Mononeuropathies: Clinical Guidelines

List of Abbreviations

VAS – visual analog scale

GC – glucocorticoids

AIN – anterior interosseous nerve (or PIN – posterior interosseous nerve depending on context)

CT – computed tomography

LACNF – lateral antebrachial cutaneous nerve

MCN – musculocutaneous nerve

MN – mononeuropathy

MRI – magnetic resonance imaging

NA – neuralgic amyotrophy

MUAP – motor unit action potential

PIN – posterior interosseous nerve

PSW – positive sharp wave

FIB – fibrillation potential

CTS – carpal tunnel syndrome

CV – conduction velocity

US – ultrasound examination

EMG – electromyography

ENMG – electroneuromyography

Terms and Definitions

Condition – body changes arising from the impact of pathogenic and (or) physiological factors and requiring medical care;

Instrumental diagnostics – diagnostics using various devices, apparatus, and instruments to examine a patient.

Level of certainty of evidence – reflects the degree of confidence that the found effect of a medical intervention is true.

Level of recommendation certainty – reflects not only the degree of confidence in the validity of the intervention's effect, but also the degree of confidence that following the recommendations will bring more benefit than harm in a specific situation.

Working group – two or more individuals of the same or different professions working together in a coordinated manner to develop clinical guidelines and bearing joint responsibility for the results of this work.

Syndrome – a set of symptoms sharing a common etiology and pathogenesis.

Surgical intervention is an invasive procedure that may be used for diagnostic purposes and/or as a method of treating diseases.

Surgical treatment – a method of treating diseases by dividing and uniting tissues during a surgical operation.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

1.1.1 Median mononeuropathy

Median mononeuropathy – a pathological condition caused by compression of the median nerve trunk or its inflammation, unrelated to direct injury or traction [1–3]

1.1.2 Ulnar mononeuropathy

Ulnar mononeuropathy – a pathological condition characterized by ulnar nerve involvement at typical compression sites, most commonly at the elbow or wrist level, manifesting as sensory and motor disturbances within the ulnar nerve innervation zone and not associated with direct nerve injury [4–6].

1.1.3 Radial mononeuropathy

Radial mononeuropathy – a pathological condition associated with involvement of the radial nerve and its main branches – the posterior interosseous nerve and the superficial branch of the radial nerve, unrelated to direct injury or traction, accompanied, depending on the level of lesion, by paresis of the forearm, wrist, and finger extensor muscles, as well as sensory disturbances in the posterior arm and forearm, and dorsolateral hand.

1.1.4 Axillary mononeuropathy

Axillary mononeuropathy – a pathological condition associated with involvement of the axillary nerve trunk, unrelated to direct injury or traction. The clinical presentation consists of sensory and motor impairments within the axillary nerve innervation zone [7].

1.1.5 Musculocutaneous mononeuropathy

Musculocutaneous mononeuropathy – a pathological condition caused by compression of the musculocutaneous nerve itself at the arm level, as well as the lateral cutaneous nerve of the forearm at the elbow crease level, not associated with direct injury or traction.

1.1.6 Mononeuropathy of brachial plexus branches

Brachial plexus branch mononeuropathy – a group of disorders associated with involvement of branches originating from the supraclavicular or infraclavicular regions of the brachial plexus, unrelated to direct injury or traction, accompanied by a combination of sensory and motor deficits or isolated motor deficits in the innervation zone of the corresponding branches [8,9].

1.1.7 Intercostal mononeuropathy

Intercostal mononeuropathy – a pathological condition caused by involvement of one or more intercostal nerves, not associated with direct injury or traction, the main manifestation of which is chest pain within the innervation area of these nerves.

1.1.8 Sciatic mononeuropathy

Sciatic mononeuropathy is a pathological condition associated with a lesion of the sciatic nerve, accompanied, depending on the level of the lesion, by paresis of the foot extensors and flexors, the posterior thigh muscles, as well as sensory disturbances in the plantar and dorsal aspects of the foot and the lateral surface of the lower leg.

1.1.9 Peroneal mononeuropathy (PMN)

Fibular mononeuropathy (common peroneal neuropathy) is a pathological condition associated with a lesion of the common fibular nerve, deep fibular nerve, or superficial fibular nerve, not related to direct injury or traction, and accompanied by paresis of the foot and toe extensors, as well as sensory disturbances along the lateral aspect of the lower leg and the dorsum of the foot [10].

1.1.10 Tibial mononeuropathy

Tibial mononeuropathy is a pathological condition associated with compression of the main trunk of the tibial nerve, the posterior tibial nerve at the lower leg level, as well as the plantar nerves and the sural nerve, not related to direct injury or traction [11]. The clinical presentation consists of sensory and motor deficits within the innervation zone of the tibial nerve [12]. Compression neuropathy of the plantar nerve in the intermetatarsal space, known as Morton's metatarsalgia, is considered separately [13].

1.1.11 Femoral mononeuropathy

Femoral mononeuropathy is a pathological condition associated with compression of the trunk and branches of the femoral nerve, but not related to direct injury or traction, accompanied by sensory disturbances within the femoral nerve innervation zone and paresis of the muscles innervated by this nerve [14–16].

1.1.12 Lateral femoral cutaneous mononeuropathy

Lateral femoral cutaneous mononeuropathy is a pathological condition caused by a lesion of the lateral femoral cutaneous nerve, but not related to direct injury or traction. It is accompanied by sensory disturbances within the innervation zone of this nerve in the anterolateral thigh region [17].

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

1.2.1 Etiology and pathogenesis of median nerve mononeuropathy

Given the anatomical features, the development of compression-ischemic neuropathies of the median nerve and anterior interosseous nerve most frequently occurs at 4 levels:

1. carpal tunnel (carpal tunnel syndrome),

2. pronator teres syndrome (Seyfarth syndrome),

3. anterior interosseous nerve neuropathy,

4. compression of the median nerve under Struthers' ligament.

Carpal tunnel syndrome (CTS) is one of the most common entrapment syndromes and mononeuropathies, manifested by a complex of clinical disorders (sensory, motor, and trophic) caused by compression or impingement of the median nerve in a narrow anatomical space (bounded by three bone walls and the transverse carpal ligament) [2,18–21].

The most common causes leading to the development of CTS are occupational factors due to static strain in the wrist joint area: pianists, painters, programmers, tennis players, and individuals exposed to local vibration [18–27]; in addition, the etiopathogenesis involves:

1. hormonal changes: hypothyroidism, diabetes mellitus, pregnancy;

2. disorders of the joint-ligamentous apparatus – rheumatoid arthritis, systemic diseases including amyloidosis (transthyretin FAP);

3. infectious diseases (tuberculosis);

4. injuries in the wrist area, tumor and cystic formations, etc.

5. weight gain.

In pediatric practice, CTS is rare. Most cases of CTS in children are genetically determined and may be associated with lysosomal storage diseases (including mucopolysaccharidosis and mucolipidosis), or be a manifestation of primary familial CTS, hereditary neuropathy with liability to pressure palsies (HNPP), Albright's hereditary osteodystrophy, and acromicric dysplasia. Other, less common causes include neoplasms (e.g., fibrolipomatous hamartoma, intraneural perineurioma, or median nerve hemangioma), metabolic disorders (pseudohypoparathyroidism), developmental malformations (macrodactyly), and idiopathic causes [28–30].

Pronator teres syndrome (Seyfarth syndrome) is a compression neuropathy of the median nerve at the forearm level caused by the pronator teres muscle. In 66% of cases, it results from a size disproportion between the head of the medial epicondyle of the humerus and the ulnar head of the coronoid process of the ulna [1].

The development of pronator teres syndrome can be triggered by rapid, repetitive gripping and pronating movements that induce hypertrophy of the pronator teres, worsened by fibrosis of the biceps aponeurosis [2].

Anterior interosseous nerve neuropathy is an isolated lesion of the anterior interosseous nerve, the most common cause of which is neuralgic amyotrophy, representing an inflammatory neuropathy [3,31,32].

Compression-ischemic neuropathy of the median nerve by Struthers' ligament is a proximal median nerve lesion resulting from nerve trunk compression by a ligament extending from the medial epicondyle to a bone spur or supracondylar process (apophysis). Due to the accessory process, the median nerve is displaced and stretched, making it vulnerable to injury, most often against the background of systemic vasculitis [33]. Isolated cases have been reported in children associated with concomitant calcification of the flexor digitorum superficialis and the presence of a congenital anomaly (Struthers' ligament and a supracondylar process) [34].

Also, in rare cases in children with congenital constriction ring syndrome, a proximal and/or distal median nerve lesion may be observed, sometimes combined with a lesion of the radial and/or ulnar nerves [34].

1.2.2 Etiology and pathogenesis of ulnar nerve mononeuropathy

The nerve is formed by roots C₈–Th₁, after which the axons pass into the lower trunk and medial cord of the brachial plexus. In the arm, the nerve runs together with the median nerve and brachial artery.

The most frequent compression sites are the elbow region and Guyon's canal. Causes of ulnar nerve compression at the elbow level may include nerve traction during prolonged elbow flexion, trauma, nerve compression in the cubital tunnel or retroepicondylar groove, elbow arthritis, synovitis, and ganglions [6,34]. Sometimes ulnar nerve neuropathy may be associated with ulnar nerve subluxation, though it should be noted that subluxation can be asymptomatic [4,35].

An association between ulnar nerve neuropathy and smoking is hypothesized; at the same time, no correlation was found between ulnar nerve neuropathy and body weight or alcohol consumption [36,37].

At the wrist level, the ulnar nerve divides into a superficial sensory branch and a deep motor branch. The causes of ulnar nerve compression at the level of Guyon's canal and the hand include external and internal etiologic factors. External factors may include repeated trauma to the wrist when working with tools or riding a bicycle, but internal factors can also occur, such as space-occupying lesions in the area of Guyon's canal or ganglions [38–42].

In pediatric practice, ulnar nerve subluxation is more common in adolescent and teenage years. Symptoms appear upon constant contact of the nerve trunk with the medial epicondyle. Compression ulnar neuropathy is more characteristic of long-term immobilized patients [43], and less frequently of athletes [44]. The nerve is formed by roots C₈–Th₁, after which the axons pass into the lower trunk and medial cord of the brachial plexus. In the arm, the nerve runs together with the median nerve and brachial artery.

The most frequent compression sites are the elbow region and Guyon's canal. Causes of ulnar nerve compression at the elbow level may include nerve traction during prolonged elbow flexion, trauma, nerve compression in the cubital tunnel or retroepicondylar groove, elbow arthritis, synovitis, and ganglions [6,35]. Sometimes ulnar nerve neuropathy may be associated with ulnar nerve subluxation, though it should be noted that subluxation can be asymptomatic [4,36].

An association between ulnar nerve neuropathy and smoking is hypothesized; at the same time, no correlation was found between ulnar nerve neuropathy and body weight or alcohol consumption [37,38].

At the wrist level, the ulnar nerve divides into a superficial sensory branch and a deep motor branch. The causes of ulnar nerve compression at the level of Guyon's canal and the hand include external and internal etiologic factors. External factors may include repeated trauma to the wrist when working with tools or riding a bicycle, but internal factors can also occur, such as space-occupying lesions in the area of Guyon's canal or ganglions [39–43].

In pediatric practice, ulnar nerve subluxation is more common in adolescent and teenage years. Symptoms appear upon constant contact of the nerve trunk with the medial epicondyle. Compression ulnar neuropathy is more characteristic of long-term immobilized patients [44], and less frequently of athletes [45].

1.2.3 Etiology and pathogenesis of radial nerve mononeuropathy

The radial nerve has several potential compression sites:

Compression in the axillary region

The most common cause of radial nerve compression in this area is the improper use of crutches, the so-called "crutch palsy" syndrome [46, 47].

Rare variants include compression in the area where the nerve passes anterior to the subteres, teres major, and latissimus dorsi muscles, associated with muscular developmental anomalies [48].

Also, a rare variant of the origin of the subscapular artery perforating the radial nerve is possible in this area. In this case, the radial nerve forms a loop around the artery, which can lead to vasoneural conflict [49].

Compression of the radial nerve in the area of entry into the spiral groove is possible, which is a triangular space bounded by the long head of the triceps medially, the teres major superiorly, and the lateral head of the triceps and the humerus laterally [50]. Compression at this site may be predisposed to by the presence of fibrous arcades between the long and lateral heads of the triceps [50, 51], as well as hypertrophy of the long head of the triceps in professional athletes—tennis players, kickboxers, bodybuilders [50, 52, 53].

Isolated case reports exist of an abnormally high origin of the superficial branch of the radial nerve in the axillary region: in the described cases, this branch may pass through the quadrangular space together with the axillary nerve and the posterior circumflex humeral artery and become involved in the pathological process during stenosis of this space [54].

Compression in the humeral shaft region

Nerve compression at the level of the spiral groove during sleep, the so-called "Saturday night palsy" or "honeymoon palsy" syndrome [55].

Compression from the application of a tourniquet due to incorrect selection of its application site and fixation method [56–58].

Compression of the radial nerve at the site of its passage through the lateral intermuscular septum distal to the lower attachment point of the deltoid muscle to the humerus [59]. Nerve damage at this site is predisposed to by individual anatomical features of the lateral intermuscular septum with a narrow opening at the site of radial nerve passage, variable attachment of the septum to the humerus, or secondary changes in its anatomy due to trauma [60–63]. Compression of the radial nerve by fibrous arches of the lateral head of the triceps at the exit from the spiral groove is also encountered [64].

