The distribution of sodium amytal and its effect on regional cerebral perfu
sion during the intracarotid amytal (Wada) test were investigated using hig
h-resolution hexamethyl propyleneamine oxime (HMPAO) SPECT coregistered wit
h the patient's MRI dataset. Methods: Twenty patients underwent SPECT after
intravenous HMPAO injection, and 5 patients had both intravenous and intra
carotid injections in a double injection-acquisition protocol. Results: All
patients had hypoperfusion in the territories of the anterior and middle c
erebral arteries. Basal ganglia perfusion was preserved in 20 of 25 patient
s. Hypoperfusion of the entire mesial temporal cortex was seen in 9 of 25 p
atients. Partial hypoperfusion of the whole mesial cortex or hypoperfusion
of part of the mesial cortex was seen in 14 of 25 patients. In 2 of 25 pati
ents, mesial temporal perfusion was unaffected. In 5 patients, the double a
cquisition showed a distribution of HMPAO delivery matching that of hypoper
fusion, except for the following: (a) HMPAO was delivered to the basal gang
lia and insula, where there was no hypoperfusion; (b) HMPAO was not deliver
ed to the contralateral cerebellum, which did show hypoperfusion; and (c) i
n 1 patient, perfusion of the mesial temporal cortex was preserved despite
intracarotid delivery of HMPAO. Conclusion: Some degree of hypoperfusion of
medial temporal structures occurs in the great majority of patients during
the Wada test. Partial inactivation of memory structures is therefore a cr
edible mechanism of action of the test. The double acquisition protocol pro
vided no evidence that mesial temporal structures are inactivated remotely
by diaschisis. Perfusion in the basal ganglia and insular cortex is not aff
ected by amytal.