Summary: The effects of thiamine (B1) deficiency on local CMRg]u (LMCRg]u) in the vestibular nuclei were studied with the '4C-2-deoxyglucose autoradio graphic method in awake asymptomatic and symptomatic rats. Animals on the B,-deficient diet for 98 days developed symptoms of ataxia and opisthotonos. The results show that B, deficiency produces: (I) bilateral vestibular nuclei lesions in symptomatic animals; (2) very low LCMRg,u rates in these lesions; and (3) limitation of glial proliferation in the lesions. Giving B, to B,-deficient symptomatic animals produced a cellular proliferative response consisting mostly of microglia in the lesioned areas of the vestibular nuclei and a high LCMRg,u rate in the regions of microglial proliferation.

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.