संपीड़न न्यूरोपैथी

This is the clinical evidence summary written for health professionals. It is technical, and it lists the research this page was built from. You do not need to read it to understand your treatment or to make a decision about it.

Overview¶

• Compression neuropathies of the upper extremity involve pathophysiology mechanisms including the double-crush mechanism and systemic factors [1].
• Validated patient-reported outcome measures are utilized in the clinical evaluation and management of upper extremity compression neuropathies [1].
• Most publications regarding uncommon compression syndromes of the radial, ulnar, and median nerves are small retrospective series or case reports [2].
• Treatment decisions for uncommon upper extremity compression neuropathies are not typically based on high levels of evidence [2].
• Complications of compressive neuropathy management include iatrogenic injury, treatment failure, and pathologic pain syndromes [3].
• Prevention of complications in compressive neuropathy management relies on a solid understanding of normal anatomy and anatomic variations [3].
• The diagnosis of compressive neuropathies is shifting towards the use of preoperative imaging with ultrasound and MRN [4].
• The management of failed decompressions for compressive neuropathies remains challenging [4].
• Minimally invasive in situ decompression is technically simple and safe for patients with severe nerve compression [5].
• Minimally invasive in situ decompression yields good results in patients with severe nerve compression [5].
• Debulking of a tumor combined with median nerve decompression resulted in relief of neurological symptoms in a case of carpal tunnel syndrome caused by collagenoma [7].
• A collagen matrix wrap technique has been reported for recurrent compression neuropathies with good success [12].
• Surgical decompression for carpal tunnel syndrome is associated with a greater decrease in median nerve cross-sectional area than nonsurgical treatment [13].
• Anterior interosseous nerve transfer combined with cubital and ulnar tunnel release results in sustained clinical and electrophysiological improvements in patients with severe chronic ulnar nerve compression [15].
• Anterior interosseous nerve transfer combined with cubital and ulnar tunnel release is encouraged as a standard treatment for severe chronic ulnar nerve compression [15].
• Satisfactory outcomes from endoscopic detection of compressing fascial bands support the perception that extensive decompression of the ulnar nerve beyond the cubital tunnel is not routinely needed [19].
• Carpal tunnel release is a reasonable first step prior to proceeding with cervical spine decompression for patients with nerve compression at both the carpal tunnel and cervical spine [20].
• Patients with and without double crush syndrome achieve similar rates of clinical improvement following carpal tunnel release [20].
• Surgical decompression remains the definitive treatment of cauda equina syndrome [47].
• The timing of surgery for cauda equina syndrome requires careful consideration to balance the urgency of intervention with the risks of complications [47].

Anatomy & Pathophysiology¶

Nerve Compression Pathophysiology¶

• The underlying pathophysiology of double crush syndrome (DCS) is widely debated [11].
• Upton and McCombs theorized that compression at one location on a nerve's axon predisposes that same axon to injury elsewhere [11].
• This increased susceptibility to injury is theorized to result from disrupted bidirectional transport of essential nutrients along the axon [11].
• Inability to obtain and utilize nutrients leads to gradual morphological and functional changes in the nerve [11].
• More proximal lesions, closer to the cell body, have a greater effect on nerve function [11].
• Evidence for disruption of axonic flow due to compression is extensive, but the resultant clinical effect remains a topic of significant debate [11].
• The term "double crush" is considered misleading because it does not account for conditions where three or more sites of a given nerve are affected [11].
• The term "crush" is considered limiting because it implies purely mechanical compression and excludes other mechanical stresses such as stretch [11].
• The term "crush" is considered limiting because it excludes medical and pharmacological factors that likely contribute to the disease process [11].
• The term "multifocal neuropathy" (MFN) is proposed to expand the scope of DCS to include non-mechanical factors and multiple sites [11].
• The clinical findings in patients with chronic nerve compression are variable and reflect a broad spectrum of histopathologic changes [36].
• Much of the information known about the histopathology of human nerve compression has been extrapolated from animal models because biopsy of neural tissue is not performed [36].
• Studies have suggested neural ischemia as a contributing factor to compression neuropathies [36].
• The continuum of neural changes seen with compression neuropathy depends on the force and duration of the compression [36].
• Histopathologic changes in chronic nerve compression begin with breakdown of the blood-nerve barrier [36].
• Breakdown of the blood-nerve barrier is followed by endoneurial edema [36].
• Endoneurial edema is followed by perineural thickening [36].
• Increased endoneurial pressure results in changes in microneural circulation and renders the nerve susceptible to dynamic ischemia [36].
• With increased compression, localized demyelination occurs, followed by more diffuse demyelination and finally axonal degeneration [36].
• Neural changes typically do not occur uniformly across the nerve and may vary depending on the distribution of compressive forces [36].
• Fascicles susceptible to greater pressure undergo changes sooner, resulting in variable patient symptoms within a nerve’s distribution [36].
• In early carpal tunnel syndrome, the superficial fascicles to the long finger and ring finger are usually affected before the fascicles to the thumb and radial side of the index finger [36].
• In cubital tunnel syndrome, the fascicles to the intrinsic muscles are located closer to the bony groove and are affected more than those to the flexor digitorum profundus and flexor carpi ulnaris [36].
• Patient sensory complaints are theorized to parallel histopathologic neural changes, progressing from intermittent paresthesia to persistent numbness [36].
• Initially, patients with nerve compression have altered threshold tests for vibration and Semmes-Weinstein monofilament testing [36].
• With more severe nerve compression, deficits progress to tactile discrimination testing, including static and moving two-point discrimination [36].

