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Assessment of spasticity in hemiplegic cerebral palsy. II: Distal lower-limb reflex excitability and function.

A clinical method for measuring the stretch reflex threshold and gain of muscles acting across the ankle joint in children with congenital hemiplegia is described. The stretch reflexes of all limbs were velocity-dependent. Hemiparetic limbs were not necessarily spastic compared with non-paretic limbs, suggesting that the term 'spastic hemiplegia' should be used more selectively and emphasis be placed on the heterogeneity of the hemisyndromes of childhood. Abnormal motor control, planning and dexterity, the hemipostures and plastic (non-electrical) muscle changes may be more important measures of impairment than reflex excitability. A general scheme for assessing reflex excitability and available treatments applicable to all types of cerebral palsy is proposed.

Ankle Joint↗

Bistability of alpha-motoneurones in the decerebrate cat and in the acute spinal cat after intravenous 5-hydroxytryptophan.

1. In the preceding paper (Crone, Hultborn, Kiehn, Mazieres & Wigström, 1988) it was shown that a short-lasting synaptic excitation ('on' stimulus) of extensor motoneurones (primarily triceps surae) in the decerebrate cat often resulted in a maintained excitability increase, which could be reset by a short-lasting inhibitory stimulus train ('off' stimulus). In the present experiments intracellular recording from triceps surae motoneurones and the electroneurogram (ENG activity) from triceps surae nerve branches were performed in parallel. 2. Sustained firing of individual triceps surae motoneurones was most often recorded in parallel with the maintained ENG activity following a synaptic 'on' stimulus. When the motoneurone was silenced, by a hyperpolarizing current through the microelectrode, there was no sign of on-going synaptic excitation during the maintained ENG activity following an 'on' stimulus. It was therefore suggested that voltage-dependent intrinsic properties of the motoneurones themselves could be responsible for the maintained firing. 3. In confirmation of this hypothesis it was found that short-lasting depolarizing current pulses through the recording microelectrode could trigger a self-sustained firing in the motoneurone provided that the bias current (i.e. the holding potential) was kept within certain limits. Hyperpolarizing current pulses terminated the firing. When the spike-generating mechanism was inactivated (by long-lasting excessive depolarization) similar depolarizing and hyperpolarizing current pulses could initiate and terminate plateau potentials in the motoneurones. By grading the depolarizing current pulses it was found that the plateau potentials were of all-or-none character, typically around 10 mV in amplitude. The two levels of excitability which can be triggered by short-lasting excitation and inhibition of the motoneurones is referred to as 'bistable' behaviour of the motoneurones. 4. After an acute spinal transection, in the unanaesthetized cat, the bistable behaviour of the motoneurones disappeared. However, it reappears following intravenous injection of the serotonin precursor 5-hydroxytryptophan (50-120 mg/kg). 5. Individual triceps surae motor units were recorded by selective EMG electrodes during tonic stretch reflexes in the decerebrate preparations. Based on an analysis of their firing pattern during lengthening and shortening (or vibration) of the muscle it is suggested that plateau potentials in motoneurones are recruited during the tonic stretch reflex. Furthermore, it is argued that a quantitatively important part of the depolarization of motoneurones during the tonic stretch reflex indeed originates from these plateau potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Hydroxytryptophan↗

Neurophysiological basis of functional recovery in the neonatal spinalized rat.

