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Nerve-fiber conduction velocity distributions in the median nerve bundle
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muscular contraction under normal and myopathic conditions. A l i n e a r array of 30 surface electrodes is f i x e d above the biceps brachii muscle and centered over the end-plate zone. The EMG is simultaneously recorded on a l l channels and displays the propagation of motor u n i t - a c t i o n p o t e n t i a l s on both sides of the innervation band. The meanlmuscle f i b e r conduction v e l o c i t y is computed by a c r o s s - c o r r e l a t i o n technique. Five adult patients in a late stage of progressive muscular dystrophy showed a h i g h l y altered propagation behaviour of motor u n i t action p o t e n t i a l s without a time s h i f t between p o t e n t i a l s of adjacent e l e c t r o des. A mathematical model is described which predicts such a behaviour and suggests that i t must be due to a pathological l o n g i t u d i n a l spread of end-plates in t h i s p a t i e n t group. In f i v e boys with Duchenne muscular dystrophy and only moderate impairment of the biceps muscle the mean muscle f i b e r v e l o c i t y was reduced (2.81+.34 m/s) compared to 17 healthy subjects (4.42+.37 m/s). Each myopathic patient-examined could be separated c l e a r l y from the g~oup of healthy subjects on the basis of the surface EMG analysis u t i l i z e d .
F134 SCANNINGEMG HILTON-BROWN,P. and STALBERG,E., Dept. of Neurophysiology, U n i v e r s i t y Hospital, Uppsala, Sweden Scanning EMG was developed to v i s u a l i z e the spatial and temporal d i s t r i b u t i o n of motor u n i t a c t i v i t y . A concentric needle EMG electrode is pulled through the muscle in 5oNm steps by a computer c o n t r o l l e d device. A c t i v i t y from one motor u n i t is obtained by t r i g g e r i n g with separate Single Fibre electrode. Scanning EMG has been performed in normals, and in patients with muscular dystrophy or motor neuron disease. The a c t i v i t y varies considerably w i t h i n u n i t s . The mean length was not s i g n i f i c a n t l y d i f f e r e n t in normals and dystrophies while the a c t i v i t y in the l a t t e r could be interrupted by s i l e n t areas. In motor neuron disease motor units had mainly unchanged t e r r i t o r y that were denser than in normal muscles.
F135 NERVE-FIBER CONDUCTION VELOCITY DISTRIBUTIONS IN THE MEDIAN NERVE BUNDLE HIROSE G, TSUCHITANI Y, HUANG J, Kanazawa Medical U n i v e r s i t y , Department of Neurology, Uchinada, Kahoku, Ishikawa Pref.,Japan, 920-02 We present a new method of estimating the d i s t r i b u t i o n of conduction v e l o c i t y (CV) w i t h i n a nerve trunk, using two compound action p o t e n t i a l s (CAP) recorded by surface electrodes. Barker, Cummins et a l . reported s i m i l a r 2 CAP methods, which use the r e i t e r a t i o n method that the solution always converges to a p a r t i cular c o n d i t i o n . This estimation becomes an issue in i t s uniqueness and convergency. Our new method does not have any of these problems. Our method requires two basic assumption, ( I ) a l l f i b e r s have a same single f i b e r action p o t e n t i a l ; (2) the sameJnumbers of f i b e r s are stimulated at two d i f f e r e n t s i t e s . The model is represented, by the f o l l o w i n g convolution: gL(t) = Mfd(t-T)pz(z)d ~ where gL(t) = CAP~ l = distance between stimulus and recording, pL~t) = latency d i s t r i b u t i o n at distance l , M = numbers of f i b e r s stimulated. This equation is expressed in terms of f a s t Fourier transform (FFT), using a microcomputer, as GI(~) = MD(oj)pl(w).
SlO0
I f stimulated at 11 and 12 , then mzl(~)/Gz2(w) = PL2(]]---~-2w)/PL2(~) • Pz2(w) is determined by a simple algorithm without i t e r a t i o n , thus, Pz2(t) is estimated by inverse FFT. The c l i n i c a l a p p l i c a t i o n of t h i s method d i f f # r e n t i a t e d nornul from patients with neuropathy in t h e i r CV d i s t r i b u t i o n .