Compression in the radial tunnel region

Currently, there is no consensus regarding the boundaries of this tunnel, nor whether this tunnel should be distinguished as a separate structure. The most common viewpoint is that this tunnel is formed by three muscles looping over the nerve: the brachioradialis, and the extensor carpi radialis longus and brevis. In this region, the brachialis muscle lies medially to the nerve, and the lateral epicondyle of the humerus lies posteriorly [65–68]. Compression of the nerve is possible in this area under the brachioradialis muscle, as well as under the extensor carpi radialis brevis. Precipitating factors in this case are significant physical loads on the forearm and arm muscles [69], as well as developmental anomalies of the brachioradialis muscle in the form of a higher origin or an accessory muscle belly [70, 71].

Compression of the forearm region

Compression of the deep branch of the radial nerve in the region of the supinator muscle—supinator syndrome or posterior interosseous nerve syndrome. This is predisposed to by an anatomical feature in the form of a tendinous ring at the site of emergence of the nerve trunk from beneath the superficial head of the supinator—the arcade of Frohse, which is observed in 60–70% of cases [72–74]. People whose professional activity is associated with repetitive, uniform movements of the forearms—tennis players, violinists, etc.—are most susceptible to radial nerve compression in this area [69, 75]. Compression of the nerve in the supinator region due to vasoneural conflict with recurrent branches of the radial artery is also encountered [76]. Among non-compressive causes of posterior interosseous nerve syndrome, the most common is neuralgic amyotrophy in both adults and children [77–80].

Compression of the superficial branch of the radial nerve—Wartenberg's syndrome or cheiralgia paresthetica. A frequent cause of lesions of the superficial branch is compression by a wristwatch strap or handcuffs. Entrapment of the superficial branch of the nerve between the tendons of the brachioradialis and the extensor carpi radialis longus is also possible, which is significantly promoted by wrist pronation and ulnar deviation, for example, during prolonged work with a computer mouse [65]. Chronic nerve compression is possible after surgery to create an arteriovenous fistula between the radial artery and the cephalic vein during hemodialysis.

1.2.4 Etiology and pathogenesis of axillary nerve mononeuropathy

Acute trauma: anterior dislocation of the humeral head, proximal humeral or scapular fractures. Risk factors: time elapsed from dislocation to reduction, presence of hematoma, age, birth trauma [81, 82].

Blunt trauma: blunt impact to the shoulder, contact sports injuries, falls onto the shoulder [83, 84].

Improper (non-physiological) limb position during sleep or general anesthesia [85].

Quadrangular space syndrome: a neurovascular entrapment syndrome manifested by pain and paresthesias in the arm (their distribution does not correspond to anatomical zones), and tenderness in the shoulder area [86].

Surgical interventions: internal fixation of the humerus with hardware, arthroscopy [87, 88].

1.2.5 Etiology and pathogenesis of musculocutaneous nerve mononeuropathy

The musculocutaneous nerve (MCN) is mixed in function, containing fibers from spinal nerve roots C₅, C₆, and C₇. In most cases, it originates from the lateral cord of the brachial plexus, but sometimes it may derive from the superior trunk, emerging in the axilla, piercing the coracobrachialis muscle in the arm and innervating it, as well as the biceps brachii and brachialis muscles, then, passing through the brachial fascia at the level of the elbow crease lateral to the tendon of the biceps brachii, it gives off the lateral cutaneous nerve of the forearm (LCNF), which provides sensory innervation to the lateral surface of the forearm. Most compressive lesions of the MCN occur at the site of nerve passage through the coracobrachialis muscle (proximal to the biceps brachii and brachialis) due to its hypertrophy or strong muscular contraction leading to mechanical and/or ischemic nerve damage [89, 90], and in rare cases due to compression by an osteochondroma of the humerus [91, 92] and after prolonged sleep in an awkward position [93]. Compression of the MCN resulting from hypertrophy or strong muscular tension is observed in armwrestlers, weightlifters, and bodybuilders [89, 94–96], in boxers and kickboxers after repeated punches [96], and in rare cases occurs after a single bout of excessive physical exertion, most often provoked by persistent training and repetitive stereotypical movements in the form of elbow flexion and forearm pronation [97].

Lesions of the LCNF occur at the forearm level most often as a result of prolonged compression, for example, carrying a heavy bag at the level of the elbow crease [98].

1.2.6 Etiology and pathogenesis of brachial plexus branch mononeuropathy

Pathogenetic mechanisms are associated with compression of brachial plexus branches in anatomical areas where the nerve can be compressed by surrounding tissues (bone, cartilage, tendinous, or muscular structures), as well as direct traumatic injury [8]. A feature of this region is a large number of anatomical anomalies, such as an accessory cervical rib, elongation of the transverse process of the C6 and/or C7 vertebra, accessory scalene muscles, anomalous origin of thyrocervical trunk arteries, dorsal scapular artery, anomalous course of the omohyoid muscle, etc. [99]. At the same time, it is extremely important to differentiate isolated lesions of brachial plexus branches from involvement of its main trunks and cords [100]. Impairment of nerve function is accompanied by motor and/or sensory deficits in the corresponding innervation zone, which subsequently determines the strategy and tactics of treatment.

1.2.7 Etiology and pathogenesis of intercostal nerve mononeuropathy

The pathogenetic mechanisms of intercostal mononeuropathy are mainly associated with mechanical compressive impact on the nerve (post-traumatic and post-inflammatory changes, neoplasms, fibrosis) [101, 102]. Another fairly common cause of this condition is herpetic infection (Herpes zoster) [101, 103]. Development of the lesion against the background of diabetes mellitus (diabetic thoracoabdominal neuropathy) is possible [104]. A relatively rare form of intercostal nerve lesion is ACNE syndrome (anterior cutaneous nerve entrapment syndrome), caused by compression of the lower intercostal nerves (T7–T11) in the lateral regions of the rectus abdominis muscle [105]. Sarcoidosis can also be classified among relatively rare causes [106].

1.2.8 Etiology and pathogenesis of sciatic nerve mononeuropathy

Main causes of sciatic mononeuropathy:

Infectious factors: abscess [107]: tubo-ovarian, pelvic abscess, psoas abscess

Inflammation: sacroiliitis [108]

Nerve tumor: neurofibroma [109], schwannoma [107], malignant peripheral nerve sheath tumor [109], intraneural perineurioma [110, 111], neurolipomatosis [110], neurolipoma [107, 109]

Sciatic nerve compression: rhabdomyosarcoma [110], leiomyosarcoma [112], lipoma [113], metastases [107].

Vascular causes: arteriovenous malformation [114], aneurysm (persistent sciatic artery, popliteal artery, hypogastric artery, common iliac artery) [115–117], iliac artery occlusion [118], vasculitis [118], gluteal varicose veins [119], ischemia [120], deep vein thrombosis [121].

Gynecological disorders: endometriosis [122, 123].

Other causes: piriformis syndrome [124], radiation therapy [125, 126], cryoglobulinemia [127], hereditary neuropathy with liability to pressure palsies [128].

Sciatic mononeuropathy in children is one of the most common neuropathies. In the past, the main cause was improper gluteal intramuscular injection technique, but nowadays such cases are reported much less frequently. The main causes of sciatic nerve injury in children are trauma, prenatal compression (especially in the setting of decreased fetal activity, oligohydramnios, uterine structural anomalies), and compression in the ischial tuberosity region due to prolonged sitting on hard surfaces against the background of relative underdevelopment of the gluteal muscles [34].

1.2.9 Etiology and pathogenesis of peroneal nerve mononeuropathy

The most frequent cause of peroneal mononeuropathy is compression of the common peroneal nerve at the fibular head level [129].

Causes of common peroneal nerve compression at this level may include prolonged immobilization during anesthesia [130], brace wear [131], habitual leg-crossing posture, or compression during sleep associated with alcohol intoxication [10]. Chronic compression of the nerve trunk by a ganglion or synovial cyst [132, 133], fibular osteochondroma, or vascular malformation [134], as well as an intraneural or extraneural neoplasm [135–137], is also possible. Other causes of mononeuropathy may include compression by a fibrous band at the fibular tunnel level [137] and nerve overstretching during squatting [138]. Predisposing factors can include asthenic body habitus, rapid weight loss [139, 140], and diabetes mellitus [141].

Another site of lesion is compression of the superficial peroneal nerve in the calf, ankle, or foot [142].

1.2.10 Etiology and pathogenesis of tibial nerve mononeuropathy

Pathogenetic mechanisms are associated with tibial nerve compression in anatomical sites where the nerve can be compressed by surrounding tissues (bone, cartilage, tendinous, or muscular structures). A specific feature of this region is the presence of the tarsal canal, where the nerve can be compressed by the flexor retinaculum or a synovial cyst [143]. Impairment of nerve function is accompanied by motor and sensory disturbances in the corresponding innervation zone, which subsequently determines the treatment strategy and tactics [144]. Symptoms of Morton's neuroma often occur during or after the forefoot has experienced significant overload during walking, standing, jumping, or running [145]. Compression occurs at the distal part of the transverse metatarsal ligament during dorsiflexion of the foot. This condition is usually caused by wearing uncomfortable, tight shoes with a narrow toe box and high heels, which causes the nerve to be squeezed between the toes, eliciting discomfort and sharp pain. The disease occurs predominantly in women [146].

1.2.11 Etiology and pathogenesis of femoral nerve mononeuropathy

The susceptibility of the femoral nerve to involvement in the pathological process is due to its topographical and anatomical features, which create conditions for nerve trunk compression at multiple levels.

The femoral nerve originates from the lumbar plexus, arising from the ventral rami of the L_II-L_IV spinal nerves.

Initially, the femoral nerve lies posterior to the psoas major muscle, then emerges from beneath its lateral border and rests in the groove between the psoas major and iliacus muscles. Here it is covered superiorly by the iliac fascia, and being in a tight and fixed space at this site, it can be subject to compression.

The nerve leaves the pelvic cavity by passing through the osteofibrous tunnel formed by the inguinal ligament (anteriorly), the pubic rami, and the ilium, which is also a potential site of femoral nerve compression. Beneath the ligament, the nerve passes through the muscular lacuna and lies beneath the layers of the fascia lata of the thigh. Here it is located in the femoral triangle, bounded superiorly by the inguinal ligament, laterally by the sartorius muscle, and medially by the adductor longus muscle. Upon emerging into the thigh in close proximity to the hip joint capsule, it divides into muscular and cutaneous branches, as well as the saphenous nerve [15, 16, 147].

Factors of retroperitoneal femoral nerve compression may include:

- inflammation and myofascial pain syndrome of the psoas major and/or iliacus muscles resulting from biomechanical overload (occupational or athletic) [148, 149];

- rare but prognostically much more unfavorable causes of femoral nerve compression can be tumors (lymphoma, sarcoma), abscesses, and hematomas (caused by hemophilia, anticoagulant therapy, etc.). Cases of nerve injury associated with common iliac and femoral artery aneurysms, as well as arteriovenous malformations, have been described [150, 151].

Factors of femoral nerve compression beneath the inguinal ligament are:

- compression of the femoral nerve by the ligament during a prolonged forced position with hyperextension, or excessive abduction, flexion, and external rotation of the hip (e.g., during gynecological surgeries, childbirth, etc.) [129, 152];

- nerve compression can be caused by a femoral hernia, inguinal lymphadenopathy, or a femoral artery aneurysm;

- it occurs as a consequence of surgery in the nerve region, in particular following hip joint manipulations.

Local compression of the nerve trunk induces intraneural ischemia and impairs intraneural venous circulation, microfluidics, and consequently edema. Persistent edema can lead to intraneural and extraneural fibrous changes. It is believed that extraneural fibrous changes account for the reduced gliding of compressed nerves during limb movements. Prolonged ischemia and mechanical impairment trigger subsequent effects such as focal demyelination and, ultimately, axonal degeneration. Along with demyelination, the architecture of the nodes of Ranvier changes, and the activity of existing ion channels is altered. Such changes are linked to spontaneous ectopic generation of action potentials, which may contribute to the onset of spontaneous pain or the appearance of symptoms elicited by Tinel's sign [153–155].

1.2.12 Etiology and pathogenesis of lateral femoral cutaneous nerve mononeuropathy

Pathogenetic mechanisms of lateral femoral cutaneous mononeuropathy are primarily associated with mechanical compressive impact on the nerve, leading to impaired function. The most frequent causes of mononeuropathy are compression beneath the inguinal ligament and at the level of the anterior superior iliac spine [17]. Compression of the nerve trunk can occur due to bony changes resulting from periostitis and iliac fractures, retroperitoneal hematoma, pelvic organ neoplasms, wearing a tight belt, tight trousers, or other clothing items causing compression in the region of the anterior superior iliac spine. Predisposing factors include ascites, diabetes mellitus, obesity, and pregnancy [156, 157].

1.3 Epidemiology of the Disease or Condition

1.3.1 Epidemiology of median nerve mononeuropathy

Carpal tunnel syndrome is the most common among entrapment neuropathies of peripheral nerves. It occurs in 1-5% of the general population and ranks sixth in the occupational disease registry [22, 158]. Among specific occupational groups, the prevalence of carpal tunnel syndrome can be up to 14.5% [159–161]. The incidence of carpal tunnel syndrome is 150 per 100,000 population. It occurs 3-6 times more frequently in women than in men, and its prevalence and severity increase with age [18, 21]. The incidence in children does not exceed 0.2% of all carpal tunnel syndrome cases [34].

Pronator teres syndrome is a rare clinical condition. It is more common in men; occupational risk factors include cycling and tennis, and it is frequently encountered in musicians and dentists [33, 162].

Anterior interosseous nerve neuropathy is a rare clinical condition that also occurs in the pediatric population [163, 164].

