Impulse conduction disorders. What indicators are recorded during conventional EMG?
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This leads to numerous types of peripheral neuropathies, the basis of which is axonal swelling and degenerative changes myel-new membranes, up to complete destruction their. Axonal degeneration is characterized by greater severity in the distal sections, with predominant damage to large-caliber sensory fibers.
There is reason to believe that the analyzer-coordination mechanism is represented not only in the brainstem, but also in the spinal cord. Here, as an analogue of this mechanism, we can consider a layer of switching neurons concentrated in the gelatinous substance spinal cord(Fig. 17), which is located at the entry point of the sensory fibers of the dorsal roots into the spinal cord. The gelatinous substance of the spinal cord directly continues into the gelatinous substance medulla oblongata, collected along the roots of the sensory nuclei of some cranial nerves.
The breakdown of myelin leads to a decrease in the speed of impulse transmission along the nerve. Damage to motor and sensory fibers initially manifests itself as intermittent sensations of tingling and numbness, and as the disease progresses, a decrease and distortion of sensitivity, weakness and muscle atrophy.
A nerve fiber, or axon, is a very long, thin tube that grows from the cell body of the brain or spinal cord and reaches a distant point, such as muscle or skin. The diameter of the fibers varies from 83 hundred thousandths to 83 hundredths of a millimeter. The diameter of most motor and sensory fibers in humans is about 25 thousandths of a millimeter. In the limbs of some large animals, the fibers can be over a meter in length. Electrical engineers, of course, will not be surprised by these figures. It is known that the length of electrical wires is often many millions of times greater than their thickness. But think about what this means for a tiny cell, which must not only grow this longest process, but also constantly take care of it, constantly look after it.
A useful adaptive result of this system is the maintenance blood pressure at a level that provides normal functioning organs and tissues. Any shift in the optimal level of blood pressure (during muscle activity, emotions) leads to irritation of special baroreceptors, which are located in large numbers inside vascular wall. The nerve signaling that occurs when blood pressure increases in these specialized receptors reaches the vasomotor center of the medulla oblongata along the sensory fibers of the depressor nerves. An increase in blood pressure dramatically increases afferent signaling to this center.
Peripheral fibers motor nerves start at motor neurons located in the anterior part of the spinal cord. Motor axons go to the periphery, to the muscles they innervate. The bodies of sensory cells are located in the dorsal root ganglia or posterior regions spinal cord. Impulses from the periphery are perceived by distal receptors and go to the center, to the bodies of neurons, from where information is transmitted along the spinal cord pathways to the brain stem and cerebral hemispheres. Some sensory fibers are directly connected to motor fibers at the level of the spinal cord, providing reflex activity and a rapid motor response to harmful influences. These sensorimotor connections exist at all levels, cranial nerves are the equivalent of peripheral nerves, but they begin not in the spinal cord, but in the brainstem. Sensory and motor fibers are combined in bundles called peripheral nerves.
Confirm dysfunction peripheral nerves, electrophysiological testing helps determine the type and severity of neuropathy. A decrease in conduction speeds along motor and sensory fibers is usually a consequence of demyelination. Normal conduction velocities, if available muscle atrophy testify in favor axonal neuropathy. An exception is some cases of axonal neuropathy with progressive decay of motor and sensory fibers: maximum conduction velocities may be reduced due to the loss of large-diameter fibers, the conduction of which is especially fast. For axonopathies on early stages recovery, regenerating fibers appear, the conduction of which is slowed down, especially in the distal parts of the fiber. When performing an electrophysiological study of patients with toxic neuropathies, it is necessary to measure conduction velocities along the motor and sensory nerves of the upper and lower extremities. Comparative study conduction along the distal and proximal sections of the nerve helps in the diagnosis of distal toxic axonopathy, as well as in determining the location of conduction blockage during demyelination.
When fed with food at a dose of 25 mg/kg daily for 26 weeks, the animals (rats) became agitated from the moment the blue color appeared. At a dose of 9 mg/kg per day, only blue coloration is detected. Pathohistologically: lipopigment granules in cells and neurons, accumulating over time in proportion to the dose. Symmetrical demyelination of axons and nerve fibers develops in the central and peripheral nervous systems, especially along the corticovisceral tract, but also in the brain stem, in sensory fibers and spinal ganglia. At a dose of 25 mg/kg, demyelination begins at 14 weeks. Over time, however, it forms thin layer myelin, which may explain the relatively slow development and stable pattern of late-stage lesions.
The speed of excitation along nerve fibers can be determined in a person in a relatively simple way. To determine the speed of conduction along motor fibers, electrical stimulation of the nerve is used through the skin in those places where it is located shallowly. Using electromyographic techniques, the electrical response of the muscle to this stimulation is recorded. The latency period of the response mainly depends on the speed of nerve conduction. By measuring it, as well as the distance between the stimulating and discharge electrodes, the conduction velocity can be calculated. It can be determined more accurately by the difference in latent response when the nerve is stimulated at two points. To determine conduction velocity, electrical stimulation is applied to the sensory fibers and the response is withdrawn from the nerve.
To measure the speed with which excitation spreads along the motor nerve, the electrical responses of the muscle to stimulation of several points along the nerve are recorded (Fig. 361.4). The conduction velocity between these points is calculated from the difference in the latent periods of the muscle action potential. To assess conduction in the distal portion of the nerve and the neuromuscular synapse, the latent period and amplitude of the muscle action potential, which occurs when the motor nerve is irritated at the distal point, is measured. To measure the conduction velocity in a sensory nerve, stimulation is applied at one point and the response is recorded at another; the speed of excitation propagation between the stimulating and recording electrodes is calculated based on the latent period of the action potential.
In healthy adults, the sensory nerves of the arms excite at a speed of 50-70 m/s, and the legs - at a speed of 40-60 m/s.
