Muscular-tonic syndrome - causes, symptoms, treatment of muscular-tonic syndrome in Moscow at the Spina Zdorova clinic

What is muscular-tonic syndrome

Muscular-tonic syndrome is characterized by a painful increase in muscle tone when the muscle is overloaded in an uncomfortable position (postural overload), reflex muscle spasm due to spinal pathology, mechanical injury to muscles and bones, and is also often found in diseases of internal organs.
Most often, back pain is associated with muscle spasm rather than with osteochondrosis and disc herniation. For example, in 96% of cases, lumbodynia occurs with muscular-tonic syndrome, which forms the basis of this condition.

One of the options for postural overload is compensatory muscle overload. An example is the lower cross syndrome, the essence of which is a compensatory overstrain of the muscles of the lower back and anterior thigh muscles in response to weakness of the abdominal muscles and gluteal muscles.

With degenerative changes in the spine, especially when a disc herniation occurs, vertebrogenic muscular-tonic syndrome is formed. This tone is aimed at fixing the damaged segment and is of a therapeutic, protective nature. But with prolonged existence of increased tone, i.e. with chronic muscular-tonic syndrome, it loses its protective function and becomes pathological, being an independent cause of back pain.

At the same time, long-term spasm of the paravertebral muscles (muscles along the spine) has a negative effect in the form of increased load on the intervertebral joints, intervertebral disc and spinal ligaments, which in itself is a prerequisite for the development of degenerative-dystrophic changes in the spine (osteochondrosis, arthrosis of the intervertebral joints , spondylosis).

Often, spasmed muscles cause compression of the neurovascular bundles, and pain is noted both at the site of pinching and in the zone of innervation of the pinched nerve fiber, where numbness and muscle weakness are also observed.

The mechanism of pain can be explained as follows: when a muscle spasms, capillaries are compressed and venous outflow is disrupted, leading to local tissue ischemia (a decrease in the level of incoming oxygen and glucose), as a result of which metabolic products accumulate, contributing to the development of edema. Edema, like the spasm itself, affects pain receptors, which results in pain. Long-term metabolic disorders lead to the destruction of the cell, in the place of which fibrous tissue grows.

Diagnostics

History of the disease, patient complaints (duration of pain, intensity of pain, nature of pain, connection with movement or other provoking factors.
Assessment of neurological status. Condition of the muscles, presence of areas of spasm or pain points (triggers), mobility of spinal segments, movements that cause increased pain.
X-ray of the spine (when examining the cervical spine, it can be carried out with functional tests. X-ray can detect pronounced degenerative changes (in bone tissue).
MRI and CT. These studies are necessary to visualize degenerative changes in soft tissues (disc herniation, protrusion, compression of neural structures)
An EMG study allows you to determine the degree of conduction disturbance in nerves and muscles.

Symptoms of muscular-tonic syndrome

Muscular-tonic syndrome with a sharp muscle spasm is characterized by acute, shooting pain, while in a chronic course the syndrome more often manifests itself as aching pain and a burning sensation. In the latter variant of development, muscular-tonic syndrome, in addition to pain, may manifest itself:

insomnia;
decreased performance;
apathy and depression;
increased irritability.

Symptoms depending on the location of the muscular-tonic syndrome

Cervical muscular-tonic syndrome is characterized by:

shooting pain in the neck;
pain in the upper neck, radiating to the temple, part of the forehead and eye socket on the same side;
numbness in the back of the head;
numbness, pain and weakness in the arms due to spasm of the scalene muscles;
tinnitus.

Muscular-tonic syndrome at the thoracic level:

more often manifested by aching, burning pain between the shoulder blades;
feeling of numbness between the shoulder blades;
pain along the ribs;
can imitate the pain characteristic of heart disease (burning sensation, compression behind the sternum).

Lumbar muscular-tonic syndrome is characterized by:

lumbago (lumbago in the lower back);
lumbodynia (lower back pain);
lumboischialgia (lower back pain radiating down the back of the thigh).

Often pain in muscular-tonic syndrome is perceived as a manifestation of diseases of the internal organs. Thus, muscular-tonic syndrome of the lumbar region can be interpreted as a manifestation of renal colic. In this case, it is important to carry out additional diagnostic measures, for example, ultrasound of the kidneys, to exclude renal pathology. At the same time, renal pathology itself can initiate the development of muscular-tonic syndrome.

How does it manifest itself in women and men?

