Search

The upper motor neuron syndrome is composed of negative, positive, and rheologic features. The positive features have to do with muscle overactivity, which results from abnormal signal processing in the spinal cord, from altered supraspinal inputs and/or dysfunctional segmental spinal modulatory mechanisms. The negative features are characterized by a reduction of muscle activity and loss of selective muscle control. Third are rheologic features characterized by changes in the physical properties of muscle. These 3 types of clinical features share perpetuating cause-and-effect relationships. This discussion highlights pathophysiology involved in muscle overactivity in the context of the upper motor neuron syndrome., (Copyright © 2018 Elsevier Inc. All rights reserved.)

In this review we describe clinical and neurophysiological features of motor control in human spinal cord injury based on two models. First, motor control is considered in subjects with injury-induced complete division of the spinal cord from brain and brainstem structures, and second, in those in which the division is partial. We describe motor control in terms of segmental and plurisegmental reflex activity that dominates motor unit output to the muscles following complete separation from the brain motor structures by accidental injury. With incomplete separation of the spinal cord from brain structures, motor control is defined as the voluntary manipulation of reflex and automatic activity integrated with internal and external feedback signals. We review here motor control found after complete spinal cord injury with paradigm of single and regular-repeating stimuli applied to elicit cutaneous and muscle stretch reflex responses. We argue, that isolated spinal cord neural circuitry is capable of organizing characteristic reflex events that depend on the characteristics of the stimulus. Also, the profile of residual brain and brainstem, modified by the reduction in descending long spinal tract fibers arriving at their targets in the spinal gray matter, produces characteristic changes in motor output to the muscles that leads to the development of new neural strategies for control of segmental and plurisegmental neural circuitry. In the second part of this review, we discuss available treatment modalities for impaired cord function and briefly outline neurobiological interventions under development for repair of spinal cord injury.

There is considerable evidence that injection of botulinum toxin (BTX) into muscles with spastic overactivity reduces resistance to passive movement in joints supplied by the injected muscles. The demonstration of improvement in active performance of the paretic limbs has been only anecdotal to date, and represents the most difficult challenge in research on BTX therapy in spastic paralysis. Data are reviewed that indicate several neurophysiological actions of BTX, other than the blocking of acetylcholine release at the neuromuscular ending: effects on the central nervous system, including retrograde axonal transport, reduced motoneuronal excitability, action on central synapses such as decreased Renshaw inhibition and increased presynaptic inhibition; action on gamma motoneuronal endings; action on most active terminals; spread of BTX to neighboring muscles; spread of BTX effects to remote muscles. Several of these neurophysiological actions are likely to contribute to improvement in active movements, as they may antagonize the primary mechanisms of functional impairment in patients with spastic paralysis: weakness, spastic cocontraction, spastic dystonia, and muscle shortening. We review the evidence for reduction of spastic cocontraction in both the injected muscle and its antagonist, and for improvement of antagonist weakness after BTX injection. The capacity of intramuscular BTX to reduce spastic dystonia and lengthen shortened muscles is also discussed based on prior literature. When injected into the more overactive of a pair of spastic antagonists around a joint, BTX should affect all the main mechanisms impairing active function around the joint., (Copyright 2004 Movement Disorder Society)

Measurable sources of muscle tension include viscoelastic tone, physiological contracture (neither of which involve motor unit action potentials), voluntary contraction, and muscle spasm (which we define as involuntary muscle contraction). The latter two depend on motor unit action potentials to generate the tension. Total muscle tension is most accurately measured as stiffness. Thixotropy of muscle is an ubiquitous and functionally important phenomenon that is not commonly recognized. A clinical pain condition associated with increased muscle tension is tension-type headache, which is largely muscular in origin; it is often caused by myofascial trigger points, but not by a pain-spasm-pain cycle, which is a physiologically and clinically untenable concept. Clinical conditions associated with painful muscle spasm include spasmodic torticollis, trismus, unnecessary muscle tension, nocturnal leg cramps, and stiff-man syndrome.

