Nerve entrapment syndrome refers to the compression of peripheral nerves by a certain peripheral tissue, which causes pain, sensory disorders, motor disorders and electrophysiological changes, and is one of the bone-fiber canal and ventricular compression syndromes.
1.Etiology
The lesion is mostly located in some specific anatomical sites, the bone-fiber canal, or inelastic muscle fiber edge, tendon arch and other nerve channel key jamming points, where the compressed nerve is difficult to avoid and buffer.
The etiology can be summarized into three main categories.
(1) Intracanalicular compression
Tendon sheath cysts, neurofibromas, and chronic inflammatory nerve injury.
(2) Extradural compression
Bone warts, bone and key injuries, ligament injuries.
(3) Systemic disorders
Rheumatoid arthritis, mucinous edema, obesity, diabetes, hyperthyroidism, Reynaud’s disease, pregnancy, etc. can be combined with nerve entrapment signs.
2.Clinical classification
(1) Carpal tunnel syndrome
This disease, also known as delayed median nerve palsy, is caused by compression of the median nerve in the carpal tunnel. The carpal tunnel is located at the root of the palm, and is composed of the carpal bones at the bottom and sides, with the transverse carpal ligament crossing it to form a bone-fiber channel.
Chronic injury caused by long-term overuse of the hand and wrist, chronic inflammation of the transverse carpal ligament and content tendons can occur, narrowing the canal lumen is the most common cause. This is followed by acute injury to the wrist, distal radius fracture, and lunate dislocation can cause acute or secondary compression of the median nerve. Certain systemic diseases can cause spontaneous median nerve damage through enlargement of the carpal tunnel contents.
The age of prevalence is 30-60 years old, five times higher in women than in men, and the onset is usually unilateral, but can be bilateral. The onset of the disease is slow, with pain, numbness, and swelling in the median nerve innervation area, often waking up after several hours of sleep and relieved by activity. The skin of the median nerve distribution area is dull and hypersensitive. There may be atrophy of the greater pisiform area and clumsiness and weakness of the thumb.
Tinel’s sign may appear on percussion of the wrist, extreme flexion of the wrist for 60 seconds, abnormal sensation of the hand may be aggravated (Phalen’s test), and intracarpal tunnel pressure is increased. Inflation of the sphygmomanometer above the systolic pressure for 30 to 60 seconds may induce pain in the affected hand. Hyperextension and flexion tests also cause sensory abnormalities and increased pain. The palmar aspect of the carpal tunnel is painful and radiating. The median nerve conduction velocity is slowed. Non-surgical treatment involves resting the wrist in a neutral position and intracarpal tunnel injection of corticosteroids. Surgical decompression is required for recurrent episodes that are not relieved by non-surgical treatment. The use of endoscopic surgery has been reported.
(2) Carpal ulnar tunnel syndrome
This disease is also known as Guyon’s canal syndrome, bean-hook cleft syndrome, and Ramsay-Hunt syndrome. The ulnar canal of the wrist is triangular in cross-section, with the anterior wall of the superficial transverse carpal ligament, the posterior wall of the deep transverse carpal ligament, and the medial wall of the carpal bean bone and bean-hook ligament. The ulnar nerve and ulnar artery and vein pass through it. Compression of the ulnar nerve within it causes ulnar canal syndrome. It is most often caused by tendon sheath cysts, with a smaller proportion of chronic injuries and contusions. Other causes are fractures, congenital malformations and generalized pain.
Superficial branch involvement causes sensory deficits in the innervated area of the ulnar nerve. Deep branch entrapment may cause intrinsic muscle atrophy and weakness of the hand, deep hand distension and burning pain, significant pain at night, thumb inversion, other four fingers retraction weakness, ring and little finger may show claw deformity, paperclip test, positive Froment test. Electrophysiological examination may reveal paralyzed muscle fiber fibrillation EMG and slowed nerve conduction velocity. If non-surgical treatment is ineffective, Guyon’s canal can be surgically incised to fully decompress and free the ulnar nerve.
(3) Rotator anterior round muscle syndrome
The median nerve is located at the proximal end of the forearm and is compressed by the tendon arch between the two heads of the pronator teres muscle. When the forearm is rotated forward, the median nerve is lifted by the ulnar head of the pronator teres muscle. The pain may be radiated to the radial side of the three fingers, and there may be weakness in flexion of the fingers. There may be pressure pain on the superior border of the anterior rotator muscle, Tinel’s sign. Weakness to the palm. Local corticosteroid injection can mostly relieve the symptoms, and when ineffective, the stuck tendon arch or fiber band can be surgically cut.
