Clinical and neurological examination of the patient includes two stages: the study of complaints, anamnesis of life and illness (questioning of the patient) and neurological status (objective study).
The study of complaints begins with the question: “What bothers you?” Questions like: “What hurts you?” Are less successful, because the disease is not always expressed only in pain.
The questioning of the patient cannot be carried out hastily. It is very important to carefully, thoughtfully and sympathetically listen to the patient’s presentation of their unpleasant sensations, if possible without interrupting it. The patient must be addressed by name and patronymic, avoiding such obsolete verbal stencils as “patient”. An in-depth study of the patient’s sensations is necessary, and not the formulation of the diagnoses that patients often resort to (“I have sciatica,” “Osteochondrosis bothers me,” etc.).
The form of the conversation and the method for studying complaints should be selected by the doctor in relation to the personality characteristics of the patient. When questioning, you should ask the patient specifically and slowly list all the complaints, and among them highlight the main disorders that are most worrying and disruptive.
After all complaints are listed and the main ones are selected, it is necessary to detail each complaint separately. Clarification of the nature, intensity and localization of a disorder is of great importance in differential diagnosis.
An in-depth analysis of one complaint (pain) allows presumably to conduct differential diagnostics based on the patient’s questioning. It helps to clarify the characteristic features of pain (“pulsating”, “bursting”, “burning”, etc.), its localization, taking into account the age at which it first appeared, its duration and persistence, the conditions in which pain occurs (lying down, after physical exertion, with a change in body position, a change in weather, etc.), as well as taking into account the symptoms that accompany pain. For example, pain in compression syndromes is almost always accompanied by paresthesia. When characterizing and analyzing pain, 4 degrees of pain are distinguished according to its intensity: 1) insignificant, disappearing at rest; 2) moderate pain at rest, but increasing with movement; 3) constant pain with periodic intensification and a senestopathic hue; 4) a sharp constant pain with a forced position of the patient, requiring urgent use of analgesics.
The localization of pain (localized, laminating on the dermatome — radicular, diffuse — in the sclerotome zone), its distribution (irradiation) to the distal or proximal limbs is specified. If possible, a connection is established with the defeat of various tissues – ligaments, joints, muscles, roots, nerves.
The presence of the patient’s forced position and posture in which pain arises and intensifies is revealed; when bending or flexing, tilting left or right, coughing or sneezing. Increased pain at rest is usually associated with a deterioration in venous blood supply around a degenerated disc.
The nature of the pain also requires clarification. Radicular pains are described as stitching, shooting, usually in a specific autonomous zone. They increase with torso, physical exertion (“straining”). In the acute stages of the disease, thermal procedures can increase pain, which is associated with hyperemia and edema of the root. The decrease in pain during thermal procedures and movements is explained by improving blood supply to the root, nerve.
Pain with a burning component is indicated as sympathetic. Most often, they are caused by irritation of the synuvertebral nerve (Lyushka’s nerve) or other autonomic formations (paravertebral sympathetic chain and autonomic plexus or nerve fibers).
Deep, aching pains occur spontaneously in the area of degeneration or neuroosteofibrosis and are aggravated by changing weather, vibration, and mechanical stresses.
Dull spilled pain and a feeling of rapid fatigue of the back occur when the muscular-ligamentous apparatus of the spine is overstrained due to overload due to instability of the vertebral motor segment.
Clarification of the anamnesis (labor, household, sports history) is aimed at clarifying the factors contributing to the disease or provoking it. These, in particular, include static-dynamic and discoordinate loads, which often lead to microtrauma of the fibrous tissues of the spine, their ruptures and later to osteofibrosis.
Objective research. In practical work, several versions of the methods of vertebral neurological research are used, which differ in one or another sequence of diagnostic techniques, as well as in larger or smaller volumes. Nevertheless, a planned and detailed study of a naked patient, as is customary in vertebral neurology, is preceded by observation of the patient’s behavior, walking, posture, movements, postures, as soon as he appears in the doctor’s office or lies in bed. This observation often allows you to see typical sparing or antalgic poses: The
patient presses his whole back against the chair, or vice versa, sits on the front of the seat, clinging to the chair only with the thoracic torso (kyphosis);
Lies on a healthy side with a bent leg;
Lies with a pillow placed under the stomach (“cushion pad” syndrome);
It is in the knee-elbow position;
Stands with a bent sore leg;
Sits on the edge of a chair on a healthy buttock with a sore leg set aside and a straightened torso in a healthy direction;
“Tripod” syndrome, when a patient sits in bed with a bent leg and an emphasis of hands behind the pelvis;
From a sitting position on the floor, the patient rises, becoming on all fours, then on his knees, finally climbing his hands on his hips (Minor’s technique);
The patient unties the shoelaces, bends the leg or kneels (lace syndrome);
Lifting an object from the floor, squats or tilts the body forward, while bending the affected leg.
