corticospinal input onto motor neurons projecting to ankle muscles in individuals with cerebral...

CORTICOSPINAL INPUT ONTO MOTOR NEURONS PROJECTING TO ANKLE MUSCLES IN INDIVIDUALS WITH CEREBRAL PALSY 4

Brenda Broiirver Eniely Sniirs .

Cerebral palsy (CP) is a general term used to describe non-progressive disor- ders of posture and movement related to damage to the developing brain during the perinatal period (Bax 1964). The neu- rophysiological mechanisms which underlie the deficits associated with voli- tional movement are largely unknown. Common abnormalities are the absence of the normal reciprocal relation between agonists and antagonists during voluntary movement (Dietz and Berger 1983, Hallett and Alvarez 1983) and agonist-antagonist co-activation during passive movement (Gottlieb et al. 1982, Myklebust er crl. 1982).

Surface electromyographic recordings of activity evoked in tibialis anterior (TA) and soleus (SOL) muscles follow- ing passive dorsal and plantar stretch have provided evidence that, in patients with CP, reciprocal innervation between the motor neurons of these muscles is facilitatory (Myklebust er nl. 1982). Reflex irradiation to other muscles as well as the antagonist suggests that a lack of supraspinally mediated inhibition is not the only factor involved (Leonard et nl. 1991). I t has been proposed that peri- natal lesions may be associated with abnormal corticospinal axonal branching (Carr et nl. 1993) or retention of exuber- ant neural projections (Leonard et nl. 1991), either or both of which may

! i

contribute to the clinical manifestations observed in CP.

Anatomical evidence for such abnor- malities i s well documented in non- human mammalian systems. In cats, unilateral lesions of the pyramidal tract during the neonatal period result in aber- rant projections to the contralateral red nucleus and thalamus arising from the intact cortex (Villablanca et 01. 1986). The terminal fields of motor cortical neu- rons are widely distributed within the neonatal spinal gray matter, then nor- mally retract during postnatal develop- ment to assume the adult projection pattern (Stanfield et 01. 1982, Theriault and Tatton 1989). Evidence has shown that following neonatal motor cortical lesions, exuberant projections are retained (Leonard and Goldberger 1987). It has been postulated that such retention may occur in humans as well and could be associated with disturbances in motor control (Theriault and Tatton 1989. Leonard et nl. 1990, Brouwer and Ashby 1991).

In humans, stimulation of cortical neu- rons has revealed abnormal bilateral corti- cospinal innervation of hand muscles in children with hemiplegic CP demonstrat- ing mirror movements (Farmer er al. 199 I , Cam et a/. 1993). Cross-correlograms of the spike trains recorded from the, homonymous muscles have demonstrated

TABLE I Summary of clinical findings in subjects with CP

~~~ ~ ~ ~~~ ~

Sitbject Clmsifcdon Age Eiiology Tone Strength . Reflexes (yrs) U E LE U E LE UE LE

1 R hemiplegia 51 Unknown + + - + + - : N + + 2 L hemiplegia 35 Preterm + +

3 Diplegia 29 Preterm L N ++ - ' R N + N - N +

4 Diplegia 40 Preterm N + + N - N N 5 Diplegia 54 Unknown N + + N - N + + 6 Diplegia 43 Preterm N + N - N ++

-

- + ++

N= normal: + = increased; ++ = markedly increased; - = decreased; UE = upper extremity; LE = lower extremity; L = left; R= right

synchrony in their firing patterns, imply- ing that the right and left motor neuron pools share common presynaptic inputs (Can er nl. 1993). In the lower limb, transcranial magnetic stimulation - which preferentially produces direct activation of the rapidly conducting corticospinal fibers (Priori er 01. 1993) - consistently evokes strong facilitation of TA motor neurons and weak or no response in SOL motor neurons in healthy subjects (Brouwer and Ashby 1990, Brouwer and Qiao 1995). In spastic CP, equivalent degrees of facilitation of both TA and SOL motor neurons is observed (Brouwer and Ashby 1991). which has not been demonstrated in subjects with spasticity due to stroke (Yang et nl. 1990) or spinal- cord injury (Brouwer et al. 1992). The neural mechanisms underlying this abnor- mality are not known.