Upper Extremity Anatomy¶

• The hand is both an organ designed to obtain information and an organ of execution [27].
• The hand functions efficiently only if the proximal joints of the limb are stable and yet mobile [27].
• The shoulder is the most mobile joint in the body and allows orientation of the upper limb as required [27].
• The movements of the clavicle amplify those of the shoulder [27].
• The elbow, through flexion–extension movements, brings the hand closer to or moves it away from the body [27].
• The combined movements of the wrist and forearm place the hand in a position for grasping [27].
• For gripping, the wrist is usually in flexion when close to the trunk and in extension when placed at a distance [27].
• Forearm rotation (pronation–supination) plays an important role, particularly for bringing food to the mouth [27].
• The hand’s blood and nerve supplies are continuous with those of the rest of the limb [27].
• Some hand muscles, the extrinsic muscles, arise in the arm and forearm [27].
• The hand consists of 19 bones, 17 articulations, and 19 muscles situated entirely within the hand [27].
• The hand contains about the same number of tendons activated by the forearm muscles [27].
• The open hand, with fingers extended and in contact, forms a balanced graceful oval in its longitudinal axis [27].
• The proximal carpometacarpal half of the hand is flattened, presenting two faces with unique anatomical and functional significance [27].
• The posterior or dorsal aspect of the hand is convex [27].
• The anterior, palmar or volar aspect of the hand is concave [27].
• The distal half of the hand is separated into five digits which flex toward the palm [27].
• Digits converge in closing by flexing and adducting, and diverge in opening by extending and abducting [27].
• The thumb has a more proximal and lateral position, allowing movement inward and outward from the palm [27].
• The four fingers are the distal extension of the carpometacarpal part of the hand [27].
• The hinges of finger movements are at the thenar crease and at the transverse distal palmar crease [27].
• When digits are fully extended and touching, their tips almost describe a regular curve, with peripheral digits being the shortest [27].
• When fingers are extended and separated, their tips lie on the circumference of a circle whose center is the head of the third metacarpal [27].
• The web space of the thumb is the largest and deepest [27].
• There are seven interosseous muscles in the hand, four dorsal and three volar [29].
• The dorsal interossei are abductors [29].
• The anatomic axis of the hand coincides with the axis of the third metacarpal [29].
• The dorsal interossei lie to the radial side of the index and middle fingers and the ulnar side of the middle and ring fingers [29].
• The little finger is abducted by the abductor digiti quinti [29].
• The volar interossei are adductors [29].
• The volar interossei lie to the ulnar side of the index finger and the radial side of the ring and little fingers [29].
• The middle finger has two dorsal interossei and no volar interossei because the central axis of the hand lies within it [29].
• Each dorsal interosseous muscle, with the exception of the third, has two muscle heads [29].
• The superficial head of the dorsal interosseous muscles arises most dorsally from the shaft of the contiguous metacarpals [29].
• The superficial head inserts deeply by a medial tendon onto the lateral tubercle of the base of the proximal phalanx [29].
• The superficial head abducts and weakly flexes the proximal phalanx [29].
• The superficial head has no direct effect on the middle or distal phalanges [29].
• The deep head of each dorsal interosseous muscle forms a lateral tendon, or lateral band, at the level of the MP joint [29].
• The deep head flexes and weakly abducts the proximal phalanx while extending the middle and distal phalanges [29].
• At the level of the middle of the proximal phalanx, transverse fibers arch dorsally from each lateral band to join each other over the dorsum of the finger [29].
• These transverse fibers flex the proximal phalanx [29].
• Oblique fibers, or spiral fibers, from the lateral bands sweep over the distal third of the proximal phalanx to insert onto the lateral tubercles at the base of the middle phalanx [29].
• The oblique fibers extend the middle phalanx at the PIP joint [29].
• The lateral bands are joined by the lateral slips of the extensor tendon to form the conjoined lateral band [29].
• The two conjoined lateral bands to each finger unite at the distal third of the middle phalanx to form the terminal tendon [29].
• The terminal tendon inserts at the base of the distal phalanx to extend it [29].
• The flexor digiti quinti brevis is structurally and functionally similar to the deep head of the dorsal interossei [29].
• The flexor digiti quinti brevis forms the ulnar lateral band of the little finger [29].
