Spinal motoneuron excitability and reciprocal inhibition in Huntington's disease

Spinal motoneuron excitability and reciprocal inhibition in Huntington's disease

Society Proceedings compare the different actions of the drugs and to quantify the clinical responses. In 10 subjects we injected BT type A, in 7 subj...

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Society Proceedings compare the different actions of the drugs and to quantify the clinical responses. In 10 subjects we injected BT type A, in 7 subjects BT type C and in 7 subjects BT type F. The dose of each BT was 3 IU and the drug was inoculated in the EBD muscle of the feet. Before and after the injection we calculated the maxima1 amplitude of the CMAP elicited by electrical stimulation of the SPE nerve at the ankle. For each subject the percentage variation was determined. Om data showed that the duration of the “percentage black” of the MAP was shorter for BT type F than for BT types A and C. With BT type C we observed an early effect, constant in time. We discuss these data and suggest that this technique is a reliable method to stress the individual sensitivity to different BTs. 92. Frequency domain source localization of EEG at rest and during photic stimulation. - S. Seri, F. Pisani, P. Sarnataro and A. Cerquiglini (Dept. of Child Neurology and Psychiatry, University “La Sapienza,” Rome) We investigated the topographic changes in electrical activity in the frequency domain during intermittent light stimulation from 5 to 16 Hz in a group of 15 normal children aged 12 years and described these changes with parameters derived from the EEG approximation method from 21-Channel recordings. The synchronizing effect of flicker stimulation was measured on the computed EEG spectra. The topography of these changes varied with stimulation frequency with a consistent and significant anteriorization of centroid location for higher harmonics of the stimulation frequency. A substantial alpha blocking was found for stimulation frequenties around 1012 Hz. These findings suggest that mechanisms underlying photic driving are much more complex than we have long thought and that neuronal networks involving thalamic relays and occipital, parietal and post-central areas are implicated in this phenomenon. These preliminary findings confirm the need for a multichannel approach even in the study of apparently localized events. 93. EEG behavioral studies in aging rats. - A. Loizzo, G. Diana, M. Luzi, S. Palazzesi and M.T. Tebano (Istituto Superiore di Sanità, Rome) EEG is a sensitive tool to explore brain activity and to study psychoactive drug effects. However, attention fluctuations or psychomotor activity during the tests may strongly influence the results. Moreover, pharmaco-EEG parameters recorded in the animals during normal activity may be altered if the EEG is recorded during the test, i.e., when a drug-stress interaction is provided. Therefore, we decided to study the effects of some drugs, which are presumed to enhance learning, in aging rats during quiet conditions and during forced walking in a slowly rotating plexiglas drum. Rats aged 20-24 months were classified according to the performance obtained in a spatial memory test (Morris water mazel. Then we recorded EEGs according to a 2 X 2 experimental protocol, i.e., in quiet/forced walking condition, and in drug/placebo condition. Preliminary results suggest that most differences found in the spectra1 EEG components between impaired and non-impaired rats disappear at the water maze during psychomotor activity. Therefore, such methods seem suitable to discriminate psychomotor stimulating effects induced by drugs during learning tests. 94. Giant somatosensory evoked potentials in benign epilepsy with rolandic spikes. - R. Plasmati, M. Volpini, A. Borghi and C.A. Tassinari (Cattedra di Neurologia, Divisione di Neurologia, Ospedale Bellaria, Bologna) In some types of myoclonus epilepsy, somatosensory evoked potentials (SEPs.1 have been reported to be of increased amplitude. On the other hand, few and scattered data are available on SEPs in other forms of epilepsy, mainly concerning shot? latency responses. We investigated middle latency SEPs in 54 children with benign epilepsy with rolandic spikes (BERS) and in 54 age matched control subjects. Short latencies

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were normal in al1 BERS patients, whereas the amplitude of middle latency was considerably increased in 15 patients and 5 controls. All the giant responses were localized in the parietal regions. In 18 patients, thc giant components disappeared at 14-18 years of age on follow-up investigations. These data suggest that giant components in BERS differ from those found in myoclonus epilepsy. Moreover, they indicate that increased middle latency amplitudes of SEPs are more frequent in BERS but can also be observed in healthy children. 95. Periodic lateralized epileptiform discharges in multiple sclerosis: report of 2 cases. - A. Primavera and F. Bandini (Department of Neurology, University of Genoa, Genoa) The term PLEDs (periodic lateralized epileptiform discharges) was coined in 1964 by Chatrian et al. This relatively uncommon EEG pattern consists of periodic or quasi-periodic spikes or sharp waves occurring at 1-2 sec intetvals in association with structural lesions (especially acute stroke) or, less frequently, with metabolic abnormalities. PLEDs have been described in conjunction with seizures, both sporadic and continuous. They have been reported, to our knowledge, only in 2 patients with multiple sclerosis (MS) (Porecha and Reilly, 1977; Awerbuch and Verna, 1987). We describe a clinical, neurophysiological and neuroradiological study of 2 patients with definite MS, respectively presenting a partial motor and an aphasic status epilepticus with a clear clinical correlation with an EEG pattern like PLEDs. We believe that the development of oedema in new cortical or subcortical demyelinated lesions may play an important role in seizure production. A cortical plaque may act itself as an irritative focus, while in subcortical lesions, expecially of the “giant” size, PLEDs might be due to a cottical-subcortical disconnection. 96. Quantified EEG, benzodiazepine-like compounds, prothrombin time: comparison in a case of fulminant hepatic failure. - V. Rossi, A. Ferrari, G. Ardizzone ‘, M. Demortini ‘, M.L. Zeneroli b, B.M. Stubinski and G. Rosadini (Dipartimento di Scienze Motorie (CNR), Genoa, ’ Servizio di Anestesia e Rianimazione, Ospedale San Martino, Genoa, and b Dipartimento di Scienze Farmaceutiche, Università di Modena, Modena)

It has been hypothesized that a failure of the liver to metabolize endogenous benzodiazepine-like compounds (EBz) may be an etiopathogenetic mechanism in acute or chronic hepatic encephalopathy. We present the evolution of a case in which the EEG, the clinical conditions and hepatic function, expressed by means of prothrombin time (PT), were monitored for 32 days. While clinical conditions improved rapidly, it was remarkable to note that the EEG pattern continued to be markedly abnormal with a low hepatic function (PT < 50’%1 and a high plasma EBz level. On day 20 EEG was normal, with a reduced plasma EBz leve1 and an improved hepatic function (PT > 50%). These observations may lead to a more detailed investigation of the correlations between EBz and EEG activity during hepatic encephalopathy. 97. Spinal motoneuron excitability and reciprocal inhibition in Huntington’s disease. - A. Priori, L. Polidori and A. Berardelli (Dipartimento di Scienze Neurologiche, Università di Roma “La Sapienza,” Rome) We studied the H reflex recovery curve and reciprocal inhibition in the upper limbs of 11 patients with Huntington’s disease. We compared the results with those obtained in a group of healthy volunteers. In the patients the recovery curve of the H reflex showed a decrease of inhibition. Reciprocal inhibition of the H reflex showed a decrease in the amount of inhibition at the conditioning test interval of 20 msec and an abnormal facilitation at 40 msec conditioning-test interval, due to the activation of radial nerve muscle afferents (possibly group 11). These findings may be explained by a reduction of presynaptic inhibition of group 1 afferents.