When walking, the patient spares the affected leg. At the same time, he bends the leg in the hip, knee and ankle joints, limps, walks in small steps, bends the body and fixes it with his hands, tilts the body forward and to the healthy side, using a stick, crutches.
A planned examination of the patient is carried out with his position with relaxed muscles of the trunk and limbs. In this case, the symmetry of the parts of the body of the healthy and sick side is assessed both at rest and during movements. Determine the height, weight, general constitution, the presence of changes in the skin, dysgraphic features, the position of the neck and lower back, the shape and structure of the spinal column, the type of posture, muscle relief, posture, range of motion in various parts of the spine and joints.
There are several types of posture: normal posture; flat back; round back; stooped back.
Evaluate the shape and length of the neck, the symmetry of the standing of the shoulder girdle and their relative position. The height of the gluteal fold and the type of the intergluteal line, the symmetry of the location of the gluteus maximus muscle, Michaelis rhombus (connected by lines to the upper end of the anal fold, the fossa above the posterior iliac bones and spinous processes of the vertebrae), trophic muscles are determined. Particular attention is paid to the symmetry of the triangles formed between the arms, hips and waist. Normally, in the standing position, symmetrical lateral waistlines and their depth are visible.
Determining the level of damage to the spine is carried out according to landmarks, which are bone protrusions. This is the mastoid process, the angle of the lower jaw, scapula, sciatic tubercle, sacroiliac joint, iliac wings, large trochanter of the thigh.
For counting the vertebrae along the posterior surface of the neck and trunk, the reference point is the most prominent spinous process of C7. The joint between the atlas and the axis is located more medially than the sternocleidomastoid muscle on the line connecting the apex of the mastoid process with the spinous process C2 and T7 – corresponds to the level of the angle of the scapula, L4 – the line of the crests of the ilium; S1 is the vertebra at the level of the posterior-lower awns of the ilium.
On the lateral surface, the transverse process C2 of the vertebra is 1.5 cm below the tip of the mastoid process, and the lower edge is on the line of the angle of the lower jaw; the transverse process of the C6 vertebra is at the level of the cricoid cartilage (in children a little higher, in the elderly lower); T2 vertebra corresponds to the level of the episternal fossa; L2 vertebra is the lowest point of the tenth rib.
When examining a patient, it is necessary to remember and take into account the physiological curvature of the spine: for the cervical and lumbar regions – physiological lordosis, thoracic and sacral – physiological kyphosis.
The top of the physiological cervical lordosis corresponds to the level of C5-C6 vertebrae, thoracic kyphosis – T6-T7, lumbar lordosis – L4 vertebra. The sacrum is usually at an angle of 30 ° with respect to the frontal axis of the body. Normally, lumbar lordosis is 18 mm. Kyphosis with a maximum forward inclination of standing is 13 mm, lordosis with a maximum deflection backward is 28-30 mm. The total range of movements in the lumbar region in the sagittal plane averages 42 mm. There are 3 degrees of severity of lordosis: I st, – up to 15 °, II st. – up to 30 °, III st. – over 30 ° (the angle of lordosis is measured by a ruler).
Determining the configuration of the lumbar spine can be carried out on a radiograph in a lateral projection according to Ferguson. Lower the perpendicular from the middle of the lower trailing plate of the III lumbar vertebra. Under normal lordosis, this line passes through the upper anterior corner of the sacrum. With decompensated myofixation in patients with hyperlordosis, it deviates by 10-15 ° and is in front of the sacrum, and with kyphosis, it is posterior to the anterior edge of the sacrum.
Flattening of lumbar lordosis (“flat back”, “plank”, “string” syndrome) is manifested more often by coherence or absence of lordosis, but sometimes it reaches the degree of lumbar kyphosis. This adaptive reaction reduces the amount of posterior hernial protrusion of the disc and leads to a decrease in pressure on the spine. Strengthening of lumbar lordosis often indicates the presence of spondylolisthesis. Hyperlordosis of the lumbar region is noted with median hernias L5.