Proximal median nerve compression beneath Struthers' ligament is a rare clinical condition, occurring in 0.5-1% of cases [33].

1.3.2 Epidemiology of ulnar nerve mononeuropathy

Ulnar neuropathy at the elbow is the most common compression-ischemic neuropathy after carpal tunnel syndrome. It includes ulnar nerve compression at the retroepicondylar groove (accounting for 75% of cases) and compression at the cubital tunnel (only 25%), which is why the term ulnar neuropathy at the elbow is preferred over cubital tunnel syndrome [4]. There is still no consensus on the anatomical structure of the cubital tunnel, as some authors prefer to include the retroepicondylar groove as part of the cubital tunnel [165].

Ulnar neuropathy affects approximately 6% of the population [81]. Ulnar neuropathy at the elbow is more common in men than in women [82], averaging 24.7 cases per 100,000 population [166]. According to various studies, the prevalence of cubital tunnel syndrome ranges from 25.2 to 32.7 per 100,000 population in men and from 18.9 to 17.2 per 100,000 population in women [166, 167].

Ulnar neuropathy at Guyon's canal is significantly less common, and the reliable prevalence of this pathology has not been established.

Non-traumatic lesions of the ulnar nerve in other segments are extremely rare.

1.3.3 Epidemiology of radial nerve mononeuropathy

Radial neuropathy is one of the most common compression-ischemic neuropathies, second only to carpal tunnel syndrome, cubital tunnel syndrome, Morton's metatarsalgia, and meralgia paresthetica. The incidence is 1.5–3 cases per 100,000 adults, and it is more frequent in men [167].

1.3.4 Epidemiology of axillary nerve mononeuropathy

Data regarding the epidemiology of axillary mononeuropathy are lacking.

1.3.5 Epidemiology of musculocutaneous nerve mononeuropathy

Isolated musculocutaneous nerve lesions are rare, and published epidemiological data are absent.

Most case report-based publications report proximal nerve involvement at the site of its passage through the coracobrachialis muscle [90].

Musculocutaneous nerve lesions are observed more frequently in men than in women [98]. The peak incidence occurs between 25 and 45 years of age, though it can occur in any age group [98]. In most cases, the condition is unilateral and predominantly affects the dominant hand. Bilateral musculocutaneous nerve lesions are extremely rare [168].

1.3.6 Epidemiology of brachial plexus branch mononeuropathy

According to a large epidemiological study, the incidence of compression neuropathies of the brachial plexus is 1.2% [8, 99, 100], with a predominance of young male patients. Compression neuropathies affecting individual branches without involving the main trunks account for only 0.38%, with the axillary and suprascapular nerves accounting for a higher proportion of these [169]. Isolated compression of the dorsal scapular nerve and long thoracic nerve is extremely rare [169].

1.3.7 Epidemiology of intercostal nerve mononeuropathy

Data on the epidemiology of intercostal mononeuropathy are absent.

1.3.8 Epidemiology of sciatic nerve mononeuropathy

Sciatic mononeuropathy is the second most frequent lower extremity mononeuropathy. Its prevalence in the general population ranges from 12% to 27% [170].

1.3.9 Epidemiology of peroneal nerve mononeuropathy

Precise data on the epidemiology of peroneal mononeuropathy are lacking.

1.3.10 Epidemiology of tibial nerve mononeuropathy

Literature results regarding the frequency of tibial compression neuropathies are contradictory. According to Rinkel W.D. (2018), the frequency of tibial nerve compression at the tarsal tunnel is 26.5% in healthy volunteers and 44.9% in patients with diabetes mellitus; however, this study used clinical evaluation methods without instrumental confirmation [143]. According to other sources, the incidence of tibial nerve entrapment in the tarsal tunnel is significantly lower [171]. Approximately 20–40% of cases are idiopathic, and up to 10% result from inflammatory conditions such as osteoarthritis, tenosynovitis, and rheumatoid arthritis [172].

1.3.11 Epidemiology of femoral nerve mononeuropathy

Data on the epidemiology of the disease are absent.

1.3.12 Epidemiology of lateral femoral cutaneous nerve mononeuropathy

The incidence is approximately 3–4 cases per 10,000 per year. It occurs in all age groups, but most frequently in the 4th and 5th decades of life [173].

1.4 Features of Coding the Disease or Condition

1.4.1 Coding features of median nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

Among median nerve neuropathies, only carpal tunnel syndrome (G56.0) is classified separately in ICD-10; all other median nerve neuropathies are coded as G56.1 – Other lesions of median nerve.

1.4.2 Coding features of ulnar nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G56.2 – Lesion of ulnar nerve

1.4.3 Coding features of radial nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G56.3 – Lesion of radial nerve.

1.4.4 Coding features of axillary nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G58.8 – Other specified mononeuropathies.

1.4.5 Coding features of musculocutaneous nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G56.8 – Other mononeuropathies of upper limb

G56.9 – Mononeuropathy of upper limb, unspecified

G58.8 – Other specified mononeuropathies

G58.9 – Mononeuropathy, unspecified

G59.8* – Other mononeuropathies in diseases classified elsewhere

1.4.6 Coding features of brachial plexus branch mononeuropathies according to the International Statistical Classification of Diseases and Related Health Problems

G54.0 – Brachial plexus disorders

G54.2 – Cervical root disorders, not elsewhere classified

G54.5 – Neuralgic amyotrophy

G54.8 – Other nerve root and plexus disorders

G54.9 – Nerve root and plexus disorder, unspecified

1.4.7 Coding features of intercostal nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G54.3 – Thoracic root disorders, not elsewhere classified

G58.8 – Other specified mononeuropathies

1.4.8 Coding features of sciatic nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G54.4 – Lumbosacral root disorders, not elsewhere classified

G54.1 – Lumbosacral plexus disorders

G57.0 – Lesion of sciatic nerve

1.4.9 Coding features of peroneal nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G57.3 – Lesion of lateral popliteal nerve

1.4.10 Coding features of tibial nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G57.6 – Lesion of plantar nerve

G57.4 – Lesion of tibial nerve

1.4.11 Coding features of femoral nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems.

G57.2 – Lesion of femoral nerve

1.4.12 Coding features of lateral femoral cutaneous nerve mononeuropathy according to the International Statistical Classification of Diseases and Related Health Problems

G58.8 – Other specified mononeuropathies

1.5 Classification of the disease or condition

1.5.1 Classification of median nerve mononeuropathy

No universally accepted classification for median nerve lesions has been developed.

1.5.2 Classification of ulnar nerve mononeuropathy

There is no universally accepted classification for ulnar neuropathy; generally, clinicians distinguish the most common ulnar neuropathy at the elbow and neuropathy at Guyon's canal. Other sites of ulnar nerve compression are rare.

At least 13 classifications of ulnar neuropathy at the elbow based on severity have been proposed, with Goldberg's classification being one of the most commonly used [174]. Grade 1 includes mild sensory disturbances (paresthesias, hypesthesia) without motor deficits; Grade 2A involves moderate sensory deficits with mild muscle weakness without significant atrophy; Grade 2B entails moderate weakness; and Grade 3 includes marked sensory disturbances and pronounced atrophy. It is also acceptable to use 3 grades of severity: 1 – mild, 2 – moderate, 3 – severe or terminal [175].

1.5.3 Classification of radial nerve mononeuropathy

There is no universally accepted classification.

1.5.4 Classification of axillary nerve mononeuropathy

There is no universally accepted classification for axillary mononeuropathy.

1.5.5 Classification of musculocutaneous nerve mononeuropathy

No universally accepted classification has been developed.

1.5.6 Classification of brachial plexus branch mononeuropathy

• Long thoracic nerve lesion

• Dorsal scapular nerve lesion

• Suprascapular nerve lesion

1.5.7 Classification of intercostal nerve mononeuropathy

There is no universally accepted classification for intercostal mononeuropathy.

1.5.8 Classification of sciatic nerve mononeuropathy

There is no generally accepted classification of sciatic nerve lesions.

1.5.9 Classification of peroneal nerve mononeuropathy

There is no generally accepted classification of fibular nerve mononeuropathy.

1.5.10 Classification of tibial nerve mononeuropathy

There is no generally accepted classification of tibial nerve lesions.

1.5.11 Classification of femoral nerve mononeuropathy

There is no generally accepted classification of femoral nerve lesions.

1.5.12 Classification of lateral femoral cutaneous nerve mononeuropathy

There is no generally accepted classification of lateral femoral cutaneous nerve mononeuropathy.

1.6 Clinical presentation of the disease or condition

1.6.1 Clinical presentation of median nerve mononeuropathy

The clinical presentation is diverse, depends on the severity of the process, and includes a number of symptoms frequently described by patients that lead to the suspicion of median nerve mononeuropathy [18,21,22,176].

Unlike in adults, the clinical presentation of carpal tunnel syndrome in children has certain features. They more frequently present with clumsiness in the hands and thenar muscle atrophy rather than sensory disturbances (including pain and tingling) [177]. Pain (including nocturnal pain) combined with numbness and paresthesias is much less frequently the primary symptom, which is more characteristic of familial or idiopathic cases and older children [177,178].

1.6.2 Clinical presentation of ulnar nerve mononeuropathy

Ulnar neuropathy at the elbow level implies hypesthesia of the ulnar area of the hand in the initial stage (grade 1 severity); muscle weakness of the ulnar muscles joins at moderate severity (grades 2A and 2B); and muscle atrophy joins the previous symptoms at the terminal stage (grade 3 severity) [174]. Patients may also complain of pain in the elbow and forearm region [35,165].

Ulnar neuropathy at the Guyon's canal level manifests with sensory and motor symptoms depending on the level of the lesion. When the ulnar nerve is affected proximal to its division into the superficial and deep branches, a clinical picture with both sensory and motor symptoms develops. When only the superficial branch is affected, the clinical picture shows sensory disturbances (hypesthesia of digits 4–5) in the absence of motor ones. When only the deep branch is affected, weakness and atrophy occur without sensory disturbances [5]. It is important to note that in lesions of the superficial branch of the ulnar nerve in Guyon's canal, sensation in the hypothenar area remains intact, which distinguishes the clinical picture from a lesion at the elbow level [5].

1.6.3 Clinical presentation of radial nerve mononeuropathy

A lesion of the radial nerve in the axillary region is characterized by paresis of the finger and wrist extensor muscles, paresis of the supinator and brachioradialis muscles, as well as paresis of the triceps brachii muscle. The triceps tendon reflex is reduced or absent. Sensory disturbances are noted as decreased sensation on the posterior aspect of the arm, forearm, and the posterolateral aspect of the hand.

A lesion of the radial nerve in the diaphyseal region leads to paresis of the wrist and forearm extensors, paresis of the supinator and brachioradialis muscles with preserved strength in the triceps brachii muscle. Sensory disturbances in the area of the posterior forearm and posterolateral hand are characteristic.

A lesion in the radial tunnel region is characterized by pain along the course of the radial tunnel due to nerve irritation by muscles, in particular the extensor carpi radialis brevis. The pain syndrome becomes more pronounced during finger extension due to increased compression of the nerve trunk by the muscle. At the same time, muscle paresis or objective sensory disturbances in the radial nerve innervation zone are typically not detected [179].

With a lesion in the forearm region, two clinical syndromes may develop:

Posterior interosseous nerve syndrome, characterized by paresis of the wrist and finger extensor muscles. In cases of neuralgic amyotrophy, neuropathic pain precedes or occurs simultaneously with the motor deficit [77,78,180].

Superficial radial nerve syndrome (Wartenberg's syndrome). This is characterized by sensory disturbances in the form of hypesthesia, hyperesthesia, or paresthesia, as well as burning pain in the posterolateral aspect of the hand [181].

1.6.4 Clinical presentation of axillary nerve mononeuropathy

Clinically, an axillary nerve lesion is characterized by the patient's inability to abduct the arm to the horizontal level, which is explained by the development of paresis and atrophy of the deltoid muscle; sensory disturbances on the skin of the outer aspect of the upper third of the arm may also occur (and can be absent). If neuralgic amyotrophy involving the axillary nerve develops, an acute neuropathic pain syndrome occurs concurrently with the development of deltoid muscle atrophy. A feature of the clinical picture is also the intensification of pain upon passive abduction of the limb [182].

1.6.5 Clinical presentation of musculocutaneous nerve mononeuropathy

Two compression syndromes of the musculocutaneous nerve are distinguished [90]:

1. Lesion of the musculocutaneous nerve prior to its division into the lateral cutaneous nerve of the forearm, causing a mixed motor and sensory deficit.

Clinical diagnosis of proximal musculocutaneous nerve lesion is suspected in the presence of biceps weakness without involvement of the deltoid muscle. This results in weakness of elbow flexion and supination, combined with hypotrophy of the biceps brachii muscle. Sensory disturbances on the radial side of the forearm may also occur.

2. Lesion of the lateral cutaneous nerve of the forearm – a lesion of the distal sensory part of the nerve, causing only sensory disturbances on the lateral surface of the forearm. The sensory part of the nerve is compressed at the level of the elbow crease. Patients are troubled by pain and a burning sensation in the antecubital fossa and along the lateral aspect of the forearm. Tenderness is noted upon palpation at the site of nerve compression – in the antecubital fossa slightly lateral to the biceps tendon. Symptoms are aggravated by pronation-supination of the forearm and by flexion-extension at the elbow joint. Moderately pronounced neurodystrophic changes in the elbow joint and manifestations of lateral epicondylitis may be observed.