The reflex mediated mechanical response was studied in the ankle flexors and ankle extensors of healthy and spastic subjects at maintained contractions from low to high concentration levels. This was done by a technique where muscle stretches could be applied during contractions with stretch reflex responses present or during contractions where the stretch reflex was absent. Stretch responses without stretch reflexes were obtained during contractions elicited by electrical stimulation. The validity of this method is discussed in details and it is concluded that the stretch responses during electrical stimulation can give a correct estimate of the non-reflex muscle response. The method is difficult to carry out in many human subjects and a number of precautions have to be taken. In healthy subjects a large reflex mediated mechanical response was found in the ankle flexors and ankle extensors, with the largest response at low and intermediate contraction levels. Surprisingly the reflex mediated mechanical response was found to be of equal size in the ankle extensors of spastic patients and control subjects at all contraction levels. In the ankle flexors no reflex mediated mechanical response was present in the patients contrary to the findings in the control subjects. A method was developed to predict the reflex mediated mechanical response from the reflex mediated EMG response. The method was successfully applied in the ankle flexors. In the ankle extensors the measured reflex mediated mechanical response was a factor of 2.5 lower than the EMG predicted mechanical reflex response. It was concluded that the method cannot be applied in situations where a large synchronized EMG response occurs--as it does in the ankle extensors. An increased EMG response was found in the ankle extensors in spastic patients, but this was not followed by an increased mechanical reflex response. This emphasizes that conclusions drawn from EMG results should be done with caution. Stretch reflexes are increased in spastic patients during clinical examination. This is in contrast to the findings under our experimental conditions, where the reflex mediated response during maintained contraction was decreased in the ankle flexors and unchanged in the ankle extensors of spastic patients. Others have found that the H-reflex is modulated in healthy subjects in relation to different motor tasks. It was proposed that healthy subjects set the reflex in a facilitated state in relation to ongoing contraction under our experimental conditions and perhaps in a more inhibited state in the clinical test situation.(ABSTRACT TRUNCATED AT 400 WORDS)

The soleus Hoffmann-reflex (H-reflex) was conditioned by a preceding stimulation of the common peroneal nerve in 74 healthy control subjects and 39 patients with spasticity in the lower extremities due to multiple sclerosis. At a conditioning-test interval of 1-3 ms a decrease of the size of the soleus H-reflex was seen in the healthy subjects. The decrease was most likely caused by disynaptic reciprocal Ia inhibition (Crone et al., 1987). In the spastic patients a similar short-latency inhibition was rarely seen. On the contrary, in several patients a facilitation was seen at a conditioning-test interval of 3-4 ms. A short-latency inhibition as pronounced as in healthy subjects was seen in four patients. These four patients did not differ from the other patients regarding the degree of spasticity or any other clinical parameter. However, they all used an external peroneal nerve stimulator daily as a walking aid. It is suggested that the lack of short-latency reciprocal inhibition reflects a deficient control of the interneurons which mediate this inhibitory spinal mechanism between antagonistic muscles in man. This might contribute to the pathophysiology of spasticity and it might be related to the frequent occurrence of co-contraction of functionally antagonistic muscles during gait in spastic patients. The existence of a pronounced reciprocal inhibition in patients receiving frequent stimulation of the peroneal nerve may suggest that regular activation of peripheral nerves is of importance for the maintenance of the activity in spinal pathways.

This study investigated the potential value of eccentric (ECC) and concentric (CONC) isokinetic testing for quantifying motor deficit in patients with spastic paresis secondary to motor neuron disease. We hypothesized that, at a moderately fast (120 degrees s-1) angular velocity, spastic patients would demonstrate different ECC-CONC torque relationships from healthy controls or patients with non-spastic neuromuscular disorders. Eleven patients with motor neuron disease having clinical evidence of spasticity, and 11 disease-control patients (with non-spastic disorders, e.g. lower motor neuron disease or myopathy) underwent isokinetic testing. One healthy subject was matched to each of the 22 patients. The average torque generated during maximal voluntary ECC and CONC knee flexion (KF) and extension (KE) was measured using an isokinetic dynamometer (Kin-Com). Reliability was established (all ICC > or = 0.97) for patient torque measurements. Relative strength (% of control subject torque) in spastic patients was significantly higher for ECC than for CONC actions in both KF and KE; conversely, in non-spastic disease-control patients relative strength was not affected by the type of muscle action. The ECC/CONC average torque ratios for KE and KF at 120 degrees s-1 were significantly greater in spastic patients than controls, but did not differ from controls in non-spastic patients. In spastic patients the ECC-CONC imbalances were related to ambulatory dysfunction. In four spastic patients followed with serial testing, the disproportion between ECC and CONC voluntary capacity persisted over time.(ABSTRACT TRUNCATED AT 250 WORDS)

A spring-loaded device that "breaks" at preset forces was used to assess readings obtained by hand-held dynamometry by three raters with varying experience in the method. Overall accuracy (3%), but not reproducibility or variability, was improved by greater experience. Readings obtained jointly by three raters had 53% greater variability than those obtained by a single rater. Nine muscle groups in 19 patients with motor neuron disease were assessed at 10 sessions (three replications per session) over six days by the experienced rater. Muscle force was expressed relative to that of 22 matched normal controls. The reproducibility was good with a mean % difference of 13.2 and repeatability coefficient of 2.17 kg-force for readings six days apart; the overall correlation coefficient was 0.98. The mean coefficient of variation (CV) of 10 readings was 9.9%. The poorer reproducibility and greater variability seen in clinically weaker muscles may account for differences in patients with bulbar palsy and classical amyotrophic lateral sclerosis; the degree of spasticity had no effect. The rater was estimated to contribute 37% of the total variability when testing patients. The use of a composite score by combining normalised dynamometry readings of eight limb muscles improved mean % difference to 6.7 and mean CV to 5.8%. The reproducibility and variability of hand-held dynamometry readings obtained by a single rater compare well with those of fixed devices. Readings from single raters, irrespective of experience, have similar reproducibility and variability. If, however, multiple raters are used in longitudinal assessments of individual patients, as occurs in clinical trials, the variability of their combined readings should be estimated when calculating the same size required.