It had been shown previously that, following spinalization of the neonatal rat on postnatal day 7 (PN7), at the middle thoracic level, there was spontaneous recovery of coordinated stepping in the hindlimbs, enabling the animal to execute quadrupedal locomotion, with an ataxic gait. No significant recovery occurred in rats that were similarly spinalized on PN14. Despite the functional recovery in the PN7 group, their hindlimbs were paralyzed when not in contact with a surface. In the present experiments, at 16-18 weeks after spinalization, muscle spindle GpIa and cutaneous afferents were tested for functional connectivity to the alpha motoneurons (a-MNs) that innervate the right triceps surae (TS) muscles. The Hoffmann reflex (H-reflex), the tonic stretch reflex (TSR), and cutaneous reflexes were recorded from the right TS muscles in the nonanesthetized, intercollicular decerebrate preparation. The H-reflex and the TSR were readily elicited from the PN7 animals, but not from the PN14 animals. The PN14 preparations were characterized by prolonged (> 18 h in 3/8 cases), spontaneous discharge of motor units, and prominent M responses. There was widespread, bilateral convergence of cutaneous afferents from the hindquarters to the a-MNs of the TS muscles in both the PN7 and the PN14 preparations. In the nonspinalized, control preparation, only ipsilateral, cutaneous afferents activated the right TS a-MNs. These results demonstrate that in the chronic (> 3 months after spinalization), spinalized PN7 rat, but not in the PN14 rat, there is a tight functional connectivity between the hindlimb GpIa afferents and their homonymous a-MNs.

Animals↗

Localization of proprioceptive reflexes in the splenius muscle of the cat.

Activity of the cat splenius muscle was modulated by sinusoidal rotation of the head around the C1-C2 joint in decerebrate cats with labyrinth intact or with all semicircular canals plugged, or, in one intact and alert cat, by rotation of the body with the head fixed in space. EMG modulation, recorded from the areas of splenius innervated by the C1-C4 nerves, was due to the cervicocollic reflex. Modulation was not uniform, but decreased with progressively more caudal recording locations; with stimuli of small amplitude it was often possible to obtain modulation of the rostral part of the muscle only. The results demonstrate localization of proprioceptive reflexes, including the stretch reflex, within the splenius muscle.

Animals↗

Different types of tremor in the human thumb.

1. The upper limbs of normal subjects were immobilized in a way that allowed measurement of forces and movements at the thumb interphalangeal joint without significant movement elsewhere in the limb. 2. When the subject attempted to maintain a steady flexing force at the joint against a rigid stop, the actual force showed the irregular 8-11 Hz fluctuations characteristic of a 'physiological tremor'. This force fluctuation increased when the mean flexing force increased. 3. If the subject exerted his flexing force against a light complaint spring, there was an analogous irregular 8-11 Hz movement at the joint. 4. When, however, an extra inertial load was added to the terminal phalanx, flexion against a complaint spring was often accompanied by a different type of tremor. This was a more regular oscillation, of lower frequency (3-6 Hz), and of much larger amplitude. 5. The precise frequency and amplitude of this type of tremor depended on the characteristics of the added inertia and spring, in a way that could have been predicted from the responses of the joint to an imposed sinusoidal movement (Brown, Rack & Ross, 1982a). The movement appeared to arise from re-excitation within stretch reflex pathways. 6. The irregular 8-11 Hz tremor at this joint could not be attributed to reflex re-excitation, since the responses to sinusoidal movement indicated a stretch reflex whose timing would not support a movement at that frequency. It is, however, emphasized that other joints of the hand and fingers may behave in different ways.

Adult↗

The effect of sectioning the trigeminal sensory root on the periodontally-induced jaw-opening reflex.

The experiment was designed to determine the pathway taken to the brain stem by periodontal afferents responsible for the digastric jaw-opening reflex induced by tooth-tapping. Cutting the trigeminal sensory roots of anesthetized decerebrate cats eliminated the ipsilateral periodontally-induced reflex, although the stretch reflexes of the jaw-closing muscles were undiminished. These results suggest that periodontal afferents causing the jaw-opening reflex reach the brainstem through the Vth sensory root, and confirm that muscle spindle afferents travel through the Vth motor root.

Animals↗

Quantitative evaluation of normal muscle tone.

Forty-eight normal subjects were evaluated for the purpose of objectively quantifying muscle tone. Flexor carpi radialis and extensor digitorum communis electromyographic (EMG) activity was simultaneously recorded during wrist movements imposed by a torque motor. Each session was subdivided into three steps: (1) measurement of the 'intrinsic stiffness index' (ISI) at 10 degrees/s; (2) measurement of the 'total stiffness index' (TSI) at 500 degrees/s; (3) evaluation of the stretch reflex threshold speed (SRTS). No stretch reflex (SR) was found in about half of the subjects, even at the highest speed. ISI was higher in males (p < 0.001); significant differences in TSI were found between subjects with SR and those without (p < 0.02); no statistical differences in SRTS were found for either age or gender. ISI, TSI and SRTS, appear to be reliable indices of the range of normal muscle tone for its quantitative assessment.

