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Parametrization of compound EMG signals at recruitment
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F368 PARAMETRIZATION OF COMPOUNDEMG SIGNALS AT RECRUITMENT MARANZANA, F.M.*, MOLINARI, R., Dipartimento di Elettronica*~ Centro di Teoria dei Sistemi CNR, Politecnico di Milano, Milano, I t a l y The morphology and the number of the motor unit potentials together with the f i r i n g rate during voluntary e f f o r t are generally considered to discriminate neurogenic lesions from myopathic disorders~ however in acute peripheral neuropathies, short polyphasic potentials may be found. For this reason, the parameters generally adopted in Quantitative EMG prove sometimes inadequate to discriminate these cases. Changes of these parameters at recruitment are u s e f u l l y taken into account because of the very d i f f e r e n t behaviour of myopathic from neurogenic muscles. The myopathic muscle r e c r u i t s early, showing high increments of the EMG turns when voluntary contraction goes from 20% to 30% of the maximum and is not able of large further recruitment from 30% to 40%, whereas the neurogenic muscle r e c r u i t s at regular pace. This work studies recruitment in the pathological muscles through the parameters of the autoregressive (AR) model. The AR class of models is chosen f i r s t in order to test possible new discriminating parameters which are easy to obtain by means of low-cost computation. F i r s t , a comparison is carried out l i t h the QEMG parameters in the case of the "a p r i o r i " selected AR(2) model. As a second step, i d e n t i f i c a t i o n with the optimal AR model is carried out. The role played by the model order is c a r e f u l l y evaluated.
F369 ULTRASTRUCTURALCHANGES IN MOTONEURONESFOLLOWING AXOTOMYAND DIPHTHERITIC INTOXICATION SEARS, T.A., PULLEN, A.H., JOHNSON, I . P . , Sobell Department of Neurophysiology, I n s t i t u t e of Neurology, Queen Square, London, W.C.1N 3BG, U.K. Neuronal death (e.g. in Motoneurone Disease) and chromatolysis are both associated with profound alterations in topographical organisation of the rough endoplasmic reticulum (RER) and polyribosomes, which comprise the morphological correlates of protein synthesis. Chromatolysis, however, does not always evoke neuronal death. A comparison therefore, between the organisation of RER and polyribosomes in normal, chromatolytic and dying motoneurones of the cat thoracic spinal cord permitted features unique to neuronal death being distinguished from those accompanying chromatolysis. Neuronal death was evoked by d i p h t h e r i t i c intoxication (Johnson, Pullen & Sears, 1983). While the mechanism responsible f o r chromatolysis remains uncertain, diphteria toxin i n h i b i t s protein synthesis by s p e c i f i c a l l y inactivating EF2, the elongation factor essential for t r a n s l a t i o n of ribosomes along mRNA (Pappenheimer & G i l l , 1973), and is f a t a l to the c e l l . The highly ordered stacks of RER lamellae interposed by rows of polyribosomes seen in normal motoneurones contrasted with the disordered RER in chromatolytic and intoxicated c e l l s . Chromatolytic motoneurones possessed numerous short fragments of RER d i f f u s e l y distributed among aggregates of polyribosomes. Degranulation was not prominent. In d i p h t h e r i t i c int o x i c a t i o n , motoneurones showed a varied response. M i l d l y affected neurones contained stacks of RER lamellae whose cisternae were dilated. In extreme cases, RER lamellae were grossely distended and fragmented with loss of associated ribosomes. Mitochondria were also vacuolated and lacked cristae. Johnson, I . P . , Pullen, A.H., Sears, T.A. (1983) J. Physiol., (In press) Pappenheimer, A.M. & G i l l , D.M. (1973), N.Y., 182, 353-358.
F368 PARAMETRIZATION OF COMPOUNDEMG SIGNALS AT RECRUITMENT MARANZANA, F.M.*, MOLINARI, R., Dipartimento di Elettronica*~ Centro di Teoria dei Sistemi CNR, Politecnico di Milano, Milano, I t a l y The morphology and the number of the motor unit potentials together with the f i r i n g rate during voluntary e f f o r t are generally considered to discriminate neurogenic lesions from myopathic disorders~ however in acute peripheral neuropathies, short polyphasic potentials may be found. For this reason, the parameters generally adopted in Quantitative EMG prove sometimes inadequate to discriminate these cases. Changes of these parameters at recruitment are u s e f u l l y taken into account because of the very d i f f e r e n t behaviour of myopathic from neurogenic muscles. The myopathic muscle r e c r u i t s early, showing high increments of the EMG turns when voluntary contraction goes from 20% to 30% of the maximum and is not able of large further recruitment from 30% to 40%, whereas the neurogenic muscle r e c r u i t s at regular pace. This work studies recruitment in the pathological muscles through the parameters of the autoregressive (AR) model. The AR class of models is chosen f i r s t in order to test possible new discriminating parameters which are easy to obtain by means of low-cost computation. F i r s t , a comparison is carried out l i t h the QEMG parameters in the case of the "a p r i o r i " selected AR(2) model. As a second step, i d e n t i f i c a t i o n with the optimal AR model is carried out. The role played by the model order is c a r e f u l l y evaluated.
F369 ULTRASTRUCTURALCHANGES IN MOTONEURONESFOLLOWING AXOTOMYAND DIPHTHERITIC INTOXICATION SEARS, T.A., PULLEN, A.H., JOHNSON, I . P . , Sobell Department of Neurophysiology, I n s t i t u t e of Neurology, Queen Square, London, W.C.1N 3BG, U.K. Neuronal death (e.g. in Motoneurone Disease) and chromatolysis are both associated with profound alterations in topographical organisation of the rough endoplasmic reticulum (RER) and polyribosomes, which comprise the morphological correlates of protein synthesis. Chromatolysis, however, does not always evoke neuronal death. A comparison therefore, between the organisation of RER and polyribosomes in normal, chromatolytic and dying motoneurones of the cat thoracic spinal cord permitted features unique to neuronal death being distinguished from those accompanying chromatolysis. Neuronal death was evoked by d i p h t h e r i t i c intoxication (Johnson, Pullen & Sears, 1983). While the mechanism responsible f o r chromatolysis remains uncertain, diphteria toxin i n h i b i t s protein synthesis by s p e c i f i c a l l y inactivating EF2, the elongation factor essential for t r a n s l a t i o n of ribosomes along mRNA (Pappenheimer & G i l l , 1973), and is f a t a l to the c e l l . The highly ordered stacks of RER lamellae interposed by rows of polyribosomes seen in normal motoneurones contrasted with the disordered RER in chromatolytic and intoxicated c e l l s . Chromatolytic motoneurones possessed numerous short fragments of RER d i f f u s e l y distributed among aggregates of polyribosomes. Degranulation was not prominent. In d i p h t h e r i t i c int o x i c a t i o n , motoneurones showed a varied response. M i l d l y affected neurones contained stacks of RER lamellae whose cisternae were dilated. In extreme cases, RER lamellae were grossely distended and fragmented with loss of associated ribosomes. Mitochondria were also vacuolated and lacked cristae. Johnson, I . P . , Pullen, A.H., Sears, T.A. (1983) J. Physiol., (In press) Pappenheimer, A.M. & G i l l , D.M. (1973), N.Y., 182, 353-358.