The severity of kyphosis, lordosis, as well as the degree of mobility of the spine forward and backward is determined using a protractor with an arrow and using a curvimetrometer. The curvimeter is represented by two supporting legs with a distance of 20 cm (this is the average distance from the XII thoracic to the I sacral vertebra) and a moving ruler with millimeter divisions between the legs. The end of one leg of the curvimeter is placed at the level I of the sacral vertebra, and the end of the other is approximately at the level of the spinous process of the XII thoracic. The patient stands at attention. The end of the scale ruler moves forward to touch the skin in the projection area of the spinous process and the degree of severity of lordosis in millimeters is determined. The shift of the ruler with respect to the zero line in millimeters in the opposite direction allows you to fix kyphosis.
First, the metacarpal beam is examined, then the elbow flexion and extensor reflexes. With relaxed muscles, a short, jerky blow is applied to the tendon or periosteum.
The ulnar flexion reflex is caused by a blow to the tendon of the biceps muscle, first one and then the other hand of the patient. The flexion-elbow and scapular-brachial (Ankylosing spondylitis) reflexes change with the pathology of the roots of C5-C6.
The ulnar extensor reflex is determined by the blow of the hammer on the tendon of the triceps muscle. In this case, the forearm and hand should hang down freely with complete relaxation of the muscles. The ulnar extensor reflex changes with the pathology of the roots of C7-C8.
The metacarpal ray reflex is caused by the impact of the malleus on the radius in the styloid process. In this case, bending of the arm in the elbow joint, slight pronation and flexion of the fingers occur. This reflex changes with damage to the roots of C5-C8.
Abdominal reflexes are caused when the stroke is directed from the periphery of the abdomen to the midline.
The upper abdominal reflex is caused by a stroke parallel to the lower edge of the costal arches and corresponds to segments D7-D8, the middle one – by a stroke along the horizontal line at the navel and corresponds to segments D9-D10 and the lower – caused by a stroke parallel to the inguinal folds and corresponds to segments D11-D12.
The cremaster reflex is caused by dashed skin irritation of the inner thigh and corresponds to segments S1-S2.
The knee-jerk reflex is examined when the hammer hits the ligament of the patella, preferably when lying or sitting. It decreases with damage to the roots of L2-L4.
The Achilles reflex is examined when the hammer hits the Achilles tendon. Decreases or disappears when the S1 root is affected.
In conclusion, the data obtained by questioning the patient and an objective study are synthesized, syndromological diagnostics, differential diagnosis are carried out and the necessary additional radiological, electrophysiological and other studies are planned to clarify the clinical diagnosis.
The basic principles of the diagnosis of tunnel neuropathies
Vertebrogenic radicular syndromes often have to be differentiated with many compression-ischemic (tunnel) neuropathies. Their recognition is based on the questioning of the patient (the study of complaints and anamnesis) and objective neurological examination. Clarification of the nature, intensity and localization of a disorder is of great importance in differential diagnosis. It is unacceptable to limit the patient to simply indicating pain or “numbness.” An in-depth analysis of complaints of pain and numbness suggests the possibility of tunnel syndrome and differential diagnosis. At the same time, clarification of the characteristic features of pain and paresthesias, their localization, the general condition of the patient and somatic diseases, the profession, the duration and persistence of disorders in their dynamics help. It is very important to find out the conditions in which paresthesia and pain arise or decrease (stop).
Analysis of complaints of patients with tunnel neuropathies shows that, despite significant clinical differences, many forms share common features. Paresthesia (the earliest sign of the disease) is provoked by prolonged physical rest and horizontal body position. Therefore, the first (manifest) paresthesia occurs in patients in the early morning hours. They are usually localized in the area of distal skin innervation: in the first three fingers during compression of the median nerve, in the fifth and sixth fingers of the hand with Guyon’s bed syndrome, etc. In this phase of the disease, paresthesias decrease or disappear under the influence of rubbing hands and repeated movements, which indicates early defective blood supply to the nerve.
In the further (natural) development of paresthesia, they appear at night, forcing patients to get out of bed several times a night. Later, pains join, also first in the morning, and then at night, with the same localization. Again, pain and its intensification are associated with prolonged physical rest. Naturally, physical stress during tunnel syndromes can increase pain, but rest does not bring relief. To an inexperienced doctor, it seems unusual to maximize paresthesia and pain, not at exertion, but at rest.
