Phasic Stretch Reflex Research Articles

Implementation of surface mechanomyography as a novel approach for objective evaluation of phasic muscle stretch reflexes in people with type 2 diabetes

IntroductionDiabetic peripheral neuropathy is the most common complication of diabetes producing metabolic disruptions in the peripheral nervous system. Alteration in the predictable nature of tendon reflexes is the most common indicator suggesting the possibility of diabetic neuropathy. Evaluation of tendon reflexes is a part of various clinical scoring systems that assess neuropathy. The conventional reflex grading scales are subjective, lack temporal data, and have high inter-rater variability. Hence, an indigenous quantification tool was developed to evaluate the tendon reflexes in order to assess diabetic peripheral neuropathy. Materials and methodsA cross-sectional study was carried out in 140 healthy volunteers and 140 patients with type 2 diabetes. The mean age of controls and diabetics (49.1 ± 8.9, 50.7 ± 7.5) years, weight (66.9 ± 9.4, 69.8 ± 11.5) kilograms and BMI (24.5 ± 3.8, 26.1 ± 4.7), respectively. All of them are subjected to evaluation of tendon reflexes using the reflex quantification tool comprised of surface mechanomyography and electrogoniometry that can provide various static and dynamic variables of tendon reflex. ResultsThe dynamic variables such as reflex amplitude, muscle velocity and angular velocity were significantly low in diabetic patients (p: <0.001) whereas latency and duration (p: <0.001) were prolonged. Furthermore, no significant difference was observed in the application of tendon striking force (p: 0.934) among the participants. ConclusionThe current study demonstrates that the proposed reflex quantification tool provides several dynamic variables of patellar tendon reflex, which are significantly affected and altered in diabetic patients suggesting the involvement of peripheral neurons.

Neural and non-neural contributions to ankle spasticity in children with cerebral palsy.

To assess the neural and non-neural contributions to spasticity in the impaired ankle of children with cerebral palsy (CP). Instrumented tapping of the Achilles tendon was done isometrically to minimize non-neural contributions and elicit neural contributions. Robot-controlled ankle stretching was done at various velocities, including slow stretching, with minimized neural contributions. Spasticity was assessed as having neural (phasic and tonic stretch reflex torque, tendon reflex gain, contraction rate, and half relaxation rate) and non-neural origin (elastic stiffness and viscous damping) in 17 children with CP (six females and 11 males; mean age [SD] 10y 8mo [3y 11mo], range 4y-18y) and 17 typically developing children (six females and 11 males; mean age [SD] 12y 7mo [2y 9mo], range 7y-18y). All torques were normalized to weight×height. Children with CP showed increased phasic and tonic stretch reflex torque (p=0.004 and p=0.001 respectively), tendon reflex gain (p=0.02), contraction rate (p=0.038), half relaxation rate (p=0.02), elastic stiffness (p=0.01), and viscous damping (p=0.01) compared to typically developing children. Controlled stretching and instrumented tendon tapping allow the systematic quantification of various neural and non-neural changes in CP, which can be used to guide impairment-specific treatment. Ankle spasticity is associated with increased phasic and tonic stretch reflexes, tendon reflex gain, and contraction and half relaxation rates. Ankle spasticity is also associated with increased elastic stiffness and viscous damping.

Ghost spasticity in multiple sclerosis

Spasticity is the velocity-dependent hypertonia frequently encountered in patients affected by Upper Motor Neuron Syndrome. It is due to a tonic stretch reflex, which is evoked in patients at rest. The aim of this study, performed using surface electromyography (EMG), was to investigate stretch reflex excitability in the hamstrings muscles of patients affected by progressive Multiple Sclerosis (MS) and to correlate EMG results with clinical findings. Thirty patients and 20 age-matched healthy controls were investigated. EMG activity was recorded from biceps femoris muscle with the patient at rest. To stretch hamstrings muscles, the patient’s leg was manually moved from maximal flexion to maximal extension at 3 different velocities to investigate both phasic and tonic stretch reflex. Only 7 patients were affected by hypertonia of the hamstrings; 4 of them showed muscle contracture. A tonic stretch reflex was present in the vast majority of the recruited patients, whether they presented hypertonia of the hamstrings or not. Tonic stretch reflex is often present in the hamstrings muscles of progressive MS patients without producing increased muscle tone. This “ghost spasticity” is likely to be, for its intrinsic features, an important risk factor for the development of contractures in the hamstrings muscles.

