Local cerebral glucose utilization (LCGU) was measured in asymptomatic rats on a thiamine (B1)-deficient diet for 70 days and in symptomatic rats on a B1-deficient diet for 98 days. LCGU increased in postcommissural fornix (F), pyramidal tracts (P), and inferior internal capsule (CAI) of symptomatic, compared with asymptomatic B1-deficient rats but decreased in thalamic nuclei, auditory structures, and lesioned vestibular nuclei. B1 administration to symptomatic rats improved symptoms; decreased LCGU in F. P, and CAI; increased LCGU in the lesioned vestibular nuclei; but decreased LCGU in mammillary nuclei, anteroventral nucleus of thalamus, and medial raphe. The results indicate that B1 deficiency symptoms correlate with LCGU changes in F and P and vestibular nuclei.