It is important to pay attention to the fact that if the pains are caused by tendovaginitis, arthritis and arthrosis, then the pain intensifies as much as possible with active movements, just in the area of the segment involved and decrease or disappear at rest. In the differential diagnosis with primary diseases of the joints and ligaments, it is necessary to take into account the retrograde spread of pain often encountered in tunnel neuropathies. We have already reported about a sailor whose pain due to compression of the tibial nerve in the tarsal canal was detected not only locally, but also spread along the projection of the sciatic nerve. At the prehospital stage, this circumstance made it possible to exclude diseases of the ankle joint, but led to an erroneous diagnosis of “sciatic nerve neuritis.”
It is possible that in cases where there is a retrograde spread of pain and the nerve is sensitive to palpation both distally and proximal to the “trap point”, we are talking about the initial stage of Waller degeneration. It is believed that this is due to secondary-induced disorders of the intraneural blood supply in the form of generalized arteriolar or capillary spasm, which in turn leads to pain and discomfort in the proximal part of the nerve trunk.
Our rheovasographic and especially thermal imaging studies convincingly testified to the spread of vegetative-vascular shifts distal and proximal to the site of nerve damage. Often with traumatic-compression neuropathies (closed nerve injury followed by compression due to a plaster cast), we observed a decrease in infrared radiation (IR radiation) not only at the site of injury, but also in the projection area of the proximal part of the nerve trunk. It should be emphasized that the reduction of infrared radiation in the proximal segment of the nerve did not appear immediately, but several hours after the moment of injury. At the same time, sensitivity disorders also intensified and paresis of the muscles innervated by this nerve increased. Another reason for the proximal spread of pain may be traction stress or tension in the proximal part of the nerve during its primary fixation in a “trap point”.
Patients notice that after morning and night paresthesias and pains, if systematic treatment is not carried out, daytime paresthesias appear. Usually they are provoked by physical activity. So, with carpal tunnel syndrome, daytime paresthesias are provoked by intense manual labor, requiring prolonged tension of the flexor muscles of the fingers (carrying weights, milking of cows, etc.), or occur after frequent stereotypical movements of the fingers and hand. Yu. E. Berzins and co-authors (1982) noted that paresthesia occurs when the hands and fingers are in an elevated position for a long time (among electricians, painters, etc.).
However, nocturnal paresthesia and pain in intensity and duration significantly exceed daytime.
In the first phase of the disease, complaints of stiffness and swelling of the fingers are not uncommon, although examination does not reveal edema. At the same time, patients in the morning, against the background of “numbness of the fingers”, experience difficulties with delicate purposeful movements (fastening buttons, tying a tie, etc.), which are necessary for the morning toilet and self-care. With careful questioning, these complaints are not caused by muscle paresis, but by sensitive neuropraxia (“afferent paresis” or movement disorders caused by impaired influx of afferent stimuli).
After the patient’s complaints are clarified in all the details, the first idea of a possible (supposed) disease is usually formed, which serves as a canvas for a focused questioning about the sequence and circumstances of the development of symptoms, that is, to study the medical history. In the recognition of compression- ischemic neuropathies, special attention should be paid to the initial symptoms, as well as an analysis of the situation and factors preceding the disease. When clarifying the history, information is needed on the presence of general systemic diseases of the connective tissue, endocrine-hormonal changes, as well as local factors. If there are assumptions about the relationship of the disease with the profession, it is advisable to inquire in detail about working conditions and the nature of muscle loads.
An objective neurological study in the initial phase of the disease does not always allow us to establish sensitive, motor, trophic and autonomic disorders typical for the defeat of a particular nerve. Therefore, it should be supplemented with special clinical tests aimed at finding a “trap point” and provoking paresthesia and pain. These tests include the Tinel-Goldberg symptom (test), the test of digital compression of a nerve in the “trap point”, the turnstile (cuff), elevation test and some other methods that are characteristic of individual forms of compression-ischemic neuroparies.
Tinel-Goldberg test. This technique was described by Jules Tinel in 1915 (symptom of Tinel I) as a sign of partial damage to the nerve trunk in the acute period of trauma or an indication of the beginning of nerve regeneration. When percussion over the projection of the nerve (in the lesion area) paresthesia appeared in the distal parts of the arm or leg. In the post-war years, D. G. Goldberg described traumatic neuromas with the same symptom, but with additional radiating pain in the distal direction. Moreover, he did not use percussion, but palpation (cited by A.V. Triumfov, 1974).
In the articles of M.V. Iretskaya et al. (1970), D.G. Goldberg et al. (1970), V.I. Kruglov (1970), E. B. Bremanis (1976, 1979) and others emphasize the great diagnostic value of the Tinel-Goldberg test for carpal tunnel syndrome.