Developmental dysgraphia is often associated with minor neurological dysfunction in children with developmental coordination disorder (DCD)

Children with developmental coordination disorder (DCD) are particularly affected by handwriting disorders, which remain poorly understood and are not clearly defined. The aim of our study is to provide a better understanding of handwriting disorders, and specifically of dysgraphia in children with DCD. Sixty-five children with DCD (5-15 years), enrolled according to DSM-5, were assessed with handwriting testing and standardized assessments of neuropsychological, neurovisual, MRI and neuropsychomotor functions, with special attention paid to muscular tone examination. While handwriting disorders were strongly represented in our sample of children with DCD (89%), dysgraphia appeared uncommon (17%) and was closely related to several specific dysfunctions of laterality establishment; mild pyramidal tract dysfunction with distal phasic stretch reflex (PSR) in lower limbs; digital praxis slowness (both P<0.05). In our sample, dysgraphia was closely related to minor neurological dysfunction (MND) suggesting a disturbance of motor control at the level of the corticospinal motor pathway. This highlights the uncommon character of dysgraphia in children with DCD for which diagnosis should be made through a particular attention to evaluation of MND with muscular tone examination. This consideration, both in the research setting and in clinical practice, appears necessary to avoid inaccurate clinical diagnosis and to optimize appropriate therapeutic management.

Developmental Coordination Disorder, An Umbrella Term for Motor Impairments in Children: Nature and Co-Morbid Disorders.

Background: Developmental Coordination Disorder (DCD) defines a heterogeneous class of children exhibiting marked impairment in motor coordination as a general group of deficits in fine and gross motricity (subtype mixed group) common to all research studies, and with a variety of other motor disorders that have been little investigated. No consensus about symptoms and etiology has been established.Methods: Data from 58 children aged 6 to 13 years with DCD were collected on DSM-IV criteria, similar to DSM-5 criteria. They had no other medical condition and inclusion criteria were strict (born full-term, no medication, no occupational/physical therapy). Multivariate statistical methods were used to evidence relevant interactions between discriminant features in a general DCD subtype group and to highlight specific co-morbidities. The study examined age-calibrated standardized scores from completed assessments of psychological, neuropsychological, and neuropsychomotor functions, and more specifically the presence of minor neurological dysfunctions (MND) including neurological soft signs (NSS), without evidence of focal neurological brain involvement. These were not considered in most previous studies.Results: Findings show the salient DCD markers for the mixed subtype (imitation of gestures, digital perception, digital praxia, manual dexterity, upper, and lower limb coordination), vs. surprising co-morbidities, with 33% of MND with mild spasticity from phasic stretch reflex (PSR), not associated with the above impairments but rather with sitting tone (p = 0.004) and dysdiadochokinesia (p = 0.011). PSR was not specific to a DCD subtype but was related to increased impairment of coordination between upper and lower limbs and manual dexterity. Our results highlight the major contribution of an extensive neuro-developmental assessment (mental and physical).Discussion: The present study provides important new evidence in favor of a complete physical neuropsychomotor assessment, including neuromuscular tone examination, using appropriate standardized neurodevelopmental tools (common tasks across ages with age-related normative data) in order to distinguish motor impairments gathered under the umbrella term of developmental coordination disorders (subcortical vs. cortical). Mild spasticity in the gastrocnemius muscles, such as phasic stretch reflex (PSR), suggests disturbances of the motor pathway, increasing impairment of gross and fine motricity. These findings contribute to understanding the nature of motor disorders in DCD by taking account of possible co-morbidities (corticospinal tract disturbances) to improve diagnosis and adapt treatment programmes in clinical practice.