• The three volar interossei arise from adjacent surfaces of contiguous metacarpal shafts [29].
• Each volar interosseous muscle has only one muscle head [29].
• None of the volar interossei insert onto the proximal phalanx [29].
• The volar interossei form the ulnar lateral band of the index finger and the radial lateral band of the ring and little fingers [29].
• The abductor digiti quinti and flexor digiti quinti brevis are similar in structure and function to the superficial and deep heads of the dorsal interossei, respectively [29].
• The abductor digiti quinti and flexor digiti quinti brevis arise from the fifth metacarpal [29].
• The abductor digiti quinti inserts onto the ulnar lateral tubercle at the base of the proximal phalanx of the little finger [29].
• The flexor digiti quinti forms the ulnar lateral band [29].
• The opponens digiti quinti lies deepest among the hypothenar muscles [29].
• The opponens digiti quinti arises from the pisohamate ligament and the hook of the hamate [29].
• The opponens digiti quinti inserts onto the ulnar side of the diaphysis of the fifth metacarpal [29].
• The opponens digiti quinti flexes and supinates the fifth metacarpal [29].
• The metacarpal arch is endowed with a great deal of adaptability because of the mobility of the peripheral metacarpals [32].
• The peripheral metacarpals form the sides of the cup or palmar gutter and can deepen the concavity as they approach each other [32].
• The peripheral metacarpals are attached to the fixed element, which is the middle metacarpals [32].
• The thumb metacarpal is independent and articulates with the trapezium [32].
• The middle metacarpals are united to the carpus by the intrinsic interlocking encasement of the bones themselves [32].
• The index metacarpal is the most firmly fixed [32].
• The ring metacarpal is a transitional element to the fifth metacarpal and has about 10 degrees of mobility in flexion and extension [32].
• The fifth metacarpal is semi-independent and articulates with the hamate [32].
• The fifth metacarpal is restrained on its radial side by its articulation with the base of the fourth metacarpal [32].
• The fifth metacarpal has a range of flexion–extension of approximately 20 degrees [32].
• The second to fifth metacarpals are bound together by various fibrous structures [32].
• The most distal fibrous structure binding the second to fifth metacarpals is the deep transverse intermetacarpal ligament [32].
• The deep transverse intermetacarpal ligament is better named the interglenoid ligament [32].
• The interglenoid ligament ties together the anterior glenoid ligaments of the metacarpophalangeal articulations, known as the volar plates [32].
• The longitudinal arches are composed of a fixed portion, the carpometacarpal, and a mobile portion, the digits [32].
• For every ray there is a longitudinal arch [32].
• The longitudinal arches diverge distally according to their different obliquities, with the thumb ray being the most divergent [32].
• The keystones of the longitudinal arches are the metacarpophalangeal articulations [32].
• The thick anterior glenoid capsules, or volar plates, of the metacarpophalangeal articulations prevent hyperextension [32].
• The volar plates are interconnected by the transverse interglenoid ligament [32].
• The stability of the metacarpophalangeal joints is essential to the support of the longitudinal arch as well as of the transverse metacarpal arch [32].
• The five rays of the hand differ in mobility and independence [32].
• Mobility and independence are considerable for the thumb, much less for the fifth ray, and even less for the others [32].
• The index ray has a certain degree of independence at the phalangeal level owing to the arrangement of its flexor and extensor muscles [32].
• The flexor retinaculum maintains and restrains the tendons of the extrinsic flexors of the digits within the carpal canal [32].
• The palmar tendons, especially the profundus, are kept close to the axis of flexion–extension of the wrist by the flexor retinaculum [32].
• The extensors of the wrist are more distant from the axis of flexion–extension than the flexors digitorum [32].
• The extensors of the wrist have a mechanical advantage that compensates for their difference in power compared to the flexors [32].
• This mechanical advantage enables the extensors to act synergistically with the flexors in the power grip [32].
• The hollow or concavity of the palm depends on changes in position of the transverse metacarpal arch [32].
• Changes in the transverse metacarpal arch are accomplished by flexion and adduction movements of the first and fifth metacarpal heads [32].
• The heads of the second and third metacarpals are fixed [32].
• Only the fourth and fifth metacarpals are mobile at their carpal articulation [32].
• The fourth metacarpal allows "flexion" of 10 degrees [32].
• The fifth metacarpal allows "flexion" of 20 degrees accompanied by a slight lateral rotational movement in the longitudinal axis of the hand [32].