The clinical picture of myotonia depends on where the lesion is located. Patients with impaired muscle activity in the arms, legs, face, shoulders, and neck experience difficulties with walking, maintaining posture, speech function, controlling facial expressions, and eating.

Common symptoms of myotonic syndrome include:

muscle weakness;
apathy;
fatigue;
enuresis;
dysfunction of the gastrointestinal tract: intestinal colic and chronic constipation;
cephalgia of unknown etiology;
hunching, stooping;
loss of stability; imbalance;
myopia;
speech disorders;
decreased intelligence;
unsteady gait during sharp descents and steep ascents.

Most often, the disease first appears in childhood. Sick babies have more difficulty holding their heads up than healthy children; they begin to walk and talk later. A child with myotonic syndrome is unable to control his or her movements normally.

They experience stool disturbances, the development of chronic constipation, dysfunction of the bile ducts and bladder.

Myotonic syndrome in adults can manifest itself as hypertrophy of overstrained muscles and an increase in their volume. Patients with myotonic syndrome often look like bodybuilders.

When the muscles of the face and neck are affected (cervical myotonic syndrome), there is a change in the patient’s appearance, a change in the timbre of the voice, a violation of swallowing and respiratory processes - shortness of breath and dysphagia develop.

Treatment of muscular-tonic pain syndrome

Vertebroneurologists are involved in the diagnosis and treatment of pathology. In most cases, the doctor, based on the history and clinical picture of the disease, can make a diagnosis based on the data obtained during examination of the patient. After making a diagnosis, the doctor determines how to treat muscular-tonic syndrome. Therapy can be based on drug and non-drug methods. Recently, preference has been given to non-drug therapy as it is more effective for this pathology:

soft manual therapy techniques;
acupuncture;
use of orthopedic collars and corsets;
physical therapy and kinesiotherapy;
deep tissue massage.

If necessary, during the acute period of pain, it is possible to use medications:

non-steroidal anti-inflammatory drugs;
muscle relaxants (to relax muscles);
B vitamins (for nutritional support of nerve structures, some of these vitamins also have an analgesic effect).

Tunnel syndromes as a cause of pain in the neck and arm

Reflex muscular-tonic syndromes are dominant among all manifestations of osteochondrosis of the cervical spine. Among reflex muscular-tonic syndromes at the cervical level, tunnel syndromes occupy a special place. Due to the fact that these syndromes manifest themselves with similar clinical symptoms, most authors of English-language scientific works use the term “the thoracic outlet syndrome” [2]. This term combines: – anterior scalene muscle syndrome (ASMS); – cervical rib syndrome; – costoclavicular syndrome; – pectoralis minor muscle syndrome (PMMS); – hyperabduction syndrome. With all of these syndromes, a combination of compression of the subclavian artery and brachial plexus is possible, which makes it possible to designate them as neurovascular syndromes. The most common are SPLM and SMGM [3]. The occurrence of SPLM, or scalenus syndrome, or Naffziger syndrome (named after the author who described it) is due to certain anatomical and topographical features. The anterior scalene muscle originates from the transverse processes of the III–VI cervical vertebrae, ending at the anterior edge of the first rib (Fig. 1). The subclavian artery and the lower trunk of the brachial plexus pass between the anterior scalene muscle and the first rib; the subclavian vein is located in front of the muscle. Tonic tension of the anterior scalene muscle causes the appearance of this syndrome. SPLM is often a symptom of cervical osteochondrosis, but this is often ignored by clinicians, because other, more striking clinical symptoms are the focus of medical attention. However, patients with subclinical forms of scalenus syndrome suffer longer, and the course of exacerbations of cervicalgia is more severe. Timely detection of scalenus syndrome has not only therapeutic and social significance, since it improves the patient’s quality of life, but also economic significance, since it reduces the number of days of disability and improves the quality of work performed by the patient. SPLM debuts predominantly (in more than 2/3 of patients) between the ages of 30 and 60 years, during the most active period. The main provoking factor in the development of SPLM is long-term static exposure of the head and upper limbs. When moving, the nerves are subjected to various loads (compression, stretching, bending), which are usually tolerated without pain or any functional impairment. As a result, in order to function adequately, the nerve must have freedom to glide through surrounding tissues and structures. Under physiological conditions, during limb movements, the nerve is capable of sliding in the longitudinal direction within a few millimeters, which provides nerve protection [4]. Even a slight decrease in the mobility of the nerve during limb movement can lead to microdamage and the formation of adhesions, further limiting the movement of the nerve. This creates a vicious circle, since adhesions, in turn, contribute to disruption of the outflow of blood and lymph, the development of swelling of the connective tissue sheaths of the nerve and compression of nerve fibers [5].