The study of the speed of propagation of excitation along the nerves complements EMG, as it makes it possible to identify and assess the severity of damage to the peripheral nerve. In case of sensitivity disorders, such a study makes it possible to determine at what level the sensory nerve is affected - proximal or distal to the spinal ganglion (in the first case, the conduction speed is normal). It is indispensable in the diagnosis of mononeuropathies, since it identifies the lesion, allows you to detect asymptomatic damage to other peripheral nerves, as well as assess the severity of the disease and its prognosis. The study of the speed of propagation of excitation along the nerves makes it possible to distinguish between polyneuropathy and multiple mononeuropathy - in cases where this cannot be done based on clinical manifestations. It makes it possible to monitor the course of a neuromuscular disease, evaluate the effectiveness of treatment, and understand the features of the pathological process.
Myelinopathies (such as chronic inflammatory demyelinating polyneuropathy, metachromatic leukodystrophy, hereditary demyelinating neuropathies) are characterized by: a significant slowdown in the speed of propagation of excitation along the nerves; an increase in the latent period of the muscle response to irritation of the motor nerve at the distal point; variability in the duration of action potentials of both sensory nerves and motor units. Acquired myelinopathies are often accompanied by conduction blocks.
With axonopathies - for example, caused by intoxication or a metabolic disorder - the speed of excitation along the nerves is normal or slightly slowed down; the action potential of the sensory nerve is reduced in amplitude or absent; EMG shows signs of denervation.
The logic of electrophysiological research is best examined with a specific example. Numbness of the little finger and paresthesia of the little finger in combination with atrophy of the intrinsic muscles of the hand can have different reasons: spinal cord damage, cervicothoracic radiculopathy, brachial plexopathy (affecting the middle or lower trunk of the brachial plexus), ulnar nerve damage. The normal sensory nerve action potential caused by irritation of the affected muscle indicates the proximal level of the lesion -
1. What is EMG?
EMG, or electromyography, - This special type studies of the neurogenic mechanisms that control the functioning of a muscle (motor unit), this study records the electrical activity of the muscle at rest and during contraction. It is also a general term covering a whole range of studies used in the field of medicine called electrodiagnostics
2. What is a motor unit?
It is an anatomical unit of function for the motor portion of the peripheral nervous system It includes motor Neuron, whose body is located in the anterior horns of the spinal cord, its axon, neuromuscular junction and muscle fibers, innervated by the peripheral nerve The electrodiagnostic specialist uses EMG, nerve conduction velocity (NCV), repetitive stimulation, and other electrophysiological tests to evaluate the condition individual components motor unit
3. What is the innervation ratio?
Everyone's axon motor neuron corresponds to a different number of nerve endings and muscle fibers. Depending on the specific requirements for the control of muscle activity, this ratio can be quite low or extremely high. The innervation ratio for the muscles of the eyeball is usually 1 3, which is explained by the need for precise control of movements that provide binocular vision In contrast, the innervation ratio of the gastrocnemius muscle can be as high as 1 2000, since most movements associated with plantar flexion of the foot are relatively crude and require more strength than precision.
4. Name other electrodiagnostic methods.
Study of the speed of nerve impulse conduction, or nerve conduction study, determines the amplitude and speed of signal propagation along peripheral nerves
Repeated stimulation study used to assess the condition of the neuromuscular junction (eg, myasthenia gravis)
Method of somatosensory evoked potentials determines the safety of conduction along the fibers of the spinal cord and brain
Other less commonly used tests include single-fiber EMG, motor-evoked potentials, and spinal root stimulation.
5. What are the clinical indications for conducting EMG and studying SPNI?
EMG is used in cases where it is necessary to determine the location and severity of neurological diseases and/or confirm the presence of myopathic disorders SPNI allows one to clarify the anatomical localization of the pathological process in the motor or sensory parts of the peripheral nervous system, as well as assess the severity of axonal pathology and the severity of demyelination
6. What indicators are recorded during conventional EMG?
Muscle in a state of relaxation: fine electrical activity of injection consists of a short-term discharge of single muscle fibers in response to the introduction of an EMG needle. If the severity this phenomenon not excessive, it does not indicate the presence of pathology Spontaneous activity due to involuntary discharge of individual motor neurons (fibrillation, positive sharp teeth), the muscle should not be in a state of relaxation
A muscle in a state of weak contraction: the subject slightly strains the muscle, which causes the appearance of isolated motor unit action potentials(PDME) Normally, PDME waves have a duration of 5-15 ms, 2-4 phases (usually 3) and an amplitude of 0.5-3 mV (depending on the specific muscle)
Muscle in a state of maximum contraction: the subject strains the muscle as much as possible. Normally, a significant number of motor units are involved in the activation process, which leads to the superimposition of PDME on each other and the disappearance of the original isoline. This phenomenon is called normal, or “complete” interference
7. What is an incremental response?
Both the sensory and motor components of the nervous system function on an all-or-nothing basis. For example, when the body of a neuron located in the anterior horn of the spinal cord and part of one motor unit is activated, the entire motor unit depolarizes. Gradients, or meaning, sensory and motor responses are assessed and controlled by the central nervous system through the progressive addition of incremental responses. In particular, when one motor unit is activated, the change muscle tone may be minimal. If other motor units are involved in the process, muscle tone increases to a visible contraction with a progressive increase in strength. Assessing the number of motor units recruited is an important element of the examination, requiring both visual and auditory skills and training on the part of the electromyographer.
8. How can you distinguish between fasciculation, fibrillation and
positive sharp teeth?
Fasciculation- this is an involuntary impulse of a single motor neuron and activation of all muscle fibers innervated by it. It manifests itself as spontaneous electrical activity of a relaxed muscle on the electromyogram and clinically in the form of short-term, non-rhythmic muscle twitches. This sign characteristic of amyotrophic lateral sclerosis.