Implicit learning and generalization of stretch response modulation in humans.

Adaptation of neural responses to repeated muscle stretching likely represents implicit learning to minimize muscle resistance to perturbations. To test this hypothesis, the forearm was placed on a horizontal manipulandum. Elbow flexors or extensors compensated an external load and were stretched by 20° or 70° rotations. Participants were instructed not to intervene by intentionally modifying the muscle resistance elicited by stretching. In addition to phasic stretch reflexes (SRs), muscle stretching was associated with inhibitory periods (IPs) in the ongoing muscle activity starting at minimal latencies of ∼35 ms. The SR amplitude decreased dramatically across 5-12 trials and was not restored after a resting period of 3-5 min, despite the increase in stretch amplitude from 20° to 70°, but IPs remained present. When SRs were suppressed, stretching of originally nonstretched, antagonist muscles initiated after the rest period showed immediate SR suppression while IPs remained present in the first and subsequent trials. Adaptation to muscle stretching thus includes features characteristic of implicit learning such as memory consolidation and generalization. Adaptation may be achieved by central shifts in the threshold positions at which muscles begin to be activated. Shifts are thought to be prepared in advance and triggered with stretch onset. Threshold position resetting provides a comprehensive explanation of the results in the broader context of the control of posture, movement, and motor learning in the healthy and damaged nervous system.

Characterizations of reflex and nonreflex changes in spastic multiple sclerosis

Spasticity, an increased resistance of a limb to movement, is associated with functional limitations and a major source of disability in neurological disorders, including multiple sclerosis (MS) and stroke. Despite the clinical significance of spasticity in brain and spinal cord injuries, it is often not clear whether the spasticity is due to reflex or non-reflex changes. Reflex and nonreflex properties of the human knee joint were studied in eight MS patients with spasticity and ten healthy subjects. A digitally controlled joint driving device was used to apply small-amplitude, and band-limited white-noise perturbations to the knee to manifest the reflex and nonreflex properties. The subjects were asked to maintain a steady level of background muscle torque during the perturbation. A nonlinear delay differential equation model was used to characterize the reflex and intrinsic properties of the knee in terms of phasic stretch reflex gain, tonic stretch reflex gain, joint elastic stiffness, and coefficient of viscosity. It was found that joint coefficient of viscosity and tonic stretch reflex gain of the spastic MS patients were significantly lower than those of normal controls. On the other hand, spastic MS patients showed higher phasic stretch reflex gains than normal controls and a trend of increased joint stiffness. Simultaneous characterizations of changes in tonic and phasic reflexes and nonreflex changes in joint elastic stiffness and viscosity in neurological disorders may help us gain insight into mechanisms underlying spasticity and develop impairment-specific treatment.

Simultaneous characterizations of reflex and nonreflex dynamic and static changes in spastic hemiparesis.

This study characterizes tonic and phasic stretch reflex and stiffness and viscosity changes associated with spastic hemiparesis. Perturbations were applied to the ankle of 27 hemiparetic and 36 healthy subjects under relaxed or active contracting conditions. A nonlinear delay differential equation model characterized phasic and tonic stretch reflex gains, elastic stiffness, and viscous damping. Tendon reflex was characterized with reflex gain and threshold. Reflexively, tonic reflex gain was increased in spastic ankles at rest (P < 0.038) and was not regulated with muscle contraction, indicating impaired tonic stretch reflex. Phasic-reflex gain in spastic plantar flexors was higher and increased faster with plantar flexor contraction (P < 0.012) than controls (P < 0.023) and higher in dorsi-flexors at lower torques (P < 0.038), primarily because of its increase at rest (P = 0.045), indicating exaggerated phasic stretch reflex especially in more spastic plantar flexors, which showed higher phasic stretch reflex gain than dorsi-flexors (P < 0.032). Spasticity was associated with increased tendon reflex gain (P = 0.002) and decreased threshold (P < 0.001). Mechanically, stiffness in spastic ankles was higher than that in controls across plantar flexion/dorsi-flexion torque levels (P < 0.032), and the more spastic plantar flexors were stiffer than dorsi-flexors at comparable torques (P < 0.031). Increased stiffness in spastic ankles was mainly due to passive stiffness increase (P < 0.001), indicating increased connective tissues/shortened fascicles. Viscous damping in spastic ankles was increased across the plantar flexion torque levels and at lower dorsi-flexion torques, reflecting increased passive viscous damping (P = 0.033). The more spastic plantar flexors showed higher viscous damping than dorsi-flexors at comparable torque levels (P < 0.047). Simultaneous characterizations of reflex and nonreflex changes in spastic hemiparesis may help to evaluate and treat them more effectively.

