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Axillary Nerve-Anatomy Arises from posterior cord of brachial plexus and runs alongside radial N behind Axillary A, separating the latter form subscapularis muscle on the floor. At lower border of muscle, it leaves radial N and turns posteriorly with the posterior humeral circumflex artery through quadrangular space to posterior aspect of humerus, where it divides into anterior and posterior branches. Posterior branch supplies to teres minor and posterior part of deltoid before it curves around the posterior border of deltoid to supply the skin over lower half of deltoid (upper lateral cutaneous nerve of arm). The anterior branch proceeds laterally and anteriorly beneath the deltoid and in contact with surgical neck of humerus about 2 inches below upper attachment of deltoid giving off numerous twigs to the muscle throughout its course. Axillary N injury-Clinical picture Injury to main nerve in axilla or at surgical neck produces complete paralysis of deltoid with loss of abduction and anesthesia of small patch of skin over lower half of deltoid (regimental badge area). First 20º to 30º abduction is initiated by rotator cuff, chiefly supraspinatus. Occasionally, with complete RD and atrophy of deltoid, the supraspinatus may hypertrophy in compensation and restore abduction. When the anterior branch is interrupted, the muscle anterior the point is paralyzed. Partial muscle paralysis is frequently compensated by hypertrophy of supraspinatus and activity of pectoralis major, especially with arm above the horizontal plane. Axillary N injury-Treatment Prophylaxis consists of avoiding unnecessary extension of operative incisions and rough handling of deltoid muscle. If the nerve is contused, spontaneous regeneration may take place in 4-6 months, during which time deltoid must be relaxed on abduction splint and light massage and electric stimulation given. Daily active exercises are done to strengthen cuff muscles. Operative repair of this nerve is exceedingly difficult and frequently impossible. Conservative treatment is advised

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unless damage to main large nerve is evident. Operative exposures of shoulder should avoid muscle splitting incisions. If unavoidable, incision should be confined to anterior third of deltoid and not beyond 1 ½ inches distal to AC joint. Axillary N injury-Arthrodesis Complete deltoid paralysis, when not compensated by other muscle action, requires arthrodesis of shoulder. Trapezius and serratus anterior will raise the arm effectively. Axillary N injury-Harmon Operation When anterior portion of deltoid is paralyzed, muscle may be seriously weakened, particularly in forward flexion and humeral head may dislocate or subluxate anteriorly. This is corrected by transposing the posterior origin of functioning muscle to new anterior position. Axillary N injury-Trapezius T Transplant Trapezius muscle insertion is transferred by fascia lata strip extension to deltoid tubercle. Prerequisite is good power in scapular muscles, including trapezius, serratus anterior, pectoralis major, rhomboids and levator scapulae. Main contraindication is subluxation of shoulder joint. Axillary N injury-Biceps & Triceps Transplant Tendons of short head of biceps and long head of triceps are fixed to anterior and posterior rims of acromion. Median N-Anatomy Formed from lateral divisions of 5th, 6th and 7th cervical roots and medial divisions of 8th cervical and 1st thoracic nerves. Enters axilla lateral to Axillary artery and lies between MC N laterally and ulnar N medially. It descends in arm with brachial A and other nerves in a groove just medial to and slightly behind the biceps muscle and gradually crosses over in front of artery (rarely it crosses behind) until it lies medial to brachial A before it reaches elbow. No branches are given off in arm. At elbow it lies deep to bicipital aponeuroses and median cubital vein. It enters forearm by passing between larger humeral and smaller ulnar