1.6.6 Clinical presentation of brachial plexus branch mononeuropathy

The clinical picture of suprascapular nerve neuropathy consists of hypotrophy (atrophy) of the supraspinatus and infraspinatus muscles [183]. Tenderness is often detected in the projection of the scapular notch, localized posterior to the clavicle in the trapezius muscle overlying the scapular spine [184,185]. A decrease in the strength of external rotation and abduction compared to the contralateral side is frequently determined. Compression of the distal part of the suprascapular nerve in the spinoglenoid notch leads to isolated atrophy of the infraspinatus muscle [183]. Tenderness in the posterior shoulder joint above the spinoglenoid notch and isolated reduction in external rotation strength may occur [185]. A lesion of the long thoracic nerve leads to the development of the scapular winging phenomenon due to weakness of the serratus anterior muscle; sensory disturbances are not characteristic. The clinical picture of a dorsal scapular nerve lesion also consists of scapular winging due to lateral displacement of its medial border resulting from weakness of the rhomboid muscles. Hypotrophy of the rhomboid muscles is detected predominantly using functional tests and is barely noticeable at rest. A lesion of the upper trunk of the brachial plexus leads to involvement of the supraspinatus, infraspinatus, deltoid, and biceps brachii muscles, and in the case of high involvement of the C5 and C6 spinal nerves, the rhomboid and serratus anterior muscles. Isolated middle trunk involvement can be asymptomatic; when combined with upper trunk lesions, paralysis of the brachioradialis, triceps brachii, and wrist and finger extensors is added. Lower trunk lesion (Klumpke paralysis) involves the pectoralis major, flexor carpi ulnaris, and the intrinsic hand muscles. In rare cases, the diaphragm may be involved [186].

1.6.7 Clinical presentation of intercostal nerve mononeuropathy

Intercostal nerve mononeuropathy frequently manifests as a sudden onset of acute burning or piercing pain, which may be associated with paresthesia and often worsens with inspiration, localized in the chest area within the innervation zone of the intercostal nerves. A girdle-like character of pain and radiation to the abdominal region are possible. When the lesion is localized below the T7 level, the pain syndrome is usually localized in the abdominal wall [105].

1.6.7 Clinical presentation of sciatic nerve mononeuropathy

The clinical picture of a sciatic nerve lesion consists of paresis or plegia of the foot extensors and flexors, the posterior thigh muscle group (semimembranosus, semitendinosus, and biceps femoris muscles), numbness and paresthesia, as well as neuropathic pain in the nerve's innervation area – the plantar and dorsal aspects of the foot, and the lateral surface of the lower leg [187].

1.6.9 Clinical presentation of peroneal nerve mononeuropathy

The clinical picture consists of acute or gradually progressive weakness of the muscles providing extension of the foot and toes, which leads to a steppage gait [131], weakness of foot eversion, and sensory disturbances in the fibular nerve innervation zone – along the lateral aspect of the lower leg, the dorsum of the foot, and the first web space [188]. Neuropathic pain is atypical for fibular mononeuropathy and develops rarely [188]. Tinel's sign may be present (percussion over the fibular head can provoke pain and paresthesia in the fibular nerve innervation area) [189].

1.6.10 Clinical presentation of tibial nerve mononeuropathy

A sensation of dull aching pain in the ankle region, sometimes shooting pain, dysesthesia along the medial aspect of the foot, and a burning sensation in this area [13]. Pain may worsen with prolonged standing, walking, or squatting. Clinical evaluation includes digital compression of the tarsal tunnel point with simultaneous dorsiflexion of the foot at the ankle joint. The clinical presentation of sural neuropathy includes pain and burning along the posterior aspect of the lower leg, radiating along the lateral aspect of the foot. Tenderness may occasionally be lancinating. Interdigital nerve compression is characteristically associated with burning pain on the plantar aspect of the foot, radiating to the corresponding digits III–IV. Sensations of shooting pain into the plantar aspect of the foot and digits are noted. Pain sometimes worsens when walking in tight shoes (improves after removing shoes and foot massage). Pain may intensify upon foot compression or palpation of the interdigital space. Morton neuroma may be asymptomatic in 33%–54% of cases [145].

The clinical presentation of tibial nerve compression in the tarsal tunnel consists of sensory disturbances along the medial and plantar aspects of the foot, and shooting pain into the foot occurring during walking or external rotation of the foot [143].

1.6.11 Clinical presentation of femoral nerve mononeuropathy

The clinical picture of femoral neuropathy depends on the site and degree of compression, the rate of compression development, the presence or absence of concomitant vascular compressive lesions, the premorbid and comorbid background, and the age and individual characteristics of the patient.

There are several potential sites of FN compression. The two most frequent locations are the iliopsoas region and the area beneath the inguinal ligament.

Retroperitoneal femoral nerve injury

In typical cases, femoral nerve injury in the iliopsoas region leads to the development of motor and sensory deficits throughout its entire innervation territory. However, anatomical variations in the formation and course of the femoral nerve (e.g., high division of the femoral nerve into muscular branches and the saphenous nerve, the trunks of which may run separately) in some cases are accompanied by predominant or even isolated involvement of the sensory or motor portion of this nerve, or a patchy distribution of motor and sensory deficits.

The initial symptoms are usually neuropathic pain in the groin, anterior thigh, and anteromedial lower leg.

Motor deficits are caused by paresis of the iliacus, psoas major, and psoas minor muscles and manifest as impaired hip flexion with external rotation and impaired trunk elevation from a supine or sitting position with fixed extremities, as well as paresis of the quadriceps femoris, which additionally impairs lower limb extension at the knee joint; walking, running, and especially climbing stairs become difficult. Patients tend not to flex the leg because they cannot extend it, and they fix the limb in hyperextension at the knee joint, leading to an altered gait.

As a rule, a decrease in thigh circumference due to hypotrophy of the quadriceps and sartorius muscles is clearly noticeable.

Sensory deficits in the form of positive and/or negative disturbances are identified on the anterior and medial surfaces of the thigh, lower leg, and foot up to the base of the first digit.

Vasomotor and trophic disorders may develop.

Patients demonstrate positive tension signs: the Wassermann and Matskevich signs.

Decreased or absent knee jerk reflex is noted on the affected side.

Femoral nerve injury beneath the inguinal ligament

The clinical presentation is generally similar to that of retroperitoneal femoral nerve injury; however, iliopsoas paresis is absent.

In the advanced stage, the specific clinical pattern usually consists of a combination of pain with prominent positive and negative sensory deficits along the anterior and medial surfaces of the thigh, lower leg, and foot, as well as paresis of the quadriceps femoris with impaired knee extension and partial weakness of hip flexion.

Along with positive tension signs, tenderness over the midpoint of the inguinal ligament (the site of femoral nerve compression) and a positive Tinel test are detected.

Decreased or absent knee jerk reflex is noted on the affected side.

Clinical manifestations of neuropathic pain syndrome include a symptom complex of spontaneous and stimulus-dependent pain in the nerve innervation zone distal to the compression site (sometimes with proximal radiation of pain). Severe shooting, throbbing pain is usually intermittent, whereas burning, aching pain may be transient and periodically of high intensity. In many cases, pain worsens with physical exertion, prolonged static loading, or exposure to cold. Spontaneous pain is typically accompanied by allodynia, as well as static and dynamic hyperalgesia [14,65,190].

1.6.12 Clinical presentation of lateral femoral cutaneous nerve mononeuropathy

Clinical manifestations of lateral femoral cutaneous mononeuropathy include sensory disturbances (hyperesthesia, hypoesthesia, paresthesia), as well as, in some cases, neuropathic pain in the nerve's innervation territory (anterolateral thigh) [191].

2. Diagnostics, medical indications and contraindications for diagnostic methods

Diagnosis of median mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for median mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of ulnar mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for ulnar mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of radial mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for radial mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of axillary mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted diagnostic criteria for axillary mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of musculocutaneous mononeuropathy, medical indications and contraindications for diagnostic methods.

Generally accepted clinical and instrumental diagnostic criteria for musculocutaneous mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of brachial plexus branch mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted diagnostic criteria for brachial plexus branch mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of intercostal mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for intercostal mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of sciatic mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for sciatic mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of peroneal (fibular) mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for peroneal mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of tibial mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for tibial mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of femoral mononeuropathy, medical indications and contraindications for diagnostic methods

Generally accepted clinical and instrumental diagnostic criteria for femoral mononeuropathy have not been developed. The diagnosis is made on the basis of characteristic complaints, medical history, and physical and instrumental examination findings.

Diagnosis of lateral femoral cutaneous mononeuropathy, medical indications and contraindications for the use of diagnostic methods

No universally accepted clinical and instrumental criteria for the diagnosis of lateral femoral cutaneous mononeuropathy have been developed. The diagnosis is established based on characteristic complaints, anamnesis, physical examination, and instrumental findings.

2.1 Complaints and Anamnesis

2.1.1 History taking and complaints in median mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

Comment: based on the patient's complaints and symptoms, the Boston Carpal Tunnel Questionnaire has been developed to assess the severity of condition in patients with suspected carpal tunnel syndrome, which is preferred for use in diagnosis (Appendix G1) [194,195].

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.1.2 History taking and complaints in ulnar mononeuropathy

The disease has a slowly progressive, recurrent course, but the onset of symptoms is often acute, "overnight" [165]. For effective diagnosis and treatment, it is necessary to identify provoking factors causing nerve damage.

2.1.3 History taking and complaints in radial mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.1.4 History taking and complaints in axillary mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.1.5 History taking and complaints in musculocutaneous mononeuropathy

2.1.6 History taking and complaints in brachial plexus branch mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.1.7 History taking and complaints in intercostal mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.1.8 History taking and complaints in sciatic mononeuropathy

2.1.9 History taking and complaints in peroneal mononeuropathy

2.1.10 History taking and complaints in tibial mononeuropathy

2.1.11 History taking and complaints in femoral mononeuropathy

Comments: characterized by intense shooting, burning, or throbbing pain that can be transient and at times highly intense. In many cases, pain is exacerbated by physical or prolonged static exertion or by exposure to cold [16,65,149,206].

2.1.12 History taking and complaints in lateral femoral cutaneous mononeuropathy

Comment: to assess the severity of pain syndrome, it is advisable to use the visual analogue scale (VAS) and the DN4 neuropathic pain questionnaire (Appendices G3, G4) [192].

2.2 Physical Examination

2.2.1 Physical examination in median mononeuropathy

Carpal tunnel syndrome

Comment: in pediatric practice, sensory assessment can be difficult due to low compliance in children under 8 years of age. Incomplete myelination processes of peripheral nerves may account for the mildness of neuropathic pain syndrome [210].

Comment: provocation tests for carpal tunnel syndrome are listed in Table 1. Provocation tests for carpal tunnel syndrome. The results of provocation tests (Tinel's, Phalen's) in children with CTS, even with prolonged neural compression, may be negative, which necessitates mandatory additional instrumental examination [177].

Table 1. Provocation tests for carpal tunnel syndrome

* – a healthy person may also develop similar sensations, but not earlier than 1 minute later.

** – in 30-50% of cases, a false-positive result is possible [27].

Pronator teres syndrome

Comment: In case of a positive test, there is an increase in pain syndrome.

Anterior interosseous nerve syndrome

Comment: in anterior interosseous nerve syndrome, sensory disturbances are absent [163,164].

Proximal compression of the median nerve under Struthers' ligament

2.2.2 Physical examination in ulnar mononeuropathy

Comment: the presence of weakness and atrophy in the ulnar muscle group in the absence of sensory changes is not entirely typical for ulnar neuropathy and requires the exclusion of other diseases, such as motor neuron disease or Hirayama disease. If sensation is impaired in digits 4-5 but preserved in the hypothenar area, the potential compression site is Guyon's canal; a test for the short palmar muscle should be performed.

Comment: the presence of disorders in the forearm rules out ulnar nerve lesion at the elbow level and at the level of Guyon's canal and indicates a higher level of lesion (the skin of the forearm is innervated by the medial cutaneous nerve of the forearm, which originates from the medial cord of the brachial plexus).

Comment: in grade 1 (mild) and grade 2 (moderate) ulnar neuropathy, muscle atrophy is absent. When the superficial branch of the ulnar nerve is affected at the level of Guyon's canal, atrophy is absent.

Comment: the presence of atrophy in the thenar muscle may suggest a higher level of lesion (e.g., the level of the brachial plexus, roots, or spinal cord segments at C₈–Th₁) or a combined lesion of the median and ulnar nerves.

Comment: observed in moderate and severe cases.

Comment: muscle weakness is not characteristic of mild ulnar neuropathy. Ulnar neuropathy is characterized by weakness of the muscles innervated by the ulnar nerve (1st dorsal interosseous muscle and other interosseous muscles, abductor digiti minimi muscle) while strength in other muscle groups remains preserved.

2.2.3 Physical examination in radial mononeuropathy

2.2.4 Physical examination in axillary mononeuropathy

Comment: compensatory abduction of the arm at the shoulder joint in axillary nerve lesions can be provided by the contraction of the supraspinatus, biceps brachii, and pectoralis major muscles. However, during abduction in the position of internal rotation, these compensatory mechanisms do not work, so deltoid muscle dysfunction is clearly revealed.

2.2.5 Physical examination in musculocutaneous mononeuropathy

2.2.6 Physical examination in brachial plexus branch mononeuropathy

Comment: the strength of the serratus anterior muscle is determined by performing the wall push-up test. The test is considered positive if the medial border of the scapula moves away from the chest wall. The arm abduction test is also used—evaluating arm abduction in the plane of the scapula at an angle of 120–130 degrees (i.e., upward rotation of the scapula). The test is considered positive if there is an inability to resist the examiner's force. When testing the strength of the rhomboid muscles, the patient lies prone, arm along the body in internal rotation. The test is considered positive when lifting the arm and shoulder causes the medial border of the scapula to move away from the chest wall. Scapular retraction test—the patient is seated, arms in internal rotation at the shoulder joints. The test is considered positive if the medial border of the scapula moves away from the chest wall during the test. The rhomboid major muscle is tested simultaneously with the rhomboid minor.

