Muscular tonic syndrome of the lumbar region treatment. Muscular-tonic syndrome: what is it? In the lumbar region

(scapular-costal syndrome)- there is a reflex structure of the muscle that lifts the scapula. Pain appears in the neck, in the scapula, in the shoulder, a crunch occurs under the scapula, movements in the upper shoulder girdle are affected, which occur with combined movement in the shoulder joint, in the collarbone and in the scapula.

Functional biomechanical disorders at the level of the cervical spine can lead to the development of compression radicular syndromes, which is associated with changes in the location of the root and local edema. Compression of the roots is manifested by symptoms of loss in the motor, sensory, reflex spheres, and the development of muscle wasting. Compressions of the roots C I, C II, C III are extremely rare and functional disorders of the biomechanics of the cervical spine are not involved in their pathogenesis. Functional biomechanical disorders are involved in the mechanisms of development of compression of the underlying roots.

C IV root compression- occurs infrequently. There is pain in the shoulder girdle and collarbone. There is weakness, decreased tone and hypotrophy in the dorsal group of neck muscles (in the levator scapulae muscle, trapezius, splenius capitis, splenius capitis) and in the prevertebral muscles of the ventral surface of the neck (longus colli and capitis muscles). Hypoesthesia is noted in the shoulder girdle. Due to the presence of phrenic nerve fibers in this root, respiratory disorders occur, a decrease in the tone of the diaphragm, which leads to pain in the heart and liver. Dysphonia and hiccups may occur.

Root compression C V- rarely noted. Clinical symptoms are associated with impaired innervation of the deltoid muscle: pain in the shoulder girdle and along the outer surface of the shoulder, impaired sensitivity along the outer surface of the shoulder, weakness of shoulder abduction, hypotrophy.

Compression of the C VI root- occurs most often.

The pain spreads from the neck to the shoulder girdle, shoulder blade, along the outer surface of the shoulder, along the radial side of the forearm to the thumb. The zone of hypoesthesia covers mainly the anterolateral surface of the thumb, in which paresthesia is also noted. Weakness of the biceps brachii muscle develops, which is manifested by weakness of flexion of the forearm at the elbow joint. There is hypotrophy of the biceps brachii muscle, a decrease or loss of the reflex from this muscle.

Compression of the C VII root- occurs slightly less frequently than the previous lesion. Clinically manifested by pain radiating from the neck to the shoulder blade, along the posterior outer surface of the shoulder and along the posterior surface of the forearm to the second and third fingers. The hypoesthesia zone is observed in the form of a thin strip above the triceps brachii muscle, in the middle of the back surface of the forearm, on the middle finger of the hand. Paresthesias are noted in the second and third fingers of the hand. Hypotrophy and weakness of the triceps brachii muscle develops, which is manifested by weakness of forearm extension at the elbow joint. The reflex from the triceps brachii muscle decreases and disappears.

Compression of the C VIII root- rarely observed. The clinical picture shows mild pain radiating from the neck to the ulnar edge of the forearm and to the little finger. The hypoesthesia zone develops along the ulnar edge of the forearm and little finger. Paresthesia also appears in the little finger. The styloradial and supinator reflexes decrease and disappear.

Arthritis is inflammation of one or more joints. The disease is a common cause of loss of ability to work and disability. Modern medicine classifies the disease as difficult to treat.

Most often, doctors alleviate the course of the disease by using non-steroidal or hormonal drugs. But in this case there is no treatment, only the appearance of it is created. Inflammation may continue, causing the joint to deteriorate.

There are several types of arthritis:

• Rheumatoid. It is an inflammatory type that can destroy cartilage in the joint. The reason for the destruction is that when a cell becomes inflamed, the immune components of the body do not attack the infected areas, but the own tissues in the joint. The disease is common in women over 30 years of age and most often affects 2 knee joints.
• Arthrosis– is a common type of arthritis that occurs in older people. Caused by disturbances in blood circulation in tissues, it occurs as an inflammatory process that progresses and leads to thinning of cartilage.
• Infectious arthritis. Appears as a result of infection.
• Post-traumatic. Happens after an injury. Similar to arthrosis, it can develop 3 to 5 years after injury.

Other types of arthritis can occur after psoriasis, tuberculosis and other diseases.

Causes of the disease

The exact cause of the appearance is unknown to doctors, but it is believed that it is an infection, the result of an injury or an allergic reaction. It sometimes appears as a result of improper metabolism, nerve diseases, or low amounts of vitamins in the body. When immune functions are impaired, the disease develops and joints are destroyed. Microorganisms enter the knee, and the immune system attacks the damaged area. With poor quality treatment, a person may remain disabled.

Knee arthritis can occur for the following reasons:

• infections that promote the appearance of bacteria;
• joint injuries;
• excessive effort when playing sports, which provokes a constant heavy load;
• excess weight;
• congenital joint deformities;
• allergic reactions;
• diseases that provoke the development of other diseases (gonorrhea, gout, tuberculosis, etc.);
• frequent consumption of alcoholic beverages;
• insect bites, resulting in poison entering the joint;
• lack of nutrients.

Knee arthritis. Symptoms of the disease

Based on certain signs, it can be determined that a person has a disease. Main symptoms:

1. Pain. In most cases, it occurs slowly. The initial stages are characterized by periodic, only after prolonged stress, unpleasant sensations. Then they become more intense, and do not stop at the last stage. In this case, treatment must be carried out, as the pain soon becomes unbearable.
2. Joint stiffness in the morning. Often combined with pain. A pulsation is felt at the site of the disease, movements are limited, and the temperature at the site of infection rises.
3. Tumor. It happens as a result of inflammatory reactions. Does not decrease in the absence of treatment, water metabolism has no effect.
4. Deformation. It first appears as a result of reflex spasms of muscle fibers due to pain. Then the incorrect location of the joints becomes stronger, due to which mobility is significantly limited. Most often, the leg takes on a semi-bent position.

Knee arthritis in children

The most common cause of knee arthritis in children is frequent colds. Due to the disease, immunity decreases, causing viruses to infect some parts of the body, for example, the knees. Tumors and redness appear after a long time, pain occurs, most often, only in the morning.

The disease progresses unevenly. Sometimes there are frequent exacerbations, and remission periods occur. In order for the treatment result to be maximum, it is necessary to carry out complex therapy, even with a decrease in the number of signs of the disease.

Often, thanks to such signs, parents suspect their children of deception, because in the evening the child feels fine, but in the morning is not able to get out of bed. It is possible to tell whether a disease exists after an examination. The spread of the disease is determined by a biochemical blood test.

Treatment of knee arthritis

Healing from a disease should not take place until the pain disappears. The causes that led to the infection must be eliminated.

Methods suitable for treating arthritis:

• use of medications;
• carrying out physiotherapeutic activities;
• special massages;
• gymnastics;
• use of folk remedies;
• surgery on the affected parts.

Medication assistance consists of using the following means:

1. Non-steroidal anti-inflammatory drugs. The drugs are used in all cases associated with inflammation of the musculoskeletal system. The substance will eliminate discomfort due to its ability to interrupt inflammatory processes. The side effects of the drugs are almost the same: gastric and intestinal disorders, intoxication of the body, bleeding.
2. Steroid hormonal substances. Capable of strengthening the body. Joints begin to become stronger, immunity improves, and the speed of recovery from illness increases. Side effects: acne on the body, increased appetite, weight gain.
3. Taking vitamin complexes and special components that strengthen the body. The body's metabolic processes are enhanced. The release of the composition filling the joint begins. It increases the elasticity of cartilage. The type of arthritis determines the medications used for treatment.
4. Use of chondroprotectors. The products help increase the amount of joint lubrication and the appearance of new cartilage cells.

Treatment with folk remedies

People have long invented remedies that will help cope with the disease. Here are some of them:

• potato tincture. To cook, you need to take one potato, which is crushed and filled with 1 tbsp. kefir. You need to take the product in periods of 10 days. The first is every day. The second one is a day later. The third one is in 2 days. The total duration will be 60 days. The pain goes away for a long time, but sometimes returns. To prevent this from happening, a preventive course is carried out once a year;
• compress. You need to take a handful of buttercup flowers and grind them until the juice appears. It will not work to use dry grass. The ground component is applied to the knees, covered with a plastic bag and secured with gauze. You need to stay in this state for 2 hours, then remove the contents.
• The compress leaves small blisters on the body, completely harmless. There is no need to tear them apart; they will disappear on their own after some time. Your knees should be wrapped in gauze daily to prevent blisters from getting wet. After they disappear, arthritis also goes away. If after using the product, burn symptoms do not occur, you need to repeat the steps with the compress;
• Apple cider vinegar is suitable for treatment. Take 1 tsp. with a glass of water 5 times a day, before meals. The course of treatment lasts 1 month. If you have a sick stomach, gastritis or similar diseases, the concentration of vinegar is halved. The course is extended by 2 times. The pain goes away, the disease disappears completely;
• mix a tablespoon of alcohol (tablespoon), 1.5 tablespoons of honey, and 1/3 spoon of radish juice. The resulting composition is applied to the knee, previously wiped with sunflower oil for 40 minutes;
• aloe leaves are crushed and mixed with brewer's yeast. The resulting mixture is applied to the joint as a compress;
• homemade ointment. It is made like this: half a kilogram of unsalted pork fat is mixed with 4 eggs, 50 g of ginger and 340 ml of vinegar. Leave to infuse for three days, then rub in in the evening for 3 weeks. The pain will subside, the disease will go away.
• A decoction made from bay leaves is quite helpful for treating arthritis. You should use half the pack and transfer the contents into a container. Everything is poured with boiling water and boiled for 5 minutes. Then the product is wrapped to keep it warm and left for 3 hours. Afterwards, the decoction is filtered and drunk 10 minutes before bedtime for 3-5 days. Every day a new remedy is prepared. The course is repeated after 7 days.