In controls and patients with different syndromes (spastic/flaccid paresis, low back pain syndrome), the myoelectrical activation patterns of complex muscles (M. biceps brachii, M. quadriceps femoris, M. masseter) or synergistic/antagonistic muscle groups in the back region during isometric muscle contractions and defined movements were determined by monopolar 16 (32) channel surface EMG recordings. On the basis of these recordings, maps of myoelectrical activation ("EMG-maps") were calculated. This method permits a detailed quantitative-topographic EMG analysis including the characterization of therapy effects.

A surface electromyogram (EMG) was recorded from four leg muscles to measure the effects of various seat inclinations and an abduction orthosis on eight children with cerebral palsy and controls during performance of an upper-extremity task and while listening to a story. EMG responses were lowest in the forward-leaning and horizontal positions with the abduction orthosis, and highest in reclined and horizontal positions without the orthosis for both groups of children during the performance of an upper-extremity task. While listening to a story, there was no median EMG activity in any muscles of the controls, but there were wide variations in those of the children with cerebral palsy. The results indicate that the use of an abduction orthosis and horizontal and forward-leaning seats decrease lower-extremity muscle activity, and so it is possible that it might also improve upper-extremity function.

Surface electromyographic "EMG" activity in biceps brachii (agonist muscle) and triceps brachii (antagonist muscle) as well as the discharge behaviour of motor units "MUs" (needle recording) in biceps brachii muscle were recorded during slow (0.33 Hz) and fast (0.66 Hz) voluntary elbow flexion movements (auditory matching task) in fifty patients with spastic hemiplegia. In the spastic limbs, a long lasting, small amplitude tonic co-contraction of antagonist muscles was seen during slow flexions (SF) in 29 cases. This effect was strongest during the fast elbow flexion movements (FF). In 33 patients a triphasic pattern of muscle activation was observed on the unaffected side but not on the spastic side. The amplitude of the agonist surface EMG was significantly reduced and the amplitudes of the MU potentials recruited during maximal effort were generally smaller on the spastic side compared to the unaffected side. The agonist-antagonist activation pattern was analysed with respect to three clinically identifiable functional recovery stages of voluntary movements in the spastic limbs, namely synergistic, isolated and useful movements. The MU amplitudes and the amplitude of the surface EMG activity in the agonist muscle recorded during FF movements became significantly larger whereas the amplitude of the antagonist tonic activity became smaller with increasing functional recovery of the limb. It is concluded that impaired recruitment of type II motor units in the agonist muscles and the inability to selectively activate the agonist muscle contribute to the deficit in motor performance in spastic paresis.

Reflex electromyographic (EMG) muscle responses were recorded from abductor pollicis brevis (APB) and tibialis anterior (TA) muscles of fifty patients with spastic hemiplegia. Responses in the muscles were evoked during voluntary muscle contraction (about 20% of maximum voluntary effort) by submaximal but suprathreshold electrical stimulation of the median (at the wrist) and common peroneal (at the neck of the fibula) nerves respectively. Three EMG peaks (R1, R2 and R3) could be recorded after the direct muscle response (M). There was only a slight difference in R1-R2 latency interval of about 5 ms between upper and lower limbs on the unaffected side of the patients making it unlikely that this late response of the lower limb involves a long loop pathway, although this possibility cannot be discounted for the later, R3, response. Reflex behaviour was analysed for three clinical identifiable recovery stages of voluntary movements in the spastic limbs (synergistic, isolated and useful movements). The major finding was that an increase in the amplitude of the early response "R1" was associated with a decreased amplitude and delayed latency of the late response "R2" on the spastic side. The amplitude of R1 in the three different recovery stages decreased significantly, whereas the amplitude of R2 increased significantly with improvement of the functional stage of the limb. A significant negative linear correlation was found between R1 and R2 amplitude changes in upper as well as lower limbs. A refractoriness of the motor neuron pool as a possible explanation for the decreased R2 amplitude could be discounted. These findings together with recent work on reflex development in children support the hypothesis of reciprocal modulation of early and late reflex signals by supraspinal motor centers.