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head of pronator teres, descending in medial part of forearm between FDS and FDP muscles. Above wrist it is radial to FDS and directly beneath PL tendon. Then it passes beneath transverse carpal ligament and after giving off motor branch to thenar muscle (OP, APB, superficial head of FPB) it inclines volarward to supply by 6 terminal branches the thumb, index, middle and ring fingers. In hand it lies in a plane superficial to tendons and deep to superficial vessels. First branches arising just above elbow are to humeral head of PT. Then below elbow, branches supply rest of PT,FCR, PL and FDS. At upper border of PT a large interosseous branch arises, penetrates between the pronator heads and supplies radial portion of FDP and FPL, and then descends on the interosseous membrane along with AIA to end in PQ. In hand, it gives off 5 palmar digital nerves. First 3 supplies both sides of thumb and radial half of index finger. Each of other 2 divide at clefts distally to supply the opposing halves of index and middle fingers and middle and ring fingers. Motor and sensory distribution of median and ulnar N frequently overlap. Normally median N supplies the palmar surface of thumb, index, middle and radial half of ring fingers and dorsal surface of distal thirds of these fingers.

Median N-Clinical Picture Above elbow results in loss of flexion of thumb, index, and middle finger, wrist flexion is weak and deviates ulnar side from unopposed action of FCU, pronation is weak or absent, thumb is in a position at the side of hand and cannot be brought into opposition, upper forearm and thenar area are atrophied, loss of sensation in volar aspect of thumb, index, middle and radial half of ring finger. Appearance of hand is similar to flat hand of monkey and is called simian hand. Trophic changes occur at distal end of index finger, which becomes thin and conical. Lesions at wrist occur from accidental cuts by knives or broken dishes or suicide attempts. It may be compressed against non yielding TCL by a dislocates lunate or by strongly grasping an object

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particularly with wrist in flexion, whereby flexor tendons are strongly displaced volarly. Inflammatory synovial swelling due to RA or neoplasm encroaches on carpal tunnel and constricts the nerve. Lesions at carpal tunnel affects short abductors (inability to abduct) opponens, superficial part of short flexors (FPB) and lumbricals to index and middle fingers. Loss of sensation is same as in higher lesions. Partial N injury or irritation is most common cause of causalgia. Severe burning pain in extremity and hand, aggravated by physical or emotional stimuli. Hand is initially swollen, red, warm, perspiring and hyper esthetic. Gradually skin becomes thinned, glossy, cold, cyanotic and dry. The hand is held fixed with fingers extended and thumb adducted and joints may ankylose in this position. Pain becomes extremely distressing . Keeping the part moist seems to reduce the symptoms temporarily. Median N-Treatment In nerve suture, better results are obtained from early intervention. Late repair leads to partial restoration, particularly of sensation and paraesthesia. Nerve should be explored and ends obtained and sutured in exact rotary apposition. Gaps can be overcome in palm by flexing MCP joint. Above wrist the nerve is freed and wrist is flexed. If elbow is also flexed and nerve is gently pulled distally, a 3 ½ inch gap can be overcome. For larger gaps, dissect the nerve in upper arm and reroute it superficial to elbow structures by detaching humeral head of PT. A plaster cast maintains flexion of joints and later very gradual extension is obtained over period of 1 month. If graft is needed, Sural N may be used. At exploratory operation in causalgia states, nerve displays a lesion in continuity (intraneural scarring). Complete division of nerve rarely causes causalgia. Treatment consists of sympathectomy, preceded by procaine block of 2nd thoracic ganglion. Complete anhidrosis and increase in warmth of hand after 10 min of block. Pain is relieved for 1 to 3 hours. A preganglionic sympathectomy is most effective. The white rami communicates to 2nd and 3rd thoracic ganglia and sympathetic trunk below 3rd are divided.

