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Neurological changes following application of Trigenics sensorimotor treatment protocols
A case study of Achilles Tendonitis |
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Written by Lauri Rannama , MSc, RTP
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Lauri Rannama , MSc, RTP
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July 27, 2009 – The present study was designed to investigate the neurological effect of using the Trigenics sensorimotor treatment system. A case of achilles tendonitis was used with Trigenics applied to the affected tendon and the soleus muscle. In a recent pilot study using 40 subjects, it was found that application of the Trigenics myoneural stengthening procedure (TS) to inhibited-weak muscles measurably increased strength from 20-70 per cent (mean average 37 per cent). This study was also designed to investigate how this might occur.
Trigenics is a neuromanual sensorimotor assessment and treatment system that uses an interactive multimodal approach. Trigenics is distinctly different than other manual treatments in that it is primarily based upon a neurological, rather than mechanical, model of treatment. Trigenics myoneural procedures involve the synergistic, simultaneous application of three treatment techniques/modalities to achieve a summative neurological effect.
These are:
1) Reflex Neurology
2) Mechanoreceptor Manipulation (deformation)
3) Cerebropulmonary Biofeedback
Its main mode of action works on the basis of integrating neurological convergence projection and amplitude summation from both segmental (PNS) and suprasegmental (CNS) pathways. The multimodal stimulation approach utilized in Trigenics is consistent with the principles of neuroplasticity and enhanced corticoneural reorganization of the somatosensory and sensorimotor systems.
The synergistic application has demonstrated that it can instantaneously relax, strengthens and/or lengthen muscles, as well as reduce inflammation and pain. It is expected that restoration of sensorimotor afferentation to the affected area will enable proper joint neurokinetics with the effect of associated pain reduction. It is known that restoring the normal length- tension relationship will affect EMG- and reflex patterns.
Surface electromyography (EMG) has a long tradition, and broad application, for measuring muscular activity8. In studies of occupational musculoskeletal disorders, EMG has been used to obtain quantitative measures of physical exposure. EMG reflects the internal load and is thus dependent on both the external load, implied by the task, and individual factors.
The surface electromyogram (EMG) provided an enticing way to examine the role of the CNS. In this study the main reason for using the EMG was to investigate the agonist-antagonist relationship during isometric contraction in low intensity level treatment. The mean frequency (MF) of the power spectrum presenting the changes in: (1) muscle fiber-conduction velocity18 and (2) synchronization of the MU firing3. A popular opinion is that MF shifts are caused by a decrease in membrane conduction velocity occurring during the fatiguing process due to local metabolic changes and ion shifts in the muscles4. At or below 30 per cent maximum voluntary contraction (MVC), when blood flow is likely maintained, MF shifts are primarily due to neural changes10.
The H-reflex technique was used to evaluate the motorneuron exitability of triceps surae muscles. The soleus H-reflex has been shown to be a monosynaptic reflex elicited by electrical stimulation of Ia afferents in the posterior tibial nerve11. The size of the reflex is thus a measure of the central gain of the monosynaptic stretch reflex and it is determined by:
1. the transmission across the synapses of the Ia afferents and
2. the exitability of the motorneuronal pool.
Changes in the amplitude of the reflex, during various voluntary tasks, express the short-term changes in these two parameters. In particular, we have measured the maximal reflex electromyographic (EMG) response (H-max) and the maximal direct EMG response (M-max) to determine the ratio between the two (H/M-response), since this is considered a suitable value for illustrating, within a pool, the efficacy of type Ia-alphamotorneuron synapses 17.
Materials and Methods
Subject
25 year old female elite sprint runner height 168 cm; weight 58 kg. Achilles tendonitis was diagnosed one month prior to her original presentation.
Protocol
Before treatment, the active plantarflexion and dorsiflexion with straight leg was measured using a standard goniometer. After that, the subject was seated in a specially designed dynamometric chair with the involved leg flexed to 90 degrees at the knee angle. The foot was strapped to an aluminum footplate and the ankle was dorsiflexed to 20 degrees. A strain-gauge transducer connected with the footplate sensed the torque acting on the footplate. The plantarflexors’ strength MVC force was measured using the dynamometer connected with the footplate. After another break, the H-reflex (Hmax) and maximum M-wave (Mmax) were elicited. Following that, the subject continued with the sustained isometric contractions 20 per cent of MVC with 60 seconds to determine EMG activity. The Trigenics strengthening treatment protocol was carried out within 15 minutes after initial measurements were recorded.