The upper motor neuron lesion that causes hemiplegia impairs the patient's selective control and exposes primitive modes of muscle activation. Significant inconsistency between the clinical findings and the patient's gait may result. Dynamic electromyography revealed the primitive mechanisms leading to these inconsistencies. The rate of stretch does not differentiate spasticity from contracture, since either a quick or slow stretch frequently causes a sustained muscle response. Using knee flexion to differentiate gastrocnemius and soleus spasticity is not reliable, since the change in neurologic input with flexion may inhibit the extensor muscle's response to stretch so that the soleus is also relaxed. The change in body position from lying supine to sitting can double the intensity of soleus spasticity, and standing further increases the tone. Primitive patterns of mass extension and flexion, while voluntary, inhibit normal progression during walking. Simultaneous activation of the soleus and gastrocnemius with the knee's quadriceps causes premature ankle plantar flexion as the limb is loaded in stance. The primitive flexion synergy between the hip, knee, and ankle (dorsiflexion) inhibits terminal swing knee extension while the hip remains flexed. Consequently, surgical planning for the hemiparetic limb must rely heavily on gait analysis findings (systematic observation or by instrumentation).

The trajectories observed for the limb during human locomotion are determined by a mixture of influences, some arising from neural circuits entirely within the central nervous system and others arising from a variety of sensory receptors. Muscle reflexes are highly modulated during locomotion in an adaptive manner within each phase of the step cycle. Furthermore, the modulation can be modified quickly for different tasks such as standing, walking and running, probably by changes in presynaptic inhibition. This modulation is often lost or severely reduced in patients with spasticity after spinal cord or head injury. In normal subjects cutaneous reflexes can be completely reversed from exciting to inhibiting a muscle during each step cycle, particularly in muscles that normally show two bursts of activity per cycle (e.g., tibialis anterior). In some patients stimulation of a mixed nerve (e.g., common peroneal) can directly produce muscle contraction, generate a reflex response (flexor reflex) and transiently reduce spasticity in antagonist (extensor) muscles. Thus, simple systems employing stimulation can enhance gait to a certain extent in patients with incomplete injuries.

The size of the soleus H-reflex was measured after a slow (17 deg/s) passive stretch of ankle plantarflexors and compared to its control size without muscle stretch in ten neurologically healthy subjects and in six spastic spinal-cord-injured patients. Two seconds after the end of the stretch, the size of the H-reflex was reduced to about 30% of its pre-stretch size in the healthy subjects. The depression remained for 10-15 s. In the spastic, spinal-cord-injured patients, stretch caused significantly less reduction in the size of the H-reflex. The H-reflex also regained its pre-stretch size much faster than in healthy subjects. We suggest that the smaller depression of the H-reflex observed in spastic patients may be involved in the pathophysiology of spasticity.

A mechanomyographic response of the hind foot to passive straightening and bending, as well as an electromyographic activity of the gastrocnemius and tibialis anterior muscles were recorded in old (35-44-month-old) and young female rats. In old rats, spontaneous, tonic electromyographic activity patterns were concurrently observed in both antagonistic muscles; they were low-amplitude, dense tonic activity and continuous, high-amplitude, sparse electromyographic activity. The tonic electromyographic activity was correlated with a decline in the strength and mass of muscles, as well as with motor disturbances, including paresis of the rigidly straightened backward hind legs, dragged behind by an animal. In muscles of old rats, morphological features of a chronic denervation atrophy were found. Baclofen (10 and 15 mg/kg, i.p.) diminished the spontaneous tonic electromyographic activity and potently decreased the whole body muscle tone, whereas Madopar (50 mg/kg of L-DOPA+12.5 mg/kg of benerazide) was ineffective. It is suggested that old rats in which the above-described pathologic alterations are observed might be a useful animal model in the search for basic etiopathological mechanisms of spasticity and similar disturbances found in humans.

Reciprocal inhibition between forearm extensor and flexor muscles was tested by means of an H-reflex technique in patients with spasmodic torticollis and normal controls. In both, patients and controls three different phases of reciprocal inhibition could be demonstrated with maximal inhibition at conditioning test intervals of 0 ms, 15 ms and 100 ms, respectively. However, the quantitative amount of this inhibition was different for the patients and the controls. Significantly less inhibition was found for the second and the third phase of reciprocal inhibition in the patient group. Discriminant analysis showed a clear separation between normal subjects and patients if the amount of reciprocal inhibition of the second and third phase were taken into account. We were not able to detect any side differences neither for the patients nor for the controls. The findings demonstrate a functional disturbance of motor control mechanisms of a clinically unaffected extremity in spasmodic torticollis. This is believed to reflect a bilateral disturbance most likely within the basal ganglia or their outflow. Therefore, our data support the idea, that spasmodic torticollis is associated with or even due to a generalized rather than a focal disturbance of motor control mechanisms.