The present study sought to examine the nature of the corticospinal projections to TA and SOL motor neurons and to determine whether evidence of abnormal axonal branching or interneuronal con- nections could be found. Since variation in background motor neuronal activity can alter the parameters of stimulus- evoked compound muscle action poten- tials. stimulus-induced changes in the firing pattern of single motor units were examined. The magnitudes of the com- posite post-synaptic potentials derived from peristimulus time histograms (PSTHs) of voluntarily activated TA and SOL motor units would more closely reflect the projection strength onto their

motor neurons (Palmer and Ashby 1992).

Method Studies were carried out on seven control subjects (four males, three females) and six subjects with CP (four males, two females), who provided their informed consent. All subjects were screened ini- tially to ensure that they had no history of epilepsy, intracranial metal implants and/or cardiac pacemakers. All subjects with CP were assessed to provide a gen- eral description of the degree of motor impairment (Table I). The presence of TA-SOL co-activation was assessed visually by observing the EMG signals on an oscilloscope during passive ankle stretch and active plantarflexion and dor- siflexion. The experimental protocol was approved by the local ethics review board.

For all procedures, subjects lay in a semi-reclining position on a hospital bed. Motor unit activity was recorded using intramuscular concentric needle elec- trodes (Dantec 13L49, Scarborough, Ontario, Canada) with a recording sur- face area of 0.07mm'. Signals were band- pass-filtered (50 to IOkHz), amplified as necessary and digitized for computer pro- cessing at 20kHz per channel. A software amplitude discriminator window allowed extraction of relevant motor units and displayed them on a computer 'oscillo- scope' (DataWave Systems, Longmont. Colorado, USA) for visual inspection and feedback for subjects. Auditory feedback of the motor-unit discharges was also

provided by a loudspeaker.

TRANSCRANIAL MAGNETIC STIMULATION A Cadwell MES-I0 electromagnetic stimulator (Kennewick, Washington, USA) with a circular coil attachment (inside and outside diameters of 7.5cm and 9cm, respectively) was used to acti- vate cortical neurons. The intensity of stimulation was adjusted according to a linear scale ranging from 0% to 100% of the stimulator output (peak flux is 2 Tesla, manufacturer's specifications), so that it was 5% below that which resulted in a phasic muscle twitch in the gently contracted TA or SOL muscle. A needle electrode was placed in each of the target muscles and positioned close to a motor unit activated by gentle isometric con- traction such that the motor unit was either isolated or clearly distinguishable from other units. Single motor-unit recordings were obtained in turn from rhythmically firing TA and SOL units following approximately 100 magnetic stimuli applied tangentially over the con- tralateral scalp. The edge of the coil over- laid the vertex (Brouwer and Ashby 1991) and stimuli were delivered at -3s intervals.

PSTHs with Ims bins recorded the fir- ing times of the motor unit relative to the time of the applied stimuli (looms). A profile of the firing probability of the motor unit time-locked to the stimulus was obtained. A period of increased firing probability was defined as a mini- mum of two consecutive bins whose con- tents exceeded the mean background bin contents plus 2 standard deviations (SD), determined from the IOOms prestimulus portion of the PSTH, or one bin whose contents exceeded the background mean plus 3SD. The area of the period of increased firing probability or PSTH peak above the mean background level was expressed as extra counts per lo00 stimuli (Mao et nl. 1984). The peak area provided an estimate of the amplitude of the underlying composite excitatory post- synaptic potential (EPSP), and the peak duration reflected the rise time of the EPSP (Ashby and Zilm 1982. Fetz and Gustafsson 1983). The latency of the EPSP was determined by subtracting the rise time of the motor unit action poten-

tial from the latency of the PSTH peak. This correction was necessary since the time of firing was detected as the time of the motor unit's peak voltage.

SYNCHRONIZATION BETWEEN MOTOR UNIT DISCHARGES To determine the degree of synchrony between the discharges of TA and SOL motor units, subjects had to maintain acti- vation of both, with the assistance of visual and aural feedback. An effort was made to record from the same SOL unit recorded during magnetic stimulation. As it was not possible to maintain a single motor unit recording in TA as well as SOL, multi-unit recordings of the activity of about three to six TA motor units were obtained.