(4) Interosseous anterolateral nerve entrapment syndrome
This disease, also known as Kiloh-Nevin syndrome, is caused by the interosseous anterior nerve branch of the median nerve being compressed by the tendon arch or fibrous band of the superficial flexor digitorum superficialis. It is characterized by pain in front of the elbow, reduced flexion force of the distal interphalangeal joint of the thumb, and “twist” sign if the thumb flexor is completely paralyzed, weakness of the anterior rotator muscle when flexing the elbow, normal hand sensation, and no intrinsic hand muscle paralysis.
(5) Radial canal syndrome
This disease is also known as radial arch syndrome, posterior rotator muscle syndrome, and interosseous dorsal nerve entrapment pain. It is caused by the deep branch of the radial nerve being stuck in the radial canal by the superficial tendon arch of the posterior rotator muscle or the tendon arch of the radial short extensor carpi radialis. The onset of the disease is slow and may occur gradually with extension of the metacarpophalangeal joint, extension of the thumb, weakness of the abducted thumb, and wrist extension to the radial side due to involvement of the ulnar carpal extensor muscle and intact radial carpal extensor muscle.
There is no sensory abnormality and no pain. The disease is positive for the middle finger test, which makes the elbow, wrist, and interphalangeal joints straight when examined, and resistance to straightening the metacarpophalangeal joint induces pain at the medial edge of the starting point of the radial carpal short extensors as positive. The pain in tennis elbow appears above and below the medial epicondyle. Surgery requires exploration of common interosseous dorsal nerve entrapment points, including the anterior radial head, the radial carpal short extensor arch, and the Frohse arch of the posterior rotator muscle.
(6) Ulnar canal syndrome of the elbow
This is the result of entrapment of the ulnar nerve within the bony fiber channel consisting of the ulnar canal at the elbow, medially at the medial epicondyle, laterally at the hawk’s mouth, with the ulnar nerve groove at the base of the canal, and covered by the tendon membrane between the medial epicondyle and the hawk’s mouth. Common causes are excessive elbow activity, sequelae of elbow trauma, and congenital deformities. In addition, elbow pain, such as osteoarthrosis, tuberculosis, and rheumatoid arthritis, can cause ulnar nerve compression.
The onset is slow, with numbness and tingling on the ulnar side of the forearm, ulnar side of the hand, and the fourth and fifth fingers. There may be intrinsic muscle atrophy, claw-shaped hand (ring little finger) deformity, positive paperclip test and Froment test. The ulnar nerve sulcus can be palpated to thicken the nerve, with pressure pain and positive Tinel’s sign. Electrophysiological examination is helpful for diagnosis. If non-surgical treatment is ineffective, ulnar nerve anterior transposition and medial humeral epicondyle resection can be used.
(7) Suprascapular nerve entrapment syndrome
This is caused by the entrapment of the suprascapular nerve in the scapular notch at the lateral superior angle of the scapula. This notch is lateral to the base of the rostral process, and the transverse ligament on the imported external transverse frame forms a bone-fiber canal. Occupations with prolonged scapular hyperactivity predispose to this disease. It manifests as persistent dull shoulder pain radiating to the cervical and interscapular regions, and the pain is aggravated by increased elbow activity in the shoulder. Shoulder abduction and external rotation is weak. The supraspinatus and infraspinatus muscles of the affected shoulder may have atrophy, but there is no localized pressure pain.
(8) Pear-shaped muscle syndrome
The sciatic nerve crosses the sciatic notch generally under the pear muscle and penetrates in the inferior foramen of the pear muscle between the inferior edge of the muscle and the superior I muscle, which causes the pear muscle syndrome by compression. The etiology is mainly acute or chronic injury of the pear-shaped muscle, complaining of hip pain and abnormal sensation, and radiating to the posterior femur, examination can reveal deep pressure pain in the pear-shaped muscle area, resistance to abduction and external rotation of the affected hip can induce pain, and feel weakness in activities, and aggravate pain in passive hip flexion, internal retraction, and internal rotation of the elbow.
(9) Lateral femoral cutaneous nerve entrapment syndrome
The lateral femoral cutaneous nerve passes through the anterior superior iliac spine and becomes entrapped in the bone-fiber canal formed between the anterior superior iliac spine and the outer end of the inguinal ligament, causing the disease. The manifestations are burning pain, numbness and hypersensitivity in the innervated area of the lateral femoral cutaneous nerve, and there may be diminished sensation of touch, pain and temperature.