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Radial N-Anatomy It is continuation of posterior cord formed by posterior divisions of brachial plexus. In axilla it lies directly behind Axillary A and runs on a floor formed by subscapularis muscle proximally and latissimus dorsi and teres major distally. Axillary (circumflex) N which originates form posterior cord, descends alongside radial N, then leaves it at lower border of subscapularis, where it passes backwards through quadrangular space. Beyond TM, it proceeds posterior to humerus by entering interval between long and medial heads of triceps and reaching spiral groove. It passes around back of humerus to lateral side, where it pierces LIMS to reach anterior aspect of arm. Here it lies in interval between brachialis medially and brachioradialis and ECRL laterally. At this level it gives off branches to lateral half of brachialis, all of brachioradialis, ECRL and PIN. It then continues distally in forearm under cover of BR till about 2” above wrist. It then pierces deep fascia and turns laterally and dorsally, crossing superficial to APL and EPB tendons and reaching dorsum of hand where it supplies digital branches of sensation to dorsum of thumb, index, middle and ring finger as far as MP. In spiral groove radial N gives off posterior and lower lateral cutaneous nerves of arm, posterior cutaneous nerve of forearm, and muscular branches to triceps and anconeus. PIN arises form radial N at level of lateral epicondyle. It descends under cover of BR and gives branches to ECRB and supinator. Then it penetrates supinator and passes obliquely around lateral aspect of shaft to reach back of forearm and travels distally of surface of APL under cover of EDL. Then it lies on IM under cover of EPL and proceeds distally to supply wrist joint. In back of forearm it supplies remainder of extensor muscles and APL. Thus it supplies all muscles on lateral and dorsal aspect of forearm except the BR and ECRL which are supplied directly by radial N. Radial N-Clinical Picture If radial N is interrupted at axilla where it is usually involved by direct compression such as arm resting over back of chair (Saturday night palsy), the extensors of elbow, extensors and

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supinator of forearm, extensors of wrist, extensors of MCP joints of fingers and extensor and long abductor of thumb are paralyzed. A strip of posterior and posterolateral surface of arm, posterior third of forearm and autonomous zone on dorsum of hand over 1st IO web space are anesthetic. Patient holds extremity at side, elbow is slightly flexed, forearm is pronated, hand dropped at wrist and fingers are dropped at MCP joints. Thumb is turned forwards into palm and interferes with flexion of fingers. Patient cannot make fist because wrist drop tenses the extensors of fingers and thereby opposes their flexion. Involvement of nerve in spiral groove may be caused by sharp jagged edge of # bone or may be delayed by callus formation and incarceration of nerve. Here it permits function of triceps and anconeus and preserves sensation at back of arm and forearm. Injury to radial N between BR and brachialis involves BR and ECRL. But the brachialis which has dual nerve supply may continue to function. If injury is at level of radius where PIN encircles the bone 1 finger breadth below the head of radius, these muscles escape. Beyond this level supinator brevis is permitted to function, whereas wrist drop, finger drop at MCP joints and thumb rolled forward into palm are the deformities. EPL, EPB & APL gain their branches of supply little more distally than EDC, ECRL & ECRB so it is possible to have thumb alone involved by properly placed point of trauma. When superficial radial N alone is severed, loss is restricted to sensation in autonomous zone. This area is main site of pain when a causalgia state results form incomplete lesions of superficial radial. Partial paralysis of one or several muscles and hypoesthesia or hyperesthesia rather than anesthesia indicate that the nerve lesion is incomplete and continuity of the nerve is preserved. Examination of extension of fingers should be limited to MCP joints only as lumbricals supplied by median and ulnar nerves extend the IP joints.

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Automatic movements at wrist like extension due to finger flexion leading to extensor tendon tightening should not be interpreted as preservation of movements. Radial N - Treatment Regardless of level, affected muscles should be kept relaxed by supportive splints and their tone maintained by galvanic stimulation and light massage until nerve regenerates. Anterior moulded splint counteracts wrist drop and should extend beyond MCP joints to support PP. An additional extension from splint holds thumb in complete extension and dorsal abduction. If paralysis is immediate and complete, nerve should be explored and sutured promptly. Good results are proportionate to early repair. Nothing is lost by early exploration and finding the nerve intact. Gaps between nerve ends may be overcome by flexing the elbow, externally rotating and adducting the arm and by freeing various branches. If distance is extensive, nerve may be transposed anteriorly. Shortening of humerus is sometimes justified to aid approximation. Compression injuries are generally temporary and almost complete restoration of function is the rule. Possibility of complete nerve tears and their serious implications certainly warrant operative exposure of # site, whereupon both nerve and bone injuries can be dealt with at the same time. Following complete cut of nerve, NCV begins to slow after 2-3 days and is maximum at 2 weeks. Therefore within 24-48 hours eliciting this findings justifies surgical exploration. If no conduction impairment develops by 1 week, nerve interruption is physiological (neuropraxia) and non surgical treatment is pursued. During this period electrical stimulation, heat and massage to maintain tone, splinting to relax affected muscles and range of motion exercises are started. When causalgia occurs, an incomplete nerve lesion should be suspected, the nerve explored, neuroma if any should be resected, if necessary by removal of portion of nerve, F/B re approximation, or adhesions if any are freed. The Tinel sign may reveal the exact site of initiation of pain impulses.