Cross-correlograms (2ms bins) were constructed between the discharge times of the TA motor units and those of the SOL unit. At each occurrence of a SOL motor unit action potential, the multi-unit TA spike train was searched for dis- charges occumng within 200ms before or after the SOL discharge. The cross-correl- ogram therefore reflects the logging of the discharge times of TA units at different lags (-200 to +200ms) relative to the dis- charge times of the SOL unit. Cumulative sums (cusums) were then calculated by subtracting the mean number of counts (occurrences) per 2ms bin in the baseline (comprising all but the central IOOms of the cross-correlogram) from each bin, and then progressively summing the residual bin contents. The duration of a cross-cor- relogram peak was determined as the time of the rising phase of the cusurn and the magnitude was calculated as the number of counts in all the bins contributing to the peak, divided by the mean bin count (Sears and Stagg 1976).

RECIPROCAL INHIBITION Surface electrodes were placed over TA and SOL muscles in addition to the needle electrode in TA (the needle in SOL was removed). Electrical stimuli ( 1 ms square- wave pulses) were delivered to the poste- rior tibia1 nerve by securing a cathode in the popliteal fossa and placing a large rec- tangular anode above the patella. Motor threshold was determined as the intensity of stimulation just sufficient to activate

CC- cc, a- m

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B

789

CONTROL ::::I ... I.'

CS

I I . TA

ES

Fig. 1. Correlogrcrrns derivedfrarn volirntcrrily activated niotor rinits from one control subject (left) cind one subject with spastic diplegici (right). Traces a and b crre PSTHs generated from single TA and SOL motor iinits in response to trciriscraniol rnagnetic stitniilaiioti (CS) applied at IOOttu. Short- latency peaks (Jucilitatiorrs) are denoted by arrows. Trcrces c correspond to PSTHs derived from sin- gle TA nioior iinits, illustrciiitig decreases in f ir ing probability in both subjects (arrows) -3Stns ajier sub-threshold electrical stitndatioti (ES) of the posterior tibiol nerve applied at 5orns. (Trough at 5Otns in control subject reflects occliision fiorn stirnirliis artefact.) Traces d elre cross-carrelograms between SOL motor irnit (reference) arid rtiiiltiple TA rnotor rinits. Solid and dotied lines correspond to ineon and 2SD of baseline bin conlents. respectively. Central IOOtns portion is expanded at bot- torn of figure and ciisirni sliown.

- - - . SOZ alpha-motor neuron axons with no concomitant activity in TA. The stimulus intensity was set to-80% of motor thresh- old and stimuli were delivered at -350ms intervals. PSTHs were constructed from the discharge times of single TA motor units, and a 50ms prestimulus portion was incorporated.

Periods of decreased firing probability were identified by comparing the bin con- tents of running 5-bin (5ms) segments to the bin contents of the prestimulus por- tion using Student t tests (Ma0 et ( i f .

1984). The number of displaced counts (below the mean background level) was

expressed as fewer counts per 10oO stim- uli. The use of different methods for analysing periods of increased and decreased firing probabilities was neces- sary as the latter is limited at zero counts.

Results All subjects tolerated the procedures well and recordings were obtained from seven neurologically healthy control subjects, with a mean age of 28.9 (SD 5.4) years, and six subjects with CP whose mean age was 42.0 (SD 9.5) years. One of those with CP had spastic diplegia, and had both legs tested. All subjects with CP

TABLE I1 a F

analyses I-

00' Control CP m 6

i * c P

I 00 I-

Characteristics of magnitudes of responses derived from correlogram

P' E Rnrtgr Menri Rnrrge Mean

Magnetic stimulation \ - - TA 102-427 227 113-294 177 >0.300

SOL 0-90 22 82401 184 <0.002 -. (extra counts/1000 s stimuli) z .-

5 Reciprocal innervation 15-57 24 3 c 9 7 38 t0.005

stimuli) 3 - SOL-TA synchrony 0 - 0- I .7 - - 3

(fewer counts/1000

2,

.? - -

' p values generated from t-tests. - Not calculated.