Spontaneous activity on the EMG examination is traditionally ascribed to disease of the lower motor neuron when present in muscles well below the level of para- or quadriplegia despite the absence of any detectable peripheral nerve injury. It is uncertain whether it reflects transient paralysis of transmission (related to clinical spinal shock) or irreversible postsynaptic damage. We performed serial EMG studies of lower extremities and paraspinal muscles on eight young, previously healthy adults, commencing 2 to 9 weeks after acute cervical cord injury. All had stimulated single-fiber EMG (SFEMG) studies at 6-month intervals to determine whether irreversible postsynaptic damage of the anterior horn cell had occurred. MRI and nerve conduction excluded patients with evidence of distal cord injury or peripheral neuropathy. All patients had spontaneous activity in all muscles tested, persisting after spinal shock had resolved. Jitter was present on SFEMG in three of eight patients 6 months after injury. Four of five patients retested 12 months after injury had abnormal jitter, including three who initially had normal SFEMG studies. We conclude that there is electrophysiologic evidence of trans-synaptic distal cord dysfunction following acute spinal cord injury. SFEMG studies suggest that anterior horn cell dropout occurs during the 1st year after injury.

The excitability of flexors and extensors of the upper and low extremities was studied in healthy people and in patients with spasticity during local thermostimulation of their receptive fields using H-reflex (HR). In healthy people the HR was inhibited during cooling and was enhanced during warming. Thermostimulation of the contralateral side caused a contraverse reaction. In patients cooling of skin followed the rise of HR. The obtained data show that the condition of the thermoreceptive fields can influence reflex excitability of motoneurons. The character of this influence depends on the initial condition of the locomotor generator.

Equinus in hemiplegic children is multifactorial. In some cases it is due to a short muscle, in others to simple foot-drop, tonic spasticity, rigidity, compensation for a short limb, fixed flexion contracture at the hip, dominantly inherited forefoot deformity, forefoot equinus secondary to chronic toe-walking, or abnormalities of the visco-elastic properties of the muscle, with true intramuscular contracture. This neurophysiological study confirms that hemiplegia in children is not a homogeneous condition. Some have tonic spasticity; some, although stiff, show electrical silence on stretching; some appear to have a short muscle, with no hypertonicity; and others have hypertonicity in relation to position (i.e. rigidity). A short muscle is not always associated with tonic spasticity with reciprocal inhibition. Weakness can occur without spasticity. Speed of movement of toes, ankle and hip is also significantly reduced.

Short, rapid dorsiflexion of the normal human ankle induces a single, synchronised reflex EMG response in the initially relaxed triceps surae muscle (TS). In subjects in whom hemiparesis is present as a result of a unilateral ischaemic cerebral lesion, a reflex EMG response can be elicited on either side with timing identical to that of the normal response. The magnitude of the response in hemiparetic subjects, however, differs from the normal on both the side contralateral and that ipsilateral to the causative lesion. Furthermore, the magnitude of this response varies over the time-course of spasticity. Contralaterally to the lesion, a gradual increase in the magnitude of the response to imposed displacement occurs. One year after stroke, the response has reached a level significantly larger than normal. Changes in the magnitude of the contralateral Achilles tendon jerk reflex EMG are apparent earlier than changes in the response to imposed displacement, with exaggerated tendon jerks already being apparent between 1 and 3 months after stroke. On the side ipsilateral to the lesion, a profound depression of the response to imposed displacement is visible as early as a month after stroke. This depression diminishes over the 1st year, but the response has not even then returned to normal values. These changes are not reflected in the ipsilateral tendon jerk response, which remains normal throughout this period.(ABSTRACT TRUNCATED AT 250 WORDS)

The consistency between patterns of lower-limb muscle strengths in children with myelomeningocele and Sharrard's classic description of segmental innervation was examined in 291 patients. Although it has been assumed that medial hamstring innervation was from a similar neurosegmental level as gluteus medius, and gluteus maximus was from a similar level as gastrocnemius-soleus, the authors found that medial hamstring strength more frequently correlated with iliopsoas and quadriceps, and glutei with anterior tibialis. It is proposed that children with myelomeningocele be grouped according to specific muscle strength rather than by neurosegmental level.

In the present study a surface-EMG investigation of the rectus femoris muscle was performed in patients with spastic hemiparesis before and after rehabilitation treatment. The EMG activity was detected during 50% of the maximum voluntary contraction by means of FFT automatic analysis; the mean power frequency (MPF) and the time-course of the frequencies of the surface-EMG signals showed significant changes after physiokinesitherapy. In hemiparetic patients a particular distribution of the frequencies of the surface-EMG signals towards the lowest values were observed. These findings could be related to the preferential atrophy of type II fibers which has been demonstrated in morphological studies. Furthermore the surface-EMG analysis after a period of rehabilitation treatment showed some significant modifications of MPF and time-course of the EMG signals. These changes corresponded to an improvement of the spasticity as evaluated by clinical rating-scale. This neurophysiological investigation seem to be a simple and reliable method for better evaluating some effects of the rehabilitation therapy.