Fibrillation- These are involuntary contractions of individual motor units. Contraction of the entire muscle, and therefore no movement, occurs. Clinically, fibrillation may be visible under the skin and resembles fasciculation. The presence of fibrillation indicates denervation. It is based on the spontaneous activation of muscle fibers, on the surface of which there is an increased number of acetylcholine receptors as a consequence of denervation (Cannon's law). Whenever acetylcholine is supplied from the outside, muscle fibers contract, which is manifested by electrical activity such as spontaneous fibrillation on the electromyogram of a relaxed muscle.
Positive sharp teeth also observed with denervation in the form of downward waves on the electromyogram of a relaxed muscle, as opposed to the upward waves characteristic of fibrillation.
9. How does a normal electromyogram differ from that of a denervated muscle?
It should be remembered that fibrillation and positive sharp teeth on the electromyogram of a relaxed muscle appear only on the 7-14th day from the moment of axon degeneration. The process of complete reinnervation of denervated muscle, characterized by large, polyphasic motor unit action potentials, can last 3-4 months.
10. How does a normal electromyogram differ from that with muscle pathology?
The EMG may appear normal in 30% of patients with non-inflammatory myopathy. Myositis (eg polymyositis) causes both neuropathic and myopathic changes on the EMG. The appearance of fibrillations and positive sharp waves on the EMG, characteristic of denervation, is due to involvement in inflammatory process nerve endings in muscles. Muscle fibers are also affected by inflammation, which leads to the appearance of low-amplitude PDMEs typical of the myopathic process.
11. Is the amplitude of the sensory nerve action potential (SNAP) higher or lower than the amplitude of normal PDME?
The magnitude of the PDSN depends on the size and accessibility of the distal nerves. It ranges from 10 to 100 µV, which is about "/20 the amplitude of normal PDME.
12. Is the normal velocity of nerve impulses (SPNI) the same on different areas nerve?
SPNI varies depending on the nerve and nerve site. Normally, conduction through the proximal parts of the nerve is faster than through the distal parts. This effect is due to a higher temperature in the torso, approaching the temperature internal organs. In addition, the nerve fibers expand in the proximal part of the nerve. Differences in SPNI are most noticeable in the example of normal SPNI values for the upper and lower extremities, 45-75 m/s and 38-55 m/s, respectively.
13. Why is temperature recorded during an electrodiagnostic study?
SPNI for sensory and motor nerves changes by 2.0-2.4 m/s with decreasing temperature by 1 °C. These changes can be significant, especially in cold conditions. If the results of the study were borderline, the following question from the attending physician might be appropriate: “What was the patient’s temperature during the study and was the limb warmed before measuring the SPNI?” Underestimation of the latter position may lead to false-positive results and erroneous diagnosis of carpal tunnel syndrome or generalized sensorimotor neuropathy.
14. What is the H-reflex and the F wave? What is their clinical significance? H-reflex is the electrical basis of the Achilles reflex and reflects the integrity of the afferent-efferent arc of the S1 segment. Disturbances of the H-reflex are possible with neuropathies, Sl-radiculopathies and mononeuritis of the sciatic nerve.
F wave is a delayed motor potential following normal PDME, which represents an antidromic response to excess stimulation
tion of the motor nerve. The F wave is recorded on any peripheral motor nerve and gives the researcher information about the state of the proximal parts of the nerve, since the excitation first spreads proximally and then returns down the nerve and causes muscle contraction.
15. How are the sensory and motor components of the peripheral nervous system studied?
Determination of conduction velocity along sensory and motor nerves is the basis for assessing the condition of peripheral nerves. The amplitude of the waves, the moment of their occurrence and the peak are compared with standardized normal values and values obtained on the opposite limb. The teeth are formed as a result of the summation of incremental depolarization of individual axons. Late phenomena (F waves and H-reflex) make it possible to assess the condition of the proximal, anatomically difficult to reach parts of the peripheral nervous system. These studies are also carried out to determine the speed of impulses along long sections of nerve fiber. In particular, identification of F waves serves as an important screening test in the diagnosis of Guillain-Barré syndrome. Less commonly used techniques for assessing peripheral nerves include somatosensory evoked potentials, dermatomal somatosensory evoked potentials, and selective nerve root stimulation.
16. What diseases affect peripheral nerves?
Functionally, peripheral nerves originate near the intervertebral foramina, where sensory and motor fibers connect. Damage to peripheral nerves at the most proximal level has the form radiculopathy(radiculitis) and is caused by compression of the nerve roots by a herniated protrusion of the intervertebral disc or bone growths. Plexus damage as a result of disease or injury, it occurs at the level of the upper (brachial plexus) or lower (lumbar or lumbosacral plexopathy) extremities.
Peripheral nerve diseases can be congenital or acquired. TO congenital disorders include hereditary sensory and motor neuropathies (for example, Charcot-Marie-Tooth disease types I and II). Acquired conditions include neuropathic disorders, such as those due to diabetes, as well as those due to intoxication and metabolic disorders.
Local nerve entrapment happens V in particular, with carpal tunnel syndrome, ulnar nerve neuropathy and tarsal tunnel syndrome. It is important for the electrodiagnostic specialist to take a good history before conducting the study.
17. What are the three main types of traumatic nerve injury?
There are three degrees of nerve damage, originally described by Seddon:
1. Neuropraxia is a functional loss of conduction without anatomical changes in the axon. Demyelination is possible, but as remyelination occurs, SPNI returns to baseline.
2. Axonotmesis- this is a violation of the integrity of the axon. In this case, Wallerian degeneration occurs in the distal region. Restoration of integrity, often not complete, is ensured by axon ingrowth at a rate of 1-3 mm/day.
3. Neurotmesis is a complete anatomical break of the nerve and the surrounding connective tissue sheaths. Regeneration often does not occur. Recovery at this degree of damage is only possible through surgical methods.
18. Is it possible to combine the three types of traumatic nerve injury?
Neuropraxia and axonotmesis often develop as a result of the same injury. Once the compression on the affected area of the nerve is relieved, recovery usually occurs in two stages. During the first, relatively short stage, neuropraxia resolves. The second stage of repair, which takes weeks or months, involves axonal ingrowth.