Clinically, SPLM is manifested by pain (in more than 85% of cases), which spreads along the inner surface of the shoulder, forearm and hand to the ring finger and little finger. Pain and sensory disorders increase with movements in the cervical spine. Sometimes pain radiates to the occipital region, especially when turning the head, sometimes to the chest, which requires the exclusion of angina. The pain intensifies during a deep breath, when turning the head in the healthy direction, at night. The pain increases significantly when moving the arm, especially when abducting it. Characterized by feelings of heaviness, weakness in the arm, and tension in the neck muscles. Vascular-trophic disorders gradually develop: coldness of the limb, cyanosis, numbness, swelling, brittle nails, decreased hair growth, weakening of the pulse, and sometimes the disappearance of the pulse when raising the arm and tilting the head in the same direction or with a maximum turn of the head in the opposite direction.

It should be noted that the neurovascular bundle can be subject to compression not only by the scalene muscle, but also by the accessory cervical rib. Cervical ribs can be 1- or 2-sided, have different sizes and degrees of clinical manifestations. The average incidence of cervical rib in the population is 6%. Cervical ribs are 3 times more common in the female population. There are 4 degrees of development of the cervical rib: 1) the cervical rib is limited by the transverse process of the 7th cervical vertebra; 2) the cervical rib extends beyond these limits, but does not reach the first rib; 3) the cervical rib is connected to the first rib through a ligament; 4) the formed cervical rib is connected to the sternum. SPLM clinically develops in every tenth owner of a cervical rib due to provoking factors. A vicious vicious circle develops, which is maintained by the tension of the anterior scalene muscle. In addition to the cervical rib, compression of the neurovascular bundle can be caused by a fracture or deformation of various origins of the clavicle and the first rib. According to B. Judovich and W. Bates, intraspinal tumors, C4–C7 radiculopathy, irritation of the phrenic nerve, myocardial infarction, etc. can lead to reflex tension of the anterior scalene muscle. The clinical picture of cervical rib syndrome is not much different from SPLM. The classic appearance of a patient with cervical rib syndrome is characterized by low shoulders and a seal-like appearance. Often in the supraclavicular region it is possible to palpate the cervical rib of one size or another. When pressing on the cervical rib or the large transverse process of the 7th cervical vertebra, pain and paresthesia in the arm arise or intensify. Less commonly, a systolic murmur can be heard during auscultation. The diagnosis of cervical rib syndrome is based on a typical clinical picture, a positive arm abduction test, as well as radiographic findings (elongated transverse processes of the 7th cervical vertebra or cervical rib).

An objective examination of scalenus syndrome in most cases reveals swelling in the supraclavicular fossa, which is explained by compression of the lymphatic vessels of this area due to changes in the anterior scalene muscle. The anterior scalene muscle itself is sharply tense. Percussion in the area of the projection of the scalene muscles provokes increased pain in the neck with possible irradiation to the arm. Neurological symptoms are manifested by a complex of sensory, motor and vegetotrophic disorders. The latter can manifest themselves in a range from swelling of the hand and mild acrocyanosis to severe trophic disorders.

Significant compression of the subclavian artery leads to a weakening of the pulse in the radial artery of the arm of the affected side. Patients in certain professions, such as plasterers, cannot work with their arms raised. During provocative tests: turning the head to the healthy side and taking deep breaths, the pulse may disappear completely, which is associated with additional tension in the scalene muscles, which are also auxiliary muscles of inhalation. When performing Dopplerography of neck vessels, it is also necessary to use a test with turning the head in the healthy direction, which significantly increases the diagnostic value of this method [6]. Objective diagnostic methods are especially necessary if SPLM manifests with symptoms of vertebrobasilar insufficiency with gradual development or acute, simulating the picture of compressive radiculopathy [7]. A possible deterioration in cerebral circulation is due to the fact that the vertebral artery, which is of cardinal importance in the blood supply to the brain, departs from the subclavian artery, which is subject to compression.

