The miogenic trigger points (MTP) are not a separate nosologic unit. Though they are frequently found in the clinical manifestations of variouns (not only neurologic) pathology there is no unanimity in understandig of the essence, pathogenesis and terminologic identification. There are more than 25 names which give different names to one and the same state of the muscle. The name - myogenic trigger point was chosen in order to achive mutual understandig among the representatives of different medical specialities. It is correct from the view-point of neurophysiology and neuropathology.

The participation of MTP in pathomorphism of the basic neurologic pathology has not been studied up till now. It was due to the simplified conception of the MTP pathogenesis as a mere local distonically dystrophic process.

The aim of our work was to study the clinical and neurophysiologic MTP characteristics in different structural lesions of the nervous system as well as the substantiation of MTP pathogenesis and the development of adequate methods of treatment.

Analysis of clinico-electrophysiological MTP characteristics was necessary under the following conditions: 1) absence of the nervous system disturbance; 2) nervous system disturbance in the efferent and afferent links; 3) affection of the central mechanisms of motor regulation.

Material and methods. According to 10 year studies there were 120 patients with MTP, 80 patients with facial nerve neuropathy, 58 - with syringomyelia, 50 - with spastik torticollis. Patients with MTP had no disturbances of the nervous system and the spinal cord neither systemic muscle diseases - "pure" MTP. In the group of 15 patients with neuropathy of facial nerves the development of contracture was estimated from paresis to contracture, the state of mimic muscles was estimated regularly during the pathologic process. In patients with algetic syringomyelia there were no arthropathies, myorrhexis and other vegeto-trophic disorders. Patients with spastic torticollis had tonic and tonico-clonic hyperkinesia, there were no MTP in the clonic form.

Investigation methods included kinetic palpation of the skeletal muscles according to the traditional method by Marsov. 1) Facial muscle palpation was estimated according to the original method of G.Ivanichev,1984. 2) The firmness of muscless was estimated by registration of the deformity pressing it using the external alternating exertion, randing from 1,0 to 5,0 kg/cm.

Electrophysiologic studies included: 1) Electromyography by the superficial and needle electrodes with presented histogram of the PMUA (potentials of motor units action) distribution in the MTP centre and periphery. 2) Registration of polysynaptic reflex reactions and the phenomenon of voluntary activity inhibition. 3) Estimation of muscle reciprocal relations-antagonists having MTP. 4) Determination of contration wave rate throughout the muscle. 5) Determination of the muscle differential stimulation when muscle being irritated with stimuli of varions duration and intensity. 6) Determination of the frequency of potential movement in the MTP centre and periphery.

Results. MTP in the basic group. The basic MTP clinic characteristics should be called the local induration of a muscle of different size, the local reflex pain (trigger phenomenon), increase of tenderness in passive muscle stretching as well as increased mechanical stimulation. The MTP localisazion in the skeletal muscle as compared to the data presented by T.Travell given in the book written with D.Simons as co author.

Accordind to our understanding the phenomenon of the reflex pain is a rather changeable clinical parametr both from view - point of intensity and direction. The phenomenon depends on the patient's emotional background and the initial muscle state. Thus following dynamic work of MTP muscle the spectrum of the reflex pain has entirely different characteristics than after the performance of the static work. The different picture of reflex pain is observed when it is induced by pressure or by stretching as well. It is worth mentioning that the maximum pain is abundant in the first seconds. Then due to adoptation the pain is localized and seems to be the secondary pains. The MTP magnitude and the extent of tenderness are incomparable indices. MTP division according to their magnitude to Cornellius', Muller's nodules, to Shade's, Lange's myogelosis have no practical sense.

In this paper we do not present the deseriptive characteristics of MTP localisazion in the different muscles. This section is kery well described in T.Travell's and D.Simon's book (1984). We should like to point here that MTP may occur in any muscle. In the structure of one muscle MTP may occur in any part but predoninantly they ara localized in the thickest (strongest) part. The most characteristic feature of hypertonicity is a significant rise in tenderness during muscle stretching. The diagnostic value of this test is perfect, it is better than the phenomenon of vibration response /reproduction of pain picture during energetic beating/. Rise in tenderness pain that is familiar to the patient and its disappearance after brief resistance of mild intensity is typical of MTP. During further stretching of the muscle MTP tenderness is again increasing to a certain degres with the following decrease when the brief efforts are resumed. This method is based on the MTP postisometric relaxation /K.Lewit, 1982/. This diagnosis may be called therapeutic diagnostics which may be of use not only in neurology.

