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Neurology 1999;53:1451
© 1999 American Academy of Neurology


Articles

Time course of frontal somatosensory evoked potentials

Relation to L-dopa plasma levels and motor performance in PD

M. Ulivelli, MD, S. Rossi, MD, PhD, P. Pasqualetti, PhD, P. M. Rossini, MD, O. Ghiglieri, MD, S. Passero, MD, PhD and N. Battistini, MD

From the Istituto di Clinica delle Malattie Nervose e Mentali (Drs. Ulivelli, Rossi, Passero, and Battistini), Università di Siena; A.Fa.R.-C.R.C.C.S. Div. Neurologia (Drs. Pasqualetti and Rossini), Ospedale Fatebenefratelli, Isola Tiberina, Rome; I.R.C.C.S. Centro S. Giovanni di Dio (Drs. Pasqualetti and Rossini), Brescia; and Istituto di Farmacologia (Dr. Ghiglieri), Università di Siena, Italy.

Address correspondence and reprint requests to Dr. Simone Rossi, Clinica delle Malattie Nervose e Mentali, Università di Siena, Policlinico Le Scotte, Viale Bracci, 53100 Siena, Italy; e-mail: ROSSISIMO{at}UNISI.IT

OBJECTIVE: To verify whether the change in L-dopa plasma levels after a single dose of carbidopa/L-dopa 50/200 (controlled-release) transiently modifies frontal components of somatosensory evoked potentials (SEPs) in patients with PD in parallel with improvement of motor performance.

BACKGROUND: Apomorphine, a potent dopamine-agonist drug, transiently increases frontal SEP components, which may be depressed in PD; however, relationships between clinical status, frontal SEPs, and therapy are still unclear.

METHODS: Nineteen PD patients (mean age 65.9 years, range 52 to 77, responders to L-dopa therapy, were studied in the same day at times T0 (baseline predose level), T1 (presumed L-dopa peak time), and T2 (end of dose-induced motor response). The following were monitored: L-dopa plasma concentration, tapping test, reaction times, peak latency (with central conduction times), and amplitude of cervical, subcortical, as well as cortical parietal and frontal SEP components elicited by median nerve stimulation of the more clinically affected arm.

RESULTS: The average amplitude of frontal components of PD patients was significantly reduced at T0 with respect to control subjects. A significant and transient amplitude increase of frontal SEPs was found at T1, in parallel with the L-dopa peak concentration and improvement in motor performance (tapping and reaction times), without significant changes in amplitude of parietal SEP waves. No latency shifts were observed in brain and spinal waves.

CONCLUSIONS: L-Dopa may influence the responsiveness of the parkinsonian brain as assessed by frontal somatosensory evoked potentials. The time course of these modifications coincides with that of the clinical response in the motor performance.

Key words: Somatosensory evoked potentials—PD—L-dopa—Pharmacodynamics.




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