Early detection and adequate treatment of SPLM will help to avoid such an urgent and dangerous complication as thrombosis in the subclavio-vertebral-basilar system, which requires urgent surgical intervention. In case of SPLM, radiography is required to exclude cervical ribs or hypertrophied transverse processes, deformities of the clavicle, and the first rib. Electroneuromyography is considered a generally accepted method for diagnosing tunnel syndromes. However, at the initial stages of compression, the insufficient information content of this study can lead to erroneous conclusions [8]. When the brachial plexus nerves are compressed, the thick myelin fibers that carry information from proprioceptors are primarily damaged, which leads to functional muscle weakness. Detection of afferent paresis by manual muscle testing is currently considered as a more promising method for early diagnosis of SPLM [9]. Since there are more similarities than differences between the clinical manifestations of various tunnel syndromes in this area, angiographic methods of radiodiagnosis are sometimes of decisive importance. It is advisable to conduct a hagiographic study in a position with the arm abducted and the head turned to the healthy side.

Differential diagnosis Differential diagnosis of SPLM should be made with Paget-Schroetter syndrome, compression of the cervical spinal root, Raynaud's disease, obliterating endarteritis. Paget–Schroetter syndrome is an acute thrombosis of the proximal subclavian vein with possible extension to the axillary and brachial veins, resulting in obstruction of venous drainage in the arm. The core of the clinical picture of Paget–Schroetter syndrome is swelling and cyanosis of the arm on the affected side. The development of the disease is facilitated by a number of features of the subclavian vein, located surrounded by bone and tendon-muscular formations. Men (4:1) with well-developed muscles and those involved in sports or heavy physical labor are more often affected. As mentioned above, aggravation of clinical disorders when turning the head in the healthy direction is typical for scalenus syndrome. If pain increases when turning the head to the painful side, it is necessary to eliminate compression of the cervical spinal root.

SPLM differs from Raynaud's disease by affecting only one limb, trophic changes and lack of response to cold; from obliterating endarteritis of the upper extremities - increased pain when pulling the arm down while simultaneously turning the head to the healthy side. A pathognomonic sign of SPLM is a noticeable improvement in the condition with novocainization of the muscle. If the clinical picture is associated only with pathological muscle tension, then after its novocainization almost all symptoms should regress. In the case of “secondary” muscle damage, for example against the background of radicular syndrome, after novocainization the situation will not change significantly [10]. SMGM and Wright–Mendlovich hyperabduction syndrome are caused by muscular-tonic, trophic disorders in the pectoralis minor muscle, provoking compression of the neurovascular bundle passing under it (subclavian artery and vein, trunk of the brachial plexus). The pectoralis minor muscle originates from the II–IV ribs, rises diagonally upward and attaches to the coracoid process of the scapula (Fig. 2). The designation “hyperabduction syndrome” is legitimate in cases where the provoking factor of the tunnel syndrome is a strong, prolonged abduction of the arm (hyperabduction during anesthesia, during sleep with the head thrown back, frequently repeated jerking movements with abduction of the arm and raising it up).

The main clinical manifestations of VMS: pain in the area of this muscle, more at the level of the III-V ribs, possible irradiation to the neck, paresthesia in the anterior chest wall, weakness in the arm, more in the distal parts, autonomic disorders. The Wright test is of great diagnostic importance for SMGM - the hand is raised and placed behind the head. With such a movement, the neurovascular bundle is subjected to even greater compression under the pectoralis minor muscle. The test is considered positive if after 30 s a pain syndrome in the corresponding localization appears or intensifies, autonomic disorders increase (pallor and swelling of the fingers), and the pulse in the radial artery weakens [11].

During palpation examination (the patient's arm is retracted posteriorly and downward), the pectoralis minor muscle can be felt through the relaxed pectoralis major muscle during a deep inspiration. Muscle infiltration with procaine can be carried out both through the axillary region and through the pectoralis major muscle [12]. The difference in the clinical manifestations of SMGM and SPLM is that for lesions of the anterior scalene muscle, a violation of the venous outflow and, as a consequence, swelling of the hand and “stiffness” of the fingers are more typical. SMHM should be differentiated from Steinbrocker syndrome (shoulder-hand syndrome), which at its onset is characterized by excruciating pain in the shoulder and hand, reflex contracture in the shoulder joint with further formation of ankylosis.

Treatment For effective treatment of tunnel syndromes, it is necessary to understand the cause and mechanisms of compression and apply an integrated approach to therapy [13]. One of the important conditions for recovery or achieving long-term remission is the elimination of stereotypic movements that contribute to compression of the neurovascular bundle. Therapy for tunnel syndromes should begin with conservative measures, such as novocaine blockades (hydrocortisone can be administered additionally), physiotherapy (diadynamic currents, ultra-high frequency therapy, procaine electrophoresis), physical therapy, massage. The decision to initiate therapy and the choice of medications in most cases is dictated by the duration of pain, the severity of symptoms, and the degree of dysfunction caused by the pain. Traditionally, initial therapy for carpal tunnel syndrome includes: non-steroidal anti-inflammatory drugs (NSAIDs), B vitamins and vasodilators. One of the well-known and time-tested drugs is the combination drug Neurodiclovit, developed and produced by the Austrian company (in Russia the holder of the registration certificate is). It contains the NSAID diclofenac and vitamins B1, B6, B12.