Changes in bioelectric MTP activity in electromyography using surface electrodes have not been detected. The expected high EMG activity corresponding to the degree of tenderness was not evident. In response to the needle electrode insertion into the MTP - the bioelectric activity is followed by plunding potencials and by a complex of discharges different in their form and duration. There are polyphase /up to 30%/ and positive sharp waves along with the fibrillation potential. The duration of this activity is from several seconds /to one minute/. Then at rest bioelectrical activity is not detected. During voluntary tension the amplitude of potentials of MTP is lower by 25-35% than in the adjacent area. During a passive stretching of the muscle there is a significant increase in the activity and it is almost equal to the bioelectrical activity of the voluntary effort. The comparison of MTP in the centre and in the periphery showed some significant differences. If EMG activity of the centre seemed to be low, with small amplitude and its quick reduction (fall), then in the periphery of hypertonicity all indicated parameters are detected in the other quantitative and qualitative ratio. Apparently, the constant muscle stretching of the transitional zone is evidently originated on the border of MTP periphery and the normal muscle which produces EMG "anxiety" even of rest, particularly during a mild muscle sretching.

Such distibution in durations is characteristic for the distorted spatial relations of MU of the terminals not resulting from the denervation processes but the distorded architectonics of the muscle with MTP.

The velosity of wave stimulation transfer through MTP is considerably reduced. This change cannot but probably influence on biomechanics of the muscle contraction. This is manifested dy the destruction of reciprocal relatios of the muscles if one of them has MTP. Electromyographic assessment of the dynamic load (50 complete flexions and extentions of the hand with increased speed showed a change in EMG structure. In the presence of MTP in the general extensor of the hand at the moment of flexor contraction of the hand the extensors are not sufficiently relaxed. During extensor contraction EMG of the contractive activity occurs. THe distrubance of the spinal cord segmental apparatus activity is found using registration of polysynaptic reflex responses and muscle voluntary activity inhibition. The characteristic feature of MTP must be considered depressed inhibition of bioelectic activity - "silence phenomenon" - absence in the MTP area.

Myogenic trigger point in clinical manifestations of contracture of mimic muscles /motor neuron affection/. Hypertonicities of mimic muscles are formed in at extent of the facial nerve affection. During the mild nerve affection they disappear as the muscle function are restored, in severe they disappear together with the affected musculature. In avarage neuropathy hypertonicities undergo a pathalogic course. The main symptom of contracture - spasm-paresis occurs on 25-30 days. When contracture is complete MTP are found in any mimic muscle, their localization is sufficiently typical. Both elongated and shortened potencials are found in hypertinicities by electromyography when contracture has been formed. This combination of durations evidently indicates the spatial change of the motor unit terminals in mimic musculature denervation. We consider some "stamped" positive potencials of 15-18 ms duration to be a specific EMG feature, they are found in the zones of junction of different muscle groups. As evidenced by Lambert and B.M.Gekht these potencials are a sigh of intermuscular impulse transmission. To prove the hypothesis of an "artificial synapse" we have presented the method of consecutive ortho antidromic stimulation of the distal branches, of the facial nerve in the region of eye angle and mouth /G.Ivanichev/. The possibility of interneural impulse transmission in the zone of affection /Waltman and co-worcers, 1956/ has not been proved by us. Thus, MTP become the site of intermuscles transmission of motor impulses that is aphatic intermuscular transmission when the muscles are denervated partially.

Miogenic trigger point in clinical manifestations of algesic syringomyelia /afferent neuron affection/. Analysis of the clinical picture of algesic syringomyelia indicated that the 75% tenderness of soft tissues and muscles first of all in the analgesia zone is due to MTP but not to irritative processes in the posterior horn of the spinal cord. The role of irritative reactions is known to be suggested by Schlesinger. Our data confirm K.Lewits view-point who was the first to assume the existence of pains in syringomyelia to be due to the functional blockades of the spinal joints and to the concomitant muscle spasms. The electromyographic picture of MTP in algesic syringomyelia has no essential differences from MTP of general origin. Thus MTP can be formed when afferent neuron is affected.