Assessment of supraspinatus muscle function is performed when raising the arm above the horizontal line. The test is considered positive if the patient is unable to hold the outstretched arm raised above 90 degrees against the examiner's pressure on the proximal arm. Drop arm test—the examiner passively abducts the straightened arm to approximately 120 degrees. Then the patient holds the arm in this position independently and then slowly lowers it down. The test is considered positive if the patient is unable to hold the arm in this position and it drops abruptly.

2.2.7 Physical examination in intercostal mononeuropathy

Comment: Carnett's test is often positive in lesions of the lower intercostal nerves (T₇–T₁₁).

2.2.8 Physical examination in sciatic mononeuropathy

2.2.9 Physical examination in peroneal mononeuropathy

2.2.10 Physical examination in tibial mononeuropathy

2.2.11 Physical examination in femoral mononeuropathy

2.2.12 Physical examination in lateral femoral cutaneous mononeuropathy

2.3 Laboratory Diagnostics

2.3.1 Laboratory diagnostic tests in median mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.2 Laboratory diagnostic tests in ulnar mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.3 Laboratory diagnostic tests in radial mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.4 Laboratory diagnostic tests in axillary mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.5 Laboratory diagnostic tests in musculocutaneous mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.6 Laboratory diagnostic tests in brachial plexus branch mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.7 Laboratory diagnostic tests in intercostal mononeuropathy

Specific laboratory diagnostic methods are absent.

The scope of investigations is variable and depends on the suspected etiological factor.

2.3.8 Laboratory diagnostic tests in sciatic mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.9 Laboratory diagnostic tests in peroneal mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.10 Laboratory diagnostic tests in tibial mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.11 Laboratory diagnostic tests in femoral mononeuropathy

Specific laboratory diagnostic methods are absent.

2.3.12 Laboratory diagnostic investigations for lateral femoral cutaneous mononeuropathy

Specific laboratory diagnostic methods are absent.

2.4 Instrumental Diagnostics

2.4.1 Instrumental diagnostic tests in median mononeuropathy

Comment: electroneuromyography is the "gold standard" of instrumental diagnostics for nerve injury. It allows objectifying the topical diagnosis as well as assessing the acuity and severity of neural lesions [18,19,27,209,217]. In pediatric cases of CTS, electrophysiological changes may be detected bilaterally even if the clinical presentation is unilateral [177,218].

Comments: The pronator teres is extremely rarely altered due to nerve compression distal to the level of its innervation. In 10% of cases, electrophysiological tests in pronator teres syndrome have low information value [220,221].

Comment: Ultrasound of the median nerve (ultrasound examination of peripheral nerves (single anatomical region)) allows visualization of the nerve and surrounding structures, helping to identify causes of compression, diagnose fascicular constriction of the nerve in the arm in anterior interosseous nerve syndrome [3,32], and perform differential diagnosis with neoplasms of the nerve or surrounding tissues.

In pediatric practice, carpal tunnel syndrome is rare. Considering the possibility of carpal tunnel syndrome developing in children due to neoplasms, it is advisable to perform nerve ultrasound (ultrasound examination of peripheral nerves (single anatomical region)) in all cases of carpal tunnel syndrome in children. In children with mucopolysaccharidoses, ultrasound (ultrasound examination of peripheral nerves (single anatomical region)) in carpal tunnel syndrome screening may be more sensitive than stimulation electromyography (median nerve stimulation electromyography) [29].

Comment: MRI (magnetic resonance imaging of joints (single joint)) of the wrist is usually used to determine the site of nerve compression after failed carpal tunnel surgeries and as a differential diagnostic method in cases with doubtful symptoms, as well as for diagnosing space-occupying hand lesions. The scan is evaluated in T1 and T2 weighted sequences with a slice thickness of 2.5 mm. The cross-sectional area of the median nerve is measured at 2 points: proximal to the carpal tunnel inlet and distal to its outlet. The sensitivity of the MRI technique for CTS diagnosis is 100% and specificity is 94%. In anterior interosseous nerve syndrome, T2-weighted MRI allows identification of its lesion in the arm [3,32,227], which is accompanied by signal intensity changes from myotomes innervated by other portions of the median nerve as well [197,228,229].

2.4.2 Instrumental diagnostic tests in ulnar mononeuropathy

The "gold standard" for diagnosing ulnar neuropathy is electromyographic study of the motor and sensory conduction function of the ulnar nerve (ulnar nerve stimulation electroneuromyography, median nerve stimulation electromyography). Neuroimaging modalities used include ulnar nerve ultrasound (ultrasound examination of peripheral nerves (single anatomical region)) and MRI of the elbow joint and ulnar nerve (magnetic resonance imaging of joints (single joint), magnetic resonance imaging of soft tissues with contrast).

Comment: The electromyographic criterion for diagnosing cubital tunnel syndrome is a decrease in conduction velocity below 50 m/s at the elbow level and/or a velocity gradient greater than 10 m/s between the forearm and the elbow level. In severe cases, a conduction block at the elbow level may be observed, and in long-standing severe cases of cubital tunnel syndrome, a progressive decrease in the amplitude of the ulnar nerve M-response upon distal stimulation is observed (which is a poor prognostic factor for conservative treatment). The study should be performed on a warm limb (skin temperature not less than 32 °C), and the arm should be positioned in flexion at the elbow joint (70–90 degrees). For a lesion at the level of Guyon's canal involving the deep branch, an increase in the distal latency of the ulnar nerve M-response is characteristic; for a lesion of the superficial branch, a decrease in sensory conduction velocity at the hand level is characteristic.

Comment: needle electromyography allows the detection of an acute or chronic denervation-reinnervation process indicating an axonal lesion. If necessary, in addition to the 1st interosseous muscle, abductor digiti minimi muscle, and thenar muscles, paraspinal muscles at the C₈–Th₁ level, as well as muscles related to the middle and upper trunks of the brachial plexus, are examined. Needle EMG allows differential diagnosis with such conditions as motor neuron disease, plexopathy, spinal cord and root lesions at the C₈–Th₁ level, Hirayama disease, distal forms of spinal amyotrophy, and distal myopathies.

Comment: Ultrasound methods allow the assessment of the structure of peripheral nerves and changes in standard characteristics depending on the zone of suspected compression. Cubital tunnel syndrome is characterized by an increase in the cross-sectional area of the nerve of more than 10 mm².

Comment: in neuropathy at the elbow level, MRI can show nerve thickening and increased signal intensity on T2-weighted or short tau inversion recovery (STIR) sequences.

2.4.3 Instrumental diagnostic tests in radial mononeuropathy

2.4.4 Instrumental diagnostic tests in axillary mononeuropathy

Comment: needle electromyography is performed 3–4 weeks after the onset of symptoms. It is after this time interval that maximal changes develop, specifically denervation spontaneous activity.

Comments: standard stimulation electromyography methodology reveals an increase in terminal latency and a decrease/absence of the amplitude of elicited motor responses when testing the axillary nerve compared to the healthy side.

Comments: MRI is a method for visualizing axillary nerve injury, including in patients with quadrilateral space syndrome. In T2 and STIR modes, increased MR signal from the nerve trunk, enlargement, and deformation of the axillary nerve are detected.

Comments: Ultrasound methods allow the assessment of the structure of the axillary nerve and changes in standard characteristics in the nerve lesion zone.

2.4.5 Instrumental diagnostic tests in musculocutaneous mononeuropathy

Comment: ultrasound examination allows visualization of the musculocutaneous nerve and surrounding structures, which helps confirm the level and identify the cause of nerve trunk compression, as well as perform differential diagnosis with other nosologies in patients with clinical and electrophysiological manifestations of musculocutaneous nerve neuropathy. When the lateral cutaneous nerve of the forearm is damaged, its cross-sectional area usually increases, and echogenicity may increase due to intreneural hemorrhage. Dynamic examination (during forearm supination/pronations) may also help detect pathological changes in the distal biceps tendon area [256].

2.4.6 Instrumental diagnostic studies for mononeuropathy of brachial plexus branches

Level of evidence recommendations C (level of reliability of evidence – 4).

Comment: if it is necessary to rule out brachial plexus trunk lesions, needle electromyography may not be limited to the evaluation of the supraspinatus and infraspinatus muscles. In this case, the deltoid, serratus anterior, and rhomboid muscles may be included in the examination protocol. If denervation changes affect only the infraspinatus muscle, involvement of the suprascapular nerve at the scapular notch must be ruled out. Isolated involvement of the serratus anterior muscle indicates ruling out involvement of the long thoracic nerve. Involvement of the rhomboid muscles indicates a lesion of the dorsal scapular nerve. In the case of denervation changes in muscles innervated by the long branches of the brachial plexus, involvement of the brachial plexus should be logically suspected.

Comment: MRI is informative in determining possible causes of compression: spinoglenoid notch cyst, benign neoplasms in the upper mediastinum, malignant lung neoplasms, and metastatic lesions.

Comments: ultrasound methods make it possible to assess the structure of peripheral nerves and changes in standard characteristics depending on the zone of suspected compression. The method allows for verifying the site of origin of the suprascapular nerve and dorsal scapular nerve from the upper trunk of the brachial plexus in the supraclavicular region, and also allows for verifying the structure of the brachial plexus itself.

2.4.7 Instrumental diagnostic tests in intercostal mononeuropathy

2.4.8 Instrumental diagnostic tests in sciatic mononeuropathy

Comment: standard stimulation electromyography technique reveals a decrease/absence of elicited motor responses when testing the peroneal and tibial nerves with normal nerve conduction parameters, as well as a decrease/absence of sensory responses when testing the sural and superficial peroneal nerves compared to the healthy side. The H-reflex may be normal if predominantly the peroneal portion of the sciatic nerve is damaged and cannot confirm the diagnosis. An increase in the minimum latency of F-waves when testing the peroneal and tibial nerves is observed in 85% and 57%, respectively.

Comment: Needle EMG is performed 3-4 weeks after the onset of symptoms. It is after this period that maximum changes develop: denervation spontaneous activity in the form of positive sharp waves and fibrillation potentials. In muscles innervated by the peroneal portion of the sciatic nerve, changes are observed in 94-100% of cases, and in the tibial portion in 74-84% of cases. To exclude L₅, S₁ radiculopathy and plexopathy, it is advisable to include the gluteus medius or tensor fasciae latae muscle (superior gluteal nerve), gluteus maximus muscle (inferior gluteal nerve), and paraspinal muscles in the study [187].

Comment: T2 and STIR images reveal an increase in the MR signal from the nerve trunk, enlargement, and deformation of the sciatic nerve. In patients with piriformis syndrome, developmental anomalies predisposing to the development of the syndrome may be detected. If necessary, gadolinium contrast enhancement is used [124, 187, 260].

• It is recommended that adult patients with suspected sciatic nerve neuropathy undergo ultrasound examination of the sciatic nerve (ultrasound examination of peripheral nerves (one anatomical region))

• for the diagnosis of neuropathy causes [111, 261].

GPP CLOE 4Grade of Recommendation C (Level of Evidence – 4).

Comment: ultrasound examination has limitations in visualizing the nerve in the pelvis. When the pathological process is localized in the thigh, ultrasound of the sciatic nerve (ultrasound examination of peripheral nerves (one anatomical region)) can be useful for detecting space-occupying lesions (schwannomas, neurofibromas, intraneural perineuriomas, lipomas).

2.4.9 Instrumental diagnostic studies for peroneal nerve mononeuropathy

Comment: Ultrasound examination is indicated to exclude soft tissue changes or formations that exert a compressive effect on the nerve.

Comment: MR imaging (magnetic resonance imaging of soft tissues) of the peroneal nerve and/or thigh is indicated to exclude soft tissue changes or intra- and extraneural formations exerting a compressive effect on the nerve.

2.4.10 Instrumental diagnostic tests in tibial mononeuropathy

Level of evidence C (confidence level of evidence: 5).

Comments: ultrasound methods make it possible to assess the structure of peripheral nerves and changes in standard characteristics depending on the area of suspected compression.

2.4.11 Instrumental diagnostic tests in femoral mononeuropathy

Comment: electromyographic examination can be useful to determine the localization of the lesion proximally or distally to the inguinal ligament and to exclude other processes that may present with proximal thigh weakness, especially high lumbar plexopathy or radiculopathy. A comparison with the unaffected contralateral side should be performed.

Comments: ultrasound allows visualization of the femoral nerve and surrounding structures, which helps identify the causes of nerve trunk compression, detect space-occupying neoplasms (schwannomas, neurinomas) causing nerve damage, as well as the presence of scar-adhesive changes, inflammatory edema, or, conversely, nerve atrophy when compared with the nerve of the intact limb [270–272].

Comments: during MRI, signs of nerve damage include its thickening beyond normal values, loss of normal fascicular appearance, or blurring of the perifascicular adipose tissue. Changes in the muscles innervated by the femoral nerve are also evaluated: in the early stages of the denervation process, the T2 and STIR signal from the muscles remains normal, but as denervation progresses, the signal intensity from the muscle tissue increases.

2.4.12 Instrumental diagnostic examinations for lateral femoral cutaneous nerve mononeuropathy

Comment: the capabilities and value of the electromyographic examination (stimulation electromyography of a single nerve) of the lateral femoral cutaneous nerve are limited, and the examination has low sensitivity and specificity, especially in the presence of well-developed subcutaneous adipose tissue [276].

