Damage to peripheral nerves. Traumatic nerve damage

A damaged nerve fiber is unable to heal. However, simultaneously with the denervation process, restoration processes begin, which can go in three directions.
(1) Nerve regeneration: the proximal stump forms axonal outgrowths (influxes of axoplasm, or “growth flasks”), which begin to move distally and grow into the endoneurial tubes (of course, only in cases where the latter have retained their integrity). The myelin sheath of the newly formed fiber is formed from strands of lemmocytes. The rate of axonal regeneration is approximately 1.5-2 mm per day. Individual nerve conductors have different abilities for regeneration: among the peripheral nerves, the function of the radial and musculocutaneous nerves is especially well restored, and the ulnar and peroneal nerves have the worst regenerative abilities [Karchikyan S.I., 1962; Weber R., 1996J. To achieve good repair, growing axons must connect to the distal nerve stump before it develops significant peri- and endoneurial scarring. In cases where a connective tissue scar is formed along the sprouting fiber, some of the axons do not spread in the distal direction, but randomly deviate to the sides, forming a traumatic neuroma.
With complete anatomical damage to the nerve trunk, an amputation neuroma forms at the central end 2-3 weeks after the injury.
Regeneration of the nerve trunk can occur heterogeneously: part of the motor fibers grows into the sensory membranes, and the same fibers grow into bundles innervating opposite parts of the limb [Gaidar B.V., 1997].
(2) In cases where not all, but only part of the nerve fibers in the nerve trunk are affected, restoration of muscle function is possible due to the branching of the surviving axons and their “capture” of those muscle fibers that were innervated by the dead axons; in this case, the motor units of the muscle are enlarged. Due to this mechanism, a muscle can maintain its performance in cases of loss of up to 50% of the axons that innervated it (and for muscles that do not develop significant efforts - even up to 90%), however, it takes about a year to complete the process of compensatory innervation restructuring.
(3) In some cases (usually with a nerve trunk injury such as a bruise), restoration or improvement of functions is associated with the reversibility of certain pathomorphological processes: with the disappearance of reactive inflammatory phenomena, with the resorption of minor hemorrhages, etc. For mild injuries, nerve conduction, even after complete loss, is restored within the first days or weeks.

7.2.2. Factors that determine the recovery forecast

The main factors that determine the speed and degree of spontaneous recovery of impaired functions in peripheral neuropathies and plexopathies (and, consequently, the volume and direction of therapeutic interventions) include the following:
- degree of damage to the nerve conductor;
- level of damage;
- the nature of the damaging agent.

7.2.2.1. Degree of damage to nerve conductors (with local trauma)

Rehabilitation specialists most often determine the degree of nerve damage in 3 categories according to the H. Seddon classification. Sometimes the classification of S. Sunderland is also used, which distinguishes 5 degrees of nerve damage; this classification is based on H.Seddon's classification, detailing it. According to H. Seddon’s classification, all local damage to nerve trunks is divided, depending on the safety of the axon and connective tissue structures, into three groups: (1) neurapraxia; (2) axonotmesis; (3) neurotmesis. (1) Neurapraxia is a nerve injury that does not lead to axon death. Often observed with nerve compression (for example, “Saturday night palsy” due to compression of the radial nerve), with mild nerve injury. Clinically characterized by a decrease in vibration, proprioceptive, and sometimes tactile sensitivity. Pain sensitivity is less affected. Motor disturbances and paresthesia are often observed. The nerve impulse conduction block observed due to local damage to the myelin sheath is transient and regresses as the myelin is restored. Restoration of motor and sensory functions can last up to 6 months.
(2) Axonotmesis (axonotmesis, English) - damage to the nerve, leading to the death of the axon while the epineurium, perineurium, endoneurium and Schwann cells are preserved. It is often observed with closed fractures or dislocations of the bones of the extremities, as well as with compression of the nerve trunks. The motor, sensory and sudomotor functions of the nerve are impaired. Functional restoration occurs due to axon regeneration. The speed and degree of recovery depends on the level of damage, age (in young people regeneration occurs faster) and the general condition of the patient. In cases where axon growth is slow, scarring of the endoneurial tube into which the axon grows may occur and repair does not occur. For the same reason, an unfavorable prognosis occurs in cases where the nerve trunk defect is of significant length. Under favorable conditions, gradual neurotization of the distal part of the damaged nerve occurs, which continues for many months, sometimes a year or more. There is a restoration of lost functions, but not always complete.
O) Neurotmesis (neurotmesis, English) - rupture of a nerve with the intersection of the axon and connective tissue sheaths of the nerve. Due to the fact that the endoneurial tubes are damaged, it becomes impossible for axons to grow into them; axonal regeneration leads to the formation of a traumatic neuroma. The prognosis for recovery is unfavorable. This classification is based on microscopic changes in the nerve trunk. It is almost impossible to discern the degree of damage macroscopically. Diagnosis is based on dynamic clinical and electrophysiological observation. In this regard, with closed injuries of the nerve trunks, domestic authors often use a different classification based on the identification of the following 4 forms of damage to the nerve trunk [Makarov A.Yu., Amelina O.A., 1998]: concussion, bruise, compression, traction. A concussion is not accompanied by morphological changes in the nerve; nerve dysfunction is short-term (no more than 1-2 weeks) and completely reversible. Nerve contusion is characterized by the occurrence of small hemorrhages, areas of crushing of nerve fibers and bundles, which leads to complete or partial disruption of conductivity, long-term and persistent loss of functions. When a nerve is compressed, the degree of conduction disturbance depends primarily on the duration of the intervention: with timely removal of the substrates compressing the nerve (hematoma, foreign body, bone fragment, etc.), a rapid and complete restoration of conductivity can be observed, whereas with prolonged compression in the nerve trunk degenerative changes develop. Failure to restore function within 2-3 months is a criterion for complete anatomical interruption of the nerve. Traction (for example, traction of the branches of the brachial plexus during reduction of a dislocated shoulder) is usually accompanied by partial dysfunction, but restoration of conduction along the nerve takes a long time (within several months).

7.2.2.2. Damage level

The more proximal the damage to the nerve trunk or plexus (i.e., the greater the distance from the site of damage to the peripheral endings), the worse the prognosis for restoration of function, since the longer it takes for the nerve fiber to grow and the greater the likelihood of irreversible development in the endoneurial tube of the peripheral segment of the nerve. Scar changes. So, for example, according to S.I. Karchikyan, with injuries to the sciatic nerve in the upper third of the thigh, the first movements of the foot and fingers appear only 15-20 months or later after the application of the nerve suture, and with injuries to the same nerve in the lower third of the thigh - 10-15 months after surgery.
The worst prognosis is observed for injuries at the radicular level, since the roots of the spinal nerves do not regenerate and cannot be restored surgically. Damage to the roots (usually a separation of the root at the cervical level), in contrast to damage to the plexus, is characterized by the following symptoms:
- intense burning pain radiating along the corresponding dermatome;
- paralysis of paravertebral muscles innervated by the posterior branches of the spinal nerves;
- paralysis of the scapula muscles due to dysfunction of the short nerves of the shoulder girdle (pterygoid scapula);
- Horner's syndrome (with damage to the C8 roots);
- trophic disorders and rapidly progressing muscle atrophy with severe secondary contractures.

7.2.2.3. Nature of the damaging agent

Peripheral neuropathies and plexopathies can have very different etiologies (Table 7.2). In peacetime, the most common form of peripheral nerve damage is tunnel neuropathies, accounting for about 30-40% of all diseases of the peripheral nervous system. Tunnel neuropathy is a local lesion of the nerve trunk caused by its compression and ischemia in the anatomical canals (tunnels) or due to external mechanical influence [Leikin I.B., 1998]. Factors predisposing to the development of tunnel neuropathies include the genetically determined narrowness of the natural nerve receptacles, acquired narrowness of these receptacles due to edema and connective tissue hyperplasia in various diseases (for example, diabetes mellitus, hypothyroidism, collagenosis), prolonged overstrain of the musculo-ligamentous apparatus in persons of certain professions, consequences herbs, muscular-tonic and neurodystrophic disorders in reflex syndromes of spinal osteochondrosis, iatrogenic traumatic effects (incorrect application of a plaster cast, hemostatic tourniquet). Nerve dysfunction occurs due to both demyelination and axonal damage (deterioration of neurotrophic control due to failure of axonal transport).
Tunnel nerve lesions are manifested primarily by pain, sensory and autonomic disorders. Motor disorders develop in only one third of patients and consist, as a rule, of decreased muscle strength, muscle wasting, and the development of contractures. The prognosis for functional restoration with early treatment is usually favorable, but this restoration can take quite a long time, up to several months. In addition, the prognosis depends on the underlying disease against which the neuropathy developed, and on whether occupational overload of the limb persists. In 30-40% of cases, tunnel neuropathies recur [German A.G. et al., 1989].
In second place in frequency are traumatic neuropathies. Among the causes of traumatic neuropathies, the most prognostically favorable are incised wounds, in which timely surgical intervention provides a good outcome. Traction and gunshot injuries have a worse prognosis, since in them the central segment of the nerve and the neuron of the spinal centers are often altered, which significantly complicates nerve regeneration. Destruction of the nerve trunk over a long distance can also be observed due to electrical trauma or chemical damage (accidental injection of various medicinal substances into the nerve). A very unfavorable condition accompanying nerve damage is circulatory disturbance in the limb (bleeding or prolonged application of a hemostatic tourniquet, thrombosis of the main artery), which can lead to the development of an atrophying sclerosing process in the muscles, tendons, joint capsules, skin and subcutaneous tissue with the formation of contractures. Secondary changes in the joints and tendons, which develop as a result of stretching of the ligaments and joint capsules during passive hanging of the limbs in the case of flaccid paralysis or paresis, can also prevent the restoration of movements.
For neuro- and plexopathies that have developed against the background of somatic diseases, due to immune, neoplastic, infectious, toxic lesions and effects, the prognosis depends on the nature of the course of the underlying disease or process.