Adult↗

Role of peripheral afferents and spinal reflexes in normal and impaired human locomotion.

For many years, electrophysiological investigations of locomotion were restricted to animals, largely the cat. They concentrated on and emphasized the role of spinal interneuronal networks responsible for the generation of the locomotor pattern. Following the introduction of perturbation impulses and electrical nerve stimulation during stance and gait, information became increasingly available concerning the role of the reflex systems involved in the regulation of gait, their afferent pathways and their control by supraspinal motor centres. During gait monosynaptic stretch reflexes are inhibited. From a knowledge of the behaviour of the cerebral potentials evoked during stance and gait, it can be deduced that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels. Polysynaptic reflex responses are mainly responsible for the compensation of perturbations introduced during gait. They are most probably mediated by group II afferents via a spinal pathway closely connected with the spinal locomotor centres. The functioning of these responses depends on an intact supraspinal control. They are suggested to be incorporated in a more complex e.m.g. pattern mainly determined by central mechanisms. In contrast to the gait condition, segmental stretch reflex activity does contribute to activation of extensor muscles of the leg during fast movements, such as running and hopping. In children at an early stage in the development of gait (around 1 to 2 years of age), as well as in patients with spastic paresis, the polysynaptic reflex responses are reduced or absent, and isolated monosynaptic reflex potentials are present. This suggests a reciprocal modulation of mono- and polysynaptic reflex mechanisms, both being dependant on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is absent and associated with a reduced facilitation of polysynaptic spinal reflexes. In spastic muscle hypertonia, the tension developed at the Achilles tendon during gait cannot be explained by gastrocnemius activation alone. In patients with spastic hemiparesis gastrocnemius e.m.g. activity is reduced in the spastic leg as compared to the unaffected one. It can be concluded that the paretic muscle undergoes changes in its mechanical properties, secondary to the supraspinal lesion, which results in the development of spastic muscle hypertonia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Subthreshold transcranial magnetic stimulation during the long latency component of the cutaneomotor reflex.

Modulation of ongoing electromyographic (EMG) activity in the small hand muscles can be induced by electrical stimulation of the digital nerves or by stimulation of the skin of the fingers. Several groups have attempted to establish a role for the motor cortex in the generation of the facilitatory component of the cutaneomotor reflex. Our aim was to establish if the facilitatory component of the reflex could be diminished by a procedure known to inhibit the motor cortex, namely, subthreshold transcranial magnetic stimulation. During sustained small contractions of the first dorsal interosseus muscle transcranial magnetic stimuli (TMS), which were subthreshold for the generation of a motor evoked potential, were delivered via a figure-of-eight coil. Inhibition of ongoing EMG was observed in all subjects. In two separate series of trials, TMS was timed so that the resultant inhibition occurred coincident with either the short or long latency stretch reflex or with the initial or later part of the facilitatory component of the cutaneomotor reflex. The short latency stretch reflex is known to involve a largely monosynaptic loop via the spinal cord, whereas the long latency response involves a transcortical loop. The long latency response was reduced in size following subthreshold TMS, whereas the short latency response was unchanged. This provides evidence of the effectiveness of subthreshold TMS in inhibiting a transcortical reflex. When the TMS was timed so that the inhibition occurred coincident with the facilitatory component of the cutaneomotor response, neither the early nor later changes were inhibited. Thus, the pathway of the long-latency cutaneomotor reflex is not similar to the transcortical pathway of the stretch reflex. Either the response does not travel via the cortex or it involves different cortical neurones.

Adult↗

Catching a ball: contributions of intrinsic muscle stiffness, reflexes, and higher order responses.

