Effects of Anterior Corpus Callosum Section on Cortical Glucose Utilization in Baboons

Abstract

Cortical glucose utilization was measured under light anaesthesia using positron emission tomography and 18F-fluorodeoxyglucose before and serially after stereotaxic anterior corpus callosum section in 3 adult baboons (Papio papio); in 1 animal needles were introduced but callosotomy was not performed ('sham' operation). Lesion efficacy was verified by x-ray computerized tomography and by postmortem examination which indicated effective anterior two-thirds callosal section in all 3 baboons, as well as a small contusional area in the medial frontal cortex. A two-way layout analysis of variance performed on the regional cerebral metabolic rate of glucose (CMRGlc) data obtained in the frontotemporal, temporal and occipital areas revealed significant effects for both the time and the region factors (P less than 0.00001 for each); the time effects indicated a significant initial metabolic depression (P less than 0.01) at day 11 and 18, and a subsequent recovery (P less than 0.01 to 0.05) at day 98. Average CMRGlc changes from preoperative values at successive studies were -23%, -27%, -17%, -8% and +2%, and -17%, -21%, -10%, -5% and +6% in the 'surgically approached' and the contralateral frontotemporal area, respectively. The frontotemporal/occipital CMRGlc ratio was significantly depressed at days 11, 18 and 32 (P less than 0.01, 0.01 and 0.05, respectively), indicating a transient postoperative alteration in the cortical metabolic pattern. In the 'sham' animal, surgery induced negligible metabolic effects. Our results indicate that effective anterior corpus callosum section induces a transient bilateral depression of cortical metabolism, which predominates in the anterior parts of the brain, while metabolic recovery suggests efficient neuronal adaptation. These functional effects in the cortex may underlie the transient behavioural changes that follow anterior callosotomy in man.

Marchiafava-Bignami disease with dementia: Severe cerebral metabolic depression revealed by PET

“…However, there are two major inconsistencies with this hypothesis. First, these effects of corpus callosotomy, both in epileptic subjects and in baboons, are transient (Spencer, 1988;Oepen et al, 1988;Yamaguchi et al, 1990), as compared to sustained in our case. Second, though the MRI suggested somewhat extensive CC lesions, the most conspicuous damage affected the splenium, which would be expected to chronically impair almost exclusively the specific transcallosal transfer functions (Geschwind et al, 1962).…”

“…In addition, the frontal and temporo-parieto-occipital transcallosal fibers cross at the level of the genu and the splenium, respectively (De Lacoste et al, 1985), which bear the brunt of the damage in this case. Finally, corpus callosotomy in epileptic subjects often induces a confusional state (Spencer, 1988;Oepen et al, 1988), and in the baboon results in a 30% reduction in CMRGlu in the fronto-temporal regions (Yamaguchi et al, 1990). However, there are two major inconsistencies with this hypothesis.…”

Effects of Unilateral Lesion of the Nucleus Basalis of Meynert on Brain Glucose Utilization in Callosotomized Baboons: A PET Study

“…1, 2, and 3, respectively (see Yamagu chi et aI., 1990, for details). Minor additional con tusion of the anterior cingulate cortex on the side of surgical approach to the CC was constantly ob served (see Yamaguchi et al, 1990). The NbM was lesioned in each of the three animals; on the coronal sections, the lesions consisted of contiguous or co alescent foci of necrosis (approximate area 10--50 mm 2 ) affecting the NbM throughout its whole ex-tent; the total lesion size was -20, 40, and 60% in baboon nos.…”

Callosal atrophy in patients with lacunar infarction and extensive leukoaraiosis. An indicator of cognitive impairment.

“…27 - 28 However, callosal transection does not irreversibly reduce intellectual function 29 or cortical glucose metabolism. 30 Therefore, callosal atrophy is not the primary factor causing intellectual impairment in Binswanger's disease but instead is a manifestation of hemispheric white matter change that results in cognitive dysfunction.…”