19. How can EMG and SPNI be used to distinguish demyelinating peripheral
neuropathy from axonal peripheral neuropathy? Demyelinating neuropathy is characterized by moderate to severe slowing of motor conduction with temporal dispersion of PDME, normal distal amplitudes, reduced proximal amplitudes, and prolonged distal latency. Axonal neuropathies manifest as slight slowing of SPNI with generally low PDME amplitudes upon stimulation at all sites. Signs of denervation on the EMG are noticeable in the early stages of axonal neuropathies and only in the late stages of demyelinating neuropathies, when axonal degeneration begins.
20. What systemic diseases predominantly cause demyelinating peripheral neuropathy? What - axonal peripheral neuropathy?
Peripheral polyneuropathies in systemic diseases can be classified as: (1) acute, subacute or chronic in onset; (2) affecting predominantly sensory or motor nerves; and (3) causing axonal or demyelinating changes. It should be noted that in most axonal neuropathies, myelin degeneration occurs over time.
Characteristic polyneuropathies in systemic diseases
C - sensory; SM - sensory-motor; M - motor. In addition to these diseases, certain medications and toxins can cause polyneuropathy.
21. How are EMG and SPNI studies used to diagnose carpal tunnel syndrome and ulnar nerve compression at the elbow?
Carpal tunnel syndrome(CTS) - the most common tunnel syndrome, affecting 1% of the total population SPNI is reduced in 90-95% of patients Latent period of the action potential of the sensory component median nerve("palmar latency") increases twice as often as that of the motor component, although as the disease progresses, the motor latency period also changes. The use of needle EMG has a limited role, but can reveal signs of denervation of the muscles of the eminence of the thumb, which indicates late stage of CTS At compression of the ulnar nerve in the elbow joint SPNI in motor and sensory nerves is reduced in 60-80% of cases EMG helps determine the degree of denervation of the muscles of the hand and forearm innervated by the ulnar nerve
22. What is “double crush” syndrome?
The syndrome of “double compression” is spoken of when carpal tunnel syndrome is combined with a degenerative lesion of the cervical spine. The first compression of the nerve occurs at the level of the roots of the cervical spine, causing disruption of the axoplasmic flow in both the afferent and efferent directions. The location of the second compression, the causes are also one physiological obstacle along the axon, located more distally, usually in the carpal tunnel area This syndrome, although it appears in electromyography reports, is difficult to quantify and diagnose in a clinical setting
23. What other diseases can be differentiated from common peripheral neuropathies using EMG and SPNI?
PERIPHERAL NEUROPATHIES DIFFERENTIAL DIAGNOSIS
CTS Pronator teres syndrome
Other areas of median nerve compression Ulnar nerve compression in the area Radiculopathy C in
elbow joint Damage to the brachial plexus
Radial nerve palsy Radiculopathy C 7
Damage to the suprascapular nerve Radiculopathy C 5 -C 6
Peroneal nerve palsy Radiculopathy C-C
Femoral nerve damage Radiculopathy L 3
24. What does EMG provide for diagnosing and predicting the course of myasthenia gravis, myotomy
nic dystrophy and Bell's palsy?
Myasthenia. Slow repetitive stimulation of motor nerves at a frequency of 2-3 Hz reveals a 10% decrease in the motor response in 65-85% of patients. Single fiber EMG measures the delay in impulse transmission between nerve endings and their corresponding muscle fibers, detects deviations from the norm in 90-95% of patients
Myotonic dystrophy. PDMEs on EMG fluctuate in amplitude and frequency and acoustically resemble the sound of an "underwater explosion"
Bell's palsy. SPNI on the facial nerve, performed 5 days after the onset of the disease, provides prognostic information about the likelihood of recovery. If at this point the amplitudes and latency periods are normal, the prognosis for recovery is excellent
Selected literature
Ball R D Electrodiagnostic evaluation of the peripheral nervous system In DeLisa J A (ed) Rehabilitation Medicine Principles and Practice, 2nd ed Philadelphia, J In Lippmcott, 1993, 269-307
MacCaen I C (ed) Electromyography A Guide for the Referring Physician Phys Med Rehabil Clm North Am, 1 1-160,1990
Durmtru D Electrodiagnostic Medicine Philadelphia, Hanley & Belfus, 1995
Goodgold J, Eberstem A (eds) Electrodiagnosis of Neuromuscular Diseases, 3rd ed Baltimore, Williams & Wilkins, 1983
Johnson E W (ed) Practical Electromyography Baltimore, Williams & Wilkms, 1980
Kimura J (ed) Electrodiagnosis in Diseases of Nerve and Muscle Principles and Practice, 2nd ed Philadelphia, F A Davis, 1989
Robinson L R (ed) New Developments in Electrodiagnostic Medicine Phys Med Rehabil Clm North Am , 5(3) 1994
Weichers D O, Johnson E W Electrodiagnosis In Kottke F J, Lehmann J F (eds) Krusen's Handbook of Physical Medicine and Rehabilitation, 4th ed Philadelphia, W B Saunders, 1990,72-107
Defeat n. medianus on any part of it, leading to pain and swelling of the hand, sensitivity disorder of the palmar surface and the first 3.5 fingers, impaired flexion of these fingers and opposition of the thumb. Diagnosis is carried out by a neurologist based on the results neurological examination and electroneuromyography; Additionally, musculoskeletal structures are examined using radiography, ultrasound and tomography. Treatment includes painkillers, anti-inflammatory, neurometabolic, vascular pharmaceuticals, exercise therapy, physiotherapy, and massage. Surgical interventions are performed according to indications.