Diclofenac has pronounced anti-inflammatory activity and powerful analgesic potential. The mechanism of action of diclofenac is associated with inhibition of the activity of the enzyme cyclooxygenase (COX), which is involved in the formation of prostaglandins from arachidonic acid and the activity of the enzyme lipoxygenase. In the early 90s of the last century, two isoforms of the COX enzyme were discovered - COX-1 and COX-2. Diclofenac inhibits both COX isoenzymes, due to which the analgesic effect of diclofenac occurs earlier than in the case of selective NSAIDs. Providing both central and peripheral antinociceptive effects, diclofenac provides effective suppression of pain of various etiologies. A pronounced analgesic effect, rapid regression of inflammatory processes, including inflammatory edema, have made this drug one of the most necessary for the treatment of compression-ischemic syndromes.

Thiamine (vitamin B1) as a result of phosphorylation is converted in the human body into cocarboxylase, which is actively involved in the processes of nerve excitation at synapses. Pyridoxine (vitamin B6) acts as a coenzyme for the most important enzymes acting in nerve tissues, ensures synaptic transmission, and normalizes the ratio of excitation and inhibition processes in the central nervous system. Cyanocobalamin (vitamin B12) has a beneficial effect on processes in the nervous system, is involved in the synthesis of the myelin sheath, helps reduce pain associated with damage to the peripheral nervous system, and is necessary for normal hematopoiesis and maturation of red blood cells, cell replication and growth. The advisability of combining NSAIDs with B vitamins is to potentiate the analgesic effect, reduce the risk of side effects of NSAID therapy, increase adherence to treatment, and also reduce the cost of a course of therapy when using Neurodiclovit compared to the separate use of NSAIDs + vitamin complexes. According to a number of independent studies [14], B vitamins potentiate the analgesic effect of NSAIDs and promote faster regression of pain than NSAID monotherapy.

Indications for the use of Neurodiclovit are: inflammatory and degenerative rheumatic diseases, many pain syndromes in neurological practice (in particular, acute back pain, tunnel syndromes), disorders of the musculoskeletal system, in addition, the drug is widely used in gynecology for dysmenorrhea, adnexitis; for inflammatory diseases of the ENT organs. The drug Neurodiclovit is enteric granules of diclofenac with delayed release and separate granules of vitamins B1, B6, B12 with immediate release. Neurodiclovit is prescribed orally, during meals, with the recommendation not to chew and drink plenty of liquid. For adults, Neurodiclovit is prescribed 1 capsule - at the beginning of treatment 3 times / day, as a maintenance dose - 1-2 times / day. The average duration of therapy is 7–14 days.

Vasodilators are an addition to the complex therapy of tunnel syndromes; the most commonly used are xanthinol nicotinate, drotaverine, and pentoxifylline (vasonite). It is advisable to continue therapy with neurotropic B vitamins (for example, Neuromultivit) to increase the effectiveness of therapy and reduce the risk of disease chronicity and relapses. Indications for the surgical treatment of tunnel syndromes: the failure of the complex of treatment measures, the presence of gross impairments of motor and sensory functions, the rapid increase in symptoms with the development of contractures, the development of secondary complications (in particular, thrombosis) [15, 16].

A radical method of treating tunnel syndromes is dissection of the tissues compressing the nerve, removal, if necessary, of the cervical rib and the creation of optimal conditions for the nerve trunk and blood vessels, preventing their injury. In case of SPLM, the preference of neurosurgeons is currently given to resection of the anterior scalene muscle over as much of its extent as possible. This reduces the risk of relapse of the disease due to fibrotic changes in the specified area, and also eliminates the focus of pathological irritation. The prognosis for tunnel neuropathies depends on timely diagnosis and initiation of therapy. In the case of the development of irreversible metabolic processes in the neurovascular bundle, as well as atrophy and contractures in the innervated muscles, the prognosis is unfavorable. Timely use of NSAIDs and B vitamins allows in some cases to prevent or at least delay the onset of irreversible changes.

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