7.2.3. Clinical and electrophysiological signs of restoration of nerve conductors

Determining the degree of restoration of the function of nerve conductors is based on data from a comprehensive clinical and electrophysiological examination conducted over time. The most complete description of the clinical patterns of restoration of the function of nerve conductors is presented in works summarizing the experience in the treatment of traumatic neuropathies accumulated during the Great Patriotic War (Karchi kyan S.I. Traumatic damage to peripheral nerves. - L.: Medgiz, 1962; Astvatsaturov M.I. Guide to military neuropathology. - L., 1951; Experience of Soviet medicine in the Great Patriotic War, 1952. - T.20). Below we will consider the patterns of functional restoration after a complete nerve break in the case of favorable regeneration or after timely neurosurgical intervention.
The earliest clinical symptoms of recovery are usually changes in the sensory sphere, which long precede signs of recovery of motor function [Karchikyan S.I., 1962]:
- paresthesia that occurs in the anesthesia zone with pressure on the nerve area immediately below the damage zone, i.e. to the area of ​​regenerating young axons;
- the appearance of sensitivity to sharp compression of the skin fold in the anesthesia zone;
- pain when pressure is applied to the nerve trunk distal to the site of injury with irradiation of pain in the distal direction along the nerve; as the axon grows, this pain is obtained from levels located more and more towards the periphery.
Restoration of sensitivity occurs earlier in more proximal sections, starting from the edges of the central zone of anesthesia. First, protopathic (primitive) pain and temperature sensitivity is restored: the ability to perceive only sharp pain and temperature irritations without accurately recognizing the quality and precise localization of the applied irritation. Therefore, painful and temperature irritations of the skin cause sensations that have the properties of hyperpathy (diffuse, difficult to localize, very unpleasant). This may be due to insufficient myelination of newly formed regenerating fibers, which leads to widespread irradiation of excitation to neighboring fibers. Then tactile sensitivity begins to recover, and only then fine temperature sensitivity, muscle-joint sense, and stereognostic sense. As epicritic (more subtle) sensitivity is restored, the hyperpathic features of perception of pain and temperature stimuli begin to disappear.
It must be remembered that a narrowing of the zone of sensitivity disorder can occur not only as a result of the beginning of regeneration, but also due to compensatory phenomena (overlapping of branches of neighboring nerves); it is important to distinguish between these processes.
The earliest signs of restoration of motor function include a slight increase in the tone of paralyzed muscles and a decrease in atrophy. Then, starting from more proximal sections, active muscle contractions appear. 5-6 months after a nerve injury, active movements occur, which are initially characterized by weakness, rapid exhaustion, and awkwardness. The restoration of small differentiated isolated movements (for example, in the interphalangeal joints) takes a particularly long time. Reflexes are the last to be restored; they often remain lost even with complete restoration of sensitivity and motor functions. In general, a damaged axon, when the cause that impedes axonal growth is eliminated, is restored within a period of 1.5-2 to 8-10 months [Lobzin V.S. et al., 1988].
Even in the absence of regeneration, partial restoration of lost movements can occur due to compensatory contraction of muscles innervated by intact nerves. On the other hand, the lack of movement recovery may not be due to a lack of nerve regeneration, but to concomitant damage to the tendons, muscles and joints.
Among the electrophysiological methods used for dynamic monitoring of the processes of restoration of nerve conduction, needle and stimulation electromyography (EMG), as well as the method of evoked potentials (Chapter 2 of the first volume) are currently used. Let us recall that a partial disruption of nerve conduction during stimulation EMG recording is characterized by a decrease in the speed of excitation, a decrease in the amplitude and frequency of action potentials of the nerve and muscle, and a change in the structure of the M-response; When recording needle EMG, a change in the structure of action potentials of the motor units of the corresponding muscles is observed. With demyelinating processes, nerve conduction velocity decreases to a greater extent, while with axonopathies, a predominant decrease in the nerve action potential and a change in the M-response are observed, and changes in conduction velocity may not be observed. When the nerve is completely interrupted, the distal segment continues to conduct impulses for up to 5-6 days. Then there is a complete absence of electrical activity in the affected nerves and muscles. After the first three weeks, spontaneous muscle activity at rest (denervation potentials of fibrillations and positive sharp waves) usually appears, recorded using needle electrodes. The first signs of reinnervation after complete denervation of the muscle are detected when recording needle EMG in the form of the occurrence of a series of low-voltage polyphasic potentials lasting 5-10 ms during an attempt to voluntarily contract [Popov A.K., Shapkin V.I., 1997]. As muscles are reinnervated, the appearance of polyphasic motor units and an increase in their amplitude and duration are also observed (the appearance of giant motor unit potentials is associated with the capture of additional muscle fibers by the remaining axons). Reinnervation potentials can sometimes be detected 2-4 months before the first clinical signs of recovery [Zenkov J1.P., Ronkin M.A., 1991].
The earliest judgments about the dynamics of recovery processes can be obtained by recording evoked potentials (EPs). Peripheral EPs are caused by stimulation of a peripheral nerve (magnetic or electrical) and are recorded as waves over various parts of the nerve. 7 or more days after the injury, peripheral EPs are compared with those observed immediately after the injury, or with their values ​​on the unaffected contralateral side. In this case, they focus not only on the amplitude of the VP, but also on the area under the VP wave. With the reversible nature of the disorders (neurapraxia), 7 or more days after the injury, sensory and motor EPs caused by stimulation of the peripheral nerve below the level of the lesion continue to be recorded in the distal part of the nerve. With axonotmesis and neurotmesis, after this period, a decrease in the amplitude and a change in the shape of VPs distal to the site of damage is observed, and after the completion of Wallerian degeneration, VPs in the peripheral segment of the nerve are not caused.
Electrodiagnostic methods make it possible to distinguish neurapraxia from axonotmesis and neurotmesis, but do not allow one to distinguish between axonotmesis and neurotmesis; This requires the use of magnetic resonance imaging.
In plexopathies, the BII method can help in the differential diagnosis of pre- and postganglionic lesions, which is important when determining indications for neurosurgical intervention. With postganglionic damage to the trunks of the plexus, the distal end loses connection with the cell body of the spinal ganglion, therefore, both sensory and motor action potentials upon irritation of the peripheral segment of the nerve are absent at any point below the site of damage. With preganglionic lesions, motor peripheral EPs are not evoked while sensory EPs are preserved in the same segments of the nerve (despite anesthesia in the corresponding innervation zones). This is explained by the following: with a preganglionic lesion, the central process of the bipolar cell is damaged, which disrupts the transmission of sensitive impulses to the cerebral cortex and, accordingly, is accompanied by anesthesia. However, the peripheral segment does not lose connection with the cell body of the spinal (sensitive) ganglion, remains viable and normally conducts sensory impulses. In this regard, with preganglionic damage, sensory action potential is recorded along the entire course of the nerve fiber up to the level of injury. Erroneous conclusions, however, can be drawn with multifocal trauma, when there is both pre- and postganglionic radicular damage; in this case, sensory peripheral EPs are not evoked, “masking” the preganglionic damage. The detection of preganglionic lesions indicates an extremely unfavorable prognosis, since, as already indicated, root regeneration is impossible and surgical intervention is not available.
Predicting the possible spontaneous recovery of impaired functions determines the direction and scope of further rehabilitation measures.

Peripheral nerve damage

What is Peripheral Nerve Injury -

Nerve damage are one of the most common and severe types of injuries that cause complete or partial disability, force patients to change professions and often become a cause of disability. In everyday clinical practice, unfortunately, a significant number of diagnostic, tactical and technical errors are made.

What provokes / Causes of Peripheral Nerve Damage:

Peripheral nerve damage can be closed or open.

Closed damage occur as a result of a blow with a blunt object, compression of soft tissues, damage from bone fragments, a tumor, etc. A complete break of the nerve in such cases is rarely observed, so the outcome is usually favorable. A dislocation of the lunate bone or a fracture of the radius in a typical location often lead to compression injuries of the median nerve in the carpal tunnel area; a fracture of the hamate bone can cause a break in the motor branch of the ulnar nerve.

Open damage in peacetime, they are most often the result of injuries from glass fragments, a knife, sheet iron, a circular saw, etc. The oncoming changes manifest themselves in various syndromes of functional disorders depending on the nature and duration of exposure to the traumatic agent.

Pathogenesis (what happens?) during Peripheral Nerve Injury:

Loss of sensitivity almost always observed with damage to the peripheral nerve. The prevalence of disorders does not always correspond to the anatomical zone of innervation. There are autonomous zones of innervation in which loss of all types of skin sensitivity is noted, i.e. anesthesia. This is followed by a zone of mixed innervation, in which, if one of the nerves is damaged, areas of hypoesthesia alternate with areas of hyperpathy. In the additional zone, where the innervation is carried out by neighboring nerves and only to a small extent by the damaged nerve, it is not possible to determine the impairment of sensitivity. The size of these zones is extremely variable due to the individual characteristics of their distribution. As a rule, the diffuse zone of anesthesia that appears immediately after a nerve injury is replaced by hypoesthesia after 3-4 weeks. Yet the process of substitution has its limits; If the integrity of the damaged nerve is not restored, then loss of sensitivity remains.

Loss of motor function manifests itself in the form of flaccid paralysis of muscle groups innervated by branches extending from the trunk below the level of nerve damage. This is an important diagnostic sign that makes it possible to determine the area of ​​nerve damage.