General information
Median nerve neuropathy is quite common. The main contingent of patients are young and middle-aged people. The most common locations of damage to the median nerve correspond to the areas of its greatest vulnerability - anatomical tunnels, in which compression (compression) of the nerve trunk is possible with the development of the so-called. tunnel syndrome. The most common tunnel syndrome is n. medianus is carpal tunnel syndrome - compression of the nerve as it passes to the hand. The average incidence in the population is 2-3%.
The second most common site of damage to the median nerve is its section in the upper part of the forearm, running between the muscle bundles of the pronator teres. This neuropathy is called “pronator teres syndrome.” In the lower third of the shoulder n. medianus may be compressed by an abnormal process humerus or Struzer's bunch. Its lesion in this place is called Struzer's band syndrome, or supracondylar process syndrome of the shoulder. In the literature you can also find a synonymous name - Coulomb-Lord-Bedosier syndrome, which includes the names of the co-authors who first described this syndrome in 1963.
Anatomy of the median nerve
N. medianus is formed by the connection of the brachial plexus bundles, which, in turn, start from spinal roots C5–Th1. After passing the axillary zone is coming Near brachial artery along the medial edge of the humerus. In the lower third of the shoulder it goes deeper than the artery and passes under the Struther ligament; when it exits the forearm, it goes through the thickness of the pronator teres. Then it passes between the finger flexor muscles. In the shoulder, the median nerve does not give off branches; sensory branches extend from it to the elbow joint. On the forearm n. medianus innervates almost all the muscles of the anterior group.
From forearm to hand n. medianus passes through the carpal (carpal tunnel). On the hand, it innervates the opponensus and abductor pollicis muscles, partly the flexor pollicis muscle, and the lumbrical muscles. Sensory branches n. medianus innervate the wrist joint, the skin of the palmar surface of the radial half of the hand and the first 3.5 fingers.
Causes of median nerve neuropathy
Median nerve neuropathy can develop as a result of injury to the nerve: its bruise, partial rupture fibers in case of cut, torn, puncture, gunshot wounds or damage by bone fragments in fractures of the shoulder and forearm, intra-articular fractures in the elbow or wrist joints. The cause of the lesion is n. medianus there may be dislocations or inflammatory changes (arthrosis, arthritis, bursitis) of these joints. Compression of the median nerve in any segment is possible with the development of tumors (lipomas, osteomas, hygromas, hemangiomas) or the formation of post-traumatic hematomas. Neuropathy may develop due to endocrine dysfunction(for diabetes mellitus, acromegaly, hypothyroidism), for diseases that entail changes in ligaments, tendons and bone tissue(gout, rheumatism).
The development of tunnel syndrome is caused by compression of the trunk of the median nerve in the anatomical tunnel and disruption of its blood supply due to concomitant compression of the vessels supplying the nerve. In this regard, tunnel syndrome is also called compression-ischemic. Most often, neuropathy of the median nerve of this origin develops in connection with professional activity. For example, carpal tunnel syndrome affects painters, plasterers, carpenters, and packers; pronator teres syndrome is observed in guitarists, flutists, pianists, and in nursing women who hold a sleeping baby in their arm for a long time in a position where its head is on the mother’s forearm. The cause of tunnel syndrome can be a change in the anatomical structures that form the tunnel, which is noted with subluxations, tendon damage, deforming osteoarthritis, rheumatic disease of the periarticular tissues. IN in rare cases(less than 1% in the entire population) compression is caused by the presence of an abnormal process of the humerus.
Symptoms of median nerve neuropathy
Median nerve neuropathy is characterized by severe pain. The pain affects the medial surface of the forearm, hand and 1st-3rd fingers. It often has a burning causalgic character. As a rule, pain is accompanied by intense vegetative-trophic disorders, which is manifested by swelling, heat and redness or coldness and pallor of the wrist, the radial half of the palm and the 1st-3rd fingers.
Most noticeable symptoms motor disorders are the inability to form a fist, oppose the thumb, or bend the 1st and 2nd fingers of the hand. Difficulty bending the 3rd finger. When the hand is flexed, it deviates to the ulnar side. A pathognomonic symptom is tenor muscle atrophy. The thumb is not opposed, but becomes on a par with the rest and the hand becomes similar to a monkey's paw.
Sensory disturbances are manifested by numbness and hypoesthesia in the area of innervation of the median nerve, i.e., the skin of the radial half of the palm, the palmar surface and the rear of the terminal phalanges of the 3.5 fingers. If the nerve is affected above the carpal tunnel, then the sensitivity of the palm is usually preserved, since its innervation is carried out by a branch extending from the median nerve before its entry into the canal.
Diagnosis of median nerve neuropathy
Classically, median nerve neuropathy can be diagnosed by a neurologist through a thorough neurological examination. To identify motor impairment, the patient is asked to perform a series of tests: clench all fingers into a fist (the 1st and 2nd fingers do not bend); scratch the surface of the table with your fingernail index finger; stretch a sheet of paper, grasping it only with the first two fingers of each hand; rotate thumbs; connect the tips of the thumb and little finger.
At tunnel syndromes Tinnel's symptom is determined - pain along the nerve when tapped at the site of compression. It can be used to diagnose the location of the lesion n. medianus. With pronator teres syndrome, Tinnel's symptom is determined by tapping in the area of the pronator teres ( upper third the inner surface of the forearm), with carpal tunnel syndrome - when tapping on the radial edge of the inner surface of the wrist. With supracondylar process syndrome, pain occurs when the patient simultaneously extends and pronates the forearm while flexing the fingers.
