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Auditory and somatosensory evoked potentials (AEPs and SEPs) and ballistic movements in parkinson disease (1985)

Rossi, L. ; Benvenuti, F. ; Pantaleo, T. ; [et al.]

Springer

Neurological sciences 6 (1985), S. 329-337

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ISSN: 1590-3478

Keywords: Auditory evoked potentials ; somatosensory evoked potentials ; ballistic movements ; Parkinson's disease

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Description / Table of Contents: Sommario Sono stati studiati in 5 pazienti affetti da sindrome di Parkinson idiopatica iniziale gli AEPs (componenti precoci e tardive), i SEPs ed i movimenti balistici (abduzione dell'omero). Lo studio è stato condotto prima dell'inizio della terapia (L-Dopa+Carbidopa), e due e sei mesi dopo l'inizio della terapia. Anomalie dei potenziali evocati sono state riscontrate prima dell'inizio della terapia in 4 pazienti. I dati elettromiografici relativi ai movimenti balistici di abduzione del braccio erano alterati in tutti i pazienti ed erano caratterizzati da un ritardo nell'inizio del movimento e da una diminuizione della velocità media. Dopo la terapia si è rivelata una riduzione delle anomalie precedentemente riscontrate per gli AEPs ed i SEPs ed anche i patterns EMG e le variabili kinematiche sono apparse notevolmente migliorati. Dall'analisi di questi risulati sembra emergere la possibilità che queste metodiche neurofisiologiche possano essere utilizzate quale mezzo per controllare la progressione della sindrome e l'efficacia di eventuali trials farmacologici.

Notes: Abstract In five patients with initial idiopathic Parkinson disease AEPs (early and late components of auditory evoked potentials), SEPs (somatosensory evoked potentials) and arm ballistic movements (abduction of the humerus) were studied. Experimental sessions were conducted before starting treatment (L-Dopa plus Carbidopa) and at two and six month intervals. Before treatment evoked potential abnormalities were found in four out of five patients; EMG patterns underlying ballistic arm abduction movements were altered in all patients; corresponding prolonged duration of initial movements and low mean velocities were found. After treatment AEP and SEP showed a reduction of previously observed abnormalities and both EMG patterns and kinematic variables consistently improved. It is suggested that the electrophysiological investigations employed in this preliminary study may be a useful tool in clinical and pharmacological researches on Parkinson disease.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF02232011

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Effect of phenylhydrazine on red blood cell metabolism (1988)

Magnani, M. ; Rossi, L. ; Cucchiarini, L. ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Cell Biochemistry and Function 6 (1988), S. 175-182

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ISSN: 0263-6484

Keywords: Erythrocytes ; glucose metabolism ; uncleotide catabolism ; phenylhydrazine ; Chemistry ; Biochemistry and Biotechnology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: In addition to the well known effect of phenylhydrazine on red blood cells (methaemoglobin and Heinz body formation, autologous IgG binding, lipid peroxidation, etc.) an increased glucose utilization was observed. Measurement of 14CO2 formation from [1-14C]-glucose showed a maximum value at 2 mM phenylhydrazine followed by a progressive inhibition on increasing the drug concentration to 16 mM. Concomitantly we found a reduction in the reduced glutathione concentration but not a corresponding increase in the level of oxidized glutathione. Phenylhydrazine also causes ATP depletion. The ATP is in part dephosphorylated to ADP and AMP and in part converted to inosine monophosphate and hypoxanthine. Measurement of the cell content of reduced and oxidized pyridine nucleotides was also performed and showed a progressive increase in the reduced forms of these coenzymes. Thus phenylhydrazine promotes cellular ATP depletion followed by adenine nucleotide catabolism that is not efficiently counteracted by an increase in glucose utilization. The relevance of these data to the mechanism of phenylhydrazine-induced anemia is discussed.

Additional Material: 6 Ill.