Manifested in disruption of the activity of the sweat glands; Anhidrosis of the skin occurs, the area of ​​which corresponds to the boundaries of impaired pain sensitivity. Therefore, by determining the presence and size of the anhidrosis zone, one can judge the boundaries of the anesthesia area.

Vasomotor disturbances are observed approximately within the same limits as secretory ones: the skin becomes red and hot to the touch (hot phase) due to paresis of vasoconstrictors. After 3 weeks, the so-called cold phase begins: the limb segment deprived of innervation is cold to the touch, the skin acquires a bluish tint. Often in this area there is increased hydrophilicity and pastiness of soft tissues.

Trophic disorders expressed by thinning of the skin, which becomes smooth, shiny and easily wounded; turgor and elasticity are noticeably reduced. There is clouding of the nail plate, transverse striations and indentations appear on it, and it fits tightly to the pointed tip of the finger. In the long term after injury, trophic changes spread to tendons, ligaments, and joint capsules; joint stiffness develops; Osteoporosis of the bones appears as a result of forced inactivity of the limb and poor circulation.

The severity of nerve damage leads to varying degrees of impairment of its function.

When a nerve is concussed, anatomical and morphological changes in the nerve trunk are not detected. Motor and sensory disorders are reversible; complete restoration of function is observed 1.5-2 weeks after the injury.

In the case of a bruise (contusion) of a nerve, the anatomical continuity is preserved, there are isolated intra-tremular hemorrhages and a violation of the integrity of the epineural sheath. Functional impairments are more profound and persistent, but after a month they are always completely restored.

Compression of the nerve can occur for various reasons (prolonged exposure to a tourniquet, in case of injury - bone fragments, hematoma, etc.). Its degree and duration are directly proportional to the severity of the lesion. Accordingly, prolapse disorders can be transient or persistent, in which case surgical intervention is required.

Partial damage to the nerve is manifested by loss of functions according to those intra-trunk formations that are injured. Often there is a combination of symptoms of loss with symptoms of irritation. Spontaneous healing in such situations is rare.

A complete anatomical break is characterized by the death of all axons and the disintegration of myelin fibers along the entire perimeter of the trunk; there is a division of the nerve into peripheral and central or they are connected by a strand of scar tissue, the so-called “false continuity”. Restoring lost functions is impossible; trophic disorders develop very quickly, and atrophy of paralyzed muscles in the denervated zone increases.

Symptoms of Peripheral Nerve Damage:

Radial nerve injuries (Cv-Cvm). Damage to the nerve in the axillary region and at shoulder level causes a characteristic position - a “falling” or hanging hand. This position is caused by paralysis of the extensors of the forearm and hand: the proximal phalanges of the fingers, the abductor pollicis muscle; in addition, supination of the forearm and flexion are weakened due to the loss of active contractions of the brachioradialis muscle. Nerve injuries in more distal parts of the upper limb, i.e., after the departure of the motor branches, are manifested only by sensory disorders. The boundaries of these disorders extend within the radial part of the dorsum of the hand along the third metacarpal bone, including the radial part of the proximal phalanx and middle phalanx of the third finger, the proximal and middle phalanges of the index finger and the proximal phalanx of the first finger. Sensitivity disorders usually occur as hyposthesia. They are almost never deeper due to the large number of connections between the dorsal and external cutaneous nerves of the forearm with the dorsal branches of the median and ulnar nerves and therefore rarely serve as indications for surgical treatment.

With a combination of injuries to the median nerve and the superficial branch of the radial nerve, the prognosis is more favorable than with the quite common combination of injuries to the median and ulnar nerves, which leads to severe consequences. If with the first option of combined nerve damage it is possible to some extent to replace the lost function with the intact ulnar nerve, then with the second option this possibility is excluded. Clinically, in the latter case, paralysis of all autochthonous muscles of the hand is expressed, and there is a claw-like deformity. Combined injury to the median and ulnar nerves has a disastrous effect on the function of the hand as a whole. A denervated, desensitized hand is unsuitable for any work.

Median nerve injuries (Cvin-Di). The main clinical sign of damage to the median nerve in the hand area is a pronounced impairment of its sensory function - stereognosis. In the early stages after nerve damage, vasomotor, secretory and trophic disorders appear; skin folds are smoothed out, the skin becomes smooth, dry, cyanotic, shiny, flaky and easily wounded. Transverse striations appear on the nails, they become dry, their growth slows down, Davydenkov’s symptom is characteristic - “suckiness” of the 1st, 2nd, and 3rd fingers; the subcutaneous tissue atrophies and the nails adhere tightly to the skin.

The degree of movement disorders depends on the level and nature of the nerve damage. These disorders are detected when there is injury to the nerve proximal to the level of the origin of the motor branch to the muscles of the eminence of the thumb or isolated damage to this branch. In this case, flaccid paralysis of the thenar muscles occurs, and with high damage to the nerve, a violation of pronation of the forearm, palmar flexion of the hand occurs, flexion of the I, II and III fingers and extension of the middle phalanges of the II and III fingers are lost. In the intrinsic muscles of the hand, due to their small mass, atrophy quickly develops, which begins within the first month after a nerve injury, gradually progresses and leads to fibrous degeneration of the paralyzed muscles. This process continues for a year or more. After this period, reinnervation of paralyzed muscles with restoration of their function is impossible. Atrophy is evident in the smoothing of the thenar convexity. The thumb is placed in the plane of the other fingers, the so-called monkey hand is formed. The paralysis affects the abductor pollicis brevis and the oppons pollicis brevis muscles, as well as the superficial head of the flexor pollicis brevis muscle. The function of abduction and, above all, opposition of the thumb to the hand is lost, which is one of the main motor symptoms of damage to the trunk of the median nerve.

Sensory impairment is the leading manifestation of damage to the median nerve and is always observed regardless of the level of damage. Skin sensitivity is absent in most cases along the palmar surface of the 1st, 2nd and 3rd fingers, as well as along the radial surface of the 4th finger of the hand; on the back of the hand, sensitivity is impaired in the area of ​​the distal (nail) phalanges of the I, II, III fingers and the radial part of the distal phalanx of the IV finger. There is a complete loss of the stereognostic sense, i.e. the ability to “see” an object with closed eyes by feeling it with your fingers. In this case, the victim can use the brush only under visual control. Replacement of sensitivity lost after a complete break in the main trunk of the median nerve occurs only to a certain level, mainly in the marginal zones of the area of ​​cutaneous anesthesia, due to the overlap of the branches of the median nerve in these areas by the superficial branch of the radial nerve, the external cutaneous nerve of the forearm, as well as the superficial branch of the ulnar nerve. nerve.

Segmental damage to the trunk of the median nerve leads to loss of sensitivity in a certain area of ​​the skin of the hand, the size of which strictly corresponds to the number of nerve fibers innervating this area. Often, partial damage to the median nerve causes excruciating pain on the palmar surface of the hand (sometimes like causalgia). Secretory disorders are characterized by severe hyperhidrosis of the skin on the palm in the branching zone of the median nerve or anhidrosis and peeling of the epidermis. The intensity of disorders (sensitive, motor, autonomic) always corresponds to the depth and extent of damage to the nerve trunk.

Ulnar nerve injury (Cvn-CVIH). The leading clinical symptom of ulnar nerve damage is motor impairment. Branches from the trunk of the ulnar nerve begin only at the level of the forearm; therefore, the clinical syndrome of its complete lesion at the level of the shoulder to the upper third of the forearm does not change. The weakening of the palmar flexion of the hand is determined, active flexion of fingers IV and V, partially III is impossible, it is impossible to bring and spread fingers, especially IV and V, there is no adduction of the thumb on the dynamometer. A significant loss of muscle strength is detected in the fingers of the hand (10-12 times less than in the fingers of a healthy hand). After 1-2 months after the injury, atrophy of the interosseous muscles begins to appear. Retraction of the first interosseous space and the area of ​​elevation of the little finger is especially quickly detected. Atrophy of the interosseous and lumbrical muscles contributes to the sharp outline of the metacarpal bones on the back of the hand. In the long term after the injury, secondary deformation of the hand occurs, which acquires a peculiar claw shape as a result of palmar flexion of the middle and distal phalanges of the IV-V fingers (due to paralysis of the lumbrical muscles that flex the proximal phalanges and extend the middle and distal ones), as well as as a result of atrophy of the muscles of the eminence little finger (hypotenar).

When the fingers are clenched into a fist, the tips of the fourth and fifth fingers do not reach the palm, and closing and spreading the fingers is impossible. The opposition of the little finger is disrupted, and there are no scratching movements with it.

Impairments of skin sensitivity when the ulnar nerve is damaged are always observed in the zone of its innervation, however, the extent of areas of complete anesthesia is variable due to the individual characteristics of the branching of the nerve, as well as depending on the distribution of branches of the neighboring - median and radial - nerves. The disorders involve the palmar surface of the ulnar edge of the hand along the IV metacarpal bone, half of the IV finger and the entire V finger. On the back of the hand, the boundaries of sensitivity disorders run along the third interosseous space and the middle of the proximal phalanx of the third finger. However, they are highly variable.

Vasomotor and secretory disorders spread along the ulnar edge of the hand, their boundaries are slightly larger than the boundaries of sensory disorders.

Segmental damage to the outer trunk of the ulnar nerve in the middle third of the forearm leads to loss of sensitivity on the palmar surface of the hand with minimal severity on the back; in case of injury to the inner part of the barrel, the ratios are reversed.

Damage to the sciatic nerve (Uv-v-Si-sh). High nerve damage leads to dysfunction of flexion of the tibia in the knee joint due to paralysis of the biceps, semitendinosus and semimembranosus muscles. Often, nerve injury is accompanied by severe causalgia. The symptom complex also includes paralysis of the foot and fingers, loss of the heel tendon reflex (Achilles reflex), loss of sensitivity along the back of the thigh, the entire lower leg, with the exception of its medial surface and feet, i.e. symptoms of damage to the branches of the sciatic nerve - tibial and peroneal nerves. The nerve is large, its average diameter in the proximal part is 3 cm. Segmental lesions of the trunk are not uncommon, manifested by a corresponding clinical picture with a predominant loss of functions in charge of one of its branches.