Assessment of Muscle Overactivity and Spasticity with Dynamic Polyelectromyography and Motion Analysis

Damage of the central nervous system often produces an upper motoneuron (UMN) syndrome. Characteristics of the UMS include the presence of positive and negative signs. Positive signs are increased phasic and tonic stretch reflexes, clonus, co-contraction, released flexor reflexes, spastic dystonia, and associated reactions, whereas negative signs signify the loss or impairment of voluntary movement assembly and production. Muscle overactivity seems to be a more suitable term than spasticity, because it evokes more an image of dynamic muscle contraction, which is the general hallmark of all positive signs of UMS. Some of the main patterns of UMN dysfunction include: equinovarus foot, hyper- extended great toe, stiff knee, adducted (scissoring) thighs, and flexed hip. The dynamic poly-EMG recordings of trunk and lower limb muscles in combination with the clinical examination provide a more detailed understanding of the genesis of these abnormal patterns in the UMN.

Characterization of a novel C8 phasic muscle stretch reflex

Muscle stretch reflexes (MSRs) are fundamental to the neurologic examination. Although the fifth, sixth, and seventh cervical roots have appropriate and easily elicited MSRs, the C8 level does not. The C8 reflex is obtained by tapping the thenar eminence, which produces flexion at the interphalyngeal joints of the fingers. To confirm that finger flexion represented an MSR, an externally triggered hammer-skin contact set-up was employed. Surface recording electrodes were placed at one third of the distance between the medial epicondyle and ulnar styloid. This montage produced distinct T-waves with latencies compatible with a reflex arc. Normative data were collected for 75 healthy subjects (150 arms), including 15 from each of five age groups (20-29, 30-39, 40-49, 50-59, > or =60 years). Distance 1 (D1) was measured from the FPL to the C7 spinous process and distance 2 (D2) from C7 to the G1 electrode. A high median neuropathy abolished the T-wave. A distal median nerve block at the carpal tunnel had no effect. Mean latencies (+/- SD) from the respective age groups were as follows: 21.73 +/- 1.16 ms; 22.50 +/- 1.70 ms; 22.19 +/- 1.52 ms; 22.66 +/- 2.13 ms; and 23.97 +/- 1.91 ms. Reflex latencies significantly correlated with age (r = 0.33, P = 0.004), height (r = 0.51, P < 0.0001), and D1 + D2 or arc length (r = 0.74, P < 0.0001). This novel MSR is generated from the FPL tendon and stimulates contraction of the long finger flexors. It therefore represents a clinically useful C8 MSR.