Cutaneous Anatomy¶

• There are functional cutaneous units in the hand similar to those customarily described in the face [28].
• One cutaneous unit on the dorsum of the hand extends from the wrist to the proximal interphalangeal joints of the fingers and the interphalangeal joint of the thumb [28].
• The dorsal covering of the interphalangeal articulations of the digits forms a unique cutaneous unit characterized by a considerable excess of skin when the digits are in extension [28].
• The fine tight skin of the dorsal aspect of the middle phalanx forms another cutaneous unit [28].
• The dorsal integument of the distal phalanx is very special because of the nail bed with its matrix [28].
• The palm forms a cutaneous unit extending from the distal transverse crease of the wrist up to the transverse crease at the base of the digits [28].
• The palmar integument may be subdivided into two separate zones by the oppositional crease of the thumb [28].
• The oppositional crease of the thumb constitutes the oblique axis of the hand [28].
• The skin of the radial portion of the palm covers the thenar eminence and the external part of the palm [28].
• The skin of the radial portion of the palm is relatively well vascularized and is the mobile portion [28].
• The skin of the ulnar and distal portion covers the hypothenar eminence where the skin has poor mobility [28].
• The distal part of the palm beyond the transverse distal palmar crease is a true hinge just at the level of the metacarpophalangeal articulations [28].
• The central triangular part of the palm has skin that is fixed and poorly vascularized [28].
• The central triangular part of the palm covers almost directly the superficial palmar aponeurosis, which inserts into it [28].
• The integument of the palmar face of the digits may be subdivided into phalangeal units separated by digital flexion folds [28].
• There are three digital flexion folds for the digits and two for the thumb [28].
• When a digit is completely flexed, the integument of the adjacent phalanges comes into contact in the zones of the flexion creases [28].
• These areas of cutaneous contact are in the form of a diamond [28].
• The sides of this diamond do not undergo variations in length during the movements of flexion and extension [28].
• Incisions made along the level of the diamond sides present a minimal chance of retraction [28].
• The web spaces are formed from the union of two nonsymmetrical cutaneous surfaces [28].
• The dorsal slope of the web space has a gradual incline and its supple skin is not adherent to the subjacent region [28].
• The palmar surface

Classification¶

• Compression neuropathies of the upper extremity are classified by the specific nerve involved, including the radial, ulnar, and median nerves [2].
• Ulnar tunnel syndrome symptoms vary based on the anatomic location of the compression within Guyon's canal [17].
• The term "double crush" is considered misleading because it implies purely mechanical compression, whereas stretch and other mechanical stresses can produce similar adverse outcomes [11].
• The term "double crush" is considered misleading because it limits the scope of the disease to purely mechanical factors, whereas medical and pharmacological factors also contribute [11].
• The term "multifocal neuropathy" (MFN) is proposed to expand the scope of double crush syndrome to include non-mechanical factors and multiple sites of involvement [11].
• Ulnar nerve pathology may precede and increase susceptibility to median nerve compression [9].
• Concurrent carpal tunnel syndrome and pronator syndrome are rarely considered, with proximal compression sites easily overlooked [14].