We studied reciprocal inhibition of H-reflexes in the forearm flexor and extensor muscles in 14 patients with spastic hemiplegia secondary to a focal cerebral lesion and 14 normal volunteers. In the spastic limb, the Hmax/Mmax ratio was increased in both flexor and particularly extensor wrist muscles. The 3 normal inhibitory phases of reciprocal inhibition between extensor and flexor forearm muscles were markedly reduced on the spastic side of patients. The early disynaptic phase showed the greatest alteration. Reduced or absent inhibition between forearm muscles associated with increased spinal motoneuron excitability may be typical to spastic hemiplegia.

Nine patients with complete cervical spinal cord injury (SCI) had their vastus medialis, tibialis anterior, and gastrocnemius muscles evaluated with an electromyographic (EMG) examination in the acute (four to eight weeks) and chronic (more than one year) phases. The hypothesis that spontaneous EMG activity changes with time was assessed. During the chronic phase evaluation, a conduction study was performed to rule out peripheral nerve damage, and the amount of reflex activity was assessed on a scale of 0 to 5 (0 = areflexia; 5 = greater than 5 beats of clonus) to estimate the amount of spasticity. Subjects demonstrated normal conduction through the sensory (sural nerve) and/or motor segments of the peroneal and tibial nerves. In the acute phase, each muscle had spontaneous activity with no significant variation between different muscles of the same patient. In the chronic phase, there was a positive correlation between the degree of spontaneous activity in a muscle and the length of its axon (p less than .01) and a negative correlation between the amount of spontaneous activity and the degree of reflex activity (p less than .01). Specifically, the lower motor neuron in the chronic phase of an SCI seems to behave much like an axonopathy where the degree of spontaneous EMG activity is dependent on the length of the axon, with the additional concept that spontaneous activity is inhibited by spasticity.

A study was made of pathological tonic reflexes (PTR) in adolescents afflicted with infantile cerebral paralysis (ICP) by means of assaying the tone of thigh muscles before and after treatment and in the presence of L-DOPA (nacom, 62.5 mg/day) intake. The drug minimized the manifestations of PTR because of changes in the function of brain structures involved in tonic reactions. It is recommended that during establishment of indications for +orthopedic-surgical treatment of ICP patients with marked PTR determining the formation of reflex contractures and deformities of limb joints, conservative treatment with L-DOPA drugs be preliminarily carried out.

The method used in the intraoperative portion of the selective dorsal rhizotomy procedure for the selection of abnormal circuits within the central nervous system of children with spasticity due to cerebral palsy is described. The decision to transect dorsal rootlets is made on the basis of electrophysiological, behavioral and medical criteria. In 100 cases the average number of rootlets transected was 64%. Of the total stimulated, 23.3% exhibited normal electrophysiological and behavioral responses. Decision making regarding the preservation or transection of the remaining 12.7% of the segments is described. This information is presented in an effort to increase understanding of this particular portion of the procedure and to encourage standardization of the procedure between centers in the future.

Canalized F-waves and H-reflexes occurring on small hand and foot muscles are to be considered symptoms of central disinhibition. Occurrence of these waves and reflexes in patients with hemispastic syndrome is analyzed and correlated with clinical aspects.

Control of elbow motion was evaluated in 45 extremities of adults with spasticity resulting from traumatic brain injury with use of dynamic electromyography. Simultaneous recording of elbow motion was obtained using a double parallelogram goniometer. Thirty-four male and 9 female patients were studied. Mean elbow flexion was 85 degrees and mean extension was 20 degrees. The average time of elbow flexion was 1.8 seconds. Extension time was prolonged to a mean of 4.0 seconds. Dynamic electromyography revealed a consistent pattern of muscle activity. Severe spasticity was noted in the brachioradialis muscle. Moderate spasticity was present in the biceps and only mild spasticity was seen in the brachialis muscle. Normal phasic muscle activity was the rule in the triceps. All patients had active elbow flexion, but the flexor spasticity limited smooth extension. Elbow flexor spasticity, especially of the brachioradialis and biceps muscles, commonly interferes with hand placement. Lengthening of the biceps and brachialis tendons combined with release of the brachioradialis enhances elbow motion and improves hand placement.