demonstrated co-activation of TA and SOL upon passive and active ankle movement as observed from EMG traces displayed on an oscilloscope.

CORTICAL PKOJECTIONS TO TA AND SOL Magnetic stimulation was applied over the contralateral scalp at intensities below the threshold for activating the gently contracting TA or SOL muscles for con- trols (mean 56. I , SD 6.0%) and subjects with CP (mean 59.3, SD 3.6%). Figure 1 gives examples of typical recordings for a control subject (top left) and a subject with diplegia (top right). In the control subjects, strong and brief short-latency facilitations (28 to 32ms) were observed in all TA motor units tested, but only two of seven SOL motor units responded at short latency (33.8 to 34.6ms) to the stimulus of the same intensity. The strength of the cortical projections to TA (in extra counts/1000 stimuli) was signif- icantly greater than that to SOL (226.6 ws 22.4) (~~0.001) . All subjects with CP showed short-latency facilitations in both TA and SOL motor neurons (TA = 25.1 to 35.0ms. SOL = 30.3 to 42.0ms) which were similar in amplitude (see Fig. 1. traces a, b; Table 11). There was no dif- ference in the mean strength of TA facil- itation between controls and subjects with CP @>0.30), but the strength of the SOL facilitation was significantly greater in CP (p<0.002). These findings are sum-

2,

3

- - - - 2 e

marized in Table 11.

SOL AND TA MOTOR UNIT SYNCHRON- IZATION Cross-comelograms of the Occurrences of TA motor unit action potentials relative to the discharge times of about 1100 to 5200 SOL spikes were constructed. In subjects with CP the recording time tended to be longer than in controls, which was associated with a greater mean number of SOL discharges (2197 for con- trols, 3375 for those with CP). although this difference was not significant (p0.34). The mean discharge rate of soleus motor units was similar in controls (6.1 Hz) to that in subjects with CP (6.9Hz).

Three of the seven SOL-TA pairs tested from subjects with CP resulted in weak central peaks, ranging in magnitude from 1.15 to 1.70 (see Method), lasting between 10 and 18 ms, and occurring at lags of 2 to 4ms. These occurred in three subjects with diplegia. None of the cor- relograms constructed from the motor units of control subjects had central peaks (see Fig. Id for examples). It was Observed that the subjects with CP had less difficulty than the controls in main- taining co-activation between SOL and TA units. Control subjects relied more heavily on the visual and aural feedback and often had periods in which the motor unit(s) of one muscle would fall silent, 791

u: E z .- r?

rq 3 B -

0 Y - 2 0 *

792

100

80

g) 10 m c 0 4 0 I

-_ - I e

8 20

0 ' SOL-TA synchrony T I SOL RCCIPIDC.1

I.Cllil.l- lYdI1.IYIII nhlblllon

Q C o n t r d I C P

Fig. 2. Freqiieiicy of occiirretice of wrioiis responses. For both groiips N= 7, tiiittiber of rniiscles (or muscle pairs) from which h t c r were collected.

followed by active phasic activity. This occurred most often in TA.

RECIPROCAL INNERVATION BETWEEN TA AND SOL Electrical stimuli of an intensity equiva- lent to 80% of motor threshold, applied to the posterior tibia1 nerve, produced inhi- bition in all TA motor neurons tested. An example is shown in Figure 1 (trace c) for a control subject (left) and a subject with diplegia (right). The mean strength of the inhibition (expressed as fewer counts/1000 stimuli) was significantly greater in subjects with CP (mean 48.1, SEM 5.9) than in controls (mean 23.6, SEM 2.3) (pcO.005; see Table 11).

Figure 2 summarizes the frequency of occurrence of discharge synchrony and responses to magnetic and electrical stimuli.

