ACR Codes: 1.3
-History: 35 yo with fever and headache
-Factoid Discussion:
-Etiology and Pathogenesis: Congenital structural abnormality
-Radiologic findings: CT demonstrates a small amount of Subarachnoid hemorrhage. MRA source image demonstrates the AVM
Treatment:
treatment planning for AVMs depends on risk of subsequent hemorrhage, which is determined by the demographic, historical,
and angiographic features of the individual patient. Prior hemorrhage, smaller AVM size, deep venous drainage, and relatively high arterial
feeding pressures make subsequent hemorrhage more likely. Treatment is recommended for the younger patient with one or more of these
high-risk features, whereas an older individual or a patient with no high-risk features may be best treated by managing the medical aspects of
the illness alone. In such a case, anticonvulsants for seizure control and appropriate analgesia for headaches may be the only treatment
recommendations necessary.
Background: Hemorrhage from cerebral arteriovenous malformations (AVMs) represents 2% of all strokes. It is imperative to have a clear
understanding of the diagnostic and treatment algorithms involved with AVM management, because AVMS are a cause of hemorrhage in young
adults. The mortality associated with a cerebral arteriovenous malformation is 10% and the morbidity is substantial at 50%.
Pathophysiology: AVMs are congenital lesions composed of a complex tangle of arteries and veins connected by fistulas. The arteries have a
deficient muscularis layer. The draining veins are often dilated due to the high velocity of blood flow through the fistulae, and there is no
intervening capillary bed. It is unknown how the abnormal vessels appear or exactly when the process begins. Deranged production of
vasoactive proteins is under investigation as the angiogenetic link to pathophysiology.
AVMs produce neurologic dysfunction through 3 main mechanisms. First, hemorrhage may occur in the subarachnoid space, the intraventricular
space, or most commonly, in the brain parenchyma. Second, in the absence of hemorrhage, seizures may occur as a consequence of AVM:
approximately 50% of patients present with seizure disorder. Finally, but rarely, a progressive neurologic deficit, over a few months to several
years, may also occur. These slowly progressive neurological deficits are thought to relate to siphoning of blood flow away from adjacent brain
tissue (the "steal phenomenon"). Neurologic deficits may be alternatively explained by the mass effect of an enlarging AVM or venous
hypertension in the draining veins.
Frequency:
In the US: The prevalence of cerebral AVM in the United States is not known. The lifetime detection rate in the general population is approximately 1:100,000.
Internationally: The worldwide prevalence is not known. It is usually assumed to be similar to the U.S. worldwide.
Mortality/Morbidity: Although 300,000 persons in the US may harbor AVMs, it is estimated that only 12% of AVMs become symptomatic.
Mortality from hemorrhage occurs in 10-15% of cases, and morbidity occurs in approximately 50%.
Hemorrhage: the overall risk of intracranial hemorrhage in patients with known AVM is 2-4% per year.
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