2.5 Other Procedures

2.5.1 Other diagnostic examinations in median nerve mononeuropathy

None.

2.5.2 Other diagnostic examinations in ulnar nerve mononeuropathy

None.

2.5.3 Other diagnostic examinations in radial nerve mononeuropathy

None.

2.5.4 Other diagnostic examinations in axillary nerve mononeuropathy

None.

2.5.5 Other diagnostic examinations in musculocutaneous nerve mononeuropathy

None.

2.5.6 Other diagnostic examinations in brachial plexus branch mononeuropathy

None.

2.5.7 Other diagnostic examinations in intercostal nerve mononeuropathy

None.

2.5.8 Other diagnostic examinations in sciatic nerve mononeuropathy

None.

2.5.9 Other diagnostic examinations in peroneal nerve mononeuropathy

None.

2.5.10 Other diagnostic examinations in tibial nerve mononeuropathy

None.

2.5.11 Other diagnostic examinations in femoral nerve mononeuropathy

None.

2.5.12 Other diagnostic examinations in lateral femoral cutaneous nerve mononeuropathy

None.

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

3.1 Conservative Treatment

3.1.1 Conservative treatment of median nerve mononeuropathy

In carpal tunnel syndrome

The treatment of CTS depends on the severity of symptoms and the duration of the disease. For mild and moderate severity, a trial of conservative treatment is advisable in order to achieve symptom regression within 2 weeks. Optimal treatment for CTS should be patient-oriented, provide symptom relief, and be comprehensive. Treatment should begin with explaining the need to modify daily hand motor activities.

Comment: immobilization is the first-line treatment for mild-to-moderate CTS due to its simplicity and good tolerability. However, there is insufficient evidence of the superiority of one immobilization device design over another.

Comment: the efficacy of perineural GCS administration in mild-to-moderate CTS has been proven. There is no convincing evidence supporting the superiority of one injection technique over others or the superiority of a specific composition and dose of GCS. Any existing GCS with a registered parenteral formulation may be used. Landmark-guided injection is generally safe, but there is a risk of damaging the median nerve, tendons, or intravascular administration of the drug. Therefore, perineural administration of glucocorticoids using ultrasound guidance may be more effective and safer, as it allows direct visualization of the entire course of the procedure. If symptoms recur after two injections, alternative treatment options should be considered.

Comment: oral GCS are more effective than nonsteroidal anti-inflammatory drugs and diuretics, but carry a high risk of more serious side effects. Currently, there is no evidence of the long-term efficacy of oral steroids.

In anterior interosseous nerve syndrome

3.1.2 Conservative treatment of ulnar nerve mononeuropathy

Conservative treatment is advisable for mild cubital tunnel syndrome [288].

Comment: Wearing an orthosis that restricts elbow flexion beyond 60 degrees for 6 months reduces symptom severity in 94% of cases and increases conduction velocity across the elbow by 6.5 m/s for motor fibers and 9.5 m/s for sensory fibers [290–292].

• It is recommended that adult patients with ulnar nerve mononeuropathy receive treatment for neuropathic pain syndrome if present [192]:

  Non-selective monoamine reuptake inhibitors:

• Amitriptyline** – 25–150 mg/day

  Other antiepileptic drugs:

• Gabapentin – 300–3600 mg/day.

• Pregabalin** – 150–600 mg/day

  Opioids (when first-line drugs are ineffective):

• Tramadol** 100–400 mg/day

Level CLevel 5Level of recommendation evidence C (reliability level of evidence – 5).

3.1.3 Conservative treatment of radial nerve mononeuropathy

3.1.4 Conservative treatment of axillary nerve mononeuropathy

Used in the absence of direct indications for surgical treatment, such as external compressive effects on the nerve trunk or pronounced irreversible changes in the nerve trunk itself, confirmed by neuroimaging methods (MRI or nerve ultrasound) [297–299].

3.1.5 Conservative treatment of musculocutaneous nerve mononeuropathy

3.1.6 Conservative treatment of brachial plexus branch mononeuropathy

Used in the absence of direct indications for surgical treatment, such as external compressive effects on the nerve trunk or pronounced irreversible changes in the nerve trunk itself, confirmed by neuroimaging methods (MRI or nerve ultrasound).

Non-selective monoamine reuptake inhibitors: amitriptyline** – 25–150 mg/day.

Other antiepileptic drugs: gabapentin – 300–3600 mg/day and pregabalin** – 150–600 mg/day.

In case of inefficacy of first-line drugs – opioids (tramadol** – 100–400 mg/day).

Level CLevel 5Level of recommendation evidence C (reliability level of evidence – 5).

3.1.7 Conservative treatment of intercostal nerve mononeuropathy

Used in the absence of direct indications for surgical treatment, such as external compressive effects on the nerve trunk (developing as a consequence of injuries and thoracic cavity neoplasms).

3.1.8 Conservative treatment of sciatic nerve mononeuropathy

Comment: the efficacy of botulinum toxin type A** administration is higher compared to injections of GCS and a local anesthetic [303].

3.1.9 Conservative treatment of peroneal nerve mononeuropathy

3.1.10 Conservative treatment of tibial nerve mononeuropathy

Conservative treatment is used in the absence of direct indications for surgical treatment, such as external compressive effects on the nerve trunk or pronounced irreversible changes in the nerve trunk itself confirmed by neuroimaging methods (MRI or nerve ultrasound).

3.1.11 Conservative treatment of femoral nerve mononeuropathy

It is advisable to limit non-surgical methods of treating femoral nerve neuropathy only when there is absolute certainty that there is no treatable cause of nerve compression (hematoma, neoplasm, etc.). Otherwise, surgery is the method of choice.

Regardless of the underlying etiological factor, femoral nerve neuropathy has no proven methods of effective non-surgical treatment. At the same time, it is accompanied by spontaneous regression of motor and sensory dysfunction within 2 to 24 months in 93% of cases. Among them, only 38% achieve a satisfactory degree of recovery [207]. During the recovery period, depending on the clinical severity of the neuropathy, auxiliary orthopedic devices such as a knee orthosis, walking cane, etc., can be used to facilitate activities of daily living.

The greatest problem in the structure of femoral nerve neuropathy is the presence of a pain component.

Comment: Blockades are used for both therapeutic and diagnostic purposes [304]. Blockades can be used as a single injection, a series of boluses performed at a certain interval depending on the duration of the effect, or using catheter techniques (paraneural catheter placement with/without subcutaneous tunneling) and continuous infusion of the anesthetic with an elastomeric pump or infusomat [305]. To increase the accuracy and safety of the blockade, it is advisable to use ultrasound guidance [306].

3.1.12 Conservative treatment of lateral femoral cutaneous nerve mononeuropathy

Comment: if lateral femoral cutaneous mononeuropathy develops during pregnancy, it is advisable to adhere to conservative treatment methods and avoid surgery, as in most cases symptoms regress after childbirth [157].

3.2 Surgical Treatment

3.2.1 Surgical treatment of median nerve mononeuropathy

Comments: The goal of surgical treatment is decompression of the median nerve in the carpal tunnel, which is achieved by complete transection of the transverse carpal ligament. Indications for decompression include the lack of a sustained adequate effect from conservative therapy, shortening of remission periods, and progression of neurological symptoms. When determining indications for surgical treatment, the clinical picture and electroneuromyography (ENMG) data should be correlated with imaging data (ultrasound). Currently, open and minimally invasive techniques (endoscopic decompression and endoscopically assisted decompression) are used. Open decompression is performed via a longitudinal approach from the transverse wrist crease to the intersection point of the 4th finger axis with Kaplan's line. Approach modifications are permissible to reduce longitudinal incisions and minimize surgical trauma. Ligament transection is performed under visual control. Unlike the former, minimally invasive techniques involve transecting the ligament under the control of an endoscope, which serves as a visualization tool for intracanalar structures. In this case, a 1.0–1.5 cm incision is made along the transverse wrist crease. A supriligamentous or subligamentous tunnel is formed subcutaneously for the endoscope. The use of a 0- or 30-degree endoscope is advisable. Transection of the carpal ligament can be performed antegrade or retrograde. The advantage of endoscopic techniques lies in minimizing surgical trauma. The disadvantage of the technique is the increased risk of incomplete transection of the carpal ligament and damage to anatomical structures. The advantage of the open technique is good visualization of all anatomical structures of the carpal tunnel. The disadvantage is the transection of the thenar and hypothenar muscles and the formation of a scar over the nerve trunk. According to literature data, the choice of decompression technique does not affect the outcome of the disease. Following carpal tunnel decompression, there is a risk of scarring and adhesion formation, which can lead to secondary compression of the median nerve trunk. Prevention of adhesions includes: meticulous hemostasis, preferential choice of minimally invasive decompression techniques, and the use of biodegradable implants during open decompression. The use of tight bandages and prolonged immobilization of the wrist joint in the postoperative period is inappropriate [319,320].

In pronator teres syndrome

Comment: Surgical treatment typically includes decompression of the median nerve, including revision of the state of Struthers' ligament and the flexor digitorum superficialis fascia.

The endoscopic technique has advantages over open surgery because it does not disrupt the blood supply to the nerves and reduces the likelihood of scar formation. In the event of a recurrence, open surgery is indicated [67].

In anterior interosseous nerve syndrome

3.2.2 Surgical treatment of ulnar nerve mononeuropathy

Surgical intervention in the form of decompression and medial epicondylectomy is advisable when conservative treatment is ineffective, as well as in severe forms of neuropathy [288].

Comment: after surgical treatment, recurrence is noted in 3% of cases, with indications for re-operation arising in 2% of cases. The risk of recurrence requiring re-intervention with submuscular transposition is 5 times higher than with open decompression with epicondylectomy [324,325].

Overall, all surgical treatment methods show sufficient efficacy (improvement in 87% of cases). Data regarding the preference for one surgical treatment method over another are contradictory, as they often depend on the surgeon's experience with each method [35,165,288,324–328].

Comment: in 83% of cases, conservative treatment for ulnar neuropathy at the elbow in children was ineffective and required surgical intervention. In situ surgical decompression in children is less effective than in adults (ineffective in 23% of cases) [29].

3.2.3 Surgical treatment of radial nerve mononeuropathy

3.2.4 Surgical treatment of axillary nerve mononeuropathy

Comment: surgical treatment for axillary neuropathy is optimal within 3–6 months after nerve injury [87]. The outcomes of surgical treatment for axillary neuropathy are poorer beyond this time period, and minimal improvement is observed when surgery is performed 12 months after nerve injury [334–336].

3.2.5 Surgical treatment of musculocutaneous nerve mononeuropathy

3.2.6 Surgical treatment of brachial plexus branch mononeuropathy

Level of evidence C (confidence level of evidence: 5).

Comments: arthroscopic decompression and open decompression of the suprascapular nerve have equal efficacy [337,338].

Level of evidence recommendations C (level of reliability of evidence – 4).

3.2.7 Surgical treatment of intercostal nerve mononeuropathy

Comment: the disadvantages of these surgical methods include the development of persistent neurological deficits in the form of anesthesia, as well as the potential development of dysesthesia in the nerve innervation zone.

3.2.8 Surgical treatment of sciatic nerve mononeuropathy

3.2.9 Surgical treatment of peroneal nerve mononeuropathy

Comment: for intraneural masses, surgical treatment should be performed using intraoperative monitoring [346].

3.2.10 Surgical treatment of tibial nerve mononeuropathy

Level of evidence recommendations C (level of reliability of evidence – 4).

Level of evidence recommendations B (reliability level of evidence – 3).

3.2.11 Surgical treatment of femoral nerve mononeuropathy

3.2.12 Surgical treatment of lateral femoral cutaneous nerve mononeuropathy

Comments: neurolysis of the lateral femoral cutaneous nerve is the most sparing method of surgical treatment, but in some cases symptom recurrence is noted [357–359].

Comments: resection of the lateral femoral cutaneous nerve provides a more pronounced and persistent reduction in symptoms, but one must account for the development of a side effect in the form of complete anesthesia in the innervation area.

3.3 Treatment, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods.

3.3.2 Treatment of ulnar nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Treatment of cubital tunnel syndrome depends on the severity degree and includes conservative and surgical treatment. In mild cases of cubital tunnel syndrome, conservative treatment helps in only 50% of cases, while surgical treatment yields nearly 100% results using any surgical method [175].

3.3.3 Treatment of radial nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.4 Treatment of axillary nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.5 Treatment of musculocutaneous nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.6 Treatment, including drug and non-drug therapies for brachial plexus branch mononeuropathies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.7 Treatment of intercostal nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used [105,360].

3.3.8 Treatment of sciatic nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.9 Treatment of fibular nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.10 Treatment of tibial nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.11 Treatment of femoral nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

3.3.12 Treatment of lateral femoral cutaneous nerve mononeuropathy, including drug and non-drug therapies, diet therapy, pain management, medical indications and contraindications for the use of treatment methods.

