Abstract
Using N-isopropyl-I-123-p-iodoamphetamine (IMP) and SPECT with acetazolamide (DIAMOX) activation test, the present study attempts to assess the regional cerebral perfusion and vasodilatory capacity in perifocal tissue of cerebral A-V malformation (AVM). Sixteen patients with cerebral AVM were studied, 10 males and 6 females, having an average age of 32. The AVM-nidus were mainly fed by cortical arteries. The angiographic diameter of AVM-nidus was classified as follows: less than 2 cm in 1 case, 2 to 2.5 cm in 6, 2.5 to 3 cm in 5, and 4.0 to 5 cm in 4. Their clinical features were divided as follows; 5 cases of hemorrhagic type (3 with a nidus of 2.0-2.5 cm in diameter, 2 with 3.0-3.5 cm), 9 cases of epileptic type and 2 cases of asymptomatic type. Regional cerebral perfusion in the perifocal area was assessed by the resting IMP SPECT in 13 patients and cerebral vasodilatory capacity was assessed by the DIAMOX-activated IMP SPECT in 12 patients.Perifocal hypoperfusion areas were observed in 11 patients but were absent in 2 cases (one with a nidus of less than 2 cm in diameter, the other with 2 cm). The incidence of the perifocal hypoperfusion was as follows: 80% in AVM nidus of 2.0 to 2.5 cm in diameter, 100% in AVM nidus of more than 3cm. The limitation of cerebral vasodilatory capacity in perifocal tissue was observed in 7 patients (1 with a nidus of 2 cm in diameter, 3 with 3.0-3.5cm, 3 with 4.0-5.0cm). In 6 of these 7 patients, a past history of seizure attack was noted. The incidence of the limitation of perifocal vasodilatory capacity was as follows: 25% in AVM nidus of 2.0-2.5cm in diameter, 60% in AVM nidus of 3.0-3.5cm, 100% in AVM nidus of 4.0-5.0cm. Preoperative limitation of cerebral vasodilatory capacity in perifocal tissue was reversed by total removal of the AVM in 2 patients. It seems likely that the perifocal hypoperfusion area is caused by both the deactivation of perifocal tissue and intracerebral steal, because the perifocal hypoperfusion is not necessarily associated with the limitation of cerebral vasodilatory capacity. The limitation of cerebral vasodilatory capacity is probably caused by reduction of cerebral perfusion pressure due to intracerebral steal, because it is more apparent in patients with larger AVMs, and can be reversed by total removal of the AVM. Assessment of vascular reactivity in perifocal tissue of cerebral AVMs using 123I-IMP SPECT activated by DIAMOX, might be a useful tool for the management of cerebral AVMs.
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