Exercises for knee arthritis

Physiotherapy procedures can be performed only during the subsidence of pain, or after recovery, to restore joints. Taking medications is combined with physical therapy. Movement helps relieve pain and strengthens the muscles and knee frame. The likelihood of developing arthritis is significantly reduced.

It is better to carry out the exercises in a supine position on a flat, solid base. Exercises:

1. The starting position is lying on your back. Legs stretch up, arms straight along the body. Movements are made as if after waking up, only with the legs. Actions will help the joints straighten.
2. The toes are extended as you inhale, and the heels as you exhale. Movements of the knee joints are carried out clockwise and counterclockwise.
3. Moving your feet in a circle. Bend at the knees and pelvis. Moves like a bicycle.
4. "Bridge". The principle is known to everyone. It is necessary, without lifting your heels and hands from the ground, lying on your back, to bend upward as much as possible.

Exercises are performed 8-10 times. If pain occurs, you must stop.

Ointments for knee arthritis

The advantage of ointments is their availability. Every pharmacy offers several treatments for knee arthritis. Compositions are made from plants that have medicinal properties. The waste products of bees, snake venoms, etc. are suitable. Most of the ointments are made up of natural substances. There are 4 types of treatments:

• Contains non-steroidal anti-inflammatory substances (Diclofenac, Ibuprofen). Pharmacies sell drugs under the names: Nise, Ketonal, Finalgel.
• With capsacin. The substance is extracted from red pepper. It is this component that makes the product taste hot. Ointments using the additive: Capsicam, Nicorflex, Finalgon, Espol.
• Low in salicylic acid. Able to eliminate inflammatory processes. Available in medications: Vpiprosal, Efkamon, Nizhvisal and others.
• On an integrated basis. The drugs use several types of additives, each of which adds the effect the knee joint needs to heal. Dimexide ointment is considered the most popular.

In addition to such funds, there are chondoprotectors. Substances can be used in the initial stages of disease development. Available in different forms, including as ointments.

Any of these remedies should be taken only after consulting a doctor. Even ointments may have contraindications and are not suitable in their composition for the treatment of arthritis. There is no need to joke with the disease; at the slightest sign, the necessary measures should be taken. Only then will you be able to always be healthy, and your joints will not bother you.

Painful arc syndrome includes several different forms, each of which has two common features: loss of normal movement between the overlying arch and underlying tubercles when the arm is abducted and disruption of the normal smoothness of the walls of the bursa.

Syndrome described in detail by Kessel and Watson, it is characterized by radiating along the outer surface of the upper limb to the region of the deltoid muscle and its insertion. It is typical that the pain worsens at night and, as a rule, intensifies when moving the hand in a certain arc. The arc, which is painful when moving, is located between 60-120° abduction, which indicates some kind of disorder in the subacromial region.

If pain worsens after 120° abduction, when the shoulder is raised almost vertically, a rupture of the acromioclavicular joint should be suspected. Although this syndrome has many causes, the common definitive definition is a complex of objective symptoms and signs, usually called “painful arc syndrome.” In this syndrome, pain is greatest along the posterior, superior, or anterior aspects of the rotator cuff.

Impact on the acromion process during abduction varies with shoulder rotation, and tenderness may resolve with external rotation of the shoulder during abduction. Injuries to the anterior and posterior structures heal better than the superior structures because the subscapularis and infraspinatus tendons are relatively well vascularized compared to the supraspinatus tendon.

All these sick should be treated with long-acting anesthetics and steroid hormone injections at the points of maximum tenderness along the anterior, superior, and posterior aspects of the rotator cuff. Multiple injections around the circumference of the rotator cuff are recommended. At the site of maximum pain, 40 mg of methylprednisolone and 5 ml of a 1% solution of bupivacaine (Marcaine) are injected once.
This disease may require several injections before the effect is achieved, so the patient should be referred to a specialist for long-term follow-up.

Scapular-costal syndrome

Syndromes This group includes a number of conditions that have a common cause and clinical symptoms and are usually the result of inflammation of the synovial bursae of the scapula or damage to the muscles attached to it. As a rule, pain in the scapula area appears at the end of the day and is usually caused by the patient being in an uncomfortable position. Scapular-costal syndrome can also occur after prolonged immobilization of the arm due to fractures and other injuries.

Clinical picture of scapular-costal syndrome

Development bursitis and stretching of the muscles surrounding the scapula occur gradually and are characterized by periods of exacerbation and remission. The most common sites for bursitis are the superior and inferior angles of the scapula. Usually the patient experiences pain when moving the latter, and the examiner, if the patient brings his hand to the chest, detects crepitus. To diagnose this disease, the doctor must retract the patient's shoulder blade by asking him to place his palm on the opposite shoulder.

After this it is possible palpate the place of pain, which is usually located at the upper corner or at the spinal column. If the disease occurs as a result of inflammation of one of the synovial bursae of the scapula, an injection of lidocaine brings relief.

Treatment of scapular-costal syndrome

Injection anesthetic it usually brings quick relief to the site of pain; it should be done in all cases accompanied by severe pain. For myositis, local heat in the form of ultrasound (for 20 minutes daily) and diathermy help. Patients with inflammation of one of the bursae of the scapula should be treated with local injection, heat and rest.

Sometimes pain in the spine is not associated with a disc herniation or protrusion, but with muscular-tonic syndrome. Muscular-tonic syndrome is a painful muscle spasm that occurs reflexively and, as a rule, with degenerative diseases of the spine, this is associated with irritation of the nerve innervating the outer part of the fibrous capsule of the intervertebral nerve (Luschka nerve). In addition, muscular-tonic syndrome can occur due to excessive stress on the back or prolonged static load (impaired posture and posture). During prolonged static load, muscles are in constant tension, which leads to disruption of venous outflow and the formation of edema of the tissues surrounding the muscles. Swelling is a consequence of muscle spasm. Dense, tense muscles affect the nerve receptors and blood vessels in the muscles themselves, which leads to the development of persistent pain. The pain, in turn, reflexively causes an increase in muscle spasm and thus further limits the range of movement. A vicious circle is formed - spasm - tissue swelling - painful manifestations - spasm. But sometimes a muscle spasm of a reflex nature is a protective reaction of the body to external influences on the bones of the skeleton (protection of nerves, blood vessels and internal organs) in various diseases. But a long-term muscle spasm turns from a protective reaction into a pathological one, and therefore it is necessary to relieve such a spasm, since a long-term spasm can lead to changes in the muscles and disruption of their functions. Muscular-tonic syndrome is characterized by muscle tension, thickening and shortening and, as a result, a reduction in the range of movements in supporting structures. Increased muscle tone can be local with diffuse involvement of a muscle area (tone in this muscle). In addition, there are regional and generalized spasms of muscles of both flexors and extensors. The intensity of increased tone can be either moderate or pronounced. With moderate hypertonicity, muscle soreness is noted on palpation and the presence of compactions in the muscle is noted. With severe hypertonicity, the entire muscle becomes very tight and painful, and massage or heat only intensifies the pain. There are complicated and uncomplicated muscle hypertonicity. With uncomplicated tone, the pain is localized only in the muscle, but with complicated tone, the pain can radiate to neighboring areas. The mechanism of pain in complicated hypertonicity is associated with ischemic manifestations in the spasmodic muscle (impaired microcirculation and compression of neurovascular formations). Often, with muscular-tonic syndrome, trigger points are formed, which are a sign of the formation of myofascial pain syndrome. The most common muscular-tonic syndromes are the following syndromes:

1. Anterior scalene syndrome. This syndrome is caused by increased tone of this muscle. With hypertonicity of this muscle, conditions arise for the formation of tunnel syndrome (between the first rib and the scalene muscle) with irritation of the neurovascular bundle with a conduction-type disorder in the zone of innervation of the ulnar nerve. When turning and straightening the head, the painful manifestations intensify. As a rule, the syndrome occurs on one side.
2. Inferior oblique capitis syndrome. This syndrome is characterized by pain in the back of the head on the side of the spasmed muscle and its intensification when turning the head. Often this syndrome is accompanied by irritation of the occipital nerve and spasm of the vertebral artery.
3. Anterior chest wall syndrome. Painful manifestations in this syndrome simulate the picture of angina pectoris, but unlike true cardialgia, there are no changes on the ECG. In addition, this syndrome is characterized by a decrease in pain when moving. Diagnosis of this syndrome is quite difficult and is possible only after accurate exclusion of heart disease.
4. Pectoralis minor syndrome. This syndrome manifests itself when the shoulder is excessively abducted and displaced towards the ribs. In this case, compression of the brachial plexus occurs in both the subclavian part and the artery, which leads to disruption of blood supply to the limb and disruption of innervation. The result is numbness, paresthesia and muscle weakness in the distal parts of the upper limb.
5. Scapular-costal syndrome. It is characterized by pain in the upper corner of the scapula, a crunch when moving the scapula, and a decrease in the range of movements. The cause of the syndrome is degenerative changes in the cervical spine (C3-C4 and C7). In addition, the cause of this syndrome may be associated with synovitis of the scapula muscles.
6. Piriformis syndrome. The cause of this syndrome is compression of the sciatic nerve by the outward rotator muscle of the femur in the area of ​​the inferior gluteal foramen (where the sciatic nerve and gluteal artery pass). The pain from piriformis syndrome resembles the pain from sciatica. In addition, there may be numbness of the lower extremity
7. Tensor fascia lata syndrome. The occurrence of this syndrome is associated with degenerative changes in the lumbar spine, and can also be of a reflex nature in diseases of the hip joint or changes in the sacroiliac joints.
8. Iliopsoas syndrome. The formation of this syndrome is associated both with degenerative changes in the lumbar spine and with muscle blocks in the thoracolumbar segment or with diseases of the abdominal cavity and pelvic organs.
9. Cramps (convulsive spasms) of the calf muscle. The duration of crumpy can be from seconds to minutes. The provoking factor may be sudden flexion of the foot. The cause of cramps is considered to be head trauma. Sometimes cramps can occur in the presence of venous or arterial insufficiency of the lower extremities.
10. Back extensor cramps. As a rule, these are spasms in some part of the muscle, most often in the middle of the back. Such spasms can last up to several minutes and the pain sometimes requires differentiation from pain of cardiac origin (angina pectoris). Trigger points are often found in the back extensor muscles.