F136 SPECTRALANALYSIS OF FORCE TREMOR IN DIFFERENTIAL DIAGNOSIS OF MOTORDISORDERS H~MBERG,V., HEFTER,H., REINERS,K. and FREUND,H.J., Neurologische U n i v e r s i t ~ t s k l i n i k , D-4ooo DUsseldorf, F.R.G. A two-component model has been proposed for the generators of physiological force tremor. The low frequency part of the tremor spectrum is produced by slow v a r i a t i o n s in force. The higherfrequency part seems to be related to motor u n i t a c t i v i t y peaking at 8-12 Hz, which corresponds to unfused twitches of muscle f i b e r s driven by motor units discharging in t h i s frequency range. The spectra f a l l o f f steeply towards higher frequencies due to increased fusion of mechanical r i p p l e s . Following t h i s model t h i s study was aimed to examine whether the analysis of force tremor could provide useful information about the discharge rates of motor units d i f f e r e n t i a t i n g physiological from various pathological conditions. Tremor spectra from high gain AC-coupled force transducer recordings of isometric f o r e f i n g e r contractions at s t e a d i l y maintained and slowly increasing forces were analyzed. The e f f e c t of mechanical damping at higher motor u n i t f i r i n g rates was compensated mathematically f o l l o w i n g an e m p i r i c a l l y determined slope. Consecutive p l o t t i n g of p a r t i a l l y overlapping spectra allowed the display of spectral changes with force v a r i a t i o n . In normal subjects spectra always peaked in the range of motor u n i t onset f i r i n g rates and spectral power s h i f t e d to higher frequencies with increasing force corresponding to concomitant increase in f i r i n g rates of motor units already recruited. Cons i s t e n t abnormalities in frequency composition of these spectra could be ident i f i e d in patient groups with various peripheral and central motor disorders. I t appears that analysis of force tremor may provide useful information on abnormalities of motor u n i t a c t i v i t y .
F137 ORDERLYRECRUITMENTOF CAT HINDLIMB MOTONEURONSDURING LOCOMOTION HOFFER,J.A., LOEB,G.E., MARKS,W.B. and SUGANO,N., Lab. of Neural Control, NINCDS, NIH, Bethesda, MD 202o5, USA In cats trained to walk on a treadmill at speeds between o.l and 1.5 m/s, the discharge of single L5 ventral root axons was recorded using implanted f l o a t i n g microelectrodes (1). Axonal conduction v e l o c i t y was determined by spiketriggered averaging onto femoral nerve c u f f electrodes (2). The destination of each recorded motoneuron was v e r i f i e d by spike-triggered averaging onto EMGelectrodes implanted in each of the a n t e r i o r thigh muscles. The r e c r u i t m e n t threshold of each motoneuron was defined by the value of the r e c t i f i e d , smoothed parent muscle EMG at the time when the u n i t f i r e d i t s f i r s t spike in each step. F u l l y characterized motoneurons (conduction v e l o c i t y range = 56.6-I18.2 m/s; mean= 91.4 m/s~=28), had p o s i t i v e l y correlated axonal conduction v e l o c i t y and recruitment threshold (p< o . o l ) . These findings demonstrate that in the normal
muscular contraction under normal and myopathic conditions. A l i n e a r array of 30 surface electrodes is f i x e d above the biceps brachii muscle and centered over the end-plate zone. The EMG is simultaneously recorded on a l l channels and displays the propagation of motor u n i t - a c t i o n p o t e n t i a l s on both sides of the innervation band. The meanlmuscle f i b e r conduction v e l o c i t y is computed by a c r o s s - c o r r e l a t i o n technique. Five adult patients in a late stage of progressive muscular dystrophy showed a h i g h l y altered propagation behaviour of motor u n i t action p o t e n t i a l s without a time s h i f t between p o t e n t i a l s of adjacent e l e c t r o des. A mathematical model is described which predicts such a behaviour and suggests that i t must be due to a pathological l o n g i t u d i n a l spread of end-plates in t h i s p a t i e n t group. In f i v e boys with Duchenne muscular dystrophy and only moderate impairment of the biceps muscle the mean muscle f i b e r v e l o c i t y was reduced (2.81+.34 m/s) compared to 17 healthy subjects (4.42+.37 m/s). Each myopathic patient-examined could be separated c l e a r l y from the g~oup of healthy subjects on the basis of the surface EMG analysis u t i l i z e d .
F134 SCANNINGEMG HILTON-BROWN,P. and STALBERG,E., Dept. of Neurophysiology, U n i v e r s i t y Hospital, Uppsala, Sweden Scanning EMG was developed to v i s u a l i z e the spatial and temporal d i s t r i b u t i o n of motor u n i t a c t i v i t y . A concentric needle EMG electrode is pulled through the muscle in 5oNm steps by a computer c o n t r o l l e d device. A c t i v i t y from one motor u n i t is obtained by t r i g g e r i n g with separate Single Fibre electrode. Scanning EMG has been performed in normals, and in patients with muscular dystrophy or motor neuron disease. The a c t i v i t y varies considerably w i t h i n u n i t s . The mean length was not s i g n i f i c a n t l y d i f f e r e n t in normals and dystrophies while the a c t i v i t y in the l a t t e r could be interrupted by s i l e n t areas. In motor neuron disease motor units had mainly unchanged t e r r i t o r y that were denser than in normal muscles.