To clarify the topic of the lesion and differentiate neuropathy n. medianus from brachial plexitis, vertebrogenic syndromes(radiculitis, disc herniation, spondyloarthrosis, osteochondrosis, cervical spondylosis), polyneuropathy helps with electroneuromyography. In order to assess the condition of bone structures and joints, bone radiography, MRI, ultrasound or CT of the joints are performed. In case of supracondylar process syndrome, an x-ray of the humerus reveals a “spur” or bony process. Depending on the etiology of neuropathy, they take part in the diagnosis:
Clinical and electrophysiological data indicate greater vulnerability of sensory fibers of peripheral nerves compared to motor ones. We attribute this to a number of reasons, the main one of which, from our point of view, is that impulses along the efferent fibers first propagate along the proximal part of the nerve, while the excitation of afferent fibers is initially carried out along the distal part of the nerve. Clinical, electrophysiological and histological data, as already indicated, indicate that the distal parts of the nerve (and above all their lemmocytes and membranes) suffer earlier and much more severely than the proximal ones. That is why the action potential of motor impulses will initially “jump” almost unhindered across the interinterceptor areas and its propagation will slow down mainly in the distal part of the nerve. However, while still having sufficient amplitude, this potential can spread even with significant demyelination, but no longer somersault, but continuously, along the entire demyelinated section of the fiber.
At the same time, predominantly distal segmental demyelination will significantly prevent both the occurrence of discharges of afferent impulses (normally, the receptor potential forms these impulses in the first node of Ranvier to the receptor), and their conduction along type I afferent fibers. It should be borne in mind that for the propagation of excitation along the pulpy fibers, the amplitude of the action potential must be 5-6 times higher than the threshold value required to excite the adjacent interception. In this regard, the amplitude of the action potential, reduced in the demyelinated area of the sensory nerve, no longer reaches the indicated value in the more intact area of the nerve, which can even lead to the extinction of the impulse.
The second reason for the greater vulnerability of sensory fibers is apparently due to the fact that the emergence of the action potential of the efferent fiber occurs in the body of the motor neuron, i.e. under much more favorable conditions (from the point of view of the safety of metabolic processes, the supply of energy material) than in the receptor , located, for example, on the dorsum of the foot, where diabetic metabolic and vascular disorders are most pronounced. These disorders lead to a significant deficiency of high-energy phosphorus compounds, which are necessary for normal functioning receptor. Thus, a deficiency of these compounds disrupts the functioning of the sodium-potassium pump, which leads to a decrease in the magnitude of the receptor potential, which, upon stimulation, either does not reach the required critical level (and, therefore, does not cause the discharge of afferent impulses), or, having reached only the lower limit of the specified level , generates only a rare frequency of afferent impulses, which, in particular, is accompanied by a decrease in the strength of sensation. It is clear that to the greatest extent this energy deficit will occur with severe vascular disorders of the lower extremities, as well as with severe decompensation of diabetes. Using special techniques, it is probably possible to identify a transient decrease in various types of sensitivity during decompensation of diabetes mellitus.
The third reason is due to the fact that motor fibers appeared phylogenetically earlier than sensory fibers and are therefore more stable.
Finally, speaking about greater safety in distal polyneuropathy motor function nerve compared to the sensitive one, in addition to the reasons noted above, one should also point out the significant compensatory capabilities of the motor function of peripheral nerves (as evidenced by clinical and electrophysiological data).
To explain the fact that the speed of excitation along nerve fibers slows down during the period of decompensation diabetes mellitus It should be taken into account that for the propagation of a nerve impulse, the work of the sodium-potassium pump is necessary, which, as already indicated, suffers greatly during this period.
The genesis of irritative pain syndrome in distal polyneuropathy, as shown by the analysis of our data, is quite complex. Clinical symptoms (pain, paresthesia and dysesthesia in the lower extremities, hyperalgesia in their distal parts, pain calf muscles etc.) indicates the presence of irritation of the peripheral neuroreceptor apparatus in this syndrome. There is reason to believe that this is primarily due to the predominant damage (mainly in the form of segmental demyelination) of thick myelinated fibers that conduct fast localized pain, with the relative preservation of non-myelinated fibers (type III) that conduct slow, diffuse pain. Segmental demyelination, in addition, contributes (as is assumed by some authors for other types of pathology) to the development of irritative pain syndrome as a result of a violation of the insulating function of the myelin sheaths, which leads both to the contact of adjacent axons by areas devoid of the myelin sheath, and to the entry of currents, spreading around axons. Pain impulses under these conditions, apparently, can arise in response to even minor irritations of tactile, temperature and other receptors.
It can be thought that in the mechanism of increasing receptor sensitivity, a significant role is played by disruption of both direct and reverse axocurrent, which occurs as part of distal polyneuropathy. Only in the later stages of development of the latter, due to the death of many axons and receptors, does such increased sensitivity give way to decreased sensitivity (hypoesthesia) and pain disappears.
In maintaining the irritative pain syndrome, we believe tissue hypoxia, characteristic of diabetes, has a certain significance, which is maximum with sharp decompensation of diabetes, somewhat less in the presence of micro- and macroangiopathies against the background of compensated diabetes, and least in compensated diabetes and the absence of vascular disorders. Severe hypoxia leads, as mentioned above, to the formation of algogenic substances (serotonin, histamine, norepinephrine, bradykinin, etc.), which increase vascular permeability. As a result, tissue swelling occurs with compression of pain receptors in the muscles, and in addition, algogenic substances, penetrating into the perivascular and pericellular spaces, themselves excite pain receptors. When diabetes is compensated (and there are no vascular disorders), the amount of such algogenic substances is small, however, due to the presence of distal polyneuropathy hypersensitivity This number of receptors is apparently sufficient to maintain pain. At the same time, it is clear why irritative pain syndrome is more pronounced with decompensation of diabetes and decreases with its compensation.
The frequent increase in pain in the lower extremities with distal polyneuropathy at rest, especially after long walking (which primarily applies to patients with arteriopathy of the lower extremities), is apparently associated with: 1) the accumulation of intermediate metabolic products in the muscles during walking and the presence of significant hypoxia, 2) weakening of the blood supply to the lower extremities at rest, 3) decreased stimulation of tactile receptors (and possibly proprioceptors). From neurophysiological studies it is known that impulses coming from tactile receptors reduce the feeling of pain. It can be assumed that this also applies to proprioceptors. That is why, when the patient gets up and begins to walk, his pain in the lower extremities decreases or disappears as a result of both an improvement in the blood supply to the muscles of the lower extremities when walking, and significant stimulation of proprioceptors and tactile receptors (the plantar surface of the foot).