In three sets of experiments in nine normal subjects and a patient with a percutaneous wrist-stabilizing splint, we quantified the open-loop gain (OLG) of the stretch reflex acting about the elbow. The subjects exerted a steady mean flexing force and were instructed not to intervene (i.e., not to resist actively) when force or displacement perturbations were imposed on the forearm. The method was either to reconstruct transmission around the entire loop in a two-part experiment, or to use the attenuation of external perturbations in normal and electrically stimulated muscle to compute gain. Across all experiments, the mean magnitude of stretch reflex OLG was close to unity in the frequency range 1-2 Hz, and declined at higher frequencies, as required to ensure stability, given that the phase lag approached 180 degrees at 5 Hz. Inherent muscle stiffness was approximately equal to reflex stiffness. In functional terms, an OLG of 1 means that the yield caused by a force perturbation is approximately halved by reflex action (prevailing inherent muscle stiffness is doubled). Automatic scaling of reflex transmission at Ia/alpha-motoneuronal synapses ensures that the OLG remains close to unity as inherent stiffness increases. Trials in the patient with the wrist fixator gave similar results, indicating that the reflexes were proprioceptive ly mediated. In a fourth experiment in which the task was to catch a heavy ball, we compared the efficacy of inherent muscle stiffness and reflexes alone, with the subject's intentional reactions, which included predictive and voluntary components of response. The latter were far more effective in maintaining the position of the hand after the ball was caught than inherent and reflex stiffnesses alone. We conclude that stability requirements limit the extent to which stretch reflexes can augment inherent muscle stiffness. When inherent muscle stiffness is low, such as in our ball-catching task, the reflex stiffness is also low, and predictive and pre-programmed reactions predominate in load compensation, thus shifting the emphasis from automatic servo or equilibrium-point behaviour to higher order control.

Elbow Joint↗

Is lower leg proprioception essential for triggering human automatic postural responses?

It is unknown to what extent automatic postural responses are triggered by lower leg proprioception. This issue was addressed by studying postural control in five carefully selected patients with subtle diabetic polyneuropathy (restricted to the lower legs) and 15 healthy subjects. All patients had bilaterally absent Achilles tendon reflexes and weak or absent patella tendon reflexes, but muscle strength was fully preserved. Subjects were tested while standing on a supporting, movable force-plate. The contribution of lower leg proprioception to automatic postural responses was investigated by randomly exposing the subjects to either a 4 degrees 'toe-up' rotational perturbation ('normal ankle input'), a simultaneous 4-cm rearward translation and 4 degrees toe-up rotation ('enhanced ankle input'), or a simultaneous 4-cm rearward translation and 4 degrees 'toe-down' rotation ('nulled ankle input'). We recorded surface EMG (stretch reflexes and balance-correcting responses) from leg and trunk muscles, ankle torque and angular velocities of the upper and lower legs and trunk. We argued that automatic postural responses that have abnormally small amplitudes in patients and are modulated in controls with the velocity of different types of ankle rotations must receive a major input from lower leg proprioception. Conversely, automatic postural responses that are weakly modified in amplitude or onset by different ankle perturbations and are present despite nulled ankle inputs and, finally, are unaffected in patients with distal polyneuropathy must be triggered or modulated by inputs other than from lower leg proprioception. Normal postural synergies and strategies were maintained in patients, although within a given synergy the timing and amplitude of some automatic postural responses were abnormal. A few automatic postural responses appeared to be triggered or modulated by lower leg proprioception. Thus, early stretch reflexes in soleus and medial gastrocnemius were severely diminished in patients, while in controls these stretch reflexes were modulated by different ankle perturbations. Furthermore, balance-correcting responses in tibialis anterior were diminished and delayed in patients, while in controls these balance-correcting responses were modulated by different ankle perturbations. Other automatic postural responses were apparently not triggered or modulated by lower leg proprioception, but likely received a major input from more proximal sensory systems. Thus, in both groups prominent balance-correcting responses were present in several muscles (soleus, gastrocnemius, quadriceps, paraspinals and trapezius) during the 'nulled ankle input' condition, where ankle position was stabilised over the first 250 ms. During the 'enhanced ankle input' condition, where prominent ankle dorsiflexion occurred during the first 200 ms, amplitudes of balance-correcting responses were only marginally weaker in patients than in controls. We analysed body segment displacements to unveil the potential nature of proximal triggers for automatic postural responses. As opposed to the 'inverted pendulum' concept of postural control, early movement occurred in the knees, hips and trunk well before the onset of automatic postural responses. For example, during the 'nulled ankle input' condition, the lower leg moved forward with early knee flexion, followed by knee extension. The trunk extended backwards at 80 ms, which was followed by forward flexion. The absent stretch reflex and weaker balance-correcting responses in patients produced changed trunk velocity profiles (mainly a reduced initial backward motion of the trunk), but lower-body segment movements showed no consistent differences between the two groups. Considering these body segment displacements, any automatic postural response with an onset within the first 200 ms could well be triggered by receptors located at the knee, hip or trunk. (ABSTRACT TRUNCATED)