61. Characterization of a novel c8 phasic muscle stretch reflex

61. Characterization of a novel c8 phasic muscle stretch reflex

THE MODE OF ACTION OF THE GABA DERIVATIVE BACLOFEN IN HUMAN SPASTICITY

Baclofen is chemically related to GABA and has proved to have a clinical effect on spasticity and on flexor spasms. The mode of action of baclofen was studied by quantitative measurements of some reflexes and of voluntary power in relation to intravenous injections of the drug (average dose 0.38 mg per kg body weight) in 44 patients with spasticity due to spinal or cerebral lesion or multiple sclerosis; a total of 53 injections were given. In most of the patients studied, depression occurred in the phasic stretch reflex (Achilles tendon), tonic stretch reflex, flexor reflex, reflexes from the pelvic floor and in the tonic vibration reflex; whereas the fl reflex changed in only a few cases, and voluntary power did not change at all. In some patients a pronounced increase was observed in the vibration-induced depression of the H reflex, which after baclofen approached normal. Baclofen can reduce the fusimotor drive, whereas a general primary effect on the α motoneurones is unlikely. It acts on the interneurones and can increase ‘presynaptic’ inhibition of the la nerve fibres. It is capable of exerting its action exclusively at the spinal level and can depress hyperactive stretch reflexes, whether they are caused by a spinal or cerebral lesion.

Pharmacologic management of spasticity in multiple sclerosis

Spasticity is very common in people with multiple sclerosis (MS). It is estimated that between 40 and 60% of all patients are affected. It consists of an abnormal, velocity-dependent increase in the phasic and tonic stretch reflexes, due to an abnormal integration of the nervous system motor responses to sensory input. The cause of spasticity could be due to an interruption of the neural network controlling the muscle stretch reflex in the central nervous system (CNS). Correct management of spasticity is essential and it must start with the identification of achievable goals. Therapeutical approaches include skilled rehabilitation strategies, pharmaceutical agents and surgery. The main objective of the treatment should be minimising the negative impact of the spasticity on disability and quality of life (QoL) of each patient.

Consequences of Uteroplacental Insufficiency on Developmental and Intellectual Performances

After completing this article, readers should be able to: 1. Explain why the difference between small for gestational age and intrauterine growth restriction is important for determining time of delivery. 2. Describe the potential developmental consequences of placental insufficiency. 3. Delineate the hypotheses underlying the association between prenatal stress and developmental outcome. Deprivation of supplies is the common pathogenic factor for fetuses experiencing placental insufficiency, even if all do not exhibit hypotrophy at birth or accelerated maturation as a response to stress. Nearly one century ago, placental insufficiency was remarkably described by the French obstetrician Pierre Budin: “They are tiny, puny infants with great vitality. Their movements are untiring and their crying lusty, for their organs are quite capable of performing their allotted functions. These infants will live, for although their weight is inferior … their sojourn in the womb was longer.” (1) Since then, normative growth curves and precise determination of gestational age (GA) have permitted consensual categorization of newborns, the last advance being the identification of an intrauterine growth restriction (IUGR) subgroup among the small-for-gestational age (SGA) group (10th percentile). (2) However, this categorization remains unsatisfactory when dealing with the very preterm group for several reasons, including unknown GA in many cases and inadequacy of the current growth curves in the low range of GA. Why is it so important to make a distinction between SGA and IUGR infants? First, the cause is different: genetic factors explain a large proportion of cases in SGA infants and epigenetic factors are involved in IUGR fetuses. This current conception is elegantly summarized by Fowden: “Normal fetal growth depends on an adequate supply of nutrients and on a strict temporal relationship between tissue accretion and differentiation. During early development, the pattern of intrauterine growth is largely determined by the fetal genome but, as size …

Starting position and stretching velocity effects on the reflex threshold angle of stretch reflex in the soleus muscle of normal and spastic subjects.

Although both starting position and stretching velocity play an important role in reflex response, their interaction with stretch reflexes has not been thoroughly investigated. This study examined the interaction effect of starting position and stretching velocity on the reflex threshold angle (RTA) of the stretch reflex in the soleus muscle of normal and spastic subjects. The spastic group included 11 ankles from 7 subjects with a history of upper motor neuron lesions. Their ages ranged from 22 to 40 years. Another 10 healthy subjects served as the control group. RTAs of the stretch reflex in the soleus muscle were measured for a matrix of starting positions and stretching velocities. The matrix design enabled the use of a 2-way analysis model to investigate the effect of starting position and stretching velocity on the RTA. No interaction effect was found in either the phasic stretch reflex (PSR) or the tonic stretch reflex (TSR) in the spastic group, or in the PSR in the normal group. The RTA of the PSR in both spastic and normal groups was significantly affected by starting position but not by stretching velocity. In contrast, the RTA of the TSR in the spastic group was affected by both starting position and stretching velocity. Stretching velocity and starting position played independent roles in determining the RTA of both the PSR and the TSR of the spastic group and in the PSR of the normal group. The lack of interaction between length-sensitive and velocity-sensitive muscle spindles in both normal and spastic subjects supports the hypothesis that they independently modulate the stretch reflex. Results for the RTA of the TSR demonstrated that spasticity results in disinhibition of motoneuron excitability with different thresholds.