Clinical Presentation¶

• Patients often have difficulty accurately describing their symptoms and may incorrectly attribute pathology to a perceived deficit [16].
• A careful physical examination is essential to direct care and future testing if indicated [16].
• Diagnostic tests such as imaging and serum laboratory studies are useful in determining pathologic processes but can be expensive, time consuming, and often nonspecific [16].
• The diagnosis of compressive neuropathies continues to evolve with technology, shifting towards preoperative imaging with ultrasound and MRN [4].
• Ultrasound measurements seem to have a limited value in clinical results of patients treated for entrapment neuropathy of the ulnar nerve [24].
• HRUS is a viable method to demonstrate a punched nerve syndrome [23].
• Surgical decompression was associated with a greater decrease in median nerve cross-sectional area than nonsurgical treatment [13].
• The most frequent described cause of compression in Guyon’s canal was ganglion cyst (16%) [10].
• Ganglia are the most common cause of ulnar tunnel syndrome [17].
• Symptoms of ulnar tunnel syndrome vary based on the anatomic location of the compression within Guyon's canal [17].
• Pseudogout should be considered a rare cause of acute neuropathic compression of the hand [8].
• There can be a delayed onset of ulnar tunnel syndrome following minor injury, in the absence of any identifiable compressive pathology [6].
• Concurrent carpal tunnel syndrome and pronator syndrome are rarely considered and proximal compression sites are easily overlooked [14].
• In case series documenting EDX severities of median neuropathy, surgeons are mostly treating and operating on moderate to severe pathophysiology [44].
• Mild median neuropathy is highly prevalent but is uncommonly considered for surgery [44].
• Compression or tension on the ulnar nerve about the elbow may cause neuropathy known as cubital tunnel syndrome [41].
• Cubital tunnel syndrome is the second most common upper extremity neuropathy with an incidence of 24.7 cases per 100,000 persons per year [41].
• Common sites of compression for cubital tunnel syndrome include Osborne's ligament, the 2 heads of the flexor carpi ulnaris (FCU), and the arcade of Struthers [41].
• The ulnar nerve encounters several vascular structures including the superior ulnar collateral and posterior ulnar recurrent arteries [41].
• There have been scarce reports of ulnar nerve compression by anomalous venous structures [41].
• Diagnostic ultrasound (US) has potential utility for the preoperative evaluation of vascular anomalies in cubital tunnel syndrome [41].

Investigations¶

Clinical Evaluation¶

• Diagnostic tests such as imaging and serum laboratory studies are useful in determining pathology but can be expensive, time consuming, and often nonspecific [16].
• A systematic method to approaching the physical examination is essential due to the number of structures in a small space [16].
• The task of the clinician is to combine patient history with a careful physical examination to pinpoint or narrow the scope of possible pathologic processes [16].

Imaging and Diagnostic Modalities¶

• The diagnosis of compressive neuropathies is shifting towards preoperative imaging with ultrasound and MRN [4].
• High-resolution ultrasound is a viable method to demonstrate a punched nerve syndrome [23].
• Modern ultrasound visualization enhances safety by enabling precise localization of the Berrettini branch during carpal tunnel release [58].
• An 8-MHz Doppler tone assessment may be used to identify superficially displaced neurovascular bundles when Dupuytren cords lie beneath soft fleshy prominences [37].
• False-negatives are possible with 8-MHz Doppler tone assessment for identifying neurovascular bundles [37].
• MRI is probably most useful in identifying additional pathology such as flexor tendon bowstringing in the context of Dupuytren's disease [37].
• MR assessment of Dupuytren's is hindered by the resolution of current equipment, orientation issues due to multiplanar deformities of the fingers, and lack of intraoperative availability [37].
• MRI may be helpful in providing a quantitative noninvasive measure of cellularity of affected areas, which is an index of biologic activity [37].

Specific Diagnostic Considerations¶

• Carpometacarpal dislocations producing transient motor neurapraxia of the ulnar nerve are likely to be missed in casualty due to extensive soft tissue swelling, apparent normal appearance of anteroposterior X-rays, and technical difficulty in testing the motor branch of the ulnar nerve in the presence of pain [56].

Treatment¶

Non-Operative Management¶

• The majority of patients with mild or moderate cubital tunnel syndrome symptoms benefit from conservative treatment [22].
• Endoscopic decompression is recommended for anterior interosseous nerve syndrome when conservative treatment fails to alleviate symptoms [25].
• Postoperative orthosis use after carpal tunnel release has been proposed to prevent flexor tendon bowstringing, nerve subluxation, and prolapse into the healing wound [46].
• Postoperative orthosis use after carpal tunnel release has been proposed to reduce immediate postoperative pain and lower rates of wound-healing complications and symptom recurrence [46].
• Randomized controlled studies comparing orthosis fabrication to no orthosis after carpal tunnel release surgery have failed to show any benefit to orthotics [46].