This measuring protocol was repeated after Trigenics treatment.
To determine the H- reflex and M-wave, the posterior tibial nerve was stimulated through a pair of surface carbon-rubber electrodes by square wave pulses of 1-ms duration. The cathode was placed over the tibial nerve in the popliteal fossa and the anode was placed under the posterior-medial side of the thigh. The evoked compound action potential (M-max) and H-reflex (H-max) of the soleus muscle was recorded using bipolar electromyography (EMG) electrodes. The following static contraction EMG activities were recorded from soleus muscle as a main mover, and from tibialis anterior as the antagonist muscle during voluntary and reflex contractions using bipolar Beckman miniature skin electrodes. The skin was dry shaved, and then cleaned with alcohol. A reference electrode was placed over the medial condyle of the tibia. The EMG signals were amplified and displayed with Medicor MG-440 preamplifiers with frequency band ranging 1 Hz-1 kHz.
The output signals from strain-gauge transducer and EMG preamplifiers were digitized on-line (sampling frequency 1 kHz) by analogue-to-digital converter installed in a personal computer. The digitized signals were stored on a hard disk for further analysis.
Results
The main results are presented in the Table 1.
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Before Trigenics
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After Trigenics
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Plantar flexion (º)
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68
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77
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Dorsal flexion (º)
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10
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12
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MVC (kg)
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104
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111
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H-max (mV)
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1,7
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2,3
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M-max (mV)
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6,2
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5,4
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H/M (m/V)
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0,27
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0,43
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PT (N)
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175
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183
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CT (s)
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0,083
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0,075
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IEMG-soleus
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0,0125
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0,0066
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IEMG-tbialis anterior
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0,0026
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0,0018
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MF-soleus (Hz)
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95,2
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87,3
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MF-tibialis anterior (Hz)
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72,3
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58,4
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Discussion
To minimize the subject’s discomfort in preparation for the experiments, two Trigenics treatments were given before the experimental session. After five days and two prior Trigenics treatments, the subject had no pain and she was ready to participate in the experiment.
As seen in the chart, the results of this study showed a significant increase in force (MVC) and electrically evoked contraction peak force (PT) of plantarflexor muscles after the Trigenics treatment. The increase in MVC may involve processes associated with central command of contraction3 as well as peripheral processes of intramuscular electrical and mechanical activity4. The ability to generate force for strength increase can also be related to neural factors (muscle activation) associated with excitation, recruitment and firing rate of motor unit. The increase of PT after Trigenics treatment, show the changes on an intramuscular level, bearing in mind that a direct relationship exists between the number of active cross bridges and the force output as well as the muscle active stiffness13. Also noted was a decrease of contraction time (CT) after Trigenics treatment showing the improvement of the intramuscular processes, specifically indicating more rapid calcium release from the sarcoplasmic reticulum.
Synchronization of motor units (MUs) has been reported by several authors3, has been shown to generate an increase in spectral components in the low frequency range of the EMG power spectrum8.A tendency towards synchronization reflects a common presynaptic input to α-motorneurons7. After the Trigenics treatment the average MF of plantarflexors and dorsiflexors shifted to lower value representing increased synchronisation of MUs or decreased muscle fiber-conduction velocity. Average IEMG of plantarflexors and dorsiflexors also shifted to lower value after the Trigenics treatment.
The increase in EMG amplitude during sustained submaximal contractions (IEMG) has been explained by: (1) facilitated motor-unit recruitment14, coupled with an increase in their average firing frequency in order to maintain the constant force reguested12 and (2) synchronization of (MU) firing9. After Trigenics, it seems that less MU recruitment is needed to maintain the same force level. Also the antagonist activity is decreased, which means less presynaptic inhibition to the plantarflexor (target) muscle. In the present study the EMG parameters showed that, after Trigenics treatment, less electrical activity is needed for a muscle to maintain the same level of isometric contraction force. This means that muscle “tone” for structural support is maintained more efficiently and movement will also occur more efficiently with less stress.