Paradoxical muscle contractions and the neural control of movement and balance

Paradoxical muscle contractions and the neural control of movement and balance

Stepping-like movements in humans with complete spinal cord injury induced by epidural stimulation of the lumbar cord: electromyographic study of compound muscle action potentials

It has been previously demonstrated that sustained nonpatterned electric stimulation of the posterior lumbar spinal cord from the epidural space can induce stepping-like movements in subjects with chronic, complete spinal cord injury. In the present paper, we explore physiologically related components of electromyographic (EMG) recordings during the induced stepping-like activity. To examine mechanisms underlying the stepping-like movements activated by electrical epidural stimulation of posterior lumbar cord structures. The study is based on the assessment of epidural stimulation to control spasticity by simultaneous recordings of the electromyographic activity of quadriceps, hamstrings, tibialis anterior, and triceps surae. We examined induced muscle responses to stimulation frequencies of 2.2-50 Hz in 10 subjects classified as having a motor complete spinal cord injury (ASIA A and B). We evaluated stimulus-triggered time windows 50 ms in length from the original EMG traces. Stimulus-evoked compound muscle action potentials (CMAPs) were analyzed with reference to latency, amplitude, and shape. Epidural stimulation of the posterior lumbosacral cord recruited lower limb muscles in a segmental-selective way, which was characteristic for posterior root stimulation. A 2.2 Hz stimulation elicited stimulus-coupled CMAPs of short latency which were approximately half that of phasic stretch reflex latencies for the respective muscle groups. EMG amplitudes were stimulus-strength dependent. Stimulation at 5-15 and 25-50 Hz elicited sustained tonic and rhythmic activity, respectively, and initiated lower limb extension or stepping-like movements representing different levels of muscle synergies. All EMG responses, even during burst-style phases were composed of separate stimulus-triggered CMAPs with characteristic amplitude modulations. During burst-style phases, a significant increase of CMAP latencies by about 10 ms was observed. The muscle activity evoked by epidural lumbar cord stimulation as described in the present study was initiated within the posterior roots. These posterior roots muscle reflex responses (PRMRRs) to 2.2 Hz stimulation were routed through monosynaptic pathways. Sustained stimulation at 5-50 Hz engaged central spinal PRMRR components. We propose that repeated volleys delivered to the lumbar cord via the posterior roots can effectively modify the central state of spinal circuits by temporarily combining them into functional units generating integrated motor behavior of sustained extension and rhythmic flexion/extension movements. This study opens the possibility for developing neuroprostheses for activation of inherent spinal networks involved in generating functional synergistic movements using a single electrode implanted in a localized and stable region.

Minor neurological signs and developmental performance in high risk children at preschool age.

The aim of this study was to establish correlations between minor neurological findings and developmental performance. A cohort of 72 preschool children was studied (38 females, 34 males; mean age 3 years 8 months, SD 1 year 2 months, range 2 to 5 years) who were considered to be at high risk due to placental insufficiency. The cohort was divided into four categories of neurological status: (1) minimal cerebral palsy (MCP) with independent walking before age 2 years; (2) Amiel-Tison triad (ATT) including imbalance of passive axial tone, phasic stretch reflex in triceps surae, and cranial signs, particularly on the squamous suture; (3) intermediate with one or two of the three ATT signs; and (4) absence of neurological findings. Six subscales of the Griffiths Mental Developmental Scales assessing locomotion, eye-hand coordination, interpersonal skills, language, performance, and practical reasoning were administered. Significant differences were found according to neurological status in three specific domains of development: coordination (F=2.84, p=0.04), language (F=3.65, p=0.02), and practical reasoning (F=3.62, p=0.02). In addition, significant differences were also found in language (L) and practical reasoning (R) performances according to the side of the abnormal stretch reflex: bilateral stretches (L=87.8; R=75.3) or an isolated right stretch (L=95.3; R=83.6) are more strongly associated with impaired developmental performances than an isolated left stretch (L=101.3; R=88.2) with F=2.94; p=0.04 for language and F=3.00, p=0.04 for practical reasoning. We concluded that a short neurological examination, easily performed by pediatricians and family practitioners, can identify permanent markers of minor brain damage occurring before, during, or soon after birth and so anticipate consequences.