Achilles Tendon↗

Peripheral mechanisms in tremor after traumatic neck injury.

Tremor is a rare manifestation after neck injury, and its physiological mechanism has not been elucidated. We studied the effects of torque loading and ischaemic nerve block on coarse postural tremor in the right upper extremity, which had developed in association with a C7-C8 radiculopathy after traumatic neck injury in a 55 year old man. Loading reduced the tremor frequency from 6.1 Hz to 4.2 Hz with corresponding electromyography (EMG) bursts at the same frequencies as the tremor. Ischaemic nerve block also reduced the tremor frequency from 6.2 Hz to 2.8 Hz, and the time course of the frequency was not in parallel with that of the size of the maximal M wave. A significant reduction of the tremor frequency by loading and ischaemic nerve block indicates a mechanical reflex mechanism underlying the tremor, and association of synchronous EMG bursts suggests an increase in gain in the stretch reflex loop. The stretch reflex loop plays an important role in generation of oscillation in tremor after neck injury.

Cervical Vertebrae↗

Stretch and Hoffmann reflexes during phasic voluntary contractions of the human soleus muscle.

Measurements were made of EMG responses in human soleus muscle, following torque disturbances of the foot during phasic voluntary plantarflexions. These were compared with measurements of the Hoffmann reflex during identical voluntary movements. We observe that stretch adequate to evoke a stretch reflex in the relaxed limb often fails to evoke any response during a phasic contraction until about 120 msec after the onset of the stimulus. During this period the H-reflex is facilitated. These findings are discussed in terms of the servo-theory of stretch reflex function and the concept of trans-cortical stretch reflexes.

Adult↗

Evidence for fusimotor drive in stroke patients based on muscle spindle thixotropy.

To study fusimotor function in stroke patients, we compared the amplitude of stretch reflexes elicited in flexor carpi radialis (FCR) after contraction of FCR with the wrist held flexed ('hold-short') or extended ('hold-long'). Seven subjects with impaired hand function and spasticity due to stroke, and seven healthy subjects were investigated. Surface electrodes recorded electromyographic activity of wrist flexors and extensors while subjects performed isometric wrist flexions with the wrist alternately in 15 degrees of flexion or extension. After contractions the wrist was moved passively to the mid-position, and stretch reflexes were elicited via controlled mechanical taps delivered over the FCR tendon. For both groups, the amplitude of the stretch reflex was greater after 'hold-short' than 'hold-long' contractions. This finding is consistent with the 'after-effects' of intrafusal fibre activation, and suggests that fusimotor neurones are activated during voluntary contractions of the paretic limb, just as in the limb of a healthy subject.

Adult↗

Reduced reflex sensitivity persists several days after long-lasting stretch-shortening cycle exercise.

