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Brain, Vol. 118, No. 6, 1485-1495, 1995
© 1995 Guarantors of Brain

research-article

Does the enhancement of cholinergic neurotransmission influence brain glucose kinetics and clinical symptomatology in progressive supranuclear palsy?

J. Blin1,3,, P. Mazetti1, B. Mazoyer3, S. Rivaud1, S. Ben Ayed2, C. Malapani1, B. Pillon1 and Y. Agid1

1INSERM U289, Nouvelle pharmacie, Hôpital de la Salpêtrière Paris 2Labouratoire de biochimie, Hôpital de la Pitié Paris 3Service hospitalier Frédéric Joliot, DRIPP, Commissariat a I'Energie Atomique Orsay, France

Correspondence to: Correspondence to: Jérôme Blin, Laboratoire de Positrons, 2 Chemin du Cyclotron, B-1348 Louvain-la-Neuve, Belgium

Chotinergic systems are markedly affected both in cortical and subcortical cerebral areas of patients with progressive supranuclear palsy(PSP). To determine whether it is possible to modify the clinical picture of PSP through the enhancement of brain cholinergic neurotransmission, we studied the effects of physostigmine, an anticholinesterase reference drug, on symptoms and brain glucose metabolism using (18F)fluorodeoxyglucose (FDG) and PET. Patients were evaluated blind in a randomized order with both placebo and physostigmine infusions after an individual determination of maximal tolerated dose. Under steady-state physostigmine infusions, although glucose consumption was not significantly modified, the entry of glucose from blood to brain was regionally increased from 8 to 32% of placebo values suggesting an increase in cerebral blood flow (CBF) or an increase in the activity of brain glucose transporter. Following physostigmine administration in the same patients: the errors in antisaccades during ocular movement testing were significantly reduced, a significant reduction in errors or performance was found in four out of seven neuropsycho-logical tests, and motor disability was not significantly altered. Although the precise pathophysiology of these physostigmine-induced effects needs further investigations, our study suggests that part of the clinical symptomatology in PSP could be relieved by the enhancement of brain cholinergic neurotransmission

physostigmine; ocular movement; neuropsychology; PET; brain glucose transporter

Received January 26, 1995. Revised May 23, 1995. Accepted July 10, 1995.


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