We believe that the reasons for the frequent absence of irritative pain syndrome in the childhood type of distal polyneuropathy (especially in those with diabetes under the age of 7 years) are: 1) significantly longer preservation (than in the adult type of development of distal polyneuropathy) of afferent fibers conducting pain impulses , and their receptors; 2) adaptation of the peripheral neuroreceptor apparatus (which grew and developed in conditions of severe diabetes) to metabolic-hypoxic disorders; 3) occurrence structural changes in those receptors whose stimulation by metabolic-hypoxic disorders in the adult type of distal polyneuropathy causes pain.
These reasons reverse the absence of neuromyalgia and the period of decompensation in long-term juvenile diabetes. As for initial period juvenile diabetes, which is also characterized by the absence of neuromyalgia, we believe that in poorly developed muscles in children under 12 years of age (and especially under 7 years of age), afferent innervation is also underdeveloped, in particular, the corresponding pain receptors of the muscles are not excited during pronounced diabetic metabolic processes. hypoxic disorders.
We associate the occurrence of neuromyalgia in adult diabetic patients with the fact that during the period of decompensation of diabetes there are significant biochemical disturbances, in particular in skeletal muscles, in which the concentrations of lactic acid and other intermediate metabolic products increase, tissue hypoxia develops, which, along with a shift in blood pH, the sour side, etc. leads to the formation of algogenic substances with the above mechanism of their painful action.
With distal polyneuropathy, a burning sensation in the feet is often observed. We carried out a detailed comparison clinical indicators in three groups of patients: 30 patients with this symptom, 56 without it, 7 patients who previously had this symptom. Summarizing the data obtained, we note that a burning sensation is observed in patients mainly over 40 years of age with a duration of diabetes of more than 10 years with moderately severe arteriopathy and severe distal polyneuropathy (which still does not reach stages VI and VII of development). As both the severity of arteriopathy (leading to significant coldness of the feet) and the pathology of sensory innervation increase, the burning sensation disappears.
Regarding the pathophysiology of the latter, we made the following assumption. If, within the framework of distal polyneuropathy, there is moderate damage to afferent fibers, in which, as we saw above, fibers 16 are predominantly affected, the addition of a macroangiopathic factor (arteriopathy) with its hypoxic effect on the nerves of the lower extremities, their receptors and foot tissues aggravates the pathology of afferent fibers (mainly 16) and their receptors and causes the formation of those algogenic substances that, activating relatively intact type III fibers, cause a burning sensation.
Now we should consider the issue of distal hypoesthesia syndrome. With this term we denote a symptom complex that is observed in the late stages of development of distal polyneuropathy of the lower extremities and is manifested by the absence of pain during mechanical, chemical and thermal effects on the feet, as well as in the presence of ulcers, gangrene and phlegmon of the foot. There is no pain in yoga either at rest or when walking (a painless form of intermittent claudication may occur when walking). In such patients, signs of pronounced distal polyneuropathy are revealed with hypoesthesia (before anesthesia) in the form of “stockings” or “socks” and the absence of pain in the lower leg muscles. In addition, their Achilles and knee reflexes are not evoked, there is a loss of vibration sensitivity in the feet and legs, and muscle-joint sensation is usually reduced. This syndrome was detected in 32 (2.4%) of 1300 patients, which was 14% among 229 patients with severe distal polyneuropathy. It was observed in patients with the adult type of development of distal polyneuropathy with a diabetes duration of more than 12 years, and in patients with the childhood type for more than 25 years.
We associate the absence of pain and intermittent claudication in patients with diabetic gangrene of the feet, noted by a number of researchers, with this syndrome. Nevertheless, these symptoms are observed, according to various authors, from 0.5 to 13.2% of cases of diabetic gangrene of the feet. One of the reasons for such a significant (25 times) discrepancy, from our point of view, is the ambiguous solution to the question of which necrotic processes on the feet should be classified as diabetic gangrene.
Our examination of 61 patients with diabetic gangrene of the feet made it possible to distinguish, based on the leading etiological factor, the following four forms of this gangrene: ischemic, neuropathic, combined (ischemic-neuropathic) and metabolic. The ischemic form was observed in 16 patients, mostly elderly with short-term diabetes. They showed signs Stage III obliterating atherosclerosis of the lower extremities (according to the classification of A. L. Myasikov), and there were also symptoms of moderately severe distal polyneuropathy mixed origin(atherosclerotic, senile and diabetic). These patients had both intermittent claudication and pain in the injured foot.
In the neuropathic form (which was diagnosed in 15 patients under the age of 45 years with an average duration of diabetes of more than 20 years), the pulsation of the arteries of the feet was either intact or somewhat weakened, the feet were warm, and polyneuropathy was manifested by the syndrome of distal hypoesthesia. In these cases, there was no intermittent claudication or pain in the affected foot.
The combined (ischemic-neuropathic) form was present in 27 mature and elderly patients with a significant duration of diabetes. They had intermittent claudication and pain in the affected foot, and objective symptoms included vascular pathology, as in patients with the ischemic form, and neurological, as in the neuropathic form of gangrene of the feet.
Finally, the metabolic form was present in 3 patients (1 with short-term diabetes and 2 with diabetes diagnosed before the onset of gangrene), in whom the necrotic process on the feet developed against the background of uncompensated metabolic disorders, which, apparently, was the reason for the decrease in the resistance of foot tissues to infection. They did not have intermittent claudication, but had intense pain in the affected foot.
Thus, intermittent claudication is characteristic only of the ischemic form of gangrene of the feet, and pain in the affected foot occurs with metabolic and ischemic forms.