The electromyographic activity evoked by forced ankle rotation in spastic patients with cerebral palsy differs markedly from that found in normal subjects or in patients with adult-onset injuries to the central nervous system. Rapid dorsiflexion can produce a strong myotatic reflex electromyogram at 30 to 50 msec in the normal adult's stretched soleus muscle, while the antagonist tibialis anterior muscle quiet. The same is true of spastic patients whose injury has an adult onset. In patients with cerebral palsy this early response is found in both muscle groups. The pattern of "reciprocal excitation" is in marked contrast to the reciprocal inhibition normally seen. This reflex behavior suggests a fundamental developmental error in neuronal interconnections of the spinal cord in cerebral palsy.

No inhibitory influence of length on the increased stretch reflex was found in the internal gastrocnemius muscle of 19 cerebral palsied children. A facilitory influence of length was found in at least five patients in which quantitative data were obtained. These results were compared with previous data on a facilitory influence in the hamstrings and inhibitory influence in quadriceps muscles.

Isometric contractile properties of human elbow flexor muscles were examined in 27 normal subjects (7 females and 20 males). Contractions of elbow flexors were elicited by application of electrical pulses to the biceps motor points. The tension development was recorded at the wrist with the elbow angle fixed at 90 degrees--100 degrees. The data for the time to peak and time to half relaxation of the twitch, the twitch tension-to-tetanus tension ratio, and the posttetanic twitch potentiation are reported. The contractile properties of spastic elbow flexor muscles from 7 subjects who had been hemiparetic for periods ranging from 4 months to 60 months were found to be similar to those of muscles in normal subjects and unaffected muscles in hemiparetic subjects.

In rats the application of 10 mg/kg 6-amino-nicotinamide (6-AN) leads to an accumulation of 6-phosphogluconate, by inhibition of 6-phosphogluconate dehydrogenase in the pentose phosphate pathway, in the cells of the spinal cord. The accumulation reaches its maximum after 18-24 h. It seems that there exists a relationship between the accumulation of 6-phosphogluconate and the lesion of the neuroglia, which is found in electron microscopic studies. Symptoms of a spastic paresis only develop later when the spinal interneurones are destroyed as a consequence of the lesion of the neuroglia. The accumulation of 6-phosphogluconate almost exceeds the 400 fold of the norm. No considerable differences are found between the effects of a dose of 35 mg 6-AN/kg and one of 10 mg 6-AN/kg. Free gluconate is identified enzymically in the cells of the spinal cords of the rats treated with 6-AN. The compound is very probably formed by dephosphorylation and diffuses into the blood. 6-Phosphogluconate is an inhibitor of the phosphoglucose isomerase. Its accumulation shifts the equilibrium towards glucose 6-phosphate. The lactate concentration decreases as compared with the untreated controls. Muscular action potentials are recorded extracellularly with a concentric needle electrode from the musculus gastrocnemius of rats treated with 6-AN. First activations of the electromyograms are found 48 h after the application of 10 mg 6-AN/kg. The electrical activities increase during the time in which a progressive destruction of the interneurones occurs. The electromyogram displays a permanent state of excitation with high amplitudes and an increased frequency. The continuity and intensity of the increased activity recorded by the electromyograph is the most important pathological finding. p-Chlorophenyl-GABA and, still more so, chlorpromazine cause temporary reduction of the excitation processes and an electromyogram nearly at rest. Under the same conditions, haloperidol is only slightly effective. The symptoms developed by the chemical destruction of the interneurones of the spinal cord, with rigidity and spasticity of the hind limbs, are suitable for testing antispastic drugs.

The prevalence of various manifestations of spasticity from questionnaire responses and from clinical examination of chronic spinal cord injured patients is reported. Extensor spasms, flexor withdrawal spasms, and clonus were reported by most subjects. Those with incomplete lesions reported more interference with activities, more pain, and less functional usefulness, than did those with complete lesions. Extensor spasms were reported to interfere more with transfers, whereas flexor withdrawal spasms were reported to be more frequent at night and to interfere more with sleep. Increased muscle tone was observed more often in extensor than in flexor muscles. Those with incomplete lesions had more hypertonus and more limited passive joint movements than did those with complete lesions. Flexor withdrawal reactions and extensor spasms were also more pronounced in those with incomplete lesions, particularly those with Frankel grade C lesions.

Quantitative electromyographic studies of the lower arm musculature before and after distal displacement of the flexor of the hand and digital flexor as well as transplantation of the m. flexor carpi ulnaris to the dorsal side of the wrist joint were conducted in 10 patients with a spastic hand. At the same time the absolute force during isometric flexing and stretching was also recorded. The results revealed that the reciprocal innervation in the paretic antagonist improves, and the efficiency of the muscle is enhanced, by the surgical relaxation of the contracted agonist. The flexor carpi ulnaris transplanted to the dorsal side will additionally safeguard the muscular balance between flexors and extensors modified towards approaching the standard values. However, the transplanted flexor does not undergo a "learning" process in cortical level in the sense of performing the tasks of an extensor.