Peroneal nerve injuries (Liv-v-Si). The nerve roots (Liv-v-Si) form the trunk. The nerve is mixed. Damage to the peroneal nerve leads to paralysis of the extensors of the foot and fingers, as well as the peroneal muscles, which ensure the outward rotation of the foot. Sensory disturbances spread along the outer surface of the lower leg and the dorsum of the foot. Due to paralysis of the corresponding muscle groups, the foot hangs down, is turned inward, and the toes are bent. The characteristic gait of a patient with a nerve injury is “cock-like” or peroneal: the patient raises his leg high and then lowers it onto his toe, onto the stable outer edge of the foot, and only then rests on the sole. The Achilles reflex, provided by the tibial nerve, is preserved, pain and trophic disorders are usually not expressed.

Tibial nerve injuries (Liv-SHI). The mixed nerve is a branch of the sciatic nerve. Innervates the foot flexors (soleus and gastrocnemius muscles), toe flexors, as well as the tibialis posterior muscle, which rotates the foot medially.

The posterior surface of the lower leg, the plantar surface, the outer edge of the foot and the dorsal surface of the distal phalanges of the fingers are provided with sensory innervation.

When the nerve is damaged, the Achilles reflex is lost. Sensory disorders spread within the boundaries of the back surface of the lower leg, the sole and outer edge of the foot, and the dorsum of the fingers in the area of ​​the distal phalanges. Being functionally an antagonist of the peroneal nerve, it causes a typical neurogenic deformation: the foot is in extension, pronounced atrophy of the posterior group of muscles of the leg and sole, sunken intermetatarsal spaces, a deepened arch, bent position of the toes and a protruding heel. When walking, the victim relies mainly on the heel, which significantly complicates gait, no less than when the peroneal nerve is damaged.

With damage to the tibial nerve, as with damage to the median nerve, a causalgic syndrome is often observed, as well as significant vasomotor-trophic disorders.

Tests of movement disorders: inability to flex the foot and toes and rotate the foot medially, inability to walk on toes due to instability of the foot.

Diagnosis of Peripheral Nerve Damage:

Making the correct diagnosis of nerve injury depends on the consistency and systematicity of the studies.

• Survey

The time, circumstances and mechanism of injury are established. Based on the referral documents and the patient’s words, the duration and volume of first aid provided are determined. The nature of the pain and the occurrence of new sensations that have appeared in the limb since the moment of injury are clarified.

• Inspection

Pay attention to the position of the hand or foot, fingers; the presence of their typical settings (positions) can serve as a basis for judging the nature and type of damage to the nerve trunk. The color of the skin and the configuration of muscle groups in the affected area of ​​the limb are determined in comparison with a healthy one; They note trophic changes in the skin and nails, vasomotor disorders, the condition of the wound or skin scars resulting from trauma and surgery, and compare the location of the scar with the course of the neurovascular bundle.

• Palpation

They obtain information about the temperature of the skin of the hand or foot, its turgor and elasticity, and the moisture content of the skin.

Pain in the area of ​​the postoperative scar upon palpation is usually associated with the presence of a regenerative neuroma of the central end of the damaged nerve. Valuable information is provided by palpation of the area of ​​the peripheral segment of the nerve, which, with a complete anatomical break, can be painful, and in the case of projection pain, partial damage to the nerve or the presence of regeneration after neurorrhaphy (Tinel’s symptom) can be assumed.

Sensitivity study. When conducting the study, it is desirable to exclude factors that distract the patient’s attention. He is asked to close his eyes in order to concentrate and not control the doctor’s actions with his eyes. It is necessary to compare sensations from similar irritations in symmetrical areas that are known to be healthy.

• Tactile sensitivity is examined by touching with a ball of cotton wool or a brush.
• The feeling of pain is determined by pricking with the point of a pin. It is recommended to alternate painful stimulation with tactile stimulation. The subject is given the task to define an injection with the word “Sharp”, a touch with the word “Dull”.
• Temperature sensitivity is examined using two test tubes - with cold and hot water; Skin areas with normal innervation are distinguished by a temperature change of 1-2°C.
• Sense of localization of irritation: the subject indicates the location of the skin prick with a pin (the prick is applied with the eyes closed).
• The feeling of discrimination between two one-dimensional stimuli is determined using a compass (Weber's method). The normal value of discrimination is taken to be the result of a study on a symmetrical area of ​​a healthy limb.
• Feeling of two-dimensional stimulation: letters are written on the skin of the area under study or figures are drawn, which must be named by the patient without visual control.
• Articular-muscular feeling is determined by giving the joints of the limbs different positions that the subject must recognize.
• Stereognosis: the patient, with his eyes closed, must “recognize” the object placed in his hand, based on the analysis of diverse sensations (mass, shape, temperature, etc.). Determination of stereognosis is especially important for injuries to the median nerve. Based on the results obtained, a functional assessment is given: if stereognosis is preserved, the human hand is suitable for performing any work.

• Electrophysiological research methods

Clinical tests to assess the state of peripheral nerve functions should be combined with the results of electrodiagnostics and electromyography, which allow us to determine the state of the neuromuscular system of the injured limb and clarify the diagnosis.

Classical electrodiagnostics is based on the study of excitability - the reaction of nerves and muscles in response to irritation by faradic and direct electric current. Under normal conditions, in response to irritation, the muscle responds with a fast, live contraction, but with injury to the motor nerve and degenerative processes, worm-like flaccid contractions are recorded in the corresponding muscles. Determining the threshold of excitability on healthy and diseased limbs allows us to draw a conclusion about quantitative changes in electrical excitability. One of the significant signs of nerve damage is an increase in the nerve conduction threshold: an increase in the strength of current pulses in the affected area in comparison with a healthy one to produce a muscle contraction response. Long-term results using this method have shown that the data obtained are not reliable enough. Therefore, in recent years, electrodiagnostics in its traditional version has been gradually replaced by stimulation electromyography, which includes elements of electrodiagnostics.

Electromyography is based on recording the electrical potentials of the muscle being studied. The electrical activity of muscles is studied both at rest and during voluntary, involuntary and caused by artificial stimulation muscle contractions. The detection of spontaneous activity - fibrillations and slow positive potentials at rest - are undoubted signs of a complete break of the peripheral nerve. Electromyography (EMG) allows you to determine the degree and depth of damage to the nerve trunk. Using the method of stimulation EMG (a combination of electrical stimulation of nerves with simultaneous recording of the resulting oscillations in muscle potential), the speed of impulse conduction is determined, the transition of impulses in the zone of myoneural synapses is studied, and the functional state of the reflex arc is studied, etc. Electromyographic recording of action potentials can provide important data not only diagnostic, but also prognostic in nature, allowing one to catch the first signs of reinnervation.

Treatment of Peripheral Nerve Damage:

• Conservative treatment

Conservative and restorative treatment is no less important than surgical intervention on the nerve, especially with combined injuries. If during the operation the anatomical prerequisites are created for the growth of axons from the central segment of the nerve to the peripheral, then the task of conservative treatment is to prevent deformities and contractures of the joints, prevent massive scarring and tissue fibrosis, combat pain, as well as improve conditions and stimulate reparative processes in the nerve , improvement of blood circulation and trophism of soft tissues; maintaining the tone of denervated muscles. Activities aimed at achieving these goals should begin immediately after injury or surgery and be carried out comprehensively, according to a specific scheme, according to the stage of the regenerative process until the function of the injured limb is restored.

The course of treatment includes drug-stimulating therapy, orthopedic, therapeutic and gymnastic measures and physiotherapeutic methods. It is performed on all patients both in the preoperative and postoperative periods; its volume and duration depend on the degree of dysfunction of the affected nerve and associated injuries. The treatment complex should be carried out purposefully, with a selective approach in each specific case.

Therapeutic exercises are carried out throughout the entire period of treatment, and to the fullest extent - after the period of limb immobilization has expired. Purposeful active and passive movements in the joints of the injured limb for 20-30 minutes 4-5 times a day, as well as movements in easier conditions - physical exercises in water have a positive effect on the restoration of impaired motor function. The use of elements of occupational therapy (modelling, sewing, embroidery, etc.) promotes the development of various motor skills that become automatic, which has a beneficial effect on the restoration of professional skills.

Massage significantly improves the condition of soft tissues following trauma or surgery, activates blood and lymph circulation, increases tissue metabolism of muscles and improves their contractility, prevents massive scarring, accelerates the resorption of soft tissue infiltrates in the area of ​​former injury or surgery, which undoubtedly promotes regeneration. nerves. The patient should be taught the elements of massage, which will allow it to be performed 2-3 times a day during the entire course of rehabilitation treatment.

The use of physiotherapeutic methods involves the rapid resorption of the hematoma, the prevention of postoperative swelling and the elimination of pain. For this purpose, on the 3-4th day after the operation, the patient is prescribed a UHF electric field and Bernard currents for 4-6 procedures, and subsequently, in the presence of pain, novocaine electrophoresis according to Parfenov’s method, calcium electrophoresis, etc., on the 22nd day - lidase electrophoresis (12-15 procedures), which stimulates nerve regeneration and prevents the formation of rough scars. During this period, daily ozokerite-paraffin applications are also indicated, which promote the resorption of infiltrates, relieve pain, as well as soften scars, improve the trophic function of the nervous system and tissue metabolism, and reduce stiffness in the joints. To maintain tone and prevent the development of atrophy of denervated muscles, it is rational to use electrical stimulation with a pulsed exponential current of 3-5 mA, a duration of 2-5 with a rhythm of 5-10 contractions per minute for 10-15 minutes. Electrical stimulation should be carried out daily or every other day; There are 15-18 procedures per course. This method helps maintain muscle contractility and tone until reinnervation occurs.

