Volume 53, Issue 1 pp. 102-108
Original Articles

Motor cortex excitability in Alzheimer's disease: A transcranial magnetic stimulation study

Florinda Ferreri MD

Florinda Ferreri MD

Department of Neurology, University Campus Biomedico

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Flavia Pauri MD, PhD

Flavia Pauri MD, PhD

AFaR, CRCCS, Department of Neuroscience, Hospital Fatebenefratelli, Isola Tiberina

Dipartimento di Neurologia e Otorinolaringoiatria, Università La Sapienza, Rome, Italy

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Patrizio Pasqualetti PhD

Patrizio Pasqualetti PhD

AFaR, CRCCS, Department of Neuroscience, Hospital Fatebenefratelli, Isola Tiberina

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Rita Fini Tech

Rita Fini Tech

AFaR, CRCCS, Department of Neuroscience, Hospital Fatebenefratelli, Isola Tiberina

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Gloria Dal Forno MD

Gloria Dal Forno MD

Department of Neurology, University Campus Biomedico

Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD

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Paolo Maria Rossini MD, PhD

Corresponding Author

Paolo Maria Rossini MD, PhD

Department of Neurology, University Campus Biomedico

AFaR, CRCCS, Department of Neuroscience, Hospital Fatebenefratelli, Isola Tiberina

IRCCS Centro S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy

Department of Neuroscience, Hospital Fatebenefratelli, Isola Tiberina 39, 00186 Rome, ItalySearch for more papers by this author
First published: 31 December 2002
Citations: 164

Abstract

Motor deficits affect patients with Alzheimer's disease only at later stages. Recent studies demonstrate that the primary motor cortex is affected by neuronal degeneration accompanied by the formation of amyloid plaques and neurofibrillary tangles. It is conceivable that neuronal loss is compensated by reorganization of the neural circuitries occurring along the natural course of the disease, thereby maintaining motor performances in daily living. Cortical motor output to upper limbs was tested via motor-evoked potentials from forearm and hand muscles elicited by transcranial magnetic stimulation of motor cortex in 16 patients with mild Alzheimer's disease without motor deficits. Motor cortex excitability was increased, and the center of gravity of motor cortical output, as represented by excitable scalp sites, showed a frontal and medial shift, without correlated changes in the site of maximal excitability (hot-spot). This may indicate functional reorganization, possibly after the neuronal loss in motor areas. Hyperexcitability might be caused by a dysregulation of the intracortical GABAergic inhibitory circuitries and selective alteration of glutamatergic neurotransmission. Such findings suggest that motor cortex hyperexcitability and reorganization allows prolonged preservation of motor function during the clinical course of Alzheimer's disease.

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