Diagnostics

1. History of the disease, patient complaints (duration of pain, intensity of pain, nature of pain, connection with movement or other provoking factors.
2. Assessment of neurological status. Condition of the muscles, presence of areas of spasm or pain points (triggers), mobility of spinal segments, movements causing increased pain.
3. 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).
4. MRI and CT. These studies are necessary to visualize degenerative changes in soft tissues (disc herniation, protrusion, compression of neural structures)
5. An EMG study allows you to determine the degree of conduction disturbance in nerves and muscles.

Treatment

Treatment for muscular-tonic syndromes is mainly aimed at treating the underlying disease that caused the muscle spasm. But often the relief of muscle spasm leads to positive dynamics of the disease itself. In addition, prolonged muscle spasm leads to the formation of a vicious pathological circle. And therefore, the patient’s task is to consult a doctor as quickly as possible and eliminate the muscle spasm. The following treatment measures are recommended:

1. Orthopedic products. Wearing a corset (lumbar region) or a Shants collar to relieve the corresponding parts of the spine. Using orthopedic pillows
2. Drug treatment. To reduce muscle spasm, it is possible to use muscle relaxants such as mydocalm, sirdalud, baclofen. NSAIDs (movalis, voltaren, ibuprofen, etc.) help reduce pain and relieve inflammation.
3. Local anesthetic injections, sometimes combined with corticosteroids, help interrupt the abnormal firing of trigger points.
4. Massage and manual therapy are quite effective for muscular-tonic syndrome. These methods make it possible to normalize muscle tone and mobility of motor segments and thus eliminate the cause of pain.
5. Acupuncture is a well-proven method of treating muscular-tonic syndromes. The method, first of all, helps to minimize the use of medications, normalizes conduction along nerve fibers and relieves pain.
6. Physiotherapy. Procedures such as electrophoresis, magnetic therapy, DDT SMT can reduce tissue swelling, improve blood circulation and reduce pain.
7. Exercise therapy. After reducing pain, a set of exercises helps normalize the muscle corset, muscle tone and is a prevention of muscle spasms.

Frequent involvement of any muscle in a reflex tonic or dystrophic process is not yet a reason to identify the corresponding syndrome. In this case, damage to the levator scapulae muscle can be designated as a syndrome only in quotation marks. The same applies to another designation - “scapular-costal syndrome” (Michele A. et al, 1950, 1968). It reflects the role of the scapular-costal, i.e. bone elements involved in this pathology together with their nearby soft structures: ligaments, mucous bursae. The role of these structures is confirmed by the fact that clinical manifestations are often found in individuals with insufficient congruence of the surfaces of the scapula and chest. These are subjects with a “round” or flat back.

According to A. Sola and R. Williams (1956), as well as J. Travell and D. Simons (1983), damage to the levator pelvis muscle

Rice. 5.10. Schematic representation of some muscles of the scapula and suprascapular nerve: 1 - semispinalis capitis; 2 - belt head; 3 - small diamond-shaped; 4 - levator scapula; 5 - suprascapular nerve; 6 - suprascapular; 7 - subscapular; 8 - large round; 9 - large diamond-shaped.

patka, is extremely common, acting as the main cause of “painful stiff neck” or torticollis.

The development of suffering is facilitated by functional factors: overstrain of the muscles that fix the scapula. The most pronounced changes are found in the levator scapulae muscle. This is the muscle of the second layer of the back. Covered by the trapezoid, it extends ribbon-like in the posterolateral parts of the neck (Fig. 5.10). Its origin is the posterior tubercles of the transverse processes of the four upper cervical vertebrae. The muscle is similar to the scalene muscle, starting from the anterior tubercles of the transverse processes of the cervical vertebrae. If the anterior scalene is attached to the first rib, the described muscle is attached to the upper part of the medial edge of the scapula and to its upper corner. Both muscles, like elastic cables, provide movement of the neck in the antero- and posterolateral directions and its dynamic fixation. In relation to the upper corner of the scapula, the muscle pulls it upward and inward, and the supraspinatus, starting from the walls of the supraspinatus fossa, especially from the upper corner of the scapula, pulls it outward with a fixed shoulder. This also applies to the infraspinatus muscle. The described relationships are extremely important, because Painful muscle compactions are often localized in the supraspinatus muscle, and spontaneous pain is often experienced here in scapulocostal syndrome. J. Travell and D. Simons (1983), as well as A. Sola and R. Williams (1956) indicate that damage to this muscle is extremely common, acting as the main cause of “painful stiff neck” or torticollis.

Patients with “scapular-costal syndrome” complain of a feeling of heaviness, aching and cerebral pain, initially in the area

the area of ​​the scapula, closer to its upper-inner corner, then into the shoulder girdle, with a return to the shoulder joint, less often, to the shoulder and along the lateral surface of the chest. At the same time, pain is experienced in the neck, especially with dynamic loads on it, often when the weather changes. These overloads largely determine the chronically recurrent course. The “trigger point” is the most painful area, when pressure is applied to it, pain radiates to the shoulder girdle and neck - the place of attachment of the levator scapulae muscle. The paravertebral points of V.G. Lazarev (1936) at the level of Tsh-Tu are apparently associated with the phenomenon of neuro-osteofibrosis at the same point and in the capsules of the corresponding transverse costal joints. Back in 1910, A. Abrams, in his book “Spondylotherapy,” drew attention to the features of physical indicators in the vertebral-paravertebral zone at the Trv-Tvi level. This is the level of tracheal bifurcation. Phonendoscopy reveals dullness, spreading more to the right, especially with enlargement of the bronchial glands. The author also points out Petrushevsky’s sign - pain between the shoulder blades. Stimulation of these points with pressure is accompanied by increased or occurrence of pain in the scapulohumeral region. When the scapula moves, a characteristic crunching sound is often detected in the area of ​​its inner corner. The diagnosis of the syndrome is also facilitated by a test with novocaine infiltration of the muscle near the site of its attachment to the scapula. E.S. Zaslavsky (1976) revealed in patients with damage to the levator scapulae muscle, electromyographic and microcirculatory changes characteristic of the neurodystrophic process.

With dystrophic lesions of the spine, upper scapular pain most often occurs in persons with damage to the SDS Cjv-v and less often - C V -vi (Popelyansky A.Ya., 1978; Zaslavsky E.S., 1979).

The described syndrome is a manifestation of pathology not only of this, but also of some neighboring muscles: the vertical portion of the trapezius, supraspinatus, infraspinatus, subscapularis, etc. Together with the osteochondral structures, the muscular-fibrous tissues of the neck, when they are affected in the upper sections, are a source of irradiating pain vegetative syndrome in the craniovertebral region. The inclusion of this, as well as other cervical muscles, in the pathology is determined not only by their local characteristics. Because the tone increases, the neck muscles are more preferentially affected than others in neurotic tension headaches. This applies in particular to levator scapulae syndrome (Chetkikh N.L., 1992). Damage to the lower SMS of the cervical spine is often the source of such brachiopectoral syndromes. Their color is determined by the corresponding anatomical and physiological features of the upper, middle and lower levels of cervical pathology (Albert I., 1963; Popelyansky A.Ya., 1978). Thus, with dystrophic pathology of the upper cervical level, vertebral syndrome is characterized by limited head rotation. Under these conditions, according to A.Ya. Popelyansky (1978), possible rotational movements of the neck have little effect on the vascular reactions that occur in response to artificial stretching of the vertebral artery plexus. During head tilts, which are sufficiently preserved in the case of upper cervical pathology, the mentioned vascular reactions are suppressed.

tens. In other words, reactions to stored but therefore dangerous reactions are suppressed, i.e. not providing protective immobilization and movement.

When the middle and lower levels are affected, when head tilts are more limited, the mentioned inhibition of vascular reactions is observed in response to head turns. Another feature of the upper level vertebral syndrome, according to the observations of the same author, is a relatively unfavorable course, often with severe exacerbation of cerebral manifestations. Features of vertebral syndrome of the lower cervical level are the predominance of suprabrachialgic and scapulalgic irradiation of pain during artificial irritation of the receptors of the affected disc, and a greater frequency and duration of exacerbations than at the upper level. Features of vertebral pathology at the mid-cervical level are the absence of algic irradiation beyond the neck, severe stiffness of the cervical spine; In the anamnesis and status of these patients, concomitant diseases of internal organs are very common.

Scapulalgia in this syndrome should not be confused with the specific Personage-Turner syndrome (see 5.1.1.5).

5.1.2.4. Pectoralis minor syndrome

The syndrome is caused by muscular-tonic, neurodystrophic disorders in this muscle and compression of the neurovascular bundle passing under it.