Drug treatment is aimed at creating favorable conditions for nerve regeneration, as well as stimulating the regeneration process itself. It is advisable to carry out a course of drug therapy as follows: on the 2nd day after surgery, vitamin B 12 injections of 200 mcg are prescribed intramuscularly, which promotes the growth of axons of the injured nerve, ensures the restoration of peripheral nerve endings and specific connections of the damaged nerve. Injections of vitamin B 12 should be alternated every other day with the introduction of 1 ml of a 6% solution of vitamin B 1 (20-25 injections per course). This method of introducing B vitamins weakens the development of inhibitory processes in the central nervous system and accelerates the regeneration of nerve fibers.

For 2 weeks, dibazole with nicotinic acid in powder is prescribed, which has an antispasmodic and tonic effect on the nervous system.

After 3 weeks from the start of the course of treatment, ATP (1 ml of 2% solution; 25-30 injections) and pyrogenal should be administered according to an individual scheme, which have a beneficial effect on the reparative process and stimulate it.

The treatment complex should also include electrophoresis of galantamine, which helps to increase the functional activity of the neuron and improves the conduction of excitation at neuromuscular synapses due to inactivation of the cholinesterase enzyme. Galantamine is administered from the anode in the form of a 0.25% solution; Duration of the procedure is 20 minutes, 15-18 procedures per course.

The duration and volume of complex conservative and restorative treatment are determined by the number, level and degree of damage to the peripheral nerve, as well as the presence of concomitant injuries. After neurolysis surgery, as well as in cases of successful neurorhaphy in the area of ​​the distal third of the palm and at the level of the fingers, one course of conservative-restorative treatment is sufficient.

After neurorrhaphy in the more proximal parts of the hand, forearm and shoulder, as well as at the level of the lower leg, thigh, taking into account the approximate period of axonal regeneration and reinnervation of the peripheral nervous apparatus, it is necessary to repeat the course of treatment after 1.5-2 months. As a rule, a course of rehabilitation treatment begun in a hospital ends on an outpatient basis under the supervision of the operating surgeon.

Initially, signs of restoration of sensitivity in the form of paresthesia appear in the area close to the level of nerve damage; over time, sensitivity in more distal parts of the limb improves. If there are no signs of regeneration within 3-5 months after surgery with full conservative-restorative treatment, the issue of repeated surgery should be considered.

Sanatorium-resort treatment in Tskaltubo, Yevpatoria, Saki, Matsesta, Pyatigorsk, etc. is indicated 2-3 months after neurography. Therapeutic factors such as mud applications and balneotherapy are used.

• Surgical treatment

Indications for surgery. The main indications for surgical intervention on damaged peripheral nerves are the presence of motor loss, impaired sensitivity and autonomic-trophic disorders in the area of ​​innervation of the nerve concerned.

Experience in treating patients with nerve injuries shows that the earlier the reconstructive operation is performed, the more completely the lost functions are restored. Nerve surgery is indicated in all cases of conduction disturbance along the nerve trunk. The time between injury and surgery should be reduced as much as possible.

In cases of failure of the primary nerve suture (increasing muscle atrophy, sensory and autonomic disorders), direct indications for reoperation arise.

The most favorable time for intervention is considered to be up to 3 months from the date of injury and 2-3 weeks after the wound has healed, although in a later period, operations on the damaged nerve are not contraindicated. In case of damage to the nerves of the hand, the optimal period for restoring their integrity is no more than 3-6 months after the injury. During this period, nerve functions, including motor functions, are most fully restored.

A complete disruption of conduction along the nerve trunk is indicated by the following: paralysis of a certain group of muscles, anesthesia in the autonomous zone of the interested nerve with anhidrosis within the same limits, negative Tinel’s symptom, absence of muscle contraction during electrodiagnostics - irritation of the nerve above the level of damage and gradually weakening and then disappearing muscle contractions under the influence of pulsed current below the level of damage.

Surgical treatment can be carried out at a later date after a nerve injury, if the intervention was not performed earlier for one reason or another. It should be noted that in this case one cannot count on a significant improvement in the motor function of the nerves. This especially applies to the muscles of the hand, where degenerative changes quickly occur due to their small size. After surgery, in almost all cases the focus of irritation is eliminated, sensitivity improves and vegetative-trophic disorders disappear. These changes have a beneficial effect on the function of the damaged organ. Restorative surgery on a damaged nerve, regardless of the time elapsed after the injury, always improves the function of the limb as a whole to a greater or lesser extent.

Neurolysis. An incomplete break or compression of the nerve trunk is manifested by mild trophic and sensory disturbances in the autonomous zone of innervation of the nerve concerned. In this case, a scar process develops in the epineurium, which can subsequently cause the formation of a scar stricture with conduction disturbances. After bruised lacerations or severe combined injuries of the extremities, especially parts, a diffuse scarring process develops, leading to compression of the nerve trunks. In such cases, sensitivity disorders and autonomic disorders are observed, the depth of which is directly proportional to the degree of compression. In these situations, if the full course of conservative treatment after a nerve injury is ineffective, neurolysis is indicated - careful excision of epineurial scars, which eliminates axonal compression, improves the blood supply to the nerve and restores conductivity in this area.

The surgical approach to the nerve must be carefully thought out and carried out with great methodicalness and the most careful treatment of tissue. The nerve trunk is first exposed in the area of ​​obviously healthy tissue and gradually mobilized towards the area of ​​damage, while maintaining the integrity of the epineurium, as well as the vessels accompanying and feeding the nerve.

The best results are obtained by early neurolysis, when the process of degeneration due to compression is less deep and reversible. The effectiveness of neurolysis, carried out according to the correct indications, manifests itself in the immediate postoperative period: the function of the nerve concerned improves or is completely restored, pain and vegetative-trophic disorders disappear, sensitivity improves, and sweating is restored.

Surgical tactics and methods of performing operations on peripheral nerves depend on the duration of the injury, the nature of the previous injury and previous surgical interventions, the degree of scar tissue changes, the level of nerve damage and concomitant injuries.

Epineural suture. Until now, the most common method of peripheral nerve reconstruction remains the classic direct epineural suture. This is the simplest operational technique, although it requires a certain amount of experience, otherwise technical errors are possible. It has a number of disadvantages, especially when restoring mixed nerves, where precise alignment of homogeneous intraneural fascicles is required. Using an epineural suture, it is difficult to maintain the achieved longitudinal orientation of the bundles after surgery. The growth of motor axons of the central end of the nerve into the sensory axon of the peripheral or inverse relationships due to mutual rotation of the ends are one of the reasons for prolonged or incomplete restoration of the main functions of the nerve. The abundance of interfascicular connective tissue complicates the opposition of bundles; there is a real danger of juxtaposing a section of the central fascicle of the nerve with the interfascicular connective tissue, which complicates the maturation and germination of regenerating axons. This ultimately leads to neuroma formation and loss of function.

Dissatisfaction with the results of surgical treatment of injuries of mixed peripheral nerves prompted doctors to search for new methods and types of surgical interventions. A big step forward was the use of magnifying optics and especially special operating microscopes. Microneurosurgery is a new direction in the neurosurgery of peripheral nerves, combining general surgical techniques with the use of qualitatively new technology under microfield conditions: magnifying optics, special instruments and ultra-thin suture material. Hemostasis during surgery is carried out using a special microelectrocoagulator. Stopping intraneural bleeding and bleeding in the wound cavity is important, and sometimes decisive, for the success of treatment.

The classic straight epineural suture can be applied to the level of the distal interphalangeal joint of the finger. It is most appropriate not only with conventional, but also with microneurosurgical techniques. The nerves of these regions contain homogeneous bundles of axons - either sensory or motor. Therefore, rotation of the ends of the nerve along the axis, the possibility of which is not excluded even with microtechniques, is not of great importance.

In areas of mixed structure of peripheral nerves, it is most advisable to apply perineural or interfascicular sutures connecting axon bundles of homogeneous function. This is necessary because after refreshing the ends of the nerve, the intra-trunk topography of the sections does not coincide, since the position and size of the bundles at different levels of the nerve are different. In order to identify intra-trunk bundles, you can use the Karagancheva scheme and electrodiagnostics on the operating table. In the process of using the epineural suture, its technique was modified: the sutures of one bundle are placed higher or lower than the other due to their resection in different planes, which greatly simplifies their suturing with two or three perineural and sutures, allows you to accurately adapt the ends of each bundle, unlike the most common the applied technique for stitching beams in one cut plane. Finally, the epineurium of both ends of the nerve is brought together with separate interrupted sutures on an overlay. Thanks to this, the line of perineural sutures turns out to be well isolated from the surrounding tissues by its own epineurium, the sutures of which are outside the zone of interfascicular sutures. The nerve bundles are not compressed, as with a conventional epineural suture.

