache, has become a relatively common occurrence. The causes for this bleeding are numerous, the most obvious being cranial trauma but a diversity of processes may be responsible including cerebral amyloid angiopathy, reversible cerebral vasoconstriction syndrome, cortical vein thrombosis, the use of cocaine, cavernous angioma, dural arteriovenous fistula, and posterior reversible leukoencephalopathy. It is interesting to note that this list largely overlaps with the causes of “thunderclap headache,” discussed earlier and in Chap. 9. Of course, in the appropriate clinical circumstances, ruptured aneurysm and mycotic aneurysm are still concerns. In a survey conducted by Kumar and associates, it was suggested that younger patients present with abrupt headache and older ones, with TIA-like symptoms and imaging findings that were consistent with cerebral amyloid angiopathy. Further notable is the later occurrence of meningeal hemosideriosis as a result of these lesions, particularly with amyloid angiopathy (see Linn and colleagues).
An arteriovenous malformation (AVM) consists of a tangle of dilated vessels that form an abnormal communication between the arterial and venous systems. These are developmental abnormalities that represent persistence of an embryonic pattern of blood vessels and not a neoplasm, but the constituent vessels may proliferate and enlarge with the passage of time. Venous malformations, consisting purely of distended veins deep in the white matter, are a separate entity; they may be the cause of seizures and headaches but less often, of hemorrhage. When a small hemorrhage occurs, it is usually the result of an associated malformation of the so-called cavernous type; these are small hamartomatous lesions of multiple juxtaposed endothelium-lined cavities without interposed neural tissue. These are discussed further on.
True vascular malformations vary in size from a small blemish a few millimeters in diameter lying in the cortex or white matter to a huge mass of tortuous channels constituting an atrioventricular (AV) shunt of sufficient magnitude to raise cardiac output. Hypertrophic dilated arterial feeders can be seen approaching the main lesion and to break up into a network of thin-walled blood vessels that connect directly with draining veins. The latter often form greatly dilated, pulsating channels, carrying away arterial blood. The blood vessels interposed between arteries and veins are abnormally thin and do not have the structure of normal arteries or veins. AVMs occur in all parts of the cerebrum, brainstem, and cerebellum (and spinal cord), but the larger ones are more frequently found in the central part of a cerebral hemisphere, commonly forming a wedge-shaped lesion extending from the cortex to the ventricle. Some lie on the dural surface of the brain or spinal cord, but these more often turn out to be direct arteriovenous fistulas, as discussed further on.