Development of Neuromuscular Coordination with Implications in Motor Control
Mark De Ste Croix, Thomas Korff in Paediatric Biomechanics and Motor Control, 2013
Muscle activation is regulated by neural mechanisms of central and peripheral origin. With regard to peripheral neural mechanisms, it is known that in the typical adult, a sudden change in muscle stretch causes firing of Ia afferent fibres, which are excitatory on the agonist alpha motoneuron by way of a monosynaptic connection in the spinal cord and inhibitory on the antagonist alpha motoneuron through an inhibitory interneuron in the spinal cord (Myklebust et al. 1986). It is not known whether this chain of events occurs similarly in the developing child; in most cases, we assume that reflexes of this type hold true for children as well. The simultaneous facilitation of the agonist muscle and inhibition of the antagonist muscle is called reciprocal inhibition. From a mechanical point of view, the presence of high muscle coactivation from muscles that act in opposite directions (antagonistic muscles) around a joint will determine the moment of force exerted around the joint and, in turn, the characteristics of joint movement. The higher the coactivation of the agonists and antagonists, the less the resultant joint moment (Kellis 2003). Consequently, changes in muscle coactivation provide useful information regarding neuromuscular development in children, which is also essential for joint stability (see Chapter 11).
Mechanisms underlying acute changes in range of motion
David G. Behm in The Science and Physiology of Flexibility and Stretching, 2018
Whereas static and PNF stretching should reduce muscle activation through some degree of reflexive disfacilitation with reduced muscle spindle receptor activity of the nuclear bag and nuclear chain (Ia afferents) and further possible inhibition from autogenic (Ib afferents) and reciprocal inhibition (Ia afferents), dynamic stretching should excite or increase activation of the system. The previously discussed myotactic reflex activity would be increased by dynamic stretching due to nuclear bag and chain excitation as a result of the higher rate and extent of muscle elongation. As dynamic muscle stretching is usually performed as a relaxed action with submaximal muscle contractions, the activation of GTOs initiating autogenic inhibition would not be expected to play a major role in increasing acute ROM. Reciprocal inhibition would be activated by the sequential movement of the limbs, similar to the well-documented reciprocal inhibition sequences found with locomotor activities such as walking and running (43,44). This reciprocal inhibition could contribute to greater dynamic movement excursions during the stretching activity, but would not persist after the activity. Hence, for the augmentation of ROM to persist after the dynamic stretching, the reciprocal inhibition would need to contribute to viscous and morphological changes, which would continue for a prolonged period after the stretching. Typically, dynamic stretching is not as uncomfortable or painful as static or PNF stretching, hence the role of stretch tolerance may not be as predominant.
Motor Deficits of Stroke: Interrelationships and Assessment
Mary C. Singleton, Eleanor F. Branch in Physical Therapy and the Stroke Patient: Pathologic Aspects and Clinical Management, 2014
Burke suggests that spasticity is a symptom, not a disease.1 The current theories on the pathophysiology of spasticity include: (a) a hyperactive stretch reflex (highly disputed by Burke),2 (b) decreased interneuronal inhibition3 and (c) hyperexcitability of the alpha motor neuron.4 In an attempt to differentiate the passive from the active components of spasticity, Lance has restricted the definition of spasticity to “a velocity dependent increase in the tonic reflex with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome.”5 Investigations into the relationship of active movement to spasticity reveal that the “spasticity” observed in active movement is not the result of a hyperactive stretch reflex of the antagonist, but rather to abnormal regulation of its motor neuron pool.6 This abnormal regulation causes prolonged recruitment of the motor units and delayed cessation of antagonist contraction at the end of the movement. Disorders of reciprocal inhibition also contribute to increased resistance during active movement.7 For example, if a patient is unable to reciprocally flex and extend the elbow, this movement dysfunction may not be a result of a hyperactive stretch reflex in the biceps but rather prolonged recruitment of the biceps motorneurons which prevents reversal into extension.
