Local cerebral glucose utilisation in treated and untreated patients with Parkinson's disease.

Abstract

SUMMARY Using the '8f-fluoro-2-deoxy-d-glucose technique and positron emission tomography (PET), the local cerebral glucose utilisation (lCMRGlc) was measured in four non-demented patients with early-onset, bilateral Parkinson's disease characterised by the predominance of akinesia. The study was done twice, first in the untreated condition, and then after levodopa had been resumed. Despite a marked clinical improvement, we found no alteration in lCMRGlc between the first and second studies in any of the brain structure analysed. Compared to control values, lCMRGlc in the basal ganglia was moderately increased in both studies. These essentially negative findings agree with most previous human or animal studies, and indicate that the functional alterations in the central dopaminergic systems of patients with Parkinson's disease have metabolic correlates that are too small to be demonstrated by current PET devices.The typical symptomatic triad of Parkinson's disease, that is akinesia, rigidity, and tremor, implies that functional alterations take place in certain cerebral structures. Since energy metabolism in the brain has been shown to be coupled to function,' changes in regional energy mnetabolism specific to the functional abnormalitves of Parkinson's disease might be expected to occur. Such changes should be found in the structures deprived of their normal dopaminergic afferences, principally the striatum2 and the cortico-limbic areas3 and, as a secondary effect, in the structures receiving projections from these structures.In the attempt to use local energy metabolism as a marker of disordered dopaminergic transmission systems, several studies of the local cerebral glucose utilisation (lCMRGlc) using '4C-2-deoxy-D-glucose ('4CDG) autoradiography in rats with unilateral destruction of the dopaminergic systems have failed to show any consistent pattern of changes,4-9 although some reported striking alterations.4 5 Human studies of Parkinson' s disease patients have been, for methodological reasons, restricted to 2-dimensional '33xenon regional cerebral blood flow (rCBF)'0-'2 or Address for reprint requests: JC Baron, MD, Service Hospitalier Fr6d&ric Joliot,

Cerebral Mitochondrial Metabolism in Early Parkinson's Disease

“…Basal ganglia metabolism in PD has been reported to be increased, decreased, or unchanged (Kuhl et al, 1984;Rougemont et al, 1984;Martin et al, 1984;Wolfson et al, 1985;Leenders et al, 1985;Mohr et al, 1992;Eidelberg et al, 1993Eidelberg et al, , 1994Eidelberg et al, , 1995Piert et al, 1996). In these studies, findings are dependent on whether analysis is performed using absolute values, relative values, or more sophisticated image analysis techniques, such as statistical parametric mapping or scaled subprofile modeling (Eidelberg et al, 1993(Eidelberg et al, , 1995Piert et al, 1996).…”

Striatal blood flow, glucose metabolism and 18F-dopa uptake: difference in Parkinson's disease and atypical parkinsonism.

“…The pure akinetic type has been considered to be a different clinical entity from idiopathic Parkinson's disease by some investigators. ' (1)(2)(3)(4)(5)(6)(7)(8) and patients with atypical Parkinsonism (PKM) (9- I I I II III III III III II III III II II III III Case 9 A 54 year old right handed man started to complain of writing difficulty at the age of 50. This was followed by dysarthria (microphonia).…”

Subcutaneous apomorphine increases regional cerebral blood flow in parkinsonian patients via peripheral mechanisms.

“…Moreover, in the present and in other studies (Leenders et al, 1985;Montastruc et al, 1987), levodopa induced a global increase in rCBF roughly similar in cortical and subcortical areas; no topographic relationship has been demonstrated between rCBF changes and central dopaminergic pathways. Finally, in man, after levodopa treatment, PET studies failed to demonstrate a significant increase in glucose metabolism or oxygen utilisation in all (Leenders et al, 1985;Rougemont et al, 1984) but one (Raichle et al, 1984) parkinsonian patients and control subjects.…”