(10) Peroneal nerve entrapment syndrome
Injury and extracorporeal compression are common causes of this disease, which manifests as pain and numbness in the lateral aspect of the foot and lower leg. Motor deficits are dorsiflexion of the ankle, weakness of toe extension, weakness or loss of valgus force, and sensory deficits in the lateral calf and lateral foot. There may be pressure pain and Tinel’s sign at the peroneal neck. Compression of the superficial peroneal nerve cutaneous branch at the outlet of the deep fascia of the distal calf is another pressure point of this syndrome. Injury and tight shoes and socks can cause this disease, which only manifests as pain and abnormal sensation in the innervated area.
(11) Tarsal tunnel syndrome
The posterior tibial nerve is compressed within the bony-fiber canal formed by the flexor support band and the heel bone under the posterior aspect of the inner ankle, causing this disease. Chronic injury caused by foot overuse is a common cause. Intermittent paresthesia, burning pain, or numbness in the sole or heel of the foot is the main complaint, and the pain can be aggravated by prolonged standing or walking, often with nocturnal pain that wakes the patient up in pain. There may be pressure pain and Tinel’s sign under the posterior aspect of the medial ankle. Weak flexion of the metatarsophalangeal joint and the tourniquet inflation test may induce foot pain.
(12) Plantar common nerve entrapment syndrome
This disease, also known as Morton’s disease and Morton’s metatarsalgia, may be caused by the entrapment of the plantar nerve between the two adjacent metatarsal heads, the deep intermetatarsal ligament and the metatarsal tendon membrane. The cause is often a chronic injury from prolonged standing and walking. The pain is aggravated by walking and standing, and is relieved by rest and shoe removal. Lateral compression of the metatarsal head can cause interval pain. Non-surgical treatment allows the patient to wear loose, flat-soled soft shoes to support the shaping of an already flat transverse arch. Traditional surgery is performed to remove the pain-causing neuroma, and in recent years it has been reported that cutting the deep interdigital ligament has obtained excellent results.
3.Clinical manifestations
(1) Pain and sensory abnormalities
Sensory loss or abnormalities may occur according to the innervated dermatome.
(2) Rest pain
The pain is aggravated at night and is also called rest pain.
(3) Radiating pain
The pain may radiate to the proximal and distal sides at the same time and needs to be differentiated from double entrapment.
(4) Movement
Muscle atrophy, weakness, and incoordination of movement.
(5) Sympathetic nerve involvement signs
The manifestations are temperature, color, sweating and nutritional disorders.
(6) Vallex phenomenon
Restricted pressure pain and radiation at the card pressure point. Vallex phenomenon is described as pressure pain on both the distal and proximal sides of the card pressure point.
(7) Tinel’s sign
Light percussion pain and tingling sensation at the pressure point.
4.Examination
It is impossible to list all of them because there are many sites and different examination methods for each site. From various common examinations, EMG examination of neurogenic disease can show fiber tremor and denervation potential, and there is generally no conduction slowdown. Peripheral nerve involvement may have conduction velocity slowing and distal latency slowing. In contrast, x-ray plain films only reveal signs of bone growth and old injury.
There are also a number of diagnostic nerve blocks that can be used, mainly in patients with atypical clinical presentation. The main nerve can be selected at the site of suspected nerve entrapment syndrome and injected with 2 ml of 1% lidocaine, which can help to diagnose if the patient’s clinical symptoms are rapidly relieved.
5. Diagnosis of neurological entrapment syndrome
Since it occurs in a very large number of parts, the diagnosis of nerve entrapment syndrome in each part needs to be differentiated from similar diseases that may occur there.
6. Complications of the disease
The complications of the disease are mainly when the compression is severe and persistent, which can cause demyelinating changes in the nerve fibers, or even disintegration of the distal axon and Waller degeneration of the myelin sheath. When the limb is active, the nerve fibers in the narrow channel undergo chronic damaging inflammation under mechanical stimulation and aggravate the vicious cycle of edema-ischemia. This causes further damage, so patients with this disease should be actively treated to prevent complications.
7.Treatment The treatment of this disease is divided into two main cases.
(1) Non-surgical treatment
Local braking, corticosteroid injection and NSAID administration are used to reduce the inflammatory response of the stuck lesion and relieve the symptoms. However, the disease is a slowly progressive disease and rarely heals on its own.
(2) Surgical treatment
For patients with this disease, surgical treatment is more often performed, usually through surgical incision of the bone-fiber channel, so that the nerve can be decompressed and released. Care should be taken at this time to avoid surgical brutality and further damage to the nerve.