The pectoralis minor muscle is triangular in shape and lies behind the pectoralis major. It begins with three to four teeth between the bone and cartilaginous parts of the II-V ribs. Rising obliquely outward and upward, it gradually narrows and is attached by a short tendon to the coracoid process of the scapula. Innervated by the anterior thoracic nerves arising from the supraclavicular part of the brachial plexus. The neurovascular bundle on the shoulder can be pressed behind the pectoralis minor muscle under the coracoid process of the scapula to the head of the humerus. In this case, the subclavian artery is compressed at the point of its transition to the axillary artery: between the muscle and the coracoid process (see Fig. 5.8). Sometimes a vein can also be compressed there. Compression of these formations can be caused by strong abduction of the arm (hyperabduction during anesthesia, immobilization of the humerus, during sleep with the arm thrown back behind the head, etc.). Hence another name for some variants of the syndrome - hyperabduction. Not only in the pathological condition of the muscle, but also in most healthy people, the pulse of the radial artery disappears or becomes weak when spreading the arms to the sides and lifting them up 45-180° almost to the temples. It was believed that pectoralis minor syndrome occurs due to macrotraumatization, as well as microtrauma due to the frequently repeated movements mentioned above (Wright P., 1945; Mendlowiz M., 1945; Lang E., 1959; HoffH., Tschabitcher, 1958). In this case, trophism in the muscle is disrupted, and contracture changes occur, which leads to compression of the trunks of the brachial plexus and subclavian artery. The most affected is the lateral secondary trunk of the brachial plexus, which innervates the pectoralis minor muscle. This circumstance further intensifies her spasm.

The clinical picture when interpreting this syndrome as local without taking into account other foci, impulses from which causes muscle tension, was presented as follows.

Patients experience aching or burning pain in the area of ​​this muscle, more at the level of the III-V ribs. Their vegetative connotation is confirmed by the fact that they often intensify at night. More often, pain is experienced during movements that require muscle contraction or stretching. The latter reveals pain upon palpation: the patient’s arm is raised above the head, the doctor clasps the pectoralis major muscle with fingers II-IV and moves it away from the axillary region in the medial direction. In this case, the muscle is defined as tense, dense, and sometimes painful nodes can be felt in it. It can also be felt through the relaxed pectoralis major muscle at the moment of a deep breath. To do this, the patient must press his hand to the body, move it backwards and downwards. With pinch palpation, you can examine the muscle through the axilla, moving your thumb under the pectoralis major muscle until the mass of the pectoralis minor is determined. It is grasped with the fingers along with the pectoralis major muscle. Soreness is also determined at the site of attachment of the muscle to the coracoid process, in the area of ​​its origin at the border between the cartilaginous and bone parts of the II-IV ribs. At the site of greatest pain, 5-10 ml of a 0.25-2% novocaine solution can be injected for diagnostic and therapeutic purposes. Infiltration of the muscle can be done both through the axillary region and through the thickness of the pectoralis major muscle. The effect occurs after 5-7 minutes: pain and paresthesia decrease, range of motion in the shoulder joint increases.

Patients are concerned about paresthesia in the area of ​​the anterior chest wall and ulnar edge of the forearm and hand, weakness in the arm, more so in the distal parts. Motor disorders usually predominate in the muscles innervated by the median nerve. Hypoalgesia is often noted in the area of ​​innervation of the ulnar nerve. Damage to the upper sections of the muscle during mammectomy is often accompanied by severe symptoms of prolapse from the entire ulnar nerve. Autonomic disorders appear in the form of pallor and swelling of the hand, as well as changes in pulse, which are a consequence of not only compression of the axillary artery, but also irritation of its sympathetic plexus. A sign of a decrease in the lumen of the axillary artery is a systolic murmur during abduction and elevation of the arm.

Studies, including electromyographic studies, conducted in our clinic by I.P. Kipervas (1975), E.S. Zaslavsky (1976), I.B. Gordon et al. (1971), as well as M.A. Chobotas (1973) and others, showed that the described picture rarely appears in isolated form and is usually accompanied by muscular-tonic, neurodystrophic symptoms of cervical osteochondrosis or lesions at the thoracic level and in other muscles and areas . Concomitant symptoms from the anterior scalene muscle and vertebral artery were noted. Injuries and other local muscle lesions are additional and provoking factors that, under the influence of impulses from a diseased spine or other focus of pathological impulses, turn the possibility of the syndrome into reality. All this is due to reflex tension

muscles. As for the cases when the neurovascular bundle is compressed under the coracoid process of the scapula by the tendon of the pectoralis minor muscle during excessive abduction of the arm, this symptom complex, characterized more by subjective disorders (pain and paresthesia) and less often by mild paresis of the arm, is predominantly of mechanical origin. Only this variant of the syndrome should be called hyperabduction.

The brachial plexus can be compressed not only by the anterior scalene and pectoralis minor, but in some cases also by the omohyoid muscle. The tendon jumper and, to a greater extent, the lateral head of its subclavian region are located above the scalene muscles along a line that seems to intersect them (see Fig. 5.8). Patients experience pain in the shoulder and neck, especially when moving the arm back and head in the opposite direction. Pain and paresthesia intensify with pressure on the area of ​​the hypertrophied lateral abdomen, which corresponds to the area of ​​the middle and anterior scalene muscles (Adson A., 1927; Fiske C, 1952; Sola A.E. et ai, 1955). Patients experience pain in the shoulder and neck, especially when moving the head to the opposite side, with pressure on the lateral head of the muscle (the area of ​​the anterior and middle scalene muscles). The pathology of this muscle should be remembered when differentiating scalene and pectoral muscle syndromes from other types of pathology manifested by compression of the brachial plexus. The extent to which the pectoralis minor syndrome is associated with cervical osteochondrosis, combined with manifestations of cervical dystrophic pathology, can be judged by its combination with glenohumeral periarthrosis. This latter syndrome is characterized by tonic tension of the shoulder adductor muscles, including the pectoralis major muscle.

5.1.2.5. Humeroscapular periarthrosis

In the past, the diagnosis of brachial plexitis was often used in neuropathology textbooks and medical documents. This diagnosis is almost never found in modern literature. The opinion about the supposedly frequent inflammation of the brachial plexus was refuted by data on a different mechanism of damage in pectoralis minor syndrome or scalenus syndrome.

In the past, the clinical picture of brachial plexitis also included pain in the shoulder joint, accompanied by contracture of the muscles that adduct the shoulder and fix it to the scapula. If such a patient was seen by an orthopedist, the diagnosis was determined as glenohumeral “periarthritis.” It is not without reason that they focused attention on the nerve plexus, because pain combined with joint stiffness (Eretskaya M.Ya., 1941). Even today, a patient with this clinical form often does not find his doctor in the clinic: the neurologist refers him to a surgeon, who then refers him to a neurologist.

Since the time of S. Duplay (1872), who described the clinical picture of glenohumeral “periarthritis,” the process in the joint capsule was considered as inflammatory (Aronovich T.D., 1928; Brzhozovsky A.G., 1930; Rotenberg L.E., 1933; Kahlmeter G., 1936; Shtremel A.Kh., 1941; Badyul P.A., Badyul A.A. , 1950; Kokhanovsky I.Yu., 1950; Farberman V.I. et al., 1959).

Orthopedic neurology. Syndromology

Rice. 5.11. Frontal cut of the shoulder joint (diagram): 1 - biceps tendon; 2 - subacromial bursa; 3 - acromion; 4 - joint cavity; 5 - transverse scapular ligament; 6 - blade.

True, the aseptic nature of the changes in the periarticular tissues was established: pieces of periarticular tissue taken during the operation turned out to be sterile. But even then, the involvement of the nerves of the periarticular tissues and trunks of the brachial plexus in the pathological process continued to be mistakenly considered as secondary neuritis.

The uniqueness of the pathology of this area is largely determined by the functional and anatomical features of the shoulder joint in connection with the humanization of the monkey.

Shoulder joint (Fig. 5.11)- this is the freest of all joints of the human body, because The surfaces of the head of the humerus and the articular fossa of the scapula vary greatly in size. The capsule is very spacious and not stressful. It itself is very thin, but almost everywhere it is reinforced by the fibers of the tendons of a number of muscles woven into it. The acromial process of the scapula is located externally above the joint capsule, and its coracoid process is located in front. Between these processes, the coracoacromial ligament is stretched over the joint capsule: it forms, as it were, a roof over the capsule of the shoulder joint. When the shoulder is abducted, rising upward in the frontal plane, the tubercles of the shoulder also go under the “roof”. The limits of this “roof” are expanded by the lower surface of the deltoid muscle.

Thus, there are two layers of anatomical formations: on top - the deltoid muscle, acromion, coracoid process and ligament, below - the joint capsule and the tubercles of the shoulder. Between these two layers, as well as between any other mobile anatomical formations, there is a mucous bursa.

To understand the genesis of pain and contracture phenomena in glenohumeral periarthrosis, one should consider the anatomical relationships that develop when the arm is abducted to the side and raised upward. This movement is not possible for the deltoid muscle alone. With it, the greater tubercle and the corresponding portion of the capsule fit under the acromion and coracoacromial ligament. Inevitably, friction of the area against the acromion and coracoacromial ligament should occur.

This compression and friction is reduced by the subacromial bursa, which, if pathological, can cause a capsule defect.

The second extremely important factor that ensures unhindered abduction of the arm, raising it upward and preventing the tubercle of the shoulder from hitting the acromion is the action of the supraspinatus and subscapularis muscles. They bring the head of the humerus closer to the glenoid cavity of the scapula, “anchoring” it, creating a point of support (rotation) for the head of the humerus. Only after this can the deltoid muscle raise the shoulder in the frontal plane.

The dynamics of the activity of the “anchor” muscles is indicated by recording the EMG activity of the subscapularis muscle as the arm is raised up to 180°. This activity increases as the arm is abducted horizontally to 90°. When the hand rises up, activity decreases (Johnman V. et al, 1944). The innervation of the joint capsule comes from the same sources from which the muscles whose tendons are woven into this capsule are innervated.