Based on the results of observations of more than 500 patients with carpal tunnel syndrome, G. Phalen (1972) considers this test to be very sensitive and the most frequent of all known methods of provoking paresthesia and pain. We did not have that impression. The symptom of Tinel-Goldberg was positive in 52.6% of our observations, according to the data of Yu. E. Berzins and co-authors (1982) – in 62% of cases.
The digital finger compression test of the nerve trap is widely used in almost all tunnel syndromes. This is the compression of the carpal tunnel along the projection of the median nerve, the Guyon canal along the projection of the ulnar nerve, the pressure in the upper third of the forearm along the projection of the median nerve with round pronator syndrome, the pressure between the heads of the metatarsal bones with Morton metatarsalgia, etc. It is recommended to exert such a thumb for 1 min In response, paresthesia and pain occur along the compressed nerve. The frequency of this symptom in our patients coincided with the frequency of Tinel I, which allowed us to combine these two methods into one Tinel-Goldberg test.
Turnstile (cuff) test. Proximal to the site of the proposed compression of the nerve (on the shoulder, thigh, lower leg, forearm) impose the cuff of the arterial tonometer and increase the pressure in it to the level of a normal systolic or slightly higher than it. Wait 1 min. In the presence of a tunnel syndrome, paresthesia appears in the autonomous zones of the innervation of the compressed nerve. This test can also be used to judge the severity of the disease by measuring the time from the onset of turnstile compression to the onset of paresthesia. It is equally applicable for monitoring the effectiveness of treatment. The turnstile test turned out to be positive in 27% of our observations.
Elevation test. With neuropathies of the hands, the patient in a sitting or standing position raises his extended arms up and holds them in this position for 1 min. At the same time, patients note paresthesia in the autonomous zones of the innervation of the compressed nerve. With neuropathies of the legs in the supine position, they alternate for 1 min. straightened one and then the other leg. It is believed that due to a decrease in hydrostatic pressure in the arteries of the arms and legs, the blood supply to the nerves is disrupted and paresthesias occur. According to our observations, this test was positive in 42% of patients.
Test with the introduction of anesthetic or corticosteroid drug. In order to verify the diagnostic assumption about the presence of nerve compression and treatment, the indicated preparations are administered paraneurally to the points of greatest pain (“trap point”) or points of alleged infringement, found according to topographic landmarks. The relief of paresthesias and pain indicates that the diagnosis is correct. The sample is very reliable (98%), provided that the blockade technique is accurately followed and the necessary manipulation skills are available.
Tests of forced and maximum passive movements. Choose a direction of movement in which the compressed nerve would be in an even greater degree of compression and additional stress. If carpal tunnel syndrome is suspected, maximum passive flexion of the wrist in the wrist joint is used and the arm is held in this position for 1 minute. The result is paresthesia in the I-III fingers. Similarly, the passive extension test is used. In case of neuropathy of the suprascapular nerve, forced cross (on the other side of the body) cast of the outstretched arm is used, which leads to increased traction and compression of the nerve and increased pain in the innervation zone of this nerve. Special methods of arm or leg movements in other clinical forms of compression neuropathies have been reported in other sections. The mechanism of this whole group of passive provocative movements, in essence, can be attributed to nerve traction, often supplemented by its compression. This traction compression test was positive in 59% of our observations.
Thus, at the first stage, which we designated as the stage of primary clinical diagnosis, a thorough study of the patient’s description of paresthesias and pain, their type and nature, localization and connection with physical activity and rest during the day and night is essential. Paresthesia and pain are the first signs of tunnel syndromes. Only later can hypersthesia, hypesthesia or dysesthesia be noted in the interested dermatomes. Anesthesia is rare and at a very late stage of the disease. The same can be said of muscle weakness or objectively observed paresis and muscle atrophy. Due to the delicacy and inconstancy of objective signs of nerve damage, the above tests play an important role, provoking paresthesia and pain. Not all of them can be detected even with a far-reaching disease. So, the symptom of Tinel-Goldberg with carpal tunnel syndrome is sometimes not possible to detect due to severe fibrosis and thickening of the transverse ligament of the wrist and its loss of elasticity. From this, the expediency of using all diagnostic tests known to the doctor is clear.
A history study may not always reveal the true causes of the development of tunnel syndromes. Specific, directly related to the formation of tunnel neuropathy, traum