Depending on the nature and severity of the lesion, conservative and surgical treatments are used.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

4.1 Medical rehabilitation and sanatorium-resort treatment, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors for median nerve mononeuropathy

4.2 Medical rehabilitation and sanatorium-resort treatment for ulnar nerve mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.3 Medical rehabilitation and sanatorium-resort treatment for radial nerve mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.4 Medical rehabilitation and sanatorium-resort treatment for axillary nerve mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.5 Medical rehabilitation and sanatorium-resort treatment for musculocutaneous nerve mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.6 Medical rehabilitation and sanatorium-resort treatment for brachial plexus branch mononeuropathies, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.7 Medical rehabilitation and sanatorium-resort treatment for intercostal nerve mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.8 Medical rehabilitation and sanatorium-resort treatment of sciatic mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.9 Medical rehabilitation and sanatorium-resort treatment of peroneal mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.10 Medical rehabilitation and sanatorium-resort treatment of tibial mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.11 Medical rehabilitation and sanatorium-resort treatment of femoral mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

4.12 Medical rehabilitation and sanatorium-resort treatment of lateral femoral cutaneous mononeuropathy, medical indications and contraindications for the use of medical rehabilitation methods, including those based on natural therapeutic factors

5. Prevention and Dispensary Observation

5.1 Prevention and follow-up (dispensary observation), medical indications and contraindications for preventive methods in median mononeuropathy

5.2 Prevention and follow-up of ulnar mononeuropathy, medical indications and contraindications for preventive methods.

5.3 Prevention and follow-up of radial mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for radial mononeuropathy. The patient does not require follow-up observation.

5.4 Prevention and follow-up of axillary mononeuropathy, medical indications and contraindications for preventive methods

No specific prevention methods have been developed for axillary mononeuropathy. The patient does not require follow-up observation.

5.5 Prevention and follow-up of musculocutaneous mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for musculocutaneous mononeuropathy. The patient does not require follow-up observation.

5.6 Prevention and follow-up of brachial plexus branch mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for mononeuropathy of the short branches of the brachial plexus. The patient does not require follow-up observation.

5.7 Prevention and follow-up of intercostal mononeuropathy, medical indications and contraindications for preventive methods

No specific prevention methods have been developed for intercostal mononeuropathy. The patient does not require follow-up observation.

5.8 Prevention and follow-up of sciatic mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for sciatic mononeuropathy. The patient does not require follow-up observation.

5.9 Prevention and follow-up of peroneal mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for sciatic mononeuropathy. The patient does not require follow-up observation.

5.10 Prevention and follow-up of tibial mononeuropathy, medical indications and contraindications for preventive methods.

No specific prevention methods have been developed for tibial mononeuropathy. The patient does not require follow-up observation.

5.11 Prevention and follow-up of femoral mononeuropathy, medical indications for preventive methods

No specific prevention methods have been developed for femoral mononeuropathy. The patient does not require follow-up observation.

5.12 Prevention and follow-up of lateral femoral cutaneous mononeuropathy, medical indications and contraindications for preventive methods

No specific prevention methods have been developed for lateral femoral cutaneous mononeuropathy. The patient does not require follow-up observation.

6. Organization of Medical Care

6.1 Organization of medical care for median mononeuropathy

Patients with median mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.2 Organization of medical care for ulnar mononeuropathy

Patients with ulnar mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.3 Organization of medical care for radial mononeuropathy

Patients with radial mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.4 Organization of medical care for axillary mononeuropathy

Patients with axillary mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.5 Organization of medical care for musculocutaneous mononeuropathy

Patients with musculocutaneous mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.6 Organization of medical care for brachial plexus branch mononeuropathy

Patients with mononeuropathy of the short branches of the brachial plexus can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.7 Organization of medical care for intercostal mononeuropathy

Patients with intercostal mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.8 Organization of medical care for sciatic mononeuropathy

Patients with mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.9 Organization of medical care for peroneal mononeuropathy

Patients with mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.10 Organization of medical care for tibial mononeuropathy

Patients with mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.11 Organization of medical care for femoral mononeuropathy

Patients with femoral mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

6.12 Organization of medical care for lateral cutaneous nerve of thigh mononeuropathy

Patients with mononeuropathy can be treated on an outpatient basis. Hospital admission is not required, except in cases requiring surgical treatment.

7. Additional Information

7.1 Additional information (including factors influencing the outcome of the disease or condition) for median mononeuropathy

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.2 Additional information for ulnar mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.3 Additional information for radial mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.4 Additional information for axillary mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.5 Additional information for musculocutaneous mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.6 Additional information for brachial plexus branch mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.7 Additional information for intercostal nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.8 Additional information for sciatic nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.9 Additional information for peroneal nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.10 Additional information for tibial nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.11 Additional information for femoral nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

7.12 Additional information for lateral femoral cutaneous nerve mononeuropathy (including factors influencing the outcome of the disease or condition)

Proper diagnosis and timely implementation of adequate treatment lead to the compensation of motor disorders in more than 80% of patients with mononeuropathy. It should be borne in mind that systematic alcohol intake can negatively affect the recovery of the affected nerve function; therefore, it is advisable to abstain from alcohol throughout the entire period of treatment and rehabilitation.

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Dmitry Alexandrovich Averyanov, Candidate of Medical Sciences, Lecturer at the Department of Military Anesthesiology and Intensive Care, S.M. Kirov Military Medical Academy. Member of the All-Russian Society of Neurologists.

2. Tatyana Alekseevna Alexandrova, Neurologist, Functional Diagnostics Physician at Tonus Medical Center (Nizhny Novgorod), member of the Association of Clinical Neurophysiology Specialists ASKLIN.

3. Vladislav Borisovich Voytenkov, Candidate of Medical Sciences, Head of the Department of Functional Diagnostics, Children's City Clinical Hospital for Infectious Diseases of the FMBA of Russia, Associate Professor at the Department of Nervous Diseases, Academy of Postgraduate Education of the FSCC of the FMBA of Russia. Member of the All-Russian Society of Neurologists. Scientific Activity Coordinator of the Association of Clinical Neurophysiology Specialists ASKLIN.

4. Alla B. Gekht, Corresponding Member of the Russian Academy of Sciences, MD, PhD, Director of the Z.P. Solovyov Scientific and Practical Psychoneurological Center of the Moscow Healthcare Department, Professor at the Department of Neurology, Neurosurgery and Medical Genetics, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Academic Secretary of the All-Russian Society of Neurologists, Member of the Presidium of the National Stroke Association.

5. Olga Valeryevna Gilvanova, Neurologist, Functional Diagnostics Physician at the Clinic of Neuromuscular Diseases. Freelance Expert in Electromyography of the Moscow Healthcare Department. Member of the All-Russian Society of Neurologists. Member of the Association of Clinical Neurophysiology Specialists ASKLIN.

6. Sergey Igorevich Dedayev, Candidate of Medical Sciences, Head of the Department for the Study of Pain and Somatoform Disorders, Solovyov Research and Practical Center for Mental Health of the Moscow Healthcare Department. Member of the All-Russian Society of Neurologists.

7. Dmitry Sergeevich Druzhinin, Doctor of Medical Sciences, Associate Professor at the Department of Nervous Diseases with a Course of Medical Genetics and Neurosurgery, Yaroslavl State Medical University of the Russian Ministry of Health. Member of the All-Russian Society of Neurologists. Neurologist, Functional Diagnostics Physician at the Clinic of Neuromuscular Diseases. Chairman of the Association of Clinical Neurophysiology Specialists ASKLIN.

8. Evgenia S. Druzhinina, PhD, Associate Professor at the Department of Neurology, Neurosurgery and Medical Genetics named after L.O. Badalyan, Faculty of Pediatrics, Pirogov Russian National Research Medical University. Neurologist, ultrasound and functional diagnostics physician at the Clinic of Neuromuscular Diseases. Functional diagnostics physician at the Russian Children's Clinical Hospital. Member of the All-Russian Society of Neurologus. Member of the Association of Clinical Neurophysiologists (ASKLIN).

9. Evgenia V. Ekusheva, DSc, Professor, Head of the Department of Nervous Diseases and Neurorehabilitation, Academy of Postgraduate Education of the Federal Center for Brain Research and Neurotechnologies of the Federal Medical-Biological Agency, neurologist at the Vейн Headache Clinic and Guta Clinic. Moscow.

10. Oksana D. Yelshina, neurologist, functional diagnostics physician at the Tonus Medical Center (Nizhny Novgorod), member of the Association of Clinical Neurophysiologists (ASKLIN).

11. Elena N. Zharova, DSc, Head of the Department of Restorative Treatment and Medical Rehabilitation, Neurosurgical Branch of the Almazov National Medical Research Centre.

12. Galina E. Ivanova, DSc, Professor, Chief freelance specialist in medical rehabilitation of the Russian Ministry of Health, Head of the Department of Medical Rehabilitation of the Faculty of Additional Professional Education, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Chairman of the Presidium of the All-Russian Public Organization for the Promotion of Development of Medical Rehabilitology "Union of Rehabilitologists of Russia", member of the Audit Commission of the National Stroke Association.

13. Maria A. Irikova, PhD, Junior Researcher at the Research Department of Neuroinfections and Organic Pathology of the Nervous System, functional diagnostics physician at the D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology of the FMBA of Russia, Member of the Association of Clinical Neurophysiologists (ASKLIN).

14. Daria S. Kanshina, PhD, Head of the Department of Neurology and Clinical Neurophysiology, Pirogov National Medical Research Center of the Ministry of Health of the Russian Federation, Associate Professor at the Department of Neurology with a Course of Neurosurgery, Institute of Advanced Training of the Pirogov National Medical Research Center of the Ministry of Health of the Russian Federation. Member of the All-Russian Society of Neurologists. Member of the Association of Clinical Neurophysiologists (ASKLIN).

15. Lyubov F. Kasatkina, DSc, Professor, specialist in functional diagnostics of peripheral nervous system diseases at the Research Center of Neurology, Member of the All-Russian Society of Neurologists. Member of the Russian Association of Specialists in Functional Diagnostics.

16. Andrey V. Klimkin, PhD, Senior Researcher at the Research Department of Neuroinfections and Organic Pathology of the Nervous System, functional diagnostics physician at the Pediatric Research and Clinical Center for Infectious Diseases of the FMBA of Russia, Member of the Association of Clinical Neurophysiologists (ASKLIN).

17. Maria O. Kovalchuk, PhD, Head of Neurology Department No. 1, Buyanov City Clinical Hospital. Neurologist at the Clinic of Neuromuscular Diseases. Member of the All-Russian Society of Neurologists.

18. Vladimir V. Krylov, Academician of the RAS, Professor, DSc, Chief freelance neurosurgeon, Head of the Department of Neurosurgery and Neuro-Resuscitation, Yevdokimov Moscow State University of Medicine and Dentistry.

19. Eduard Yu. Maletsky, PhD, Associate Professor at the Department of Radiology and Radiation Therapy, North-Western State Medical University named after I.I. Mechnikov, Saint Petersburg, member of the Russian Association of Specialists in Ultrasound Diagnostics in Medicine.

20. Olga V. Malysheva, neurologist at the Neurosurgery Clinic of the Kirov Military Medical Academy of the Ministry of Defense of the Russian Federation. Member of the All-Russian Society of Neurologists. Member of the Association of Clinical Neurophysiologists (ASKLIN).

21. Sergey A. Malmberg, DSc, Professor at the Department of Clinical Physiology and Functional Diagnostics, Academy of Postgraduate Education of the Federal Medical and Biological Center of the FMBA of Russia, Moscow, member of the Association of Clinical Neurophysiologists (ASKLIN), member of the Russian Association of Specialists in Functional Diagnostics.

22. Mikhail Yu. Martynov, Corresponding Member of the RAS, Professor, DSc, First Deputy General Director of the Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency, Acting Head of the Department of Neurology, Neurosurgery and Medical Genetics, Faculty of General Medicine, Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Scientific Secretary of the All-Russian Society of Neurologists, Board Member of the National Stroke Association.

23. Andrey S. Nikitin, PhD, Head of Academic Affairs at the Department of Neurosurgery and Neuro-Resuscitation, Yevdokimov Moscow State University of Medicine and Dentistry.

24. Nikolay A. Pavlov, Candidate of Medical Sciences, Leading Researcher at the Department of Neurology, Neurosurgery and Medical Genetics, N.I. Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation, Member of the Presidium of the All-Russian Society of Neurologists.

25. Elena N. Plastunenko, neurosurgeon, researcher at the Department of Neurosurgery and Neurotrauma, Research Institute of Emergency Pediatric Surgery and Traumatology of the Moscow Healthcare Department.

26. Andrey P. Rachin, DSc, Professor, Deputy Director for Scientific Work, Head of the Department of Neurorehabilitation and Clinical Psychology, National Medical Research Center for Rehabilitation and Balneology of the Ministry of Health of the Russian Federation.

27. Victoria G. Saltykova, DSc, Professor at the Department of Ultrasound Diagnostics, Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation, Moscow, Vice President ofilin the Russian Association of Specialists in Ultrasound Diagnostics in Medicine.

28. Ekaterina G. Seliverstova, functional diagnostics physician at the Neurosurgical Department of the Sklifosovsky Research Institute of Emergency Medicine. Member of the All-Russian Society of Neurologists. Member of the Association of Clinical Neurophysiologists (ASKLIN).

29. Mikhail V. Sinkin, PhD, Senior Researcher at the Department of Emergency Neurosurgery, Head of the Clinical Neurophysiology Group, Sklifosovsky Research Institute of Emergency Medicine. Member of the All-Russian Society of Neurologists. Member of the Association of Clinical Neurophysiologists (ASKLIN).

30. Maria A. Surma, neurologist, functional diagnostics physician at the Pirogov National Medical and Surgical Center of the Ministry of Health of Russia, Moscow. Member of the Association of Clinical Neurophysiologists (ASKLIN).

31. Dmitry A. Tumurov, PhD, Leading Researcher at the Department for the Study of Pain and Somatoform Disorders, Solovyov Research and Practical Center for Mental Health of the Moscow Healthcare Department, neurologist at the outpatient clinic for patients with myasthenia gravis, Buyanov City Clinical Hospital of the Moscow Healthcare Department, Member of the All-Russian Society of Neurologists.