Discussion Transcranial magnetic stimulation of the motor cortex leg area preferentially pro- duces direct activation of the rapidly conducting corticospinal fibers which project monosynaptically or oligosynap- tically onto motor neurons (Priori et a / . 1993). The present study provides evi- dence that the corticospinal projections to the soleus muscle, an ankle plantarflexor. are abnormal in spastic CP. Further, these projections are as strong as those inner- vating the dorsiflexor (TA) motor neu- rons, corroborating earlier work involving a similar patient population

(Brouwer and Ashby 1991). This is not a reflection of the stimulus parameters, since increasing the intensity and altering the coil position fails to produce similar SOL activation in control subjects (Brouwer and Ashby 1991, Brouwer and Qiao 1995). In subhuman primates, motor cortical areas projecting to motor nuclei of synergistic or antagonistic muscles often overlap extensively (Jankowska et al. 1975, Asanuma et al. 1979). However, there are differences i n projection strength and activation thresholds of these neurons; specifically, motor neu- rons of distal muscles receive more extensive projections than those of proxi- mal muscles and dorsiflexors more than plantarflexors (Jankowska et al. 1975). The pattern of muscle activation evoked by transcranial magnetic stimulation in healthy human subjects is similar (Brouwer and Ashby 1990, Palmer and Ashby 1992). However, this is not the case in patients with CP, as evidenced by equivalent evoked responses in TA and SOL. This may be related to differential spread of the magnetically induced cur- rents due to structural abnormalities, although radiographic images have failed to support this argument in a comparable group of subjects (Brouwer and Ashby 1991).

The functional implications of exces- sive corticospinal input to the soleus muscle are not clear, largely because the underlying neural circuitry has not been identified. The activation of both TA and SOL motor neurons by identical stimuli may reflect divergence of corticospinal axons, reciprocal excitation (Gottlieb et al. 1982, Myklebust et al. 1982) or aber- rant corticospinal projections (Brouwer and Ashby 1991). Determining the mech- anism(s) involved may well be important in selecting or developing appropriate intervention strategies.

Short-term discharge synchrony between motor neurons and their motor units i s attributed to shared input from common branched-stem presynaptic fibers (Sears and Stagg 1976, Bremner et ( I / . 1991. Datta et a/ . 1991). In healthy subjects the frequency of occurrence and the strength of discharge synchrony between non-homonymous motor units decreases when units are selected from

different anatomical compartments (Bremner et al. 1991, Datta et al. 1991, Carr et al. 1993) such as TA and SOL. Synchronization strength increases as the recruitment thresholds of the units con- verge toward similar levels (Datta and Stephens 1990). Although the relative recruitment thresholds of TA and SOL motor neurons to natural synaptic drive is not known, normally alpha motor neu- rons projecting to TA are activated at lower intensities of cortical stimulation applied to various scalp sites (Brouwer and Ashby 1990). Taken in combination. it is not surprising that synchronization between voluntarily activated TA and SOL motor units was not found in the control subjects in this study. I t was observed in three of seven muscle pairs in subjects with CP.

Where SOL-TA synchrony was observed, the central peaks were of dura- tions consistent with those reported for .I single TA motor units (3 to 25ms) in healthy subjects (Datta e r cil. 1991). ' When the synchronization is of short duration and occurs with negligible lag, it is likely that the common presynaptic fiber represents a first-order neuron. However, it is unlikely that corticospinal axons branch to both SOL and TA motor neurons, since the shorter peripheral con- duction distance to TA would place the synchronization peak to the left of zero (SOL discharges serving as the refer- ence). This did not occur.

Alternatively, it is possible that the fir- ing of the cortical cells themselves may have been synchronized (Smith and Fetz 1989) via cortical afferents. If so. the efferent central conduction times would probably be dispersed sufficiently such that the detection of short-duration syn- chrony would be unlikely (Carr er 01. 1993). However, this mechanism may account for the occurrence of cortically evoked responses in both TA and SOL muscles at a given stimulus intensity, as observed in all subjects having CP. Control subjects also reported difficulty in sustaining simultaneous motor unit activity in both muscles, whereas all sub- jects with CP accomplished the task with relative ease.