Nerve plastic surgery. Particularly great difficulties in reconstructing a nerve arise in cases where there is a defect between its ends. Many authors abandoned the mobilization of the nerve over a long distance, as well as excessive flexion in the joints of the limb to eliminate diastasis in order to suture the nerve end to end. The blood supply to peripheral nerves is segmental, with most nerves having a longitudinal direction along the epineurium and between the fascicles. Therefore, mobilization of the nerve to eliminate diastasis is justified when separating them for no more than 6-8 cm. Increasing this limit leads to impaired circulation, which in such cases can only occur due to the ingrowth of new blood vessels from the surrounding soft tissues. There is no doubt that developing fibrosis in the nerve trunk interferes with the maturation and growth of regenerating axons, which will ultimately negatively affect treatment results. Such disorders are caused by tension along the line of sutures due to incompletely eliminated diastasis between the ends of the nerve. For these reasons, a diastasis between the ends of the main trunks of peripheral nerves of 2.5-3.0 cm, and of common digital and digital nerves - more than 1 cm, is an indication for neuroautoplasty. The external cutaneous nerve of the leg should be used as a donor nerve, since due to its anatomical and functional characteristics it is most suitable for these purposes. When plasticizing the main nerve trunks, the defect is filled with several grafts, usually 4-5 depending on the diameter of the trunk, collected in the form of a bundle, without tension in the average physiological position of the limb joints. Between the nerve bundle and the graft, 3-4 stitches are applied with a 9/0-10/0 thread, and this area is additionally covered with epineurium. For plastic surgery of the common digital and digital nerves, one graft is usually required due to their similar diameter.

In most cases, damage to peripheral nerves is combined with damage to blood vessels, which is explained by their anatomical relationship. Along with suture or plasty of the nerve, it is necessary to simultaneously suture or plasty the damaged blood vessel, which will optimize the conditions for regeneration of the restored nerve in anticipation of a favorable final result of treatment.

Thus, microsurgical techniques for operations on peripheral nerves make it possible to create optimal anatomical conditions for restoring nerve function. The use of microsurgical techniques is especially important in operations on mixed nerves, where precise comparison of the ends of the nerve with subsequent suturing of its identical bundles is required.

Which doctors should you contact if you have Peripheral Nerve Damage:

• Traumatologist
• Surgeon

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Other diseases from the group Trauma, poisoning and some other consequences of external causes:

Injuries to peripheral nerves, including bruises, are much more common in wartime, and armed conflicts, sadly, make an invaluable contribution to their study. In comparison, during the First World War, damage to nerves and plexuses amounted to (in relation to all types of wounds) 1-5%, and in modern wars - already 13-16%, due to mine-fragmentation weapons and frequent concussions. Of course, their damage to the nerves is not limited to military injuries, and in peacetime there are also natural disasters, road accidents and many other factors leading to injuries.

About the frequency of occurrence

In first place in terms of frequency of occurrence are neuropathies of the radial nerve and peroneal nerve. Then, in second place are lesions of the sciatic nerve and ulnar nerve, and closing the “honorable top three” are median neuropathies and lesions of the lumbosacral plexus. With a large “lag” there are lesions of the axillary nerve, musculocutaneous, and femoral nerves.

As a rule, nerve injuries occur, as already mentioned, in the form of neuropathies (damage to individual nerves), and in the form of plexopathies, or damage to bundles and plexuses.

On the classification of nerve lesions

There are many different classifications of nerve damage:

• etiological: gunshot, concussion, sports, road transport, industrial, household and even medical (post-injection, tourniquet) injuries;

The classification according to the mechanism of action of the traumatic factor is much richer. So, there are:

• cut, chopped, punctured open wounds of nerves;

• traction, for dislocations of limbs;

• compression during falls and impacts;

• compression-traction (for example, in car accidents);

• compression-ischemic (for example, tourniquets, crutches when moving incorrectly on crutches), shoulder straps when wearing incorrectly selected bags and backpacks, cicatricial syndromes when a nerve is compressed by scar tissue, tunnel syndromes when a nerve is compressed in the area of ​​“narrow” anatomical formations.

Due to the richness of the impact of damaging factors, anything can happen to the nerve, from rupture to complete degeneration, to the appearance of reflex-dystrophic syndromes due to neuroapraxia (its concussion).

Known law: the further away from the central nervous system the nerve is damaged, the greater the chance of its recovery: That is, more distal injury promotes better and faster recovery. Nerve conduction changes due to nerve contusion, and this change occurs for several reasons:

• long segments, or sections of nerves are affected due to its stretching when the limb is displaced;

• due to compression or crushing of areas of nervous tissue, sometimes due to blunt blows;

• sometimes the nerve can be compressed under a tourniquet, cuff, or tight bandage, including a plaster cast. This may result in iatrogenic or medical injuries;

• After the fracture has healed, the nerve may enter the area of ​​the callus as it grows.

In case of nerve injury, even a very short-term but strong impact can lead to disruption of the myelin sheath and disruption of impulse transmission. Progressive distal atrophy of the nerve fiber develops, and, as a consequence, dysfunction of the underlying part.

About the clinical picture of nerve damage in bruises and injuries

Like other disorders, plexopathies and neuropathies of traumatic origin can manifest themselves:

• sensory disorders, which are also painful in nature, with the development of various paresthesias;

• motor disorders, which consist of muscle weakness, progressive or persistent wasting of the muscles innervated by this nerve, or a decrease in skin turgor over the area of ​​paretic muscles;

• vegetative-trophic disorders: increased fragility of nails, hair loss, the appearance of a marbled skin color or its cyanosis, due to a violation of the regulation of vascular tone, with injury to the part of the nerve that carries vegetative-trophic fibers;

• it is important that in addition to the classic triad (sensitive, motor and autonomic loss of functions), symptoms of excessive pathological production of nervous tissue may develop. These include reflex muscle contractures, the appearance of excess hair growth, or hypertrichosis, the appearance of excessive keratinization of the skin (hyperkeratosis), or disorders such as hyperpathia and causalgia.

Hyperpathy is a state of pathological pain that involves more ancient types of sensitivity, called protopathic, as opposed to the newer, more precise and localized - epicritic sensitivity. In this case, the applied irritation feels inaccurate, vague, painful, and unpleasant, that is, an emotional coloring of sensations appears.

This type of “perverted pain” occurs precisely after nerve injuries, in conditions where nerve insulation (or remyelination processes) have not gone through enough. A hallmark of hyperpathy is that the sensation of the effect lasts longer than it actually lasts: there is a “deception” of the nervous system. The second option for the appearance of hyperpathy is pathological processes in higher, but subcortical pain analysis centers, for example, in the visual thalamus or in the thalamus.

Causalgia is the name given to burning, intense pain. Most often, they occur with injuries to the sciatic nerve in the leg and the median nerve in the arm. A characteristic feature of such a peripheral injury is that moisturizing the limb (applying a wet towel) reduces discomfort. It is even more unpleasant that this pain goes “beyond the scope” of the physiological innervation of a given nerve and affects neighboring areas.

These pathological types of pain are often accompanied by chronic insomnia, depression, and can even lead to suicide in special cases.

Some typical signs of damage to individual plexuses and nerves

When the cervical plexus is damaged, first of all, the neck begins to bend and straighten poorly, sensitivity in the area of ​​the skin behind the ears, in the area of ​​the shoulders and shoulder girdle, and even to the subclavian region and the area of ​​the 1st intercostal space is often reduced.

Damage to the brachial plexus leads to striking symptoms: upper Erb's palsy is manifested by loss of function of the scapular muscles, proximal parts, arm and shoulder, while the movements of the muscles of the hand and fingers are preserved.

Damage to the inferior fasciculus, or Dejerine-Klumpke palsy, causes distal paralysis of the small muscles of the hand, with their atrophy. As a rule, the upper muscles work without change. In some cases, Horner's symptom may occur: ptosis (drooping of the upper eyelid), miosis (constriction of one pupil), and enophthalmos, or a decrease in the size of the eyeball with its retraction.

With pathology of the nerves of the lumbosacral plexus, the following common symptoms occur:

Roth's disease, or meralgia paresthetica. Occurs when the external cutaneous nerve of the thigh is compressed. This often happens when wearing tight trousers with a trouser belt. It manifests itself as a violation of sensitivity on the outer thigh, “crawling goosebumps.”

In case of bruise and injury to the femoral nerve, such activities as simple climbing stairs are disrupted, namely, it becomes difficult to extend and straighten the leg at the knee joint. Gradually, as a result, weight loss and atrophy of the anterior femoral muscles develop.

If the sciatic nerve, as the longest and thickest nerve in our body, is damaged, many disorders can occur. Thus, with disorders in the pelvic cavity, there is a violation of the rotation of the hip, drooping of the foot and toes, and hypotrophy of the muscles of the thigh and lower leg along with the foot appears, since both the peroneal and tibial nerves, which make up the sciatic nerve, are affected.

As for damage to the tibial nerve, it is characterized by deterioration of flexion in the ankle joint, and the patient cannot stand on his toes. A “claw-shaped” foot occurs, and sensitivity in the heel area is impaired.

When the common peroneal nerve is damaged, the foot drops and the foot “slaps” when walking, or “cock’s gait.”

Of course, these examples do not limit the variety of nerve damage due to trauma and bruises. It is important for us, ordinary people, to know one thing: that the treatment of damage to peripheral nerves should be quick.

So, with “garden bench paralysis”, when a person sleeps with his hand under his head, and then realizes that his hand is “dangling”, you need to immediately consult a doctor, or the neurology department in the morning. But what is typical is that people who have been drinking heavily usually fall asleep this way, and the next morning, they prefer to recover from their hangover, instead of starting urgent treatment. And alcohol itself is a factor that significantly worsens the course of any neuropathy and plexopathy.

Quite often, in addition to conservative treatment, surgery is required, for example, to decompress the nerve trunk or remove it from the callus.

This is done by neurosurgeons who specialize in the peripheral nervous system - a rather rare medical specialty, since “regular” neurosurgeons work on the central nervous system - the brain and spinal cord. Sometimes the intervention of microsurgeons specializing in the hand is required, since the structure of this organ is very complex, and in case of compression-ischemic neuropathies it is necessary to go there, if they are located near the hand.

Causes of hand deformation due to nerve damage.