Electrical stimulation of the posterior tibial nerve in the popliteal fossa at various intensities evokes two electromyography responses in the soleus muscle: the M and the H wave. Whereas the M wave is due to direct activation of the axons of the soleus α-motorneuron pool, the H wave is the reflex discharge of the same pool in response to the orthodromic afferent volley traveling in the large diameter Ia fibers originating in the muscle spindles. The maximal H-reflex (Hmax) is elicited by submaximal nerve stimulation and is mainly due to the activation of the slow-twitch motor units6. The maximal M wave (Mmax) is elicited by supramaximal nerve stimulation and is the electrical counterpart of the activation of all motor units of the pool, including the fast-twitch units.
The Hmax to Mmax ratio is considered a suitable index for illustrating the level of reflex excitability of the motor pool, which in turn is dependent on the facilitation of the transmission between the Ia fibers an the α-motorneuron17. The Hmax/Mmax increases after endurance type training15, indicating an association between endurance and the capacity to recruit a large proportion of the whole motor pool in response to the electrically elicited Ia afferent volley.
Our result shows that the efficacy of the reflex transmission between Ia spindle afferent input and soleus α-MN, as witnessed by the Hmax/Mmax was increased after Trigenics treatment. This, in turn, shows an increased number of MNs excited and activated following Trigenics by way of an electrically evoked Ia afferent volley. The processes of altering afferent input and efferent output have been coined “resafferentation” and resefferentation by the originator of the Trigenics treatment system, Dr. Allan Oolo Austin.1
His concept is that a relative state of “dysafferentation’ develops in mechanoreceptors embedded in tissues which have become damaged or stressed and that these mechanoreceptors require “re-setting” through multi-pathway stimulation. (Oolo Austin hypothesizes that this is what occurs with Trigenics multimodal approach and draws an analogy to the “resetting” of a computer when it malfunctions by way of “freezing”.) In terms of performance augmentation for athletes, this would indicate that Trigenics treatments applied immediately prior to participation to specific muscles used in different sports, would increase performance and outcome.
Due to direct synaptic connection of Ia afferents and α-motorneurons it has been tempting for researchers to assume that the H-reflex represents faithfully the excitability of the motorneuron pool under study. However, the synaptic connection between Ia afferents and α-motorneurons is itself subject to modification. It is sensitive to mechanisms that cause changes in the presynaptic inhibition (PSI) of Ia afferent transmission which has a direct affect on neurotransmitter release at the Ia/α-motorneuron synapse5. The primary reason for this is the effect of presynaptic inhibition. PSI is mediated by the action of the inhibitory interneuron acting on the Ia afferent terminals, leading to a reduction in neurotransmitter release and a concomitant reduction in motorneuron depolarization induced by Ia activity. There is evidence that PSI could selectively alter transmission in a monosynaptic reflex pathway, and it has recently been demonstrated that this mechanism is selective enough to affect different collaterals from the same muscle spindle afferent 16.
Many spinal mechanisms will come into play secondarily, particularly through changes in reciprocal inhibition and the many reflex effects evoked by the increasingly widespread contractions. In the case of this study, the reduction in H-reflex excitability, as found before Trigenics treatment in our study, may also represent a beneficial adaptation to avoid further injury of the Achilles tendon, possibly reflecting an increase in presynaptic inhibition of Ia afferents as a result of reciprocal inhibition mechanisms associated with co-contraction of opposing muscle groups such as the tibialis anterior and soleus muscles.
Based on this study, the Trigenics treatment system may also have effect of reducing the PSI to decrease risk of injury in the elite athlete.
Although the results of this pilot study are very promising, it must be noted that it was done with one subject only, and that the results must be conclusively validated by way of further scientific research. For the clinician, one of the most challenging aspects of providing optimum rehabilitative is understanding the effect on proprioceptively mediated sensorimotor control after joint or muscle injury. As complex as the proper management of athletic-related or personal injuries can be, the neuromanual Trigenics sensorimotor treatment system appears to provide advanced, leading edge methodology for accelerated resolution and injury prevention.