Operative Management¶

• Minimally invasive in situ decompression is technically simple, safe, and yields good results in patients with severe ulnar nerve compression [5].
• In-situ release is an alternative for managing McGowen grade 3 ulnar nerve compression neuropathy at the elbow with a similar success rate to submuscular and intramuscular transpositions [18].
• In-situ release for McGowen grade 3 ulnar nerve compression neuropathy at the elbow is associated with a lower complication rate than submuscular and intramuscular transpositions [18].
• Surgical decompression of carpal tunnel syndrome is associated with a greater decrease in median nerve cross-sectional area than nonsurgical treatment [13].
• Debulking of a collagenoma tumor along with median nerve decompression provides relief of neurological symptoms in cases of carpal tunnel syndrome caused by the tumor [7].
• A collagen matrix wrap is a novel technique used in recurrent compression neuropathies with good success [12].
• Extensive decompression of the ulnar nerve beyond the cubital tunnel is not routinely needed based on satisfactory outcomes from endoscopic detection of compressing fascial bands [19].

Complications and Special Considerations¶

• Delayed onset of ulnar tunnel syndrome can occur following minor closed wrist injury in the absence of identifiable compressive pathology [6].
• Pseudogout is a rare cause of acute neuropathic compression of the hand, including acute carpal tunnel syndrome and acute Guyon canal syndrome [8].
• Milder variants of reflex sympathetic dystrophy are common in conjunction with digital replantations (DRFs) [40].
• Early recognition of pain, finger stiffness, swelling, allodynia, or paresthesia during the first or second week may prevent the development of full-blown complex regional pain syndrome (CRPS) [40].
• Removal or splitting of a dressing or cast to relieve pressure, elevation of an edematous hand, and intensive hand therapy are frequently helpful in preventing the development of full-blown CRPS [40].
• An irritated or entrapped median nerve is frequently the cause of CRPS [40].
• Surgeons should have a low threshold for performing electrodiagnostic studies and/or surgical decompression for suspected nerve entrapment in patients with CRPS [40].
• Preemptive treatment with a long-acting sympathetic block or indwelling catheter for regional nerve blockade may be valuable for patients with a history of CRPS undergoing surgical procedures [40].
• Surgery on neural structures compromised by neuromas, neuroma-in-continuity, or compression is indicated if symptoms persist after nonoperative modalities, including sympatholytic medications, provided symptoms can be controlled medically in the perioperative period [42].
• Surgical options for neural injury in CRPS include neurolysis, neurorrhaphy, neural relocation, and modification of the neural bed [42].
• Nerve grafts from the sural nerve or a branch of the medial or lateral antebrachial cutaneous nerve are used to avoid tension on the repair site in cases of complete nerve transection or neuroma-in-continuity [42].
• Adhesions between the skin and nerve are managed by Z-plasty local flaps or distant flaps [42].
• Modification of the neural bed with autologous fat, rotational muscle flaps, pedicled muscle or fascial flaps, free muscle transfer, autologous or allograft venous wraps, or nerve conduits is an option if excessive scarring or adhesions develop [42].
• Internal neurolysis should be minimized during surgical management of neural injury in CRPS [42].
• Postoperative care for neural injury in CRPS includes sympatholytic intervention, pharmacologic palliation, physical therapy, and early active and passive range of motion [42].
• Hemostasis must be established to prevent hematoma formation during surgical management of neural injury in CRPS [42].
• Constrictive postoperative dressings should be avoided during surgical management of neural injury in CRPS [42].