The mechanisms related to the acute and delayed secondary impairment of the stretch reflex function were investigated after long-lasting stretch-shortening cycle exercise. The results demonstrated a clear deterioration in muscle function immediately after fatigue, which was accompanied by a clear reduction in active and passive reflex sensitivity. For active and passive stretch reflexes, this reduction was biphasic (P < 0.05 to P < 0.001). However, for the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential, only one significant reduction was seen immediately after fatigue (71.2%, P < 0.01). A similar significant (P < 0.01) decrease in the stretch-resisting force of the muscle was also detected. Clear increases were found in the indirect markers of muscle damage (serum creatine kinese activity and skeletal troponin I), which could imply the occurrence of ultrastructural muscle damage. It is suggested that the acute reduction in reflex sensitivity is of reflex origin and due to two active mechanisms, disfacilitation and presynaptic inhibition. However, the delayed second decline in the sensitivity of some reflex parameters may be attributable to the secondary injury, because of some inflammatory response to the muscle damage. This might emphasize the role of presynaptic inhibition via group III and IV muscle afferents.

Adult↗

Tremor in the tension developed isometrically by soleus during the tonic vibration reflex in the decerebrate cat.

1. Irregularities in the development of tension during the tonic vibration reflex of the soleus muscle of the decerebrate cat have been analysed into their frequency components. The reflex was recorded isometrically and elicited by longitudinal vibration, normally at 150 Hz. The amplitude of vibration was set so as to elicit a maximal reflex response, suggesting 1:1 driving of the majority of the Ia afferents at the frequency of vibration. 2. The resulting power spectrum regularly showed a well marked tremor peak separated by a trough from any slow irregularities. The predominant frequency of this tremor varied from 4 to 11 Hz in different preparations, with a mean of 7.4 Hz; on average, frequencies within 1.7 Hz on either side contained over half the power of the predominant frequency. Altering the frequency of vibration did not alter the distribution of tremor frequencies. 3. The root mean square value of the tension irregularities, over the range 4-14 Hz, varied from 12 to 110 mN in different preparations (median value, 23 mN); this was superimposed on mean active reflex tensions varying from 2 to 10 N. 4. The 'tremor' due to a single motor unit was estimated from spectral analysis of tetanic contractions of the whole muscle and decreased with increasing frequency of activation. Comparison of the single unit values with the tremor seen during vibration in the same preparations showed that equivalent amounts of tremor to the latter could typically have been produced by the continued synchronous contraction of about five 'average' motor units firing at the predominant tremor frequency. 5. When a tonic stretch reflex was present its tremor frequencies did not differ consistently from those of the tonic vibration reflex. On average, the tremor was smaller for the stretch reflex than for the tonic vibration reflex; the difference was usually slight and might have been related to the stretch refex tension being smaller. 6. Evidence was obtained that the tremor was not due to any insecurity of 1:1 driving of the Ia afferents by the vibration. First, the tremor did not increase when the amplitude of vibration was decreased sufficiently to ensure that the degree of 1:1 driving must have been reduced. Secondly, the introduction of a comparable 'artificial tremor' by sinusoidally oscillating the muscle at low frequency did not produce the e.m.g. response that would have been expected if the applied 'tremor' had been modulating the firing of the Ia or any other group of afferents. 7. It is concluded that the observed tremor cannot be attributed to 'oscillation in the stretch reflex arc', though without prejudice to the role of this mechanism under other conditions and especially when the recording is not isometric. However, the genesis of the tremor has not been established and much of it might result simply from the chance synchronization of motor units that are firing below their tetanic fusion frequency.

Action Potentials↗

Spatio-temporal separation of roll and pitch balance-correcting commands in humans.