The excitability of a lower limb myotatic reflex arc is modulated by the antecedent activation of another myotatic arc in the same limb; the changes can be represented by heteronymous excitability curves. This work compares heteronymous excitability curves in spastic and normal subjects. Eighteen patients who showed clear signs of pyramidal tract lesions at a chronic stage were studied. Three myotatic arcs of the lower limb (soleus, quadriceps, and short biceps) were activated either by mechanical percussion (T Sol-T Quad-TSBi) or by electrical stimulation of the afferent nerve (H Sol-H Quad). They were used as conditioning and test responses in six different combinations, and the results compared to those obtained previously in normal volunteers. In spastic patients, heteronymous excitability curves are more obviously modified than homonymous ones. The changes are most prominent in the thigh muscles and less marked when the soleus reflex is conditioned by activation of quadriceps and biceps femoris myotatic reflex arcs.

The article describes the results of electromyographic examination of the muscles of the neck in 26 patients with spasmodic torticollis. Electromyography was performed before and after stereotaxic operative interventions on the nucleus of Cajal or in combination with the diencephalic structures. It is shown that electromyographic examination of patients, especially with the use of functional motor and oculomotor tests, widens essentially the possibilities of the diagnosis by facilitating the identification or specification of the predominantly involved group of muscles. The discovery of concurrent oculographic and electromyographic changes in the dominant muscles of the neck during oculomotor tests is evidence of the connection of the system of concurrent movements of the eyes and head with the motor systems participating in the pathology of torticollis. Analysis of the dynamics of electromyographic changes in patients with predominance of the tonic component in the early and late postoperative periods is indicative of gradual increase of positive changes in the motor sphere, which, evidently, is due to the dynamic reorganizations in the previously formed stable pathological system.

Clinical evaluation of clonus in spastic muscles was performed by comparing reflex path length with clonus frequency for different muscles in the same patient. It was found that clonus frequency varied inversely with reflex path length (r = 0.84, p less than 0.001). The findings confirm that clonus is generated by a peripheral mechanism of self re-excitation rather than a central spinal pacemaker.

This article reviews the experimental foundations of EMG biofeedback with the upper extremity. Considered are investigations on recruitment and training of single and multiple motor units in both normal and nonnormal subjects, on transfer of training effects from trained to untrained muscles, and on the relationship of reduced muscle output to relaxation. Examined are procedures, results, and conclusions of these basic studies. Problems noted in the research are discussed and suggestions are made for further work in the area.

Length changes of gastrocnemius muscle belly and tendon at different passive tensions and ranges of motion (ROM) were measured in 31 healthy persons and 15 hemiplegic patients with clinically demonstrated ankle joint plantar flexion (PF) contractures. Preliminary studies were done to obtain accurate determination of gastrocnemius muscle insertion and origin points on x-ray films, to calculate the magnification factor due to x-ray beam divergence and to measure the length changes in muscle belly by the use of a wire hook placed at the muscle-tendon junction. Our results revealed: (1) change in length at different passive tensions is in the muscle belly, not in the tendon, (2) in hemiplegic patients no statistical difference in elongational characteristics of affected gastrocnemius muscle bellies with clinically demonstrated ankle PF contractures and of the contralateral nonaffected muscle bellies, (3) spastic and flaccid gastrocnemius muscle bellies are not statistically different in respect to passive elongations, (4) gastrocnemius muscle bellies of both affected and nonaffected legs of hemiplegic patients were statistically different from the muscle bellies of healthy persons in regard to maximal ROM and maxinum muscle belly length changes, (5) there was approximately .5 mm change in the belly length for each degree of ankle ROM, (6) age is not a factor influencing passive elongation of muscle belly, (7) average muscle belly lengths were consistently shorter in hemiplegic muscles while their tendon lengths did not change. The enumerated findings suggest that the limitation of ankle ROM in spastic hemiplegic legs obtained by the standard clinical measurements technique represents a change in muscle belly rest length without a structural contracture of the muscle fibers.

Indirect motor responses with the characteristics of the H wave were recorded from the flexor carpi radialis and the palmaris longus muscles in normal adults. A series of experiments has been performed, constituting circumstantial arguments for the monosynaptic nature of these reflex responses. The findings in pathological conditions, which corroborated this point of view, are documented briefly.

The inhibitory effect of IB interneurons on motoneurons was tested in both legs of six hemiplegic adults. On the normal side, an inhibition of 10 ms, (14.6%) was observed in all cases and was similar to that described previously. On the spastic side, the same technique results in a facilitation of same duration reaching a maximum of 15%. Hence the IB inhibitory effect is, at least functionally, absent in spasticity. Disappearance of IB inhibition is an additional mechanism to be considered in interpreting spasticity.