Miogenic trigger point in clinical manifestations of spastic torticollis /central mechanism affection in tonus regulation/. MTP are revealed only in the tonic form of torticollis are more coarse than the "usual". They are detected against the background of the tense muscle as a considerable indurations. The long tonic spasm of the neck muscle rotators produces the combined coarse fuctional blocade of the cervical vertebto-motor segments.

The most vulnerable levels are the cranio-cervical transition and mid cervical segments. These mechanisms underlie a stable pathologic dynamic stereotype which can support the head faulty posture without pathologic affect on the central mechanisms. In this sense the peripheric pathologic mechanism of torticollis (MTP plus articular blockades) has a far higher pathologic activity than the central structural tonus regulations.

The regularity of polysynaptic reflexes manifestations in the tonically strained muscles is rudely distorted. There was no bioelectric activity inhibition of the strained muscles when the polysinaptic reflexes were produced.

The study of the cerebral blood flow showed the essential disturbance of hemodynamics in patients with torticollis. These disturbances are detected in the vertebro-arterial system: the blood flow is the poorest one on the side opposite to the head turn. This pathologic hemodynamics is due to a stable cervical musculature tension and to the change of the main vessels tonus.

Thus MTP in spastic torticollis are detected against the background of the previously tonically strained musculature of the neck, finally forming a complex system of active peripheral pathogenetic factor.

Pathogenesis of myogenic trigger point. The trigger moment of MTP development is static /isometric/ work of the muscle with minimal intensity within a long period of time. This kind of work may be due to the reflex tension of the muscle in the pathology of an internal organ, functional blocades of joints etc. The space deformation of the working muscle occurs during prolonged static work. The most strong, the more active part from view-point of innervation streches the most thin and weak one /Beritov I.S., 1947/. When the tension is off this deformity disappers due to the natural muscle elasticity. During continuous static work of the muscle the induced deformity produces the next stage of the pathologic changes. First of all this is the distortion of proprioceptive afferentation due to the spatial reorganization of the receptors. The main tendency of afferent disorganization is the disbalance of impulses of the dynamic and static madality. This pathologic situation is responsible for the following changes in the activity of the segmental apparatus of the spinal cord.

1) The disorder of the presynaptic inhibition mechanisms providing "gate control" at aditis medulla spinalis. As a result the primary pattern of nociceptive impulsation is formed which corresponds to the muscle hypertonicity.

2) The disturbance of the motor neuron impulse activity. As a result a territorial change of the motor unit, distortion of coordinative relations, muscular contraction rate delay, descrease of strength occur.

3) The disturbance of non impulsive activity /neurotrophic control/. This is evidenced by the muscle metabolism change and the development of dystrophic processes in it.

The pathologic changes in the activity of the segmental apparatus are the basis of pathologic alterations, regulating the suprasegmental structure influence. This means the change in the program motion that is the formation of the pathologic dynamic stereotypes. These changes may provide varions emotional stresses in MTP that is a personal estimation of the tenderness and other MTP manifestations. As a result of these complicated changes uniting the periphery, segmental apparatus, the suprasegmental structures, a stable pathologic sensomotor system is formed , MTP being its generator. In mimic musculature contraction the development of the muscle hypertonicities occurs according to another schema.

The main stages are:

1. At any extent of facial nerve affection hypertonicities in the muscles are formed on the 3-4 day according to Vulpian's tonomotor effect. In the mild nerve affection these hypertonicities dysappear as the muscles are regenerating while in severe - they disappear together with degenerative muscle.

2. At the average extent of affection hypertonicities have a chance for further development - they bring together different muscle bundles, they cause the deformity of the receptor apparatus. As a result there is a possibility of intermuscular transmission of impulses. Pathologic sinkinesias of different muscles are explained by this pathologic intermuscular synapse. The disbalance of proprioception is also a base of formation of the pathologic sensomotor system "trigeminal-facial nerve" with the secondary involvement of the limbicoreticular system.

The details of this process were presented in monography by G.Ivanitchev (1992).

Treatment of myogenic trigger point. It includes a complex of therapeutic measures in order to eliminate the distruction of the pathologic sensomotor system. First it must eliminate MTP (pressure, extension, postisometric relaxation, irrigation). Second, normalization of the activity of the spinal cord segmental apparatus - physiotherapeutic procedures, drugs, acupuncture. Third normalization of suprasegmental influence on the motor activity and sensor systems, physical training, treatment of psychic disorders.