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Radial N - Prognosis Prognosis of radial N repair is usually very good. Failure of some portion to regenerate necessitates tendon transplantations. Triceps paralysis needs no compensation other than that provided by gravity. Supination of forearm may be restored by osteotomy of radius and by rotating the distal fragment. Tubby operation transplants the insertion of PT from volar to dorsal aspects of radius. Radial N - Treatment Extension and abduction of thumb which stabilizes the thumb at CMC joint is necessary for proper apposition. FCR may be transplanted to APL and EPL and EPB. FCU is transferred to EDC. If no tendons are available, dorsiflexion of wrist is provided by arthrodesis of wrist or by cutting tendons of EDC and tenodesing the proximal ends of distal segment to dorsum of radius. Active flexion at MCP joints thereby tightens these tenodesed tendons and automatically dorsiflexes the wrist. The CMC joint of thumb may also be stabilized by arthrodesis. Ulnar N - Anatomy Largest branch of medial cord, arising under cover of PMn, and descending along medial side of Axillary A and proximal half of brachial A. At middle of humerus it leaves brachial A and in company with UCA it passes backwards through the MIMS to posterior aspect of arm. Then it descends along medial head of triceps to back of medial epicondyle and passes between heads of FCU to enter forearm. Under cover of FCU (which it supplies) it lies on FDP (supplies its medial half) and is immediately lateral to ulnar A. Near pisiform bone it emerges through deep fascia lateral to FCU and descends anterior to FR, where it divides into superficial and deep branches. Deep branch passes medial to hook of hamate and along with deep branch of ulnar A, enters interval between ADM and FDM to gain the deep area of palm. It supplies to hypothenar muscles and turns laterally across

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palm deep to flexor tendons giving off 3 branches, each of which runs distally in front of IS, supplying the interosseous muscles. Medial 2 branches also medial 2 lumbricals muscles. At lateral side of palm, main deep branch of ulnar N ends by breaking up into nerves of supply to adductor pollicis and 1st dorsal IM. Superficial branch of ulnar N runs under PB, which it supplies, and then divides into 2 digital branches, which provide sensation to palmar aspect of little and ulnar half of ring finger. Dorsal branch arises at middle of forearm and descends with parent nerve to carpus, where it becomes superficial and inclines backwards to gain to dorsum of hand. Here it divides into 2 dorsal digital nerves, which supply skin of medial third of back of hand and little finger and ulnar half of ring finger as far as second phalanx. Ulnar N – Clinical picture If FCU is paralyzed, on attempting flexion at wrist, hand deviates radially, S/O interruption of ulnar N above elbow. Otherwise ulnar N paralysis leads to extension of ring and little fingers at MCP joints and flexion at IP joints, because of lack of lumbricals. When lesion is sufficiently low in forearm, FDP is spared and unopposed by intrinsic, exerts strong flexion on DP, clawing of ring and little fingers is pronounced. When FCU and ulnar portion of FDP are paralyzed by a high lesion, atrophy over ulnar aspect of forearm is very apparent. Flexion of DP of ring and little finger is lost. Demonstrated best by placing hand palm down where inability of little finger to scratch the surface of table is evident. Hypothenar eminence is thinned and hollowing of IS suggests atrophy of interosseous. Abduction and adduction of fingers is lost to great extent. Index and middle finger may still abduct because their lumbricals innervations is through median N. Pinch between thumb and index finger normally depends on ability to stabilize MCP joint in flexion (adductors and flexor brevis) so that action is strong and apposed fingers form letter O. in ulnar paralysis, PP is hyper extended, IP joint of thumb hyper flexes and pinch is weak. Failure of stabilization at CMC joint by APL will likewise interfere with pinch.