It has long been noted that in patients with diabetic gangrene of the feet, when walking, instead of pain, increased fatigue of the legs occurs. Indeed, in our patients with neuropathic and ischemic-neuropathic forms of gangrene of the feet (as well as with pronounced arteriopathy of the lower extremities in the absence of gangrene, but with symptoms of distal hypoesthesia), weakness and severe fatigue of the legs were observed even with short-term walking (according to these patients, " legs can't walk at all"), i.e. this fatigue was equivalent to the pain of intermittent claudication. In other words, in these groups of patients, according to our terminology, a “painless form of intermittent claudication” occurred.
Finally, it should be noted that severe damage to sensory fibers as part of the syndrome of distal hypoesthesia (approaching deafferentation of the distal parts of the lower extremities) is directly related not only to symptoms, but also to the occurrence of diabetic gangrene of the feet. From numerous works on neurogenic dystrophies it is known that severe dystrophic and autoallergic processes develop in deafferented tissues. To this should be added the increased trauma to the anesthetized foot due to mechanical and thermal factors, as well as the fact that such patients usually seek medical help late. That is why there is every reason to believe that these sensory disorders are one of the leading factors in the occurrence of significantly more frequent gangrene of the feet in the presence of diabetes than in its absence.
The question of the mechanism of one of the most common symptoms distal polyneuropathy - reduction and loss of tendon and periosteal reflexes, is very controversial. Our earlier clinical and electromyographic studies, including the results of determining the speed of excitation propagation along the motor fibers of peripheral nerves, confirmed the point of view of those authors who associate these reflex disorders with damage to the afferent part of the reflex arc. Further study of this issue, taking into account data on the H-reflex and the speed of propagation of excitation along afferent fibers tibial nerve, as well as the possibility in some cases of restoring lost proprioceptive reflexes, led us to the idea that these reflex disorders are associated with the pathology of the primary afferent fibers of the muscle spindles, which primarily consists of a distal type of demyelination of these fibers.
We also associate the decrease and loss within the framework of distal polyneuropathy of the plantar reflex with damage to the afferent fibers of the reflex arc. Since the afferent fibers of the Achilles and plantar reflexes pass as part of the tibial nerve and the distal sections of these fibers are almost equally distant from the cell bodies of their neurons, it would seem that they should suffer from diabetic metabolic and vascular disorders almost equally. However, as we saw above, plantar reflexes within the framework of distal polyneuropathy fall out much later than Achilles reflexes. We attribute this to the action of two main factors. Firstly, judging by neurophysiological studies, hypoxia primarily affects the thickest myelin fibers, and since in development diabetic polyneuropathy Since hypoxia is one of the pathogenic factors, it is clear that afferent fibers 1a (related to the reflex arc of the Achilles reflex) will be affected earlier than less thick myelinated fibers and especially non-myelinated ones.
Secondly, we believe that the number of afferent fibers in the reflex arc of the plantar reflex is significantly greater than that of the Achilles reflex. Indirect confirmation of this assumption is provided by the results of our study of the sensitivity of the plantar surface of the foot, which is the receptive field of the plantar reflex. As we saw above, hypoesthesia on the sole occurs several years after its appearance on the dorsum of the feet, which is similar in topographical position (and therefore in the vulnerability of afferent fibers). This situation can arise only if the number of skin receptors and corresponding afferent fibers per 1 cm2 of the surface of the sole of the foot is greater than on the dorsum of the foot, which is apparently associated with a significantly larger biological role sensitivity on the sole.
In the literature, there are isolated reports of recovery of lost knee reflexes in diabetic patients after a cerebral stroke on the side of hemiparesis. The analysis of our observations, described in detail earlier, confirmed this fact, but at the same time showed that, firstly, it concerns not only the knee, but also the Achilles reflexes, which are restored less frequently and to a lesser extent than the knee, and secondly, the restoration knee and Achilles reflexes are not observed in all patients with cerebral stroke (it was absent in patients with pronounced hypoesthesia in the form of “stockings”), and thirdly, this recovery occurs not only after a stroke, but also (albeit to a lesser extent ) after prolonged hypoglycemic comas, as well as after meningoencephalitis.
When discussing the mechanism of recovery in patients with distal polyneuropathy of the knee and Achilles reflexes under the influence of cerebral stroke, encephalitis and hypoglycemic comas, we proceeded from the fact known in neurophysiology that lesions of the pyramidal and extrapyramidal tracts, causing a violation of descending cerebrospinal tonogenic influences, increase the excitability of segmental motor neurons (about This is also evidenced by our data). In this case, activation of motor neurons leads to increased afferent impulses from muscle spindles. Such enhancement in many cases is sufficient to compensate for the disruption of nerve impulse conduction (arising mainly as a result of demyelination) by the afferents of these spindles, leading to an increase in the influx of proprioceptive impulses to alpha motor neurons and restoration of lost Achilles reflexes. These ideas make it possible to understand that the possibility of this restoration depends on two factors: on the degree of damage to the reflex arc of the proprioceptive reflex and on the degree of activation of the loop game. The latter will be more significant after a massive cerebral stroke than after hypoglycemic comas. In cases where the loss of Achilles reflexes occurred relatively recently and is associated only with demyelination of spindle afferents, restoration of these reflexes occurs relatively easily. On the contrary, with gross damage to the axial cylinders of spindle afferents (and even more so if there is already damage and efferent fibers reflex arc), even maximum stimulation of the yre-fibers, which, apparently, also suffer in severe distal polyneuropathy, cannot lead to the restoration of lost reflexes.
A more significant restoration of the knee reflexes than the Achilles reflexes is due to the fact that reflex arc the first is shorter and more proximally located. To an even greater extent than to the knee reflex, the above applies to the mandibular reflex, the arc of which is even shorter and located much more orally than that of the knee reflex. This is partly why, in the presence of the above factors, patients often have a preserved or increased mandibular reflex with loss of the knee and Achilles reflexes.
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