32. Nikolay A. Shamalov, MD, PhD, Professor, Chief Freelance Neurologist of the Ministry of Health of the Russian Federation, Chief Freelance Neurologist of the Moscow Healthcare Department, Director of the Institute of Cerebrovascular Pathology and Stroke, Federal Center of Brain Research and Neurotechnologies of the Federal Medical-Biological Agency, Executive Secretary of the National Stroke Association.

Conflict of interest

The members of the working group declared no financial or non-financial conflicts of interest regarding the topic of these clinical guidelines. Working group member(s) who reported circumstances that could potentially lead to a conflict of interest were excluded from the discussion of sections related to the conflict of interest.

Appendix A2. Methodology for Developing Clinical Guidelines

Target audience for these clinical guidelines:

1. Neurologists, general practitioners, family physicians;

2. Medical students, residents, postgraduate students;

3. Faculty members, researchers.

Table 1. Scale for evaluating levels of evidence (LE) for diagnostic methods (diagnostic interventions)

Table 2. Scale for assessing levels of evidence (LE) for prevention, treatment and rehabilitation methods (preventive, therapeutic, rehabilitation interventions)

Table 3. Grade of Recommendation (GoR) scale for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Procedure for updating clinical guidelines.

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

1) Federal Law No. 323-FZ of November 21, 2011 "On the Basics of Protecting the Health of Citizens in the Russian Federation".

2) Federal Law No. 61-FZ of April 12, 2010 "On Circulation of Medicines".

3) Federal Law No. 489-FZ of December 25, 2018 (latest edition) "On Amendments to Article 40 of the Federal Law 'On Compulsory Medical Insurance in the Russian Federation' Regarding Clinical Guidelines".

4) Procedure for the provision of medical care to the adult population for nervous system diseases (Order of the Ministry of Health of the Russian Federation No. 926n of November 15, 2012).

Appendix B. Physician Action Algorithms

Management algorithms for a patient with mononeuropathy

Appendix C. Patient Information

Mononeuropathy is a condition associated with damage to a peripheral nerve. The patient may experience numbness in the limb, tingling or a "pins and needles" sensation, pain, burning, changes in temperature sensitivity, as well as clumsiness and weakness. In more severe cases, muscle wasting occurs in the muscles innervated by the affected nerve.

The most important diagnostic method for mononeuropathy is a neurological examination, during which the neurologist can suspect damage to a specific nerve and assess the severity.

Diagnosis is confirmed using electromyographic research methods, nerve conduction study is performed, and needle electromyography is carried out if necessary.

An additional diagnostic method is ultrasound examination of the nerve; in some cases, MRI of joints and nerves may be necessary.

Depending on the type of mononeuropathy and severity of the condition, conservative or surgical treatment is chosen. First of all, the patient should avoid positions that compress the nerve (for example, for the fibular nerve, do not sit with legs crossed or in a squatting position; for the ulnar nerve, do not rest the arms on an armrest and do not bend the elbow by more than 90 degrees, and so on). In many cases, orthoses are prescribed; with proper use of the orthosis, a gradual reduction of neuropathy symptoms is observed within 1–3 months, whereas improper use may have the opposite effect. For many neuropathies, local administration of glucocorticosteroid drugs ("blockade") is effective. Blockades are administered directly into the osteofascial canals exclusively by a physician and may be performed under ultrasound guidance. The patient should keep in mind that blockades often contain an anesthetic, so numbness of the limb may increase for 1–4 hours, which is a normal drug effect and should not alarm the patient. If conservative therapy is ineffective for 3–6 months, the patient may be referred for a neurosurgical consultation to address the issue of surgical treatment. Operations are performed under local anesthesia, or general anesthesia if necessary; open or endoscopic access may be used (when the surgery is performed through small skin incisions). In general, surgical treatment for mononeuropathies is very effective, but in late stages, the effect of surgery may be incomplete.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Appendix G1. Boston Carpal Tunnel Questionnaire (BCTQ).

Source:

Levine DW, Simmons BP, Koris MJ, Daltroy LH, Hohl GG, Fossel AH, Katz JN., A self-administered questionnaire for the assessment of severity of symptoms and functional status in carpal tunnel syndrome; J Bone Joint Surg Am. 1993 Nov;75(11):1585-92.

Yusupova D.G., Suponeva N.A., Zimin A.A., Zaitsev A.B., Belova N.V., Chechetkin A.O., Gushcha A.O., Gatina G.A., Polekhina N.V., Bundhun Pratish, Ashrafov V.M. Validation of the Boston Carpal Tunnel Questionnaire in Russia. Neuromuscular Diseases. 2018;8(1):38–45.

Type: rating scale.

Purpose: evaluation of symptom severity and functional impairment in carpal tunnel syndrome.

Content (template):

Symptom Severity Scale (SSS)

The following questions refer to symptoms you have experienced at different times of the day over the past few weeks (choose one answer per question).

How severe is the pain in your hand or wrist at night?

1. I do not have pain in my hand/wrist at night

2. Mild pain

3. Moderate pain

4. Severe pain

5. Very severe pain

How often did you wake up due to pain in your hand/wrist over the past two weeks?

1. Never

2. Once

3. Two or three times

4. Four or five times

5. More than five times

Do you typically experience pain in your hand/wrist during the day?

1. I do not have pain during the day

2. I have mild pain during the day

3. I have moderate pain during the day

4. I have severe pain during the day

5. I have very severe pain during the day.

How often during the day do you experience pain in your hand/wrist?

1. Never

2. One to two times a day

3. Three to five times a day

4. More than five times a day

5. I have pain constantly

What is the average duration of a daytime pain episode?

1. I do not have pain during the day

2. Less than 10 minutes

3. From 10 to 60 minutes

4. More than 60 minutes

5. I have pain constantly throughout the day

Do you have a feeling of numbness (decreased sensitivity) in your hand?

1. No

2. There is a mild feeling of numbness/decreased sensitivity

3. There is a moderate feeling of numbness/decreased sensitivity

4. There is a pronounced feeling of numbness/decreased sensitivity

5. There is a very pronounced feeling of numbness/decreased sensitivity

Do you have weakness in your hand/wrist?

1. No

2. There is mild weakness

3. There is moderate weakness

4. There is pronounced weakness

5. There is a substantial loss of strength in the hand/wrist

Do you feel a tingling sensation in your hand/wrist?

1. No

2. Mild tingling

3. Moderate tingling

4. Pronounced tingling

5. Very severe tingling

How severe is the numbness (loss of sensitivity) or tingling sensation during the night?

1. I do not have numbness or tingling at night.

2. Mild

3. Moderate

4. Severe

5. Very severe

How many times over the past two weeks have you woken up from numbness or a tingling sensation in your hand/wrist?

1. Never

2. Once

3. Two or three times

4. Four or five times

5. More than five times

Do you experience difficulty picking up and using small objects (keys, pencil)?

1. No

2. I experience slight difficulty

3. I experience moderate difficulty

4. Experience great difficulty

5. Experience very great difficulty

Functional Status Scale (FSS):

Have you experienced any difficulty performing the following activities due to hand or wrist problems over the past two weeks? Please circle one number in each row that best describes your ability to perform the activity.

Key (Interpretation): The scores for the SSS and FSS scales are calculated independently; scores from the two scales are not summed.

The score for each scale is calculated as the arithmetic mean of the item scores (from 1 to 5).

Examples:

SSS scale: Total score = 16. Sum/number of items = 16/11 = 1.5. FSS scale: Total score = 14. Sum/number of items = 14 / 8 = 1.8.

Notes: The scale allows for an objective assessment of the severity of carpal tunnel syndrome clinical manifestations and tracking the patient's condition over time.

Appendix G2. Medical Research Council (MRC) Scale

Source: Medical Research Council Scale, R. Van der Ploeg, et al 1984.

Type: rating scale

Purpose: assessment of muscle strength

Content (template):

Key (Interpretation): Muscle strength of the tested muscles is scored according to the data provided in the table.

Notes: The scale allows assessing the strength of the tested muscles at the time of examination using points and determining the pattern of muscle weakness distribution.

Appendix G3. Visual Analogue Scale (VAS) for pain assessment

Source: Huskisson, E. C. Measurement of pain / E. C. Huskisson // Lancet. - 1974. - Vol. 304, Issue 7889. - P. 1127-1131.

Type: rating scale.

Purpose: assessment of pain intensity.

Content (template):

0–0.5 points     0–4 mm         no pain

0.5–4.5 points    5–44 mm       mild pain

4.5–7.5 points  45–74 mm      moderate pain

7.5–10 points   75–100 mm   severe pain

Notes: The scale allows assessing the severity of subjective pain sensations.

Appendix G4. DN4 Diagnostic Questionnaire for Neuropathic Pain (Douleur Neuropathique en 4 Questions)

Source:

Bouhassira D., Attal N., Alchaar H., Boureau F., Brochet B., Bruxelle J., Cunin G., Fermanian J., Ginies P., Grun-Overdyking A., Jafari-Schluep H., Lanteri-Minet M., Laurent B., Mick G., Serrie A., Valade D., Vicaut E. Comparison of pain syndromes associated with nervous or somatic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4)// Pain: March 2005 - Volume 114 - Issue 1 - p 29 - 36 doi: 10.1016/j.pain.2004.12.010.

Type: rating scale

Purpose: identification of neuropathic pain or a neuropathic component of pain in mixed nociceptive-neuropathic pain syndromes

Content (template):

PATIENT INTERVIEW

Does the pain experienced by the patient meet one or more of the following definitions?

Is the pain accompanied by one or more of the following symptoms in its localization area?

PHYSICAL EXAMINATION

Is the pain localized in the same area where examination reveals one or both

of the following symptoms:

Can the pain be provoked or exacerbated in the area of its localization:

Total score (number of "Yes" answers): _____

Key (interpretation): A score of 4 or more indicates that the patient's pain is neuropathic, or that there is a neuropathic pain component (in mixed nociceptive-neuropathic pain syndromes).

Notes: The scale is used to detect neuropathic pain, as well as a neuropathic pain component in mixed-character pain syndromes.

Appendix G5. Leeds Assessment of Neuropathic Symptoms and Signs (LANSS)

Source:

Bennett M, The LANSS Pain Scale: the Leeds assessment of neuropathic symptoms and signs, Pain. 2001 May; 92(1-2):147-157; 

Yusupova D.G., Suponeva N.A., Zimin A.A., Zaytsev A.B., Bennett M., Belova N.V., Chechetkin A.O., Gushcha A.O., Gatina G.A., Polekhina N.V., Bundhun P., Ashrafov V.M.,

Piradov M.A. Validation of the Leeds assessment of neuropathic symptoms and signs (LANSS) scale in Russia. Neuromuscular Diseases. 2018;8(3):43-50.

Type: rating scale

Purpose: identification and assessment of neuropathic pain.

Content (template):

A. PAIN ASSESSMENT (Questionnaire)

Think about what your pain sensations have been like over the past week.

Please select the statements that best describe your pain.

1. Does your pain present as strange, unpleasant sensations in the skin? Can these sensations be compared to tingling?

a) NO – The pain I experience cannot be described in this way (0)

b) YES – I am troubled by such sensations quite frequently (5)

2. Does the skin change in the area where the pain is localized? Does it become blotchy? Does it appear red?

a) NO – Pain does not affect the appearance of the skin (0)

b) YES – Where the pain bothers me, the appearance of the skin differs from normal (5)

3. Is sensitivity to touch increased in the affected skin area? Could it be said that light stroking of the skin or contact with clothing causes unpleasant or painful sensations?

a) NO – Sensitivity is unchanged in the affected skin area (0)

b) YES – Skin sensitivity is increased in the affected area (3)

4. Does the pain appear suddenly, at rest, for no apparent reason? Can it be described as throbbing, bursting, or resembling an electric shock?

a) NO – My sensations cannot be described in this way (0)

b) YES – I am troubled by such sensations quite frequently (2)

5. Does the skin temperature in the affected area differ from the temperature of the rest of the skin surface? Can such sensations be described as burning or heat?

a) NO – I am not troubled by such sensations (0)

b) YES – I am troubled by such sensations quite frequently (1)

B. SENSITIVITY ASSESSMENT

Superficial sensitivity is examined for the presence of allodynia and changes in the pain sensitivity threshold (using pinprick testing) in the affected skin area compared to a symmetrical area on the opposite side of the body or another skin area.

1. Allodynia

Assess sensitivity to light touch with cotton wool on the affected and healthy skin areas. The presence of allodynia can be stated if touching the affected skin area causes pain or other unpleasant sensations (tingling, nausea), whereas performing the test on the healthy skin area does not cause such sensations.

a) NO – Sensitivity is identical in both areas (0)

b) YES – Allodynia only in the affected area (5)

2. Change in the pain sensitivity threshold

Determine the pain sensitivity threshold in the healthy and affected skin areas using a 23-gauge needle inserted inside the barrel of a 2 ml syringe.

If pinprick on the healthy area feels like a sharp touch, while on the affected area it feels different — for example, the touch is not felt at all, feels like a dull touch (increased pain threshold), or is very painful (decreased pain threshold) — then a change in the pain sensitivity threshold can be stated.

If the prick is not felt anywhere, attach the needle to the syringe to increase the weight and repeat the test.

a) NO – Sensations from the needle prick are identical in both areas (0)

b) YES – Altered sensation from the needle prick in the affected area (3)

SCORING:

To obtain the total sum, the values of the pain and sensitivity assessment parameters are added up.

TOTAL SCORE: ______________ (maximum 24 points)

Key (Interpretation): If the score is <12, a neuropathic mechanism of pain is unlikely. If the score is ≥12, a neuropathic mechanism of pain is likely.

Notes: The scale helps identify dysfunction of nerves responsible for pain, which is important for determining further management tactics.