• For the treatment of compression neuropathy in CRPS, the dystrophic response is managed by sympatholytic medications or autonomic blockade or both [42].
• Location of the compression neuropathy is confirmed by peripheral nerve conduction velocities or interstitial pressure measurements if symptoms justify intervention [42].
• Complete release of the involved nerve is important in the surgical treatment of compression neuropathy in CRPS [42].
• Modification of the neural environment is appropriate if there is damage to the neural bed or the neural bed is compromised [42].
• Postoperative management of CRPS patients involves sympatholytic intervention with parenteral or oral agents to minimize postoperative pain and prevent a dystrophic flare-up [42].
• Patients undergoing surgical treatment for compression neuropathy in CRPS should expect prolonged rehabilitation, continued use of oral nonnarcotic agents for 3 to 6 months, and some residual disability [42].
• Surgical release of intrinsic muscles by myotomy or tenotomy about the MCP or PIP joints decreases stiffness but does not restore full range of motion, with an average improvement of 50% [42].
• Indications for surgical management of a painful median nerve with CRPS include quiescent or stable sympathetically maintained CRPS with mechanical pain and previous neurolysis with scar and decreased nerve mobility [43].
• Preoperative evaluation for surgical management of a painful median nerve with CRPS includes demonstrating painful nerve gliding and evaluating peripheral nerve conduction velocities [43].
• When vein wrapping is selected for median nerve treatment, the autogenous saphenous vein or allograft is wrapped directly around the median nerve with an opening to allow the palmar cutaneous branch to exit [43].
• The palmar cutaneous branch may be separately wrapped if it is scarred or injured [43].
• The vein graft should be sutured proximally and distally with a 5-0 or 6-0 nonreactive suture [43].
• Chromic suture should be avoided for vein wrapping because chemicals released from the suture can create a nociceptive neural focus [43].
• An injured palmar cutaneous branch of the median nerve can be resected and moved to an unscarred area or repaired by using an end-to-end interposition antebrachial cutaneous nerve [43].
• Repair of a short palmar cutaneous nerve branch is accomplished under the operating microscope with 9-0 to 10-0 nonabsorbable suture on 75- to 130-µm needles [43].
• A suction drain is placed before completion of the procedure for median nerve surgery in CRPS [43].
• Postoperatively, the limb is protected from pain and dystrophic flare-up by the use of continuous autonomic blockade [43].
• Motion of the affected extremity is initiated in a controlled active therapy program or by using continuous passive motion over the 3- to 5-day period of hospitalization [43].
• Perioperative pain control with continuous epidural or peripheral catheters should be maintained for 3 to 5 days after surgery for chronic deformities following CRPS [43].
• Continuous field block catheters can be used as an alternative for pain control after surgery for chronic deformities following CRPS [43].
• Surgery on contracted joints should not be performed until maximal nonoperative improvement has been achieved [43].
• The waiting period for surgery on contracted joints should be a minimum of 3 to 6 months after successful elimination of the active dystrophic pain [43].
• Indications for surgery on contracted MCP or PIP joints include joint pain without diffuse dystrophic symptoms and arthrofibrosis that interferes with function [43].
• All four MCP joints and all four PIP joints can be released in a single operation if necessary [43].
• Restoration of full flexion or extension is an unreasonable goal or expectation for surgery on contracted MCP or PIP joints [43].
• The range of motion achieved during surgery for contracted MCP or PIP joints is rarely maintained after surgery as some loss is expected [43].