Damage to the peripheral nerves of the upper limb, in addition to impaired sensitivity and autonomic-trophic functions, leads to movement disorders due to flaccid paralysis of the muscles innervated by the motor branches of these nerves. Despite the attempted restoration of the nerves, motor impairments may remain persistent and cause neurogenic deformities and contractures of the fingers.

Within 4-6 months, a denervation process begins in the intrinsic muscles of the hand with the replacement of myofibrils with adipose fibrous connective tissue. The ability of muscles to reinnervate is lost, despite the restoration of peripheral nerve trunks using careful microsurgical techniques. According to leading experts, changes in both muscles and peripheral nerves remain irreversible. In human muscles after damage to tendons and nerves, atrophy, homogenization, fragmentation, a decrease in the number of mitochondria, and a sharp decrease in glycogen content were found already by the 4-16th day. The motor end plates are atrophic, and motor neurons show typical Wallerian degeneration.

With persistent damage to the radial nerve, paralysis of the extensor muscles of the hand and fingers develops. There is no active extension of the hand, fingers or abduction of 1 finger. The hand hangs in a flexed position; active extension of the fingers is impossible.

The median nerve from the distal third of the forearm provides motor innervation to the I-II lumbrical muscles, as well as the muscles of the opponensus, abductor brevis and superficial head of the flexor brevis of the first finger. Due to denervation, the intrinsic muscles of the hand quickly undergo atrophy and fibrosis. In this regard, motor disorders in 70-75% of cases remain persistent and become the cause of the formation of neurogenic deformities of the hand and fingers.

The lumbrical muscles perform flexion and radial abduction of the proximal phalanges of the II-III fingers and participate in extension at the interphalangeal joints. With paralysis of the I-II lumbrical muscles, active flexion and radial abduction of the proximal and extension of the middle and distal phalanges of the II-III fingers are lost. Hyperextension of the proximal phalanges of the second and partially third finger develops.

When the group of thenar muscles innervated by the median nerve is paralyzed, a very important function is disrupted - opposition of the first finger. This movement of the first finger is carried out by nine muscles.

Each thenar muscle, innervated by the median nerve, reproduces its characteristic function. The abductor brevis performs palmar abduction of the first finger with moderate flexion of the main and extension of the distal phalanges. The flexor brevis flexes the proximal 1st metacarpal bone and extends the distal phalanx of the 1st finger. The muscle opposing the first finger produces palmar stabilization, flexion and pronation of the first metacarpal bone, participating in the opposition of the first finger to the II-V fingers.

With persistent damage to the median nerve, the function of these muscles is lost and neurogenic deformation of the metacarpophalangeal joint develops with a limitation of palmar abduction by 50-60%. The first finger in the supination position is in the same plane relative to the hand, with radial adduction limited to 40-50%. Pronation and opposition of the first finger are impaired. The ball grip is limited, it is performed by the side surface of the finger. The cylindrical grip is partially compensated by the long flexor and extensor muscles of the fingers. The strength of the pinch grip is reduced by 30-40%. Due to paralysis of the I-II lumbrical muscles, hyperextension of the II-III proximal phalanges occurs, and precise types of grip with the fingertips are affected. Not only the function, but also the shape of the hand is disrupted.

The ulnar nerve from the distal third of the forearm innervates 14 intrinsic muscles of the hand:

deep head of the flexor brevis and adductor muscles of the first finger;

abductor, contralateral muscles and short flexor of the fifth finger;

all interosseous muscles;

III-IV lumbrical muscles.

The action of the interosseous muscles is extremely diverse: in the metacarpophalangeal joints they carry out radial and ulnar abduction of the corresponding fingers. The dorsal interosseous muscles flex the proximal phalanges. The palmar interosseous muscles promote extension of the proximal phalanges. The III and IV lumbrical muscles, starting from the deep flexor tendons of the III-IV-V fingers, at the level of the heads of the metacarpal bones, pass to the rear of the proximal phalanx and are woven into the extensor tendon apparatus of the corresponding fingers. They flex the proximal phalanges, and also, when contracting, pull the deep flexor fingers distally, relaxing them, thereby facilitating the extension of the distal phalanges of the fingers.

The interosseous and lumbrical muscles of the hand are a kind of regulators of the function of the long flexors and extensors of the fingers, stabilizing and balancing their function.

Thus, with persistent damage to the ulnar nerve, the following components of deformation and limitation of the function of the hand and fingers develop:

atrophy of the ulnar edge of the hand develops;

atrophy and retraction of the intermetacarpal spaces develop, followed by fibrosis and contraction of the transverse arch of the hand;

the contractile activity of the interosseous muscles is lost, their role as flexors of the proximal and extensors of the middle and distal phalanges of the fingers ceases;

paralysis of the III-IV lumbrical muscles is accompanied by loss of the function of active flexion of the proximal phalanges and extension in the interphalangeal joints of the III-IV-V fingers.

adduction, flexion and pronation of the first finger, flexion, adduction and opposition of the fifth finger are impaired;

flexion, ulnar and radial abduction of the proximal phalanges, extension of the middle and distal phalanges of the IV-V and partially III fingers are limited.

When the hand remains in a vicious position for a long time, secondary fibrogic changes occur in the tissues of the hand. They form a persistent claw-like deformity, predominantly of the ulnar half of the hand with supination of the first finger, hyperextension of the proximal phalanges of the III-IV-V fingers, flexion of the middle and distal IV-V and partially III fingers; excessive abduction of the fifth finger.

Flexor carpi ulnaris

With persistent damage to the median and ulnar nerves, all the intrinsic muscles of the hand are switched off from function, and a kind of control panel for the coordination of finger movements is lost. Hyperextension-flexion deformation of the hand occurs. The longitudinal arch is deformed, the transverse arch becomes flat, and the opposition of the first finger disappears. Hyperextension of the proximal phalanges and flexion contracture in the interphalangeal joints develop. The main types of grip are impaired: pinch, ball, interdigital, planar.

Reconstructive surgeries for persistent damage to the radial nerve

In case of paralysis of the extensor muscles of the fingers and hand caused by persistent damage to the radial nerve, various types of muscle-tendon transpositions are performed. S.Bunnell proposed his own version of moving muscles - the tendon of the ulnar flexor of the hand - to the extensors of the III-V fingers; flexor carpi radialis - to the extensors of the 1st and 2nd fingers. I. Matev et al. Transposition of the pronator teres to the extensor carpi radialis, the flexor ulnaris to the extensor digitorum communis, and the palmaris longus to the extensor brevis and abductor muscles of the first finger are considered effective.

A.M.Volkova uses the operation according to Yu.Yu.Dzhanelidze. From an incision along the dorsal surface of the forearm to the wrist joint, the tendons of the common extensor of the II-V fingers and the long extensor of the first finger are exposed.

From two parallel incisions along the ulnar and radial edges of the distal third of the forearm, the tendons of the ulnar and radial flexors of the hand are exposed and cut off from the attachment site of the palmar surface and transferred through the subcutaneous channels to the dorsum of the forearm. Both wounds on the palmar surface of the forearm are sutured.

The tendon of the long extensor of the first finger is isolated after dissection of the third osteofibrous canal. The hands and fingers are placed in an extension position.

The flexor carpi ulnaris is passed under the tendons of the common extensor digitorum and sutured side to side with the tendon of the extensor pollicis longus in the position of maximum extension. All extensor tendons of the II-V fingers are sutured to the flexor carpi radialis tendon.

After suturing the wound, the hand and fingers are fixed with a plaster cast in the position of maximum extension for 5-6 weeks. The described operations in most cases provide a positive functional outcome.

Reconstructive operations for persistent damage to the median nerve. To date, all methods of reconstructive surgery on the hand for persistent paralysis of the ulnar and median nerves are divided into:

stabilizing;

dynamic.

During stabilizing operations, a functionally advantageous position is created for the fingers to grasp objects. During dynamic operations, active function is restored due to muscle-tendon transposition of functional muscles.

One of the reasons for impaired grasping function in case of paralysis of the intrinsic muscles of the hand is a violation of the opposition of the first finger. To stabilize the first finger in the opposition position, many authors performed arthrodesis of the metacarpal joint. Synostosis of the I-II metacarpal bones using a bone graft-spacer in the opposition position was performed by Ch. Thompson, B. Boychev et al., R. E. Raie.

Opinions about stabilizing operations are mixed. Currently, they are used very rarely - only in the absence of conditions for muscle-tendon transpositions.

More than 40 methods are known to restore the active opposition of the first finger of the hand in case of paralysis of the thenar muscles. S.Bunnell performed transposition of the elongated tendon of the flexor ulnaris of the hand through a “block” with fixation to the base of the proximal phalanx of the first finger. A similar method, only using the superficial flexor tendon of the fourth finger, was proposed by C. Thompson and W. Blauth, who used various options for muscle-tendon transposition to restore the opposition of the first finger. E. Paneva-Kholevich transplanted the elongated tendon of the flexor carpi radialis, V. Sook, L. Schneider, J. Zweig, S. A. Goloborodko transferred the extensor tendon of the fifth finger. K. Tsuge performed transposition of the extensor carpi radialis longus.

With persistent damage to the ulnar and median nerves, not only the opposition of the first finger suffers, but also a claw-like deformity of all fingers develops. E. Zancolli believes that with paralysis of the interosseous and lumbrical muscles, the stabilization of the metacarpophalangeal joints is impaired. In this regard, the extensors overextend the proximal phalanges of the II-V fingers and lose the ability to extend the middle and distal phalanges. On this basis, he developed an operation to stabilize the proximal phalanges of the II-V fingers. The essence of the Zancolli operation is capsuloplasty: the palmar capsule of the metacarpophalangeal joints is shortened by cutting out a flap and fixing it with shortening and flexion of the proximal phalanx. However, the author himself, as well as other surgeons, noted recurrence of the deformity in 50% of cases.