Clinical care and therapeutic trials in PLS
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Mary Kay Floeter, Deborah Warden, Dale Lange, James Wymer, Sabrina Paganoni, Hiroshi Mitsumoto
Ideally, clinical trials for PLS should be based on a scientific rationale. Because the cause(s) and even pathogeneses of PLS are currently unknown, current clinical trials focus on symptomatic, rather than disease-modifying treatments. There are three general categories of hypotheses underlying symptomatic treatments. The first category involves enhancing existing corticospinal function, for example by improving conduction in axons with secondary demyelination (20). In other disorders with spasticity, it is known that maladaptive changes occur in subcortical and spinal neural circuits following the loss of corticospinal input. The second category involves interventions aimed at reducing spasticity and are hypothesized to enhance circuits for reciprocal inhibition thus reducing muscle co-contraction. The third category involves facilitating adaptive neuroplasticity in unaffected or less affected circuits outside the corticospinal system. This approach is particularly promising for PLS, given the relative sparing of motor pathways outside the corticospinal system and the long duration of disease. Facilitating spinal neuroplasticity, as has been piloted in spinal cord injury (21–24) and activating brainstem motor pathways, for example with rhythmic cueing (25) may be ways to improve ambulation in PLS. There is sufficient scientific rationale to support clinical trials using activity-based and noninvasive stimulation interventions in PLS to promote neuroplasticity.
Do functional hamstring to quadriceps ratio differ between men and women with and without stroke?
Published in Topics in Stroke Rehabilitation, 2018
Rodrigo Rodrigues Gomes Costa, Jefferson Rosa Cardoso, Clarice Bacelar Rezende, Gustavo Christofoletti, Rodrigo Luiz Carregaro
To the best of our knowledge, there is a lack of studies focusing on FH/Q ratio measurements in individuals with stroke. We found only a previous study in which the FH/Q ratio was assessed in children with cerebral palsy, demonstrating that the ratio was lower compared to children with a normal development.16 After stroke, due to the central nervous system injury, the reciprocal inhibition mechanism is limited by a cortical disinhibition.17,18 Thus, the lack of reciprocal inhibition may result in hypertonia of the flexor system (hip flexors, hamstring and ankle flexor muscles) or coextension of the extensor and hip flexor muscles, which restrain the knee and hip range of motion during gait.19 Such neuromuscular imbalance may result in a premature and increased recruitment of the hamstrings, in addition to a delayed activation of the quadriceps.17 Consequently, this could result in an insufficient quadriceps strength and abnormal hamstring co-contraction during the gait balance phase, for instance. Hence, the FH/Q ratio can be a useful functional measure that can easily detect knee muscular imbalances and might help to ascertain whether individuals are exposed to risky conditions.
The effects of locomotor training in children with spinal cord injury: a systematic review
Published in Developmental Neurorehabilitation, 2019
Jennifer Glenna Donenberg, Linda Fetters, Robert Johnson
Evidence suggests that the circuitry for the CPG is present at birth. The ability to elicit a stepping response in infants, while in supported standing and shifting their weight forward to yield a hip extension moment in the stance phase of gait, supports the activity of the CPG.16 This stepping observed is not volitionally controlled due to immature supraspinal centre development and additional gross motor skills not yet obtained through cortical development to independently step.17 As children grow and develop, the supraspinal centres begin to mature and influence stepping. Reciprocal inhibition further develops and modulates the ability to walk. For example, this means taking a step with active dorsiflexion present and simultaneous relaxation of the plantarflexors. This synchronous relationship allows for coordination of stepping reciprocally between limbs.18 Another important supraspinal centre that is developing is the vermis located in the cerebellum. The vermis is responsible for developing intra- and inter-limb coordination as well as the initiation of stepping.14 As a child grows and the spinal cord continues to develop, the supraspinal centres become more refined and locomotion becomes more modulated based on cortical input. The evidence, however, does suggest that training in those with an injured spinal cord can yield modulated stepping without higher centres’ input. Therefore, stimulation of the neuromuscular system through the CPG below the level of a SCI, with a variety of sensory input, could lead to the reoccurrence or development of walking after injury. This statement holds true even with compromise to the communication between the supraspinal centres, descending tracts, and the spinal cord.13,19
Related Knowledge Centers
- Alpha Motor Neuron
- Stretch Reflex
- Joint
- Skeletal Muscle
- Allied Health Professions
- Anatomical Terms of Muscle
- Quadriceps
- Hamstring
- Pulled Hamstring
- Strain