References
1. Austin AO. Trigenics Clinical Applications. 2000.
2. Bigland-Ritchie B. EMG and fatigue of human voluntary and stimulated contractions. Ciba Found Symp 82: 130-156, 1981.
3. Bigland–Ritchie B., Furbush F., Woods J.J. Fatigue of intermittent submaximal voluntary contractions: central and peripheral factor in different muscles. J. Appl. Physiol. 1986, 61: 421-429.
4. Brody L.R., Pollock M.T., Roy S.H., DeLuca C.J., Celli B. pH- induced effects on median frequency and conduction velocity of the myoelectric signal. J. Appl. Physiol. 1991, 71: 1878-1885.
5. Brook JD, Cheng J, Collins DF, McIlroy WE, Misiaszek JE, Staines WR. Sensori-sensory afferent conditioning with leg movement: gain control in spinal reflex and ascending paths. Prog Neurobiol 51: 393-421, 1997.
6. Calancie B and Bawa P. Motor unit recruitment in humans. In: The segmental Motor Systems, edited by Binder MD and Mendell LM. Oxford, UK: Oxford Univ. Press, 1990, pp 75-95.
7. Farmer SF, Halliday DM, Conway BA, Stephens JA, Rosenberg JR. A review of recent applications of cross-correlation methodologies to human motor unit recording. J Neurosci Methods 74:175-187, 1997.
8. Hagg GM Interpretation of EMG spectral alterations indexes at sustained contraction. J Appl Physiol 73:1211-1217, 1992.
9. Krogh-Lund C., Jorgensen K. Myo-electric fatigue manifestations revisited: power spectrum, conduction velocity, and amplitude of human elbow flexor muscle during isolated and repetitive endurance contractions at 30 % maximal voluntary contraction. Eur. J. Appl. Physiol. 1993, 66: 161-173.
10. Löscher W.N. Cresswell A.G., Thorstensson A. Electromyographic responses of the human triceps surae and force tremor during sustained submaximal isometric plantar flexion. Acta Physiol. Scand. 1994, 152: 73-82.
11. Magladery J.W., McDougal D.B. Electrophysiological studies of nerve and reflex activity in normal man. I. Identification of certain reflexes in electromyogram and the conduction velocity of peripheral nerves. Bull. John Hopkins Hosp. 1950, 86: 265-290.
12. Maton B, and Gamet D. The fatigability of two agonistic muscles in human isometric voluntary submaximal contraction: an EMG study. II. Motor unit firing rate and recruitment. Eur J Appl Physiol 58: 369-374, 1989.
13. Metzger JM, and Moss RI. Shortening velocity in skinned single muscle fibres. Biophys J. 1987, 52 127-131.
14. Moritani T, Muro M, NagataA. Intramuscular and surface electromyogram changes during muscle fatigue. J Appl Physiol 60:1179-1185, 1986.
15. Pérot C, Goubel F, and Mora I. Quantification of T and H responses before and after a period of endurance training. Eur J Appl Physiol 63: 368-375, 1991.
16. Rudomin P, Jimenez I, Quevedo J. Selectivity of the presynaptic control of synaptic of effectiveness of group Ia afferents in the mammalian spinal cord. In: Rudomin P, Romo R, Mendell LM (eds) Presynaptic inhibition and neural control. Oxford University Press, New York, pp 282-302, 1998.
17. Schieppati M. The Hoffmann reflex: a means of assessing spinal reflex excitability and its descending control in man. Prog Neurobiol 1987, 28: 345-376.
18. Stulen F., DeLuca C.J. Frequency parameters of the myoelectric signal as a measure of muscle conduction velocity. IEEE. Trans. Biomed. Eng. 1981, 28: 515-523.
Author Bio
Lauri Rannama , MSc, RTP. 31 year-old, Physiotherapist of Estonian National Ski Team. Lecturer at University of Tartu and University of Tallinn.
As physiotherapist, participated in Olympic Games, in Salt Lake City, Torino and Beijing.
Co-author of 3 sport medicine books. Last article : Pääsuke M., Rannama L., Ereline J., Gapeyeva H., Ööpik V. (2007). Changes in soleus motorneuron pool excitability and surface EMG parameters during fatiguing low- vs. high-intensity isometric contractions. Electromyogr. Clin. Neurophysiol. 47 (7-8): 341-350.
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