To restore the opposition of the first finger, the following surgical technique has been proposed. From the incisions along the ulnar and radial edges of the forearm, the tendons of the radial and ulnar flexors of the hand are isolated and cut off from the attachment sites. The distal end of the flexor carpi radialis tendon is sutured with an intra-trunk suture. The flexor carpi ulnaris tendon is lengthened by longitudinal splitting, and the distal end is sutured in the same way. From the incision along the dorsal radial surface, the first metacarpal bone is exposed. The tendons of the radial and ulnar flexors of the hand are passed through the subcutaneous tunnels to the first metacarpal bone. The flexor carpi radialis tendon is fixed to the upper third of the metacarpal bone, and the flexor carpi ulnaris tendon is fixed to the proximal phalanx of the first finger.

Some surgeons prefer an operation, the essence of which is that the tendon of the long flexor of the first finger is split in half. The ulnar part is left in place, and the radial part is moved to the dorsulnar surface of the main phalanx of the first finger.

Reconstructive operations for persistent damage to the ulnar nerve. As already mentioned, the main complaints from patients with damage to the ulnar nerve are claw-shaped deformities of the ulnar half of the hand, which prevents the palm from opening for grip. Various methods of surgical treatment of a claw-shaped hand have been described, but preference is given to dynamic operations that restore active flexion of the proximal phalanges of the fingers. The most functionally effective are two methods of muscle-tendon transposition of the superficial flexor from the middle phalanx to the proximal one.

In the first method, both legs of the superficial flexor tendon are cut off from the place of attachment to the middle phalanx. The tendon is removed from the fibroaponeurotic canal and split lengthwise into two halves. One leg is sutured and passed through the bone canal in the middle third of the proximal phalanx. The middle phalanx is extended, and the proximal phalanx is brought out of hyperextension by tensioning the superficial flexor tendon to a flexion position of 20°. Both legs of the superficial flexor muscle are sutured.

In the second method, at the level of the IV-V metacarpophalangeal joints, the proximal part of the annular ligament is exposed and transversely dissected. The pedicles of the superficial flexor tendon are cut off and enclosed in the form of a loop around the proximal part of the fibrous ring. After tension and flexion of the proximal phalanx to an angle of 20°, the distal end of the tendon is sutured to the same tendon.

The use of the described methods of dynamic operations ensures restoration of the longitudinal arch of the hand, anginal differentiated flexion of the proximal phalanges of the IV-V fingers, elimination of flexion contracture of the middle and distal phalanges.

Considering the deficiency of adduction of the first finger for a stable power grip, the following technique of muscle-tendon transposition is advisable. From a longitudinal incision along the ulnar edge of the distal third of the forearm, the flexor carpi ulnaris tendon is isolated, mobilized, and cut off from its attachment site. The latter is lengthened by longitudinal dissection and passed through the subcutaneous tunnel to the proximal phalanx of the first finger. From an incision along the neutral radial line at the level of the metacarpophalangeal joint, transosseous attachment of the flexor ulnaris tendon to the proximal phalanx is made in the position of adduction and pronation of the first finger. Thus, the function of the flexor carpi ulnaris provides stability and grip strength, and hyperextension of the proximal phalanx is corrected.

To eliminate excessive involuntary abduction of the fifth finger, it is possible to cut off the extensor tendon from its attachment site. Methods of operations are described that are aimed not only at eliminating excessive abduction, but also at restoring active adduction of the fifth finger to the fourth. The operation consists of cutting off the extensor tendon of the fifth finger and fixing it to the extensor tendon aponeurosis of the fifth finger on the radial side.

The listed surgical interventions allow for effective correction of all components of hand deformity in case of persistent damage to the ulnar nerve.

Restoring sensitivity in cases of old damage to the nerves of the hand. A feature of old injuries of the common and intrinsic palmar digital nerves is the increase in diastasis between the ends of the nerve trunk and the formation of a neuroma on the proximal segment of the nerve. In this regard, it is often necessary to perform plastic surgery of the nerves of the hand.

If the number of damaged nerves is significant, then it is advisable, if possible, to perform plastic surgery on the maximum number of nerves using one of the sural nerves as grafts. With a small number of damaged nerves, the use of a donor area can be dispensed with, thus not creating additional scars. In these cases, the own nerves of the hand, innervating functionally less significant zones, can be used as grafts. You can also use the nerves on the dorsal surface of the hand for this. Finally, in case of deep tissue defects, the defects in the nerves of the hand can be replaced by a nerve trunk taken as part of a free complex of tissues transplanted into the defect.

The second option for restoring sensitivity in functionally important areas of the hand is to transplant innervated island flaps from the non-dominant surface of the finger. Isolation is possible in two versions: on a wide skin base or on a neurovascular pedicle. One of the innervated flaps transplanted to the palmar surface of the first finger is a graft from the dorsal radial surface of the second finger, supplied with blood from the first dorsal artery of the wrist, which includes the superficial branch of the radial nerve.

To restore the full sensitive skin of the hand, various donor sources of tissue complexes, including branches of nerves, can be used. One of the most suitable grafts for the hand are flaps fed from the 1st dorsal metatarsal artery. Tissue reinnervation is carried out through the deep branch of the peroneal nerve, which is sutured to the sensory nerve of the hand.

The described methods of surgical treatment provide a good functional effect for chronic injuries of the nerves of the hand in children.

The peripheral nervous system consists of a huge number of nerves, nerve fibers and nerve endings that provide sensory and motor abilities to all organs of the body. Any damage, no matter how minor, to one of these nerves or one of its branches will affect sensory and motor abilities at a specific point in the body and even in entire organs or areas. In some cases, the nerve can heal on its own, but if the peripheral nerve is severely damaged, microsurgery will be required to repair the nerve.

Prof. Shimon Rochkind, one of the world's leading neurosurgeons in the field of the peripheral nervous system, conducts at the hospital's Center of Advanced Neurosurgery "Herzliya Medical Center" various operations to restore the affected peripheral nerve.

Peripheral nerve damage: types and consequences

In most cases, the cause of peripheral nerve damage is an external factor: a cut, a knife blow, a gunshot wound, severe stretching, compression, or strong and constant pressure. Such injuries can result in partial or complete disruption of the nerve—the long, thin fiber that carries electrical signals from the brain to the organ it innervates and back again.

The severity of nerve damage is divided into five levels on the Sunderland scale:

• Level 1: minor damage, amenable to complete recovery, without irreversible damage to nerve tissue
• Degree 2: Trauma will cause some damage to nerve tissue, but if prompt medical attention is provided to correct the problem that caused the injury, full recovery is possible and the damage will only be temporary.
• Level 3: a more serious injury that will actually result in some permanent nerve damage. With this degree of damage, recovery will only be partial.
• Degree 4: severe damage to the nerve, contributing to the formation of a scar that interferes with the process of nerve repair. Although the nerve damage is not always complete (that is, the nerve is not completely severed), in such a situation the nerve can only be restored through surgery
• Level 5: complete damage - complete disconnection of the nerve requiring surgery

Injury to peripheral nerves can be critical: disruption of the integrity of the nerve leads to the fact that electrical signals emanating from the brain do not reach their destination, and vice versa - the nerve signal in response to an external stimulus is not transmitted in full (or not at all) into the brain. As a result, various symptoms may occur, including:

• Acute neuropathic pain (long-lasting pain, in most cases characterized by a burning or electrical sensation where the nerve is damaged)
• Sensory impairments
• Complete loss of sensation
• Movement disorders (movement disorders) - to the point of paralysis
• Damage to the autonomic nervous system (the system responsible for the involuntary actions of the body, including sphincter function, blood pressure, etc.).

Treatment for peripheral nerve damage

Treatment methods depend on the injury and, of course, its severity. When it comes to a minor injury (usually grade 1 - 2), recovery of the nervous system will occur naturally: due to the natural characteristics of the peripheral nervous system, the affected nerve undergoes a process of reinnervation (regrowth), which leads to improved function and sensitivity in the affected area. The rehabilitation process can be “helped” by undergoing physical therapy, which helps speed up the process and ensures that rehabilitation is carried out in an optimal manner.

However, in some cases, natural recovery and various treatment methods will not improve the situation. This occurs in cases of very serious injuries that do not allow the body to recover on its own. Therefore, if after some time there is no improvement, or if the nerve damage is complete and the distance between the nerve endings is too large, microsurgical intervention is necessary.

Prof. Rochkind He is considered one of the leading doctors in the field of peripheral nerve repair, and over the years he has performed countless surgical procedures to correct this type of damage. Prof. Rochkind has also spent many years researching and developing new methods and approaches for optimal recovery from peripheral nerve injury.

The operation itself is carried out using microsurgical techniques and mainly concentrates on freeing and restoring the damaged nerve because, in most cases, as noted earlier, the surgical procedure will be required when the grass is most severe, up to the complete cutting off of the affected nerve fibers.

During the operation, the nerve will be repaired by freeing it from the scars formed after the injury, which will facilitate the recovery of the nerve. The operation uses a surgical microscope and additional precision microsurgical instruments to ensure optimal results.

An additional action to allow the nerve to recover is to implant healthy nerves in the affected area or create an anastomosis: suturing and connecting the proximal part of the nerve (close to the center of the body) to the distal part (far from the center of the body), which will allow the future conduction of electrical signals.

It should be noted that sometimes such nerve damage will also lead to the development of a tumor (neuroma), which is removed during surgery. Tumor removal is also carried out using microsurgical instruments in order to preserve the health and integrity of the nearby nervous tissue and nerve canal.

Do you suffer from peripheral nerve damage?

Are you experiencing severe localized pain, weakness, or even paralysis?

Contact us today to the hospital's Center of Advanced Neurosurgery "Herzliya Medical Center".