In spastic CP, reciprocal excitation between SOL and TA has been attributed

to primary (Ia) afferents arising from the spindles of the soleus muscle (Gottlieb et al. 1982, Myklebust et al. 1982). If this were the case, SOL-TA synchrony may also be evident if the interneuronal circuit shared a common input. All subjects in this study, however, demonstrated recip- rocal inhibition in TA motor neurons, unlike previous studies using surface recordings from subjects with severe functional involvement (Myklebust et al. 1982). Other studies used stretch-induced reflex activity (Gottlieb et al. 1982, Myklebust et nl. 1982), and the associ- ated proprioceptive and cutaneous input may have reduced reciprocal inhibition (Berbrayer and Ashby 1990).

The inhibition observed was in the presence of TA activation. which should obscure the effect due to Renshaw cell activity. The fact that the inhibition was greater than that observed in controls (see also Berbrayer and Ashby 1990) may be associated with abnormal Renshaw cell activation as reported by Katz and Pierrot-Deseilligny (1982) in patients with spasticity due to stroke or spinal- cord lesion. In the absence of studying Renshaw cell activity, this cannot be determined, nor can its association with the occurrence of SOL-TA synchrony be established.

The electrophysiological data showed no apparent differences between those subjects with CP in whom discharge syn- chrony was observed and those in whom it was not. Clinically, however, the three subjects in whom synchrony was found had diplegia and exhibited very brisk ten- don reflexes and elevated tone (see Table I). Based on a small number of cases, the implication is that SOL-TA synchroniza- tion may be related to the degree of impairment, i.e. of spasticity. Shefner et 01. (1992) reported that measures o f recurrent inhibition may correlate with clinical measures of spasticity in patier& with spinal-cord injuries. Further study is needed to determine whether this is a sub- strate for short-term synchrony in CP.

The findings of this study support the theory that individuals with spastic CP have abnormal corticospinal projections to soleus motor neurons. While it is unlikely that these axons branch to both TA and SOL motor neurons to any

a QI r- I r-

X r- oo' F,

z : 2 s -

793

794

significant degree, the possibility that cortical ncurons projecting to each motor neuron pool (TA and SOL) are activated concurrently through cortical afferents cannot be refuted. In spastic diplegia (though not hemiplegia), short-term dis- charge synchrony was evident between SOL and TA motor units, a finding which may reflect abnormal supraspinal modu- lation of spinal neurons, but not an absence of reciprocal inhibition. Onc or both of these mechanisms could con- tribute to the disordered movement pat- terns, including co-activation, observed in this population. Further study is

required to determine the prevatence of SOL-TA synchrony and whether dissoci- ation occurs during various tasks or in response to different task strategies.

Accepted for pitblictrtiori 3/31 Airyiist 1995.

Ackrio~vle~lXetrrer It This research was funded by the Ontario Easter Seal Kescarch Institute (grant 9156).

Aiithors ' Appoiri/trretlts ' Brenda Brouwer, PhD. School of Rehabilitation - Therapy, Queen's University. Kingston. Ontario, Canada K7L 3N6. Emely Smits. PhD. School of Occupational Therapy. Dalhousie University. Halifax, Nova Scotia.

*Correspoi~det~ce to J r ~ t critthor.

SUMMARY Cross-comelograms between voluntarily active soleus (SOL) and tibialis anterior (TA) motor units were gencrated from scven control subjects and six subjects with spastic cerebral palsy (CP). Short- duration central peaks were observed in three subjects with spastic diplegia only All subjccts demonstrited reciprocal inhibition in TA following electrical stimulation of group 1 afferents to SOL, and all subjecds with CP demonstrated strong activation of both TA and SOL in response to transcranial magnetic stimulation. Responses in SOL were stronger than those observed from controls. Thesc data support the existence of abnormal corticospinal projections to soleus motor neurons in individuals with spastic CP. In spastic diplegia, short-term discharge synchrony between SOL and TA motor units may reflect abnormal interneuronal modulation at the spinal level. Abnormal corticospinal projections andlor modulation of spinal interneurons may contribute to the disordered movement patterns and to-activation observed in this population.