Minor neurological signs and developmental performance in high risk children at preschool age

The aim of this study was to establish correlations between minor neurological findings and developmental performance. A cohort of 72 preschool children was studied (38 females, 34 males; mean age 3 years 8 months, SD 1 year 2 months, range 2 to 5 years) who were considered to be at high risk due to placental insufficiency. The cohort was divided into four categories of neurological status: (1) minimal cerebral palsy (MCP) with independent walking before age 2 years; (2) Amiel‐Tison triad (ATT) including imbalance of passive axial tone, phasic stretch reflex in triceps surae, and cranial signs, particularly on the squamous suture; (3) intermediate with one or two of the three ATT signs; and (4) absence of neurological findings. Six subscales of the Griffiths Mental Developmental Scales assessing locomotion, eye‐hand coordination, interpersonal skills, language, performance, and practical reasoning were administered. Significant differences were found according to neurological status in three specific domains of development: coordination (F=2.84,p=0.04), language (F=3.65,p=0.02), and practical reasoning (F=3.62, p=0.02). In addition, significant differences were also found in language (L) and practical reasoning (R) performances according to the side of the abnormal stretch reflex: bilateral stretches (L=87.8; R=75.3) or an isolated right stretch (L=95.3; R=83.6) are more strongly associated with impaired developmental performances than an isolated left stretch (L=101.3; R=88.2) with F=2.94;p=0.04 for language and F=3.00,p=0.04 for practical reasoning. We concluded that a short neurological examination, easily performed by pediatricians and family practitioners, can identify permanent markers of minor brain damage occurring before, during, or soon after birth and so anticipate consequences.

Reciprocal and Renshaw (recurrent) inhibition are functional in man at birth

The aims were (1) to determine when in human postnatal development Group Ia reciprocal and Renshaw inhibition can be demonstrated; (2) to explore the relationship between the expression reciprocal inhibition and the disappearance of Group Ia excitatory reflexes between agonist and antagonist muscles. Studies were performed on 99 subjects, aged 1 day to 31 years, of whom 53 were neonates. A longitudinal study was also performed on 29 subjects recruited at birth and studied 3 monthly until 12 months of age. Reciprocal inhibitory and excitatory reflexes were recorded in the surface EMG of contracting biceps brachii (Bi), evoked by taps applied to the tendon of triceps brachii (Tri). Reciprocal excitatory reflexes were recorded in all but one neonate. Reciprocal inhibition was observed in 25% of neonates; evidence is provided that it was likely to have been masked by low threshold reciprocal excitation in the remaining neonates. Reciprocal inhibition was demonstrated in all subjects after 9 months of age. In four neonates there was depression of inhibition of Bi during co-contraction of Bi and Tri implying that Group Ia interneurones may be under segmental and suprasegmental control at birth. Renshaw cells, identified in human postmortem cervical spinal cord by their morphology, location and calbindin D28K immunoreactivity, were present at 11 weeks post-conceptional age (PCA) and by 35 weeks PCA had mature morphological characteristics. In four neonates reciprocal inhibitory responses in Bi disappeared when the tap to Tri evoked its own homonymous phasic stretch reflex, providing neurophysiological evidence for Renshaw inhibition of Group Ia inhibitory interneurones.