10 Inability of thumb to scrape across distal palm suggests loss of

thumb adductors. Instead it comes forward into opposed position. Another test is failure to resist attempts to extract a sheet of paper held between apposed sides of thumb and index finger. Trophic changes in ring and little fingers reflect sensory loss. Very frequently innervations form median N preserves function of intrinsic and thumb adductors. Fibers innervating these muscles proceed distally in median N to distal 3rd of forearm and by a connecting branch enter ulnar N. in such case a high ulnar lesion fails to eliminate intrinsic action.

Ulnar N –Treatment Repair should be done with care. Nerve contains both motor and sensory fibers. Gaps are overcome by flexing wrist and elbow. Nerve at elbow may be transposed anteriorly, and branches freed, permitting mobilization distally. Recovery of function requires > year in following order, forearm muscles, sensations, hypothenar muscles, interossei and thumb adductors. During this period, hand is splinted with MCP joint in flexion and IP joint in extension to keep paralyzed muscles relaxed and prevent joint contractures. When ulnar N paralysis is permanent, tendon transplantation is the treatment of choice. Ulnar N –Repair of clawed fingers Claw hand is due to intrinsic muscle paralysis while long extensors and flexors are still functioning. Loss of flexor power on PP allows extensors to pull PP into hyperextension, tension on long flexors pull DP into flexion, unopposed by lost extension of intrinsic. Extension of distal 2 phalanges takes place synergistically by long extensors and intrinsic. Action of long extensors is lost when PP is hyper extended. Any procedure that prevents hyperextension of PP preserves extension of distal 2 phalanges and eliminates claw deformity.

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Bunnell Technique : Transplants multiple slips of sublimis

through lumbrical canals into aponeurotic expansion. This procedure is not effective in claw hand of long standing in which patient has developed habit of flexing wrist to extend DP automatically, thereby rendering the sublimis ineffective. Fowler Technique : Splits EIP and EDQ into 2 strands each, next each individual slip is passed through IOS anterior to TMCL and inserted into aponeuroses. Riordan technique : Tenodesis procedure. Half of ECRL & ECU is separated and each half is split longitudinally into 2 slips and then each slip is passed and attached into aponeuroses. Tendon should be under tension so as to obtain restriction of extension. Post operatively wrist is in dorsiflexion, MCP joints in flexion and distal 2 joints in extension. Ulnar N –Restoration of thumb adduction and arches When grasping small round objects, hand cups into arch and enables fingers to converge during flexion, thus strength of grasp is obtained. These arches are produced mainly by thenar and hypothenar muscles. They are reduced considerably in ulnar paralysis and completely flattened in combined ulnar and median paralysis. It is essential to restore functions of pinch and grasp. Tendon Loop operation : EIP is removed just before its insertion and is prolonged by tendon graft around ulnar border of hand, placed volar to hypothenars and beneath finger flexors and inserted into ulnar side of base of PP of thumb. The distal remaining stump of tendon is attached to EI to avoid adduction and rotation deformity of index finger. This procedure only adduction and is suitable only in pure ulnar paralysis. Tendon T Operation : Provides strong adduction to both thumb and index finger and reforms arches. Tendon graft is placed transversely across palm beneath flexor tendons and is attached to neck of 5th MC and ulnar side of base of PP of thumb. To its centre is attached motor tendon, usually one of sublimis. Contraction of motor tendon pulls