RESUME 1rflii.v corticospiriairx siir les iieiirotics iwteurs des mitscles de la clreiillc chez les IMC Les correlogrammes croises des unites motriccs stirnukes volontairement sur le soleaire (SOL) et le jambier anttricur (TA) ont kte releves chez sept sujets contr6les et six IMC a fome spastique (CP). Des pics centraux de courte duree ne furent observes que chez trois sujets avec diplkgie spastique. Tous les sujets montrerent une inhibition rkciproque sur les TA klcctrique des afferents du groupe I du soleaire. et tous les sujets CP montrerent une forte activation conjoinre dcs TA CI des SOL en rkponse A une stimulation magnktiquc transcrinienne. Les reponses SOL etaient plus fortes que chez les contrbles. Ces donnkes favorisent I'hypothkse de I'existence de projections corticospinales anormales sur les neurones moteurs du soleaire chez les CP spastiques. Dans la diplegie spastique, le synchronisme des decharges A court terme entre les unites motriccs SOL et TA pourrait traduire une modulation interncurale anormale au niveau spinal. Les projections corticospinalcs anormales et/ou la modulation des interneurones medullaires peuvent contribuer a I'allure perturb& du mouvement et h la co-activation observke dans cette population.

ZUSAMMENFASSUNG Corticospirialer Ittipuls fiir Motonieurotie iler UtitersclieriX.eItniisklr/citnr bei Patienten mit Cerebralparese B& sieben Kontrollpersonen und sechs Patienten mil spastischer Cerebralparese (CP) wurden Kreuzkomelogramme zwischen den willkurlich innervierbaren Motor Units der Mm soleus (SOL) und tibialis anterior (TA) hergestellt. Nur bei drei Patienten mit spastischer Diplegie wurden kurze zentrale Entladungen beobachtet. Alle Probanden zeigten eine reziproke Inhibition im TA nach

, dektrischer Stimulation der Afferenten der Gruppe I zum SOL und alle Patienten mit CP zeigten T. eine starke Aktivierung von TA und SOL als Reaktion auf eine transkranielle magnetische _Stimulation. Die Reaktionen im SOL waren stiirker ausgepragt als bei den Kontrollen. Die Daten bestatigen. daD es bei Patienten mit spastischer CP abnorme kortikospinale Projektionen zu den SOL Motorneuronen gibt. Bei der spastischen Diplegic kann eine kurze Entladungssynchronisation zwischen SOL und TA Motor Units Ausdruck einer abnormen interneuronalen Modulation auf spinaler Ebene sein. Abnorme kortikospinale Verbindungen undIoder Beeinflussung der spinalen lnterneurone konnen zu dem gestorten Bewegungsmuster und der Co-Aktivierung beitragen. die bei dicsen Patienten beobachtet werden.

la suite d'une stimulation

RESUMEN Arcidn corticoespinul sohe Ins iieirronus inororus flue s e proyeciati eri 10s muscirlos del robillo, eri individictis colt paralisis cerebrd Se generaron correlogramas cruzados entre el sbleo voluntariamente activo (SOL) y el tibia1 anterior (TA) en sus unidades motoras, en sicte sujetos control y seis con parilisis cerebral (PC). Se observaron espigas centrales d e corta duraci6n en Ires individuos con diplegia espistica sola. Todos 10s individuos rnostraron una inhibicion reciproca e n TA tws la estimulacion clectrica del grupo 1 d e aferentes al SOL, y todos 10s individuos con PC demostraron una fuerte activacibn al mismo tiempo d e TA y SOL como respuesta a la estimulaci6n magnetics transcraneal. Las respuestas en el SOL eran mlis intensas que las observadas e n controles. Estos datos refuerzan la existencia de proyecciones corticoespinales anormales sobre las neuronas motoras del s6leo en individuos con PC espistica. En la diplegia espistica. la descarga a corto plazo sincrbnica entre SOL y \as unidades motoras del TA puede reflejar una modulacibn interneural a n h a l a a nivel espinal. Las proyecciones cortico-espinales anbmalas ylo la modulaci6n interneuronal espinal. puedcn contribuir P 10s patrones d e desorden motor y a la co-activacibn observadas en esta poblacion.

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Manual of methods for recording and analyzing sleep-wakefulness states

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