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they may be the cause of seizures and headaches but seldom of hemorrhage When a small hemorrhage occurs in relation to venous malformation, it is usually due to an associated cavernous malformation 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 AV shunt of suf cient magnitude, in rare instances, 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 tangled blood vessels interposed between arteries and veins are abnormally thin and do not have the structure of normal arteries or veins Arteriovenous malformations 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 most often turn out to be direct arteriovenous stulas, as discussed further on When hemorrhage occurs, blood may enter the subarachnoid space, producing a picture almost identical to that of ruptured saccular aneurysm, but generally less severe; since most AVMs lie within cerebral tissue, bleeding is more than likely to be intracerebral as well, causing a hemiparesis, hemiplegia, and so forth, or even death Arteriovenous malformations are about one-tenth as common as saccular aneurysms and about equally frequent in males and females The two lesions AVM and saccular aneurysm (on the main feeding artery of the AVM) are associated in about 5 percent of cases; the conjuction increases with the size of the AVM and the age of the patient (Miyasaka et al) Rarely, AVMs occur in more than one member of a family in the same generation or successive ones For a review of the embryologic theories of formation of AVMs, the reader is directed to the article by Fleetwood and Steinberg Clinical Features Bleeding or seizures are the main modes of presentation Most AVMs are clinically silent for a long time, but sooner or later they bleed The rst hemorrhage may be fatal, but in more than 90 percent of cases the bleeding stops and the patient survives The rate of hemorrhage in untreated patients is established to be 2 to 4 percent per year, far lower than for aneurysms The mortality rate in two major series (Crawford et al, Ondra et al) has been 1 to 2 percent per year but as high as 6 to 9 percent in the immediate year following a rst hemorrhage The matter of an increased risk of AVM rupture during pregnancy has been disputed The weight of evidence suggests that the risk is not raised by pregnancy alone, but as with saccular aneurysm that parturition and Valsalva activity is always a source of concern Before rupture, chronic, recurrent headache may be a complaint; usually the headache is of a nondescript type, but a classic migraine with or without neurologic accompaniment occurs in about 10 percent of patients probably with greater frequency than it does in the general population Most of the lesions associated with migraine-like headaches lie in the parieto-occipital region of one cerebral hemisphere, and about two-thirds of such patients have a family history of migraine Huge AVMs may produce a slowly progressive neurologic de cit because of compression of neighboring structures by the.

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enlarging mass of vessels and by shunting of blood through greatly dilated vascular channels ( intracerebral steal ), resulting in hypoperfusion of the surrounding brain (Homan et al) When the vein of Galen is enlarged as a result of drainage from an adjacent AVM, hydrocephalus may result Not infrequently one or both carotid arteries pulsate unusually forcefully in the neck A systolic bruit heard over the carotid in the neck or over the mastoid process or the eyeballs in a young adult is almost pathognomonic of an AVM However, such bruits have been heard in fewer than 25 percent of our patients Exercise that increases the pulse pressure may bring out a bruit if none is present at rest The blood pressure may be elevated or normal; it is axiomatic that the occurrence of intracranial bleeding with a previously normal blood pressure should raise the suspicion of an AVM, but also of ruptured saccular aneurysm, bleeding diathesis, cerebral vessel amyloidosis, or hemorrhage into a tumor Rarely, inspection of the eye grounds discloses a retinal vascular malformation that is coextensive with a similar lesion of the optic nerve and basal portions of the brain Cutaneous, orbital, and nasopharyngeal AVMs may occasionally be found Rarely, skull lms show crescentic linear calci cations in the larger malformations The natural history of AVMs has been studied by Ondra and colleagues, who have presented data on a large and comprehensive series of untreated malformations in Finland over a 30-year period, and another similar series has been reported by Crawford and coworkers in Great Britain In the latter study, comprising 343 patients, 217 were managed without surgery and observed for many years (mean, 104 years) Hemorrhage occurred in 42 percent and seizures in 18 percent By 20 years after diagnosis, 29 percent had died and 27 percent of the survivors had a neurologic handicap Although the lesion is present from birth, onset of symptoms is most common between 10 and 30 years of age; occasionally it is delayed to age 50 or even beyond In almost half of patients, the rst clinical manifestation is a cerebral subarachnoid hemorrhage; in 30 percent, a seizure is the rst and only manifestation; and in 20 percent, the only symptom is headache Progressive hemiparesis or other focal neurologic de cit is present in about 10 percent of patients In a series of 1000 patients referred mainly for proton beam radiation of an AVM and studied by our colleague R D Adams, 464 had a hemorrhage as the rst manifestation and 218 had a seizure (mainly with frontal and frontoparietal lesions) In 139, the lesion came to attention as a result of a progressive neurologic de cit; most of these were situated in the posterior fossa or axially in the cerebrum Headaches were an early symptom in 212, but only 59 of these patients had a subsequent hemorrhage The combination of a prolonged history of headaches, seizures, and a progressive de cit almost always indicated a large malformation Fully 95 percent of AVMs are disclosed by CT scans if enhanced and an even larger number by MRI (Fig 34-25) Magnetic susceptibility MRI shows small areas of previous bleeding around AVMs Arteriography is usually necessary to establish the diagnosis with certainty and will demonstrate AVMs larger than 5 mm in diameter (Fig 34-26); MRI may fail to reveal smaller lesions Small ones may be obscured by hemorrhage; even at autopsy, a careful search under the dissecting microscope may be necessary to nd them Treatment The preferred approach in most centers is surgical excision Some 20 to 40 percent of AVMs are amenable to block dissection, with an operative mortality rate of 2 to 5 percent and a morbidity of 5 to 25 percent (see Fleetwood and Steinberg for a.

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