Complications¶

• A delayed onset of ulnar tunnel syndrome can occur following a minor closed wrist injury in the absence of any identifiable compressive pathology [6].
• The most frequent described cause of compression in ulnar nerve release at Guyon’s Canal was ganglion cyst, accounting for 16% of cases [10].
• The term "crush" in double crush syndrome is considered limiting because it implies purely mechanical compression and does not account for other mechanical stresses such as stretch or medical and pharmacological factors [11].
• The phrase "double crush" has been expanded to multifocal neuropathy to emphasize that the disease process involves complex interactions beyond purely mechanical compression [11].

Recovery¶

• Long-term improvement in patients with diabetes remained after carpal tunnel release to the same extent as for patients without diabetes [26].
• Minimally invasive in situ decompression gives good results in patients with severe nerve compression [5].
• Anterior interosseous nerve transfer, along with cubital and ulnar tunnel release, results in sustained clinical and electrophysiological improvements in patients with severe chronic ulnar nerve compression [15].
• Complete electrophysiological recovery may not occur if symptoms have been present for a prolonged period [61].
• The management of failed decompressions remains challenging [4].

Key Evidence¶

• [L4] This article reviews uncommon compression syndromes of the radial, ulnar, and median nerves, noting that most publications are small retrospective series or case reports and treatment decisions are not typically based on high levels of evidence. [2] (10.1016/j.hcl.2013.04.014)
• [L5] Complications of compressive neuropathy management include iatrogenic injury, treatment failure, and pathologic pain syndromes, with prevention relying on a solid understanding of normal anatomy and anatomic variations. [3] (10.1016/j.hcl.2015.01.012)
• [L5] The diagnosis and treatment of compressive neuropathies continue to evolve with technology, shifting towards preoperative imaging with ultrasound and MRN, while the management of failed decompressions remains challenging. [4] (10.1016/j.jhsg.2022.10.009)
• [L3] Minimally invasive in situ decompression is technically simple, safe and gives good results in patients with severe nerve compression. [5] (10.1177/1753193411416426)
• [L5] This case report highlights that there can be a delayed onset of this syndrome following minor injury, in the absence of any identifiable compressive pathology. [6] (10.1016/0020-1383(95)00013-y)
• [Case_report] Debulking of the tumor along with median nerve decompression was performed with relief of neurological symptoms. [7] (10.1016/j.jhsa.2013.07.004)
• [L4] Pseudogout should be considered a rare cause of acute neuropathic compression of the hand. [8] (10.1016/j.jhsg.2022.07.010)
• [L2] This supports the hypothesis that ulnar nerve pathology may precede and increase susceptibility to median nerve compression. [9] (10.1016/j.jhsg.2026.100970)
• [L3] The most frequent described cause of compression was ganglion cyst (16%). [10] (10.1177/15589447251325827)
• [L5] [11] (10.1016/j.jhsa.2016.09.009)
• [L4] The authors report on the novel technique of using a collagen matrix wrap in recurrent compression neuropathies with good success. [12] (10.1097/sap.0b013e3182956475)
• [L3] Surgical decompression was associated with a greater decrease in median nerve cross-sectional area than nonsurgical treatment. [13] (10.1016/j.jhsa.2010.06.010)
• [L4] Concurrent carpal tunnel syndrome and pronator syndrome are rarely considered and proximal compression sites are easily overlooked. [14] (10.1016/j.otsr.2016.10.009)
• [L4] Anterior interosseous nerve transfer, along with cubital and ulnar tunnel release, results in sustained clinical and electrophysiological improvements in patients with severe chronic ulnar nerve compression, which encourages its adoption as a standard treatment for severe chronic ulnar nerve compression. [15] (10.1177/17531934251381023)
• [L5] The article provides a comprehensive review of the anatomy, pathophysiology, and causes of ulnar tunnel syndrome, noting that ganglia are the most common cause and that symptoms vary based on the anatomic location of the compression within Guyon's canal. [17] (10.1016/j.hcl.2007.06.006)
• [L4] Thus, in-situ release could be an alternative in management of patients with McGowen grade 3 ulnar nerve compression neuropathy at the elbow with a similar success rate as the submuscular and intramuscular transpositions with a lower complication rate. [18] (10.1016/j.jhsa.2015.06.068)
• [L4] The satisfactory outcomes support the perception that extensive decompression of the ulnar nerve beyond the cubital tunnel is not routinely needed. [19] (10.1007/s11552-011-9377-x)
• [L3] For patients with nerve compression at the carpal tunnel and cervical spine, CTR is a reasonable first step prior to proceeding with cervical spine decompression. [20] (10.1177/15589447241233764)
• [L2] The majority of patients suffering from cubital tunnel syndrome with mild or moderate symptoms benefit from conservative treatment. [22] (10.1177/1753193408098480)
• [L4] HRUS is a viable method to demonstrate a punched nerve syndrome. [23] (10.1007/s00402-015-2216-8)
• [L3] Ultrasound (US) measurements seem to have a limited value in clinical results of patients treated for entrapment neuropathy of the ulnar nerve. [24] (10.1177/1558944719857816)
• [L4] The authors recommend endoscopic decompression when conservative treatment fails to alleviate symptoms. [25] (10.1016/j.jhsa.2013.07.026)
• [L2] Long-term improvement in patients with diabetes remained after carpal tunnel release to the same extent as for patients without diabetes. [26] (10.1016/j.jhsa.2014.01.012)
• [L4] [41] (10.1016/j.xrrt.2023.04.001)
• [L2] The observation that in case series documenting EDX severities of median neuropathy, surgeons are mostly treating and operating on moderate to severe pathophysiology, emphasizes that while mild median neuropathy is highly prevalent it is uncommonly considered for surgery. [44] (10.1177/15589447241284776)
• [L1] [46] (10.1016/j.jhsa.2018.01.016)
• [L5] Surgical decompression remains the definitive treatment of CES, though the timing of surgery requires careful consideration to balance the urgency of intervention with the risks of complications. [47] (10.2106/jbjs.rvw.24.00156)
• [L4] Such injuries are likely to be missed in casualty because of the extensive soft tissue swelling, the apparent normal appearance of anteroposterior X-rays and the technical difficulty in testing the motor branch of the ulnar nerve in the presence of pain. [56] (10.1016/s0020-1383(96)00207-0)
• [L4] Modern ultrasound visualization enhances safety by enabling precise localization of this tiny nerve. [58] (10.1177/17531934261428976)
• [Case_report] Early diagnosis and careful excision of epineural ganglia are associated with satisfactory outcomes, although complete electrophysiological recovery may not occur if symptoms have been present for a prolonged period. [61] (10.1007/s11552-006-9013-3)

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