Chapter V. Syndromes of cervical osteochondrosis

Age-related dystrophic changes developing in the periarticular tissues of the shoulder joint are accelerated due to the severity and originality of the loads, as well as due to micro- and macrotraumas falling on this joint. According to V.A. Shirokov (1995), in recent years, in connection with the mechanization and automation of production, it is not overloads that play a major role, but violations of the control and regulation of technological processes. Due to traumatic injuries and hemorrhages, the joint capsule shrinks and the mucous bursae become infected. Age-related changes in the capsule of the shoulder joint, according to the anatomical data of I.L. Krupko (1959), are reduced to its thinning, fiber disintegration with the formation of cracks, especially at the greater tubercle of the shoulder, to the deposition of lime in it, deforming changes on the areas of the acromial and coracoid processes and greater tubercle of the humerus. The outer wall of the subacromial bursa, covering the lower surface of the acromial process and the coracoacromial ligament, is erased, and the ligament itself in its lower surface is disintegrated. A slight concavity is often found radiographically on the lower surface of the acromion. (Kamalov I.I., 1993). All these changes are found almost constantly in preparations of corpses of persons who died at the age of 40 years and older. Microscopic age-related changes in the ligamentous tendon region of the capsule begin with swelling of collagen fibers and their disintegration. Fiber degeneration intensifies over the years, the fibers become thinner or hyalinosis occurs in them, followed by necrosis and calcification. While the localization of calcification foci was based on radiographic data alone, they were associated with the subacromial bursa. Hence the common term “stone bursitis” - bursitis calcarea. Later it turned out that this term is not accurate. E.Codman (1934), J.Lecapere (1950), A.Ya.Shnee (1951) indicate that “stone bursitis” is calcification not of mucous bursae, but of muscle tendons and their sheaths, most often the supraspinatus tendon near its attachment to the bone. Therefore, it would be fairer to talk not about bursitis, but about tendinitis or peritendinitis, tendinosis (Sandstrom S, 1938; Zharkov T.A., 1966, 1983). Among patients with polytendoperiosteitis, this form is observed on average in every fifth (Schindel E., 1951).

Although local disorders in periarticular tissues have been studied by orthopedists, orientation in the corresponding manifestations is no less necessary for a neurologist in order to provide therapeutic effects on these local foci while simultaneously taking into account other neurological, radicular, cerebral or other mechanisms of the disease. Arthrosis of the joint is inevitably accompanied by reactive changes in the periarticular tissues. There is no true or pseudoperiarthrosis, there are its variants. The following local manifestations may predominate in the picture of periarthrosis.

Tendinosis of the supraspinatus tendon. In the case when lime is deposited in areas of necrosis and fibrinoid degeneration of the tendon (tendinosis calcarea), the disease, if clinically manifested, usually takes an acute course. Following the feeling of discomfort and heaviness in the shoulder, severe gnawing pain appears, especially at night. They radiate proximally and distally

directions. Quite soon, movement is limited, up to the appearance of “frozen shoulder.” A positive Dovborn sign is detected, pain in the area of ​​the greater tubercle, intertubercular groove, in the supraspinatus fossa, along the tendon and up to the muscle itself. Pain decreases and range of motion increases when the shoulder is abducted in the position of maximum impaired rotation (Abdrakhmanov A.Sh., Orzhovsky N.B., 1984).

The flow becomes especially acute when calcium salts break into the bag (subacromial bursitis). Then a painful bulge is detected in the area of ​​the bag, and a clear yellowish liquid is found in the area. Acute bursitis lasts 1-4 weeks, chronic - up to 1-6 months. When salts break into the joint, a picture of arthritis develops. Usually, in the absence of calcification, tendinosis develops gradually, and the arm begins to get tired when working, especially when abducting the shoulder. Müller's nodes are detected in the supraspinatus muscle, pain at the site of its attachment. Often happens gap or tear of dystrophically changed tendons (Codman E.A., 1934; Bosworth V.. 1941). Most often - in 80% - this happens after an awkward movement, falling on an adducted arm, etc. (Abdrakhmanov A.Zh., Orlovsky N.B., 1984), but after 40 years, spontaneous onset was also observed in 50% of ruptures. At When the tendon ruptures, the “anchoring” of the head of the shoulder is disrupted and the joint capsule is stretched. In acute cases, swelling appears at the site of the rupture, and in the second or third week - muscle wasting. The shoulder girdle is lowered due to stretching of the deltoid muscle, pain is also noted in nearby areas. Active abduction of the shoulder is impossible, the patient cannot keep the arm passively abducted in a horizontal position - a sign Leclerc falling hand or “lash symptom”. The pain intensifies with tension in the passively abducted shoulder due to irritation of the soft tissues between the acromion and its head. After blocking the supraspinatus nerve, active abduction of the shoulder is restored in a position with the head of the humerus pulled down, i.e. with subacromial decompression If, after novocainization of the rupture site, shoulder abduction becomes possible, one can think that the gap is incomplete ny, there is only a tear. Much less often, according to R. A. Zul-karneev (1979) - in 6%, the predominant tendinosis is not the external rotators of the shoulder, but its biceps muscle. However, these processes can only be distinguished in the initial stages of periarthrosis. Damage to the long head of the biceps muscle is characterized by pain in the her at the moment supination of the forearm bent at the elbow and simultaneous clenching of the hand into a fist (Jurgenson's symptom). A.M.Brixman(1984) noted pain when flexing the forearm in a pronated position, as well as when abducting the arm posteriorly. A muscle protrusion forms above the ulnar fossa. There is a variant of glenohumeral periarthrosis with damage to the long head of the triceps brachii muscle at its origin - at the subarticular tubercle of the scapula (Frolich E. 1989). Next It is necessary to take into account the susceptibility of the specified area to neuroosteofibrosis, because this head is a biarticular muscle. In addition, the long head, like the supraspinatus muscle, participates in anchoring the head of the humerus when it is abducted to the side, in adducting the shoulder with the teres major muscle. When stimulating the long head of the triceps brachii muscle, its main function is adduction

Orthopedic neurology. Syndromology

(Duchenne G.B., quoted by TravellJ., Simons D., 1982). Thus, she is an active participant in the formation of glenohumeral periarthrosis. Other rare forms, accompanied by corresponding local pain and swelling, are acromial clavicular arthrosis and coracoiditis.

Separately, capsulitis (capsulosis) is isolated, more often in women over 40 years of age (Neviaser J., 1945; Batenam J., 1972; Agababova E.R. et al., 1985; Shirokov V.A., 1995). Characterized by a gradual onset, a monotonous course for more than 6 months, and no history of trauma. The pain is constant, worsening at night. The shoulder is raised, muscle atrophy is not severe. Periarticular tissues are painful. Passive and active movements are very limited. The fatigue test and the “braces fastening phenomenon” - pain when rotating the shoulder inwards - are positive (Ro&oky S. et al, 1978; Vischer T.L., 1979; Agababova E.R. et al., 1983).

Recognizing this differentiation, which should be reflected when making a diagnosis, after the work of I.L. Krupko (1959), tendinitis in the shoulder joint, as well as coracoiditis, ligamentitis, tendon ruptures and stone bursitis, previously described as independent nosological units, are considered a single process - glenohumeral periarthritis, more precisely periarthrosis (Friedland M.R., 1934).

The sequence of local lesions in glenohumeral periarthrosis, according to A.Ya. Popelyansky (1993), is as follows: “trigger” zones in the subscapularis muscle and scapulocosteal changes in the supraspinatus muscle, its tendon and in the suprascapular nerve.

Recently, a form with predominantly bone-dystrophic lesions has also been identified. It is characterized by unevenly distributed dystrophic disorders of the humerus, the spread of this process to other bones (Kuznetsova I.E., Veselovsky V.P., 1994).

To what extent glenohumeral periarthrosis is an independent form of damage to the musculoskeletal system and what is the participation of the nervous systems in the process, we will discuss after analyzing the clinical picture.

The disease is sometimes associated with macrotrauma, but most often with microtrauma under conditions of professional overload. This explains the predominant suffering of the right hand (Schnee A.Ya., 1931; Sheikin A.I., 1938; Werkgartner F., 1955; Farberman V.I., 1959; Elkin M.K., 1963; Shirokov V.A., 1995, etc.). As at the lumbar level, one should distinguish between cervical reflex vascular syndromes with a predominance of vasospasm and vasodilation in the wide and cervicocranial and cervicomembral zones and local vasodistonia or compression. Thus, among operators of rolling shops, as well as those working in drawing thin tubes, according to our clinic, the manifestation of glenohumeral periarthrosis is caused by the frequency of arm movements and unfavorable working posture (Koltun V.Z., 1971; Vasilyeva L.K., 1975). Among those who stand to the left of the machine and make significantly more movements with their right hand, glenohumeral periarthrosis occurs in the right hand in 85% of cases, while those standing to the right of the machine have pain in their left hand. Suffering was described among knitters, carpenters, typists, pipe drawers, laundresses, weavers, loaders, and blacksmiths. A. Dortheimer and O. Popescu (1959) emphasize

or the provocative role of some sports: javelin, discus, shot put. In athletes who come in such cases with “muscle strain”, a picture of coordinator myopathy according to V.S. Marsova (1935) is found. E.V. Usoltseva and N.K. Kochurova (1953) found thickening of the muscles in the places where they pass into the tendon, lengthening of the chronaxy and uneven fluctuations of the electromyographic curve.

Until recently, the premorbid features of the periarticular tissues of the joint and, in particular, the residual effects of their neonatal pathology were not sufficiently taken into account. Meanwhile, the circumference of the fetal shoulder girdle is often larger than the circumference of its skull: difficult removal of the shoulders is a common feature of the birth of injured children. When removing the head during breech presentation, the shoulder girdle serves as a support for the obstetrician's hand. Often the shoulder is injured when throwing the handle behind the head of the fetus during birth in a breech presentation. In injured newborns, pain and limitation of movements in the joint are detected, an increase in its circumference, pain in the periarticular tissues, and morphologically they are soaked in blood, fiber ruptures, dystrophy, thickening of the deltoid muscle, widening of the joint space (Dergachev KS, 1964; Kholkina G.F. et al., 1993).