This study was designed to provide evidence for the hypothesis that human balance corrections in response to pitch perturbations are controlled by muscle action mainly about the ankle and knee joints, whereas balance corrections for roll perturbations are controlled predominantly by motion about the hip and lumbro-sacral joints. A dual-axis rotating support surface delivered unexpected random perturbations to the stance of 19 healthy young adults through eight different directions in the pitch and the roll planes and three delays between pitch and roll directions. Roll delays with respect to pitch were no delay, a short 50-ms delay of roll with respect to pitch movements, (chosen to correspond to the onset time of leg muscle stretch reflexes), and a long 150-ms delay between roll and pitch movements (chosen to shift the time when trunk roll velocity peaks to the time when trunk peak pitch velocity normally occurs). Delays of stimulus roll with respect to pitch resulted in delayed roll responses of the legs, trunk, arms, and head consistent with stimulus delay without any changes in roll velocity amplitude. Delayed roll perturbations induced only small changes in the pitch motion of the legs and trunk; however, major changes were seen in the time when roll motion of the trunk was arrested. Amplitudes and directional sensitivity of short-latency (SL) stretch reflexes in ankle muscles were not altered with increasing roll delay. Small changes to balance correcting responses in ankle muscles were observed. SL stretch reflexes in hip and trunk muscles were delayed, and balance-correcting responses in trunk muscles became split into two distinct responses with delayed roll. The first of these responses was small and had a directional responsiveness aligned more along the pitch plane. The main, larger, response occurred with an onset and time-to-peak consistent with the delay in trunk roll displacement and its directional responsiveness was roll oriented. The sum of the amplitudes of these two types of balance-correcting responses remained constant with roll delay. These results support the hypothesis that corrections of the body's pitch and roll motion are programmed separately by neural command signals and provide insights into possible triggering mechanisms. The evidence that lower leg muscle balance-correcting activity is hardly changed by delayed trunk roll also indicates that lower leg muscle activity is not predominant in correcting roll motion of the body. Lower leg and trunk muscle activity appears to have a dual action in balance corrections. In trunk muscles the main action is to correct for roll perturbations and the lesser action may be an anticipatory stabilizing reaction for pitch perturbations. Likewise, the small changes in lower leg muscle activity may result from a generalized stabilizing reaction to roll perturbations, but the main action is to correct for pitch perturbations.

Adult↗

Alterations in group Ia projections to motoneurons following spinal lesions in humans.

1. The hypothesis that the exaggerated tendon jerks and stretch reflexes that follow chronic spinal cord lesions in humans result from alterations in transmission from group I muscle afferents to motoneurons was tested by making observations on nine normal subjects and 25 patients with spinal cord lesions. All the patients had increased tendon jerks, one-third of them had both increased tendon jerks and increased, velocity-dependent stretch reflexes (i.e.g spasticity). 2. Changes in the firing probability of single, voluntary-activated soleus or tibialis anterior motor units during stimulation of the muscle nerve below the threshold of the alpha-motoneuron axons were used to derive the characteristics of the postsynaptic potentials produced by group I volleys in single motoneurons. Paired stimuli were used to test how multiple volleys in group I muscle afferents were transmitted to motoneurons. 3. Stimulation of the posterior tibial nerve produced a short-latency period of increased firing probability representing the homonymous composite Ia excitatory postsynaptic potential (EPSP) in all soleus motoneurons tested. There was no detectable alteration in the magnitude, duration, or profile of the short-latency facilitation in the patients with spinal lesions when compared with normal subjects. 4. In patients with traumatic spinal cord lesions less than 8 wk in duration the magnitude of the facilitation representing the composite Ia EPSP was significantly larger than normal, although only one out of the four patients in this group had spasticity. 5. In the patients with the greatest spasticity, group I volleys produced a second period of facilitation 11-15 ms after the facilitation representing the composite Ia EPSP. This is presumed to represent enhanced transmission through polysynaptic pathways from group I afferents to motoneurons. 6. In normal subjects the facilitation of motoneurons produced by the second of two group I volleys is greater 5 and 10 ms after the first volley and less 20, 30, and 50 ms after the first volley. These changes involve at least two factors: 1) changes in excitability of peripheral nerves and 2) changes in transmission at the Ia-motoneuron synapse. 7. In patients with spinal lesions the facilitation produced by the second of two muscle-afferent volleys was less depressed at the 30-ms interstimulus interval. 8. Thus two separate abnormalities have been uncovered in human subjects with chronic spinal lesions: 1) a change in the transmission of multiple volleys from muscle afferents to motoneurons and 2) an increase in transmission through polysynaptic pathways from Ia afferents to motoneurons. Both could contribute to the increased tendon jerks and exaggerated stretch reflexes.

Afferent Pathways↗