F135 NERVE-FIBER CONDUCTION VELOCITY DISTRIBUTIONS IN THE MEDIAN NERVE BUNDLE HIROSE G, TSUCHITANI Y, HUANG J, Kanazawa Medical U n i v e r s i t y , Department of Neurology, Uchinada, Kahoku, Ishikawa Pref.,Japan, 920-02 We present a new method of estimating the d i s t r i b u t i o n of conduction v e l o c i t y (CV) w i t h i n a nerve trunk, using two compound action p o t e n t i a l s (CAP) recorded by surface electrodes. Barker, Cummins et a l . reported s i m i l a r 2 CAP methods, which use the r e i t e r a t i o n method that the solution always converges to a p a r t i cular c o n d i t i o n . This estimation becomes an issue in i t s uniqueness and convergency. Our new method does not have any of these problems. Our method requires two basic assumption, ( I ) a l l f i b e r s have a same single f i b e r action p o t e n t i a l ; (2) the sameJnumbers of f i b e r s are stimulated at two d i f f e r e n t s i t e s . The model is represented, by the f o l l o w i n g convolution: gL(t) = Mfd(t-T)pz(z)d ~ where gL(t) = CAP~ l = distance between stimulus and recording, pL~t) = latency d i s t r i b u t i o n at distance l , M = numbers of f i b e r s stimulated. This equation is expressed in terms of f a s t Fourier transform (FFT), using a microcomputer, as GI(~) = MD(oj)pl(w).
SlO0
I f stimulated at 11 and 12 , then mzl(~)/Gz2(w) = PL2(]]---~-2w)/PL2(~) • Pz2(w) is determined by a simple algorithm without i t e r a t i o n , thus, Pz2(t) is estimated by inverse FFT. The c l i n i c a l a p p l i c a t i o n of t h i s method d i f f # r e n t i a t e d nornul from patients with neuropathy in t h e i r CV d i s t r i b u t i o n .
F136 SPECTRALANALYSIS OF FORCE TREMOR IN DIFFERENTIAL DIAGNOSIS OF MOTORDISORDERS H~MBERG,V., HEFTER,H., REINERS,K. and FREUND,H.J., Neurologische U n i v e r s i t ~ t s k l i n i k , D-4ooo DUsseldorf, F.R.G. A two-component model has been proposed for the generators of physiological force tremor. The low frequency part of the tremor spectrum is produced by slow v a r i a t i o n s in force. The higherfrequency part seems to be related to motor u n i t a c t i v i t y peaking at 8-12 Hz, which corresponds to unfused twitches of muscle f i b e r s driven by motor units discharging in t h i s frequency range. The spectra f a l l o f f steeply towards higher frequencies due to increased fusion of mechanical r i p p l e s . Following t h i s model t h i s study was aimed to examine whether the analysis of force tremor could provide useful information about the discharge rates of motor units d i f f e r e n t i a t i n g physiological from various pathological conditions. Tremor spectra from high gain AC-coupled force transducer recordings of isometric f o r e f i n g e r contractions at s t e a d i l y maintained and slowly increasing forces were analyzed. The e f f e c t of mechanical damping at higher motor u n i t f i r i n g rates was compensated mathematically f o l l o w i n g an e m p i r i c a l l y determined slope. Consecutive p l o t t i n g of p a r t i a l l y overlapping spectra allowed the display of spectral changes with force v a r i a t i o n . In normal subjects spectra always peaked in the range of motor u n i t onset f i r i n g rates and spectral power s h i f t e d to higher frequencies with increasing force corresponding to concomitant increase in f i r i n g rates of motor units already recruited. Cons i s t e n t abnormalities in frequency composition of these spectra could be ident i f i e d in patient groups with various peripheral and central motor disorders. I t appears that analysis of force tremor may provide useful information on abnormalities of motor u n i t a c t i v i t y .
F137 ORDERLYRECRUITMENTOF CAT HINDLIMB MOTONEURONSDURING LOCOMOTION HOFFER,J.A., LOEB,G.E., MARKS,W.B. and SUGANO,N., Lab. of Neural Control, NINCDS, NIH, Bethesda, MD 202o5, USA In cats trained to walk on a treadmill at speeds between o.l and 1.5 m/s, the discharge of single L5 ventral root axons was recorded using implanted f l o a t i n g microelectrodes (1). Axonal conduction v e l o c i t y was determined by spiketriggered averaging onto femoral nerve c u f f electrodes (2). The destination of each recorded motoneuron was v e r i f i e d by spike-triggered averaging onto EMGelectrodes implanted in each of the a n t e r i o r thigh muscles. The r e c r u i t m e n t threshold of each motoneuron was defined by the value of the r e c t i f i e d , smoothed parent muscle EMG at the time when the u n i t f i r e d i t s f i r s t spike in each step. F u l l y characterized motoneurons (conduction v e l o c i t y range = 56.6-I18.2 m/s; mean= 91.4 m/s~=28), had p o s i t i v e l y correlated axonal conduction v e l o c i t y and recruitment threshold (p< o . o l ) . These findings demonstrate that in the normal