When describing the clinical picture of glenohumeral periarthrosis, they primarily point to pain symptoms: 1) pain, often spontaneous, more at night when lying on the affected side, aggravated by movements and radiating to the neck and arm; 2) pain that appears when the arm is abducted and when the arm is placed behind the back; 3) soreness of the periarticular tissues when palpated.

Pain can occur acutely, for example, during awkward movement, after an injury, but more often it increases gradually and radiates from the shoulder joint to the arm or neck. There is pain on the outer surface of the shoulder in the area of ​​its tubercles, coracoid process, and upper edge of the trapezius muscle.

The second important group of symptoms is associated with contracture phenomena in the joint area. Unlike diseases of the joint itself (infectious monoarthritis, tuberculosis, giant cell and malignant tumors), not all movements in the joint are difficult. If the abduction of the arm to the side is sharply limited, pendulum-like movements of the shoulder within 30-40° always remain free. When you try to move your arm to the side and up, a sharp pain appears in the area of ​​the tubercles of the humerus and acromion. In some patients, however, it is possible to overcome this pain by passively raising the arm up. From the moment when the greater tubercle of the humerus and the altered tissues in the area of ​​the subacromial bursa go under the acromion and their friction stops, the pain disappears. This entire sequence of subjective and objective manifestations is defined as Dovborn's symptom. Holding the arm in the lateral abduction position is impossible. Shoulder rotation, especially the rotation of the shoulder, is severely difficult.

As the disease progresses, atrophy of the deltoid, supra- and infraspinatus, and subscapularis muscles increases more and more, which was confirmed pathomorphologically (Schaer H., 1936), long head of the biceps muscle (Hitchcoc H., Bechtol S, 1948). Because joint capsule, supra- and infraspinatus

Chapter V. Syndromes of cervical osteochondrosis

muscles are innervated by the suprascapular nerve, it is interesting that when it is stimulated, the latent period of the M-response of the supraspinatus muscle is prolonged (Berzinsh Yu.E., Tsiparsone R.T., 1983). Along with this, contracture phenomena also progress - the shoulder is pressed to the chest, its abduction becomes more and more limited, carried out at the expense of the scapula. A forced posture occurs: the arm is pressed to the body, the shoulder is raised, the tone in the trapezius, subscapularis and teres muscles, the latissimus dorsi muscle, etc. increases - “a symptom of the forced position of the arm” (Karlov V.A., 1965). With a long course of the disease, the restriction of movement in the joint becomes very pronounced - “frozen shoulder”, “capsulitis” (Beetham W.P., 1978).

Sometimes hypoalgesia is detected along the outer surface of the shoulder. W.Bartschi-Rochaix (1953) describes a zone of hyperesthesia the size of “two francs” in case of humeroscapular periarthrosis. This zone is located above the painful area of ​​the greater tubercle of the shoulder. I.L. Krupko (1943), having carried out an anatomical study of the axillary nerve, found that its intertubercular branch comes very close to the ligamentous-tendon part of the capsule. He admits the possibility of damage to this branch, which can cause an “echo” through the axillary nerve in the form of cutaneous hypoalgesia. Yu.E.Berzins and R.T. Tsiperson (1983) found an extension of the latent period of the M-response of the deltoid muscle in half of the patients with such sensitivity disorders. Following J. Kirbi and G. Kraft (1972), they admit the possibility of compression of the nerve in the area of ​​fibrously changed muscles - the teres major and minor (top and bottom), the long head of the triceps muscle outward from the humerus, i.e. in the area of ​​the four-sided hole. It is possible that these mild hypoalgesias in some cases have a vegetative origin. Radiographic symptoms, according to J. King and O. Holmes (1927), are rarely detected. The data of most radiologists, especially those using polypositional studies, do not agree with this (Isaenko E.I., 1966); A.S. Vishnevsky (1938) emphasizes the importance of identifying traces of trauma. Decalcification is often found in areas of the bone adjacent to the joint, and lucidity of the greater tuberosity of the humerus. Foci of calcification for the most part lie just opposite the greater buffalo, they can remain for years without clinically manifesting themselves, or disappear under the influence of treatment, and sometimes on their own. It is now known that this shadow most often corresponds to the calcified supraspinatus tendon. Symptoms of deforming arthrosis of the shoulder joint are often noted: spikes on the area of ​​the greater tuberosity, sclerosis of the marginal parts of the greater tuberosity, sclerosis of the subchondral layer in the area of ​​the glenoid cavity of the scapula - “ring symptom” according to V.S. Maykova-Stroganova and D.G. Rokhlin (1957 ).

We have presented the main picture of glenohumeral periarthrosis as it seemed possible before the pathogenetic connection of this process with cervical osteochondrosis was established.

Already in 1932, D.C. Keyes and E. Compere drew attention to the combination of dystrophic lesions of the cervical spine with glenohumeral periarthrosis. A. Oppenheimer described the swollen hand syndrome in 1938, pointing out the connection between the process and the pathology of the cervical spine.

night light At the same time, he emphasized that before the onset of symptoms in the hand area, patients had pain in the shoulder girdle and deltoid muscle long before (from several weeks to 20 years). In 1941, E.Fenz found pain in the shoulder joint (“neurogenic arthralgia”) in 18 out of 49 patients with “cervical spondylosis.” In 1948, P. Duus reported on an X-ray and subsequent anatomical study of one patient who had suffered from severe glenohumeral periarthrosis for 7 years. A sharp narrowing of the intervertebral foramina of the cervical spine was detected. The same connection was noted in observation No. 5 from the work of W.Brain et al. (1952). F. Reischauer (1949) found symptoms of cervical osteochondrosis in almost all patients with glenohumeral periarthrosis, and in 2/3 he also identified radicular symptoms. Similar data were cited by J. Yong (1952).

J.Lecapire (1952), R.Gutzeit (1951), H.Passler (1955), H.Mathiash (1956), A.Stuim (1958), G.Chapchal (1958) wrote about the close connection of cervical osteochondrosis with glenohumeral periarthrosis. etc. They also indicate different percentages of patients with glenohumeral periarthrosis with cervical osteochondrosis (15% - Metz U., 1955; Arutyunov A.I., Brotman M.K., 1960; 19% - Bente D. et al., 1983; 23% - Bente D. et al., 1953; 28% - Tonnis W., Krenkel, 1957).

The observations of R. Frykholm (1951) are especially demonstrative regarding the proportion of radicular pathology in glenohumeral periarthrosis. 9 out of 30 patients with cervical-radicular syndrome had a picture of glenohumeral periarthrosis. The results of the facetectomy operation in 2 patients who had symptoms of glenohumeral periarthrosis for 2-3 years were striking: 10-12 days after decompression of the root, these symptoms disappeared.

In the practice of a neurologist, glenohumeral periarthrosis, according to our data, occurs very often, acting as one of the symptoms of cervical osteochondrosis (in 26.35 Of the 79 patients we examined with this manifestation of osteochondrosis, there were 40 men and 39 women. In 46, periarthrosis was on the right, in 28 - on the left, in 5 - bilateral, in 4 of them - with a predominance on the right.

Everything spoke in favor of the fact that the symptoms of cervical “radiculitis” that we observed with periarthrosis are not associated with the initial damage to the joint capsule, as some of the authors mentioned above believed. However, perhaps cervical osteochondrosis is only a concomitant pathology with glenohumeral periarthrosis, given the prevalence of osteochondrosis in people over 40 years of age? So, in particular, P. Matzen wrote in a manual on orthopedics from 1968. He believed that the positive effect of therapeutic effects on the cervical nerve formations is due not to their etiological or pathogenetic role, but to the fact that effects on the neck simultaneously improve blood flow and in hand.

To answer the questions posed, in our work from 1960, we paid attention to the initial symptoms of the disease. In more than half of the observations, suffering began not with symptoms of periarthrosis, but with other manifestations of cervical osteochondrosis: with lumbago, pain in various parts of the arm, but not in the shoulder joint, with paresthesia in the fingers and with vertebral artery syndrome. In a minority of cases, the disease is present from the very beginning

Orthopedic neurology. Syndromology

Soreness of typical pain points in 300 patients with osteochondrosis, including patients with glenohumeral periarthrosis (in absolute numbers and %)

Table 5.3

manifested itself by symptoms of glenohumeral periarthrosis. However, in these patients, later or simultaneously with periarthrosis, radicular and other symptoms of cervical osteochondrosis developed, and radiography of the cervical spine revealed cervical osteochondrosis or spondyloarthrosis.

So, the first evidence of the pathogenetic connection of periarthrosis with osteochondrosis is the development of glenohumeral periarthrosis against the background of symptoms of cervical osteochondrosis or spondyloarthrosis.

The second evidence is the development in patients with cervical osteochondrosis of other disorders that are close in their pathogenetic essence to glenohumeral periarthrosis. We are talking about the commonality of a number of neurodystrophic disorders in the area of ​​​​bone protrusions in the places where muscle tendons are attached to them - the phenomena of neuroosteofibrosis. On the arm, according to A. Merlini (1930), the expression of such dystrophic disorders is “epicondylitis” of the shoulder, “styloiditis”, lesions in the area of ​​the epiphyses of the ulna and radius. As shown above, with glenohumeral periarthrosis, the main pathology occurs in the places of attachment of muscle tendons and ligaments to the tubercles of the humerus and to the coracoid process. Immediately there is pain in the points of the deltoid muscle and the Naderbian point that we described.

The coexistence of these neurodystrophic disorders in cervical osteochondrosis and glenohumeral periarthrosis indicates that And humeroscapular periarthrosis is related to cervical osteochondrosis.

Let's look at the relevant data (Table 5.3).

The table shows that pain at the point of the vertebral artery occurs almost equally often both in patients with cervical osteochondrosis in general and in those with glenohumeral periarthrosis (P>0.05). Points in the areas of bony protrusions are more often painful in case of glenohumeral periarthrosis than in other groups. Naderbov's points and the point of the anterior scalene muscle are painful somewhat more often with glenohumeral periarthrosis (P<0,05). Несомненно, в группе больных пле­челопаточным периартрозом чаще болезненны верхняя точка Эрба, область клювовидного отростка, точка при­крепления дельтовидной мышцы (Р<0,01); чаще в этой группе отмечались и болезненность в области наружного надмыщелка плеча (Р<0,02). Весьма демонстративны раз­личия в отношении точки прикрепления дельтовидной мышцы к плечу: у лиц с плечелопаточным периартрозом она болезненна в 2 раза чаще, чем у прочих больных (44 и 21%). Это наблюдение позволяет объяснить давно извест­ный факт: при форсированном отведении руки в сторону или вперед, при напряжении передней или средней головки

deltoid muscle, patients with glenohumeral periarthrosis often complain of pain not so much in the area of ​​the shoulder joint, but in the upper and middle part of the shoulder.

With the development of glenohumeral periarthrosis, the pain phenomena associated with it become dominant, and radicular pain, spreading in the area of ​​any dermatome, recedes into the background. The pain associated with glenohumeral periarthrosis is concentrated mainly in the places of attachment of tendons and ligaments to bone protrusions; these are “deep”, sclerotomal pains. That is why V. Inman and J. Saunders (1944) noted the spread of pain along the sclerotomes not only with injuries of bones and tendons, but also with glenohumeral periarthrosis.

As it should from rice. 3.26, sclerotomes in the area of ​​the shoulder joint and shoulder are not limited to just the Su level. These sclerotomes correspond to the levels of Cvi and Sup, so often affected in cervical osteochondrosis. Referral of pain to the area of ​​the shoulder joint due to irritation of disc receptors was observed when fluid was introduced into it and at the level Ciii.iv and Qy_y, Cv-vi and Cvi-vn (Popelyansky A.Ya., Chudnovsky N.A., 1978). The syndrome of glenohumeral periarthrosis occurs with cervical osteochondrosis of any localization. Therefore, the opinion of A.D. Dinburg and A.E. Rubasheva (1960) about the connection between glenohumeral periarthrosis and glenohumeral pain in general with the pathology of the Civ_y disc alone is undoubtedly erroneous. The appearance of lesions in the bone-periosteal-tendon tissues changes the nature and zone of distribution of sensations.

Humeral periarthrosis is associated with pathology of both the upper thoracic spine and the corresponding spinal-costal joints (Steinrucken H., 1981), and also With pathology of the muscles located directly on the chest, in particular the pectoral, subscapularis (Johnman V. et al, 1944).

Here it is appropriate to point out the tests proposed by the authors for thoracogenic limitation of range of motion in the shoulder joint. With blockade of the SDS T w_|y or Tn-sh, it is possible: a) limiting the volume of active posterior abduction of the shoulder; limitation of the volume of passive abduction of the straightened shoulder (taken into account in the absence of damage to the rotator cuff, “frozen shoulder” and diseases of the chest organs); b) limiting the volume of active clasping of the head with the palm when the shoulder is abducted.

The above allows us to join the opinion of the authors who believe that damage to the nerve trunks is secondary to glenohumeral periarthrosis (Shtremel A.Kh., 1941; Badyul P.A., Badyul A.A., 1950; Kokhanovsky I.Yu., 1960). This does not mean, however, that the process, as the mentioned authors believe, is of the nature of ascending neuritis. One also cannot agree with the denial of the primary

Chapter V. Syndromes of cervical osteochondrosis

the role of nerve damage. The reflected phenomena in the nerves and plexus are secondary to periarthrosis, but it itself is secondary to nerve damage due to osteochondrosis. This mutually supporting ring mechanism is to some extent reflected in the statement of E. Fenz (1941) about neurogenic arthralgia and arthrogenic neuralgia in patients with pathology of the cervical spine. This does not mean, however, that the pathology of the nervous system necessarily develops as a result of damage to the nerve trunks.

Both in the case of damage to the roots in the spine and nerve trunks in the area of ​​the capsule of the shoulder joint, and when they are intact on the periphery, foci of neuroosteofibrosis are formed according to reflex mechanisms. The periarticular tissues of the shoulder joint are only one of the recipients of pathological nerve impulses from the spine or other foci.

Thus, the second evidence of the possible vertebral genesis of glenohumeral periarthrosis should be considered the fact that it is a component of other vertebrogenic syndromes.

The third evidence of a possible neurogenic rather than local mechanism of periarthrosis is its uniqueness in patients with cerebral focal diseases.

Humeroscapular periarthritis is detected in patients on the side of post-stroke hemiparesis in 15-20% (Stolyarova L.G. et al., 1989). Their pathogenesis was studied experimentally at our department (Veselovsky V.P., 1978). The creation of a brain lesion contributed to the development of characteristic extravertebral syndromes in the presence of spinal lesions. Thus, in patients with hemiplegia, in whom there can be no talk of either “ascending” or “descending” neuritis, pain often occurs in a shoulder joint that is loose or affected by contracture. The source of these pains in many cases is irritation of the sensitive nerve endings of the periarticular tissues, as well as tonically tense muscles (Wang-Xin-de, 1956; Anikin M.M. et al., 1961). Subsequently, we established that the source of these pains is not an organically affected optic tubercle, but cervical osteochondrosis accompanying the cerebral lesion.

Shoulder pain with hemiplegia cannot be considered “thalamic.” The time of their occurrence, weeks and months after a stroke, also speaks against this, according to J. Budinova-Smela et al. (1960), 1-3 months after the stroke. The same is indicated by their localization not in all tissues and joints on the side of hemiplegia, and the dependence of pain on posture and movements. Also, motor disorders that form in this area during the recovery and residual periods of hemiplegia cannot be explained by cerebral influences alone. It is known that the Wernicke-Mann position is characterized by spastic hypertension of the extensors of the leg, foot, and adductor muscles of the thigh, and in the arm - the flexors, pronators, and adductor muscles. However, the muscle-tonic relationships in the area of ​​the shoulder joint turn out to be very peculiar. Regardless of the problem of osteochondrosis or glenohumeral periarthrosis, the possibility of contracture of the muscles of the shoulder joint with hemiplegia was emphasized by E.Brissaud (1880), L.O.Darkshevich (1891). Along with tension in the adductor muscles, as well as some muscles in the shoulder girdle,

the shoulder is often lowered and the joint space gapes: the distance between the acromion and the head of the humerus increases (Tkacheva K.R., 1968; Smith R.G. etal, 1982). A special clinical study conducted in our clinic by M.M. Aleksagina (1972) made it possible to establish the presence of a significant peripheral nervous component in the development of pain. Muscle tone in the paralyzed limbs was increased in 13 out of 22 subjects, and decreased in 9. In 2 patients, the previously elevated tone decreased from the day the pain syndrome appeared in the arm (on the 4th and 11th days of the underlying disease). Other features of the clinical picture made it possible to clearly define the pain syndrome as glenohumeral periarthrosis and speak in favor of its connection with cervical osteochondrosis. The medical history of all patients revealed pain or crunching in the neck, “radiculitis”, some had wounds in the arm, and one had Dupuytren’s contracture. Simultaneously with the appearance of pain, neurovascular, neurodystrophic and muscular-tonic disorders characteristic of glenohumeral periarthrosis developed on the side of brachialgia. In 12 patients, the limitation of the range of movements of the head and all typical points on the neck were very pronounced. All of them had swelling, cyanosis and coldness of the hand, the anterior scalene muscle was sharply painful, tense and thickened. 20 had tenderness of the coracoid process, the deltoid muscle attachment to the humerus, the brachioradialis muscle, and other tendon and ligament attachments to bony prominences. Painful Müller or Cornelius nodes were palpated in the muscles of the shoulder girdle. A sharp pain appeared when actively and passively moving the arm to the side, forward, or when placing it behind the back. Dovborn's symptom was observed in 11 patients. An increase in skin temperature was noted in the area of ​​the adductor muscles of the shoulder. Thus, in all our patients, on the side of hemiparesis, a typical picture of glenohumeral periarthrosis with anterior scalene muscle syndrome developed.

X-rays of the cervical spine revealed straightening of the lordosis, flattening of the discs, anterior and posterior exostoses, i.e. changes of II-III degrees according to Zecker. On the images of the shoulder girdle there was diffuse porosity of the bone tissue on the side of brachialgia, in 4 cases there was a “ring symptom” according to V.S. Maykova-Stroganova (1957).

Pain in the paralyzed arm occurred within 2 to 45 days, in 3 patients - 2-3 months after the onset of cerebral disease. They developed gradually over 3-4 days, were more often aching, cerebral in nature, bothered during active and passive movements, and less often occurred spontaneously at night. All of them had a decrease in palpation tone on the side of brachialgia, and in 13 this was combined with an increase in tone of the pyramidal or extrapyramidal type during passive movements, hypotrophy of the hypothenar and interosseous muscles. In 19 subjects whose muscle tone was decreased or slightly increased (grades I-II), an increase in the coraco-acromio-brachial gap on the side of brachialgia was found.

Taking into account the complex neurogenic features of muscle-tonic mechanisms, the concept of periarthrosis after stroke as arthropathy with stretching of the joint capsule due to the heaviness of the arm should be considered simplified

Orthopedic neurology. Syndromology

(Tkacheva G.R. et al., 1966). It is enough to point out the fact that pain in the joint capsule also occurs in bed, when gravity has nothing to do with the arm.

According to P. Henning (1992), the tone of the muscles that fix the head of the humerus plays a role (the author distinguishes two constitutions: varus hypertonicity, more often in men, and valus, hypotonic, more often in women).

Accordingly, when lifting the shoulder, the head touches the “roof” of the joint to a greater or lesser extent. Next, we focused on the muscles that showed the greatest palpation tenderness and density in this group of patients: the teres major, pectoralis major, and subscapularis. Research by L.S. Lerner (1977, 1978) found that the most severe electromyographic shifts, as well as the most severe decrease in lability, were noted in the adductor muscles compared to the abductor muscles. Assessment of the condition of the cervical spine and associated glenohumeral periarthrosis made it possible to obtain an adequate explanation of pain in the shoulder area and with hemiplegia. It is caused by emerging vertebrogenic syndromes of glenohumeral periarthrosis and scalene muscle in patients with hemiplegia in the presence of age-related changes in the joint capsules.

Our observations are consistent with the electromyographic data of those authors who showed that with hemiplegia, not only central, but also peripheral neurons are involved in the process (Goldcamp O., 1967; Bhala R., 1969)- denervation potentials are detected. According to Yu.S. Yusevich (1958), K. Krueger and G. Wyalonis (1973), they are caused by alteration of peripheral motor neurons due to the switching off of the trophic influence of corticospinal fibers. This interpretation in itself did not explain the fact that the arm muscles are involved in the pathology while the peripheral motor neurons innervating the leg muscles are intact. All of the above observations, as well as the data that we will dwell on below, showed the significance of central influences in hemiplegia in the presence of a peripheral focus in the area of ​​the shoulder joint.

Thus, the third proof of the not local, but neurogenic nature of the syndrome of glenohumeral periarthrosis is the possibility of its occurrence in cerebral patients on the side of other manifestations of focal brain pathology.

In itself, the reflex tension of the muscles fixing the shoulder joint in vertebrogenic pathology is initially protective as a component of regional myofixation (Veselovsky V.P., Ivanichev G.A., Popelyansky A.Ya. et al., 1984).

Below we will see that the source of impulses that form this, like any other vertebrogenic syndrome, in addition to vertebral and cerebral foci, can be other affected organs or tissues: any source of impulses from the upper quadrant of the body, under certain conditions, can cause defence of the adductor muscles of the shoulder, as well as corresponding neurodystrophic disorders, sclerotomy pain and other autonomic disorders.

The fourth evidence of not a local, but a neurogenic mechanism of this syndrome is the possibility of its occurrence in response to impulses from any source, not just the vertebral one.

By the period of development of glenohumeral periarthrosis with cervical osteochondrosis, radicular pain, if it occurs, is replaced by sclerotomy. These pains, as well as radicular hypoalgesia and reflex disturbances, did not disappear completely. The combination of “primary” sclerotomy symptoms makes the clinical picture very complex, but quite accessible to neurological analysis. Because humeroscapular periarthrosis is a neurodystrophic process; it is important to establish to what extent other autonomic, in particular neurovascular, changes are expressed in it. Many consider autonomic disorders to be the leading factors in the pathogenesis of glenohumeral periarthrosis. Some authors put stellate ganglion damage at the forefront of glenohumeral pain, including periarthrosis. (Reischauer Shch 1949; Leriche R., 1955; Brotman M.K., 1962, etc.). Pain in the glenohumeral region occurs with artificial irritation of the stellate ganglion (Leriche R., Fontaine R., 1925; Polenov A.Ya., Bondarchuk A.B., 1947). Contracture phenomena are also related to autonomic disorders, without which there is no picture of glenohumeral periarthrosis. With passive contractures, a decrease in skin temperature in the distal parts of the affected limb, sometimes cyanosis, and an increase in the vasoconstrictor adrenaline reaction are noted - a picture of sympathetic irritation (Rusetsky I.I., 1954). When measuring skin temperature in 15 patients with cervical osteochondrosis with a picture of glenohumeral periarthrosis, O. Stary (1959), Ya. Yu. Popelyansky (1960) discovered hypothermia in these parts of the limb. Sensorine pain adaptation and the reactivity of the skin of the hand to ultraviolet irradiation are disrupted (Razumnikova R.L., 1969). The results of our study of some neurovascular changes in glenohumeral periarthrosis are presented in table 5.4.

From the table above it follows that neurovascular disorders in the hand area in patients with glenohumeral periarthrosis are more common than in the general group of patients with cervical osteochondrosis without this syndrome. The same applies to muscular dystrophic changes, which should also be considered as a consequence of autonomic disorders.

As for the reflex processes that lead to stiffness, depending on muscle contractures in articular and periarticular lesions, here we encounter the same mechanisms that were discussed in connection with cervical lumbago, contracture of the anterior scalene, pectoralis minor and other muscles. The muscles in the area of ​​the shoulder joint are, on the one hand, the recipient where pathological impulses from the spine are sent, on the other hand, being in a state of contracture, they are also the source of pathological impulses sent to the spinal cord. Such a source can be overworked muscles suffering from microtrauma, and impulses from internal organs, in particular, during myocardial infarction (Osier W., 1897; Karchikyan S.N., 1928; Howard T., 1930; Rotenberg L.E., 1933; Edeiker J., Wilfarth S., 1948; Askey J., 1941; Jonson A., 1943; Steinbrocker O. etal, 1948; Bayer H. et ai, 1950; Albov N.P., 1951; 1952; Jarvinen, 1952; Parade G., Bockel P., 1955; Steinbrocker O., Argyros N., 1957; , 1959; Somerville W., 1959;

Chapter V. Syndromes of cervical osteochondrosis

Table 5.4 Distribution of the frequency of various neurovascular changes in the area of ​​the affected hand in patients with cervical osteochondrosis, including in patients with glenohumeral periarthrosis (in absolute numbers and %)

Symptoms	Nosological form
Cervical osteochondrosis (300 people)	Humeroscapular periarthrosis (79 people)
Decreased skin temperature	54(18%)	12(15,2%)
Decreased skin temperature + cyanosis + swelling	29 (9,7%)	13(16,5%)
Decreased skin temperature + swelling	32(10,7%)	12(15,2%)
Decreased skin temperature -U- paleness	8 (2,7%)	6(7,6%)
Increased skin temperature	59(19,7%)	2 (2,5%)
Increased skin temperature + cyanosis + swelling	13 (4,3%)	6 (7,6%)
Increased skin temperature + swelling	3(1%)	2(2,5%)
Dry hand skin	5(1,7%)	2(2,5%)
Hyperhidrosis of the skin of the hand	8 (2,8%)	4(5%)

Lyansky Y.Yu., 1961; Welfling Y., 1963; Dubrovskaya M.K., 1965; Gordon K.B., Popelyansky Ya.Yu., 1966; Yurenev P.N., Semenovich K.K., 1967; Bosnev V., 1978; Chetkikh N.L., 1992, etc.). Similar neurodystrophic syndromes in the shoulder and anterior chest wall occur, according to various authors, in 10-20% (Gordon I.B., 1966). They have also been described in pleuropulmonary diseases (Jonson A., 1959; Zaslavsky E.S., 1970; Morandi G., 1971). They are very often observed with damage to the hand, in particular, with a fracture of the ray in a typical place (Logachev K.D., 1955; Kohlrausch W., 1955; Dietrich K, 1961; Strokov B.C., 1978, etc.).

Thus, the fourth evidence of the neurogenic nature of glenohumeral periarthrosis and, in particular, in connection with impulses from the vertebral lesion, is the possibility of developing the same syndrome from other lesions - from various tissues of the upper quadrant zone on the ipsilateral side. Other examples of the participation of the viscerogenic mechanism in the development of glenohumeral periarthrosis will be given below.

In order to consider in more detail the question of the relationship between various foci of irritation and reflex contractures in the area of ​​the shoulder joint, it is necessary to first establish the nature of contracture phenomena in glenohumeral periarthrosis. Considering the well-established fact of the presence of dystrophic changes in the periarticular capsular-tendon tissue, it should be recognized that this syndrome has a component of passive tendon-muscular contracture with all its characteristic autonomic-vascular reflex influences. However, even in the stage of pronounced phenomena, the volume of possible active movements in the shoulder joint with glenohumeral periarthrosis is less than the volume of passive movements. Therefore, this is not only a passive, but also an active contracture. Reducing active contracture manifestations with the help of therapeutic effects leads to a decrease in pain. In such cases, it becomes clear that the decisive moment in the syndrome was not the changes in the periarticular connective tissue themselves, but reflex muscle tensions. The most common source of reflex action on the muscles of the shoulder joint, the cause leading to their tonic tension, is the affected disc. Removing the affected disk, as already mentioned, h some observations

yah leads to the disappearance of symptoms of glenohumeral periarthrosis. In this regard, we, together with A.I. Osna (1966), traced the effect of novocainization of the affected disc. Under X-ray control, which specifies the position of the needles inserted into the discs, a 2% solution of novocaine (from 0.5 to 2-3 ml) is injected through them. Within two to three minutes, contractures in the muscles of the shoulder joint significantly decrease or disappear, and the range of movements, hitherto sharply limited, increases significantly. The pain of typical points usually remains unchanged. After a few days, if the procedure is not repeated or other therapeutic measures are not applied, contracture phenomena are restored, although in a less pronounced form. Here is a typical example.

Patient P., 55 years old. For four years he suffered from cervical disease, and a year before admission to the hospital съг experience pain in the right forearm and arm: a picture of typical glenohumeral periarthrosis. Upon admission, the right arm was abducted no more than 50°, and then only at the expense of the scapula (Fig. 5.12). On the spondylogram, osteochondrosis Cy-vi, pneumomyelography showed protrusion of the Simu disc, and discography showed a rupture of the fibrous ring Civ-v- 2 ml of a 2% novocaine solution was injected into this last disc. After 2 minutes, the range of movements in the hip joint increased sharply. After two hours, I raised my hand slightly above the horizontal - an effect that remained after. The compression force increased from 40 to 50 kg. Subsequent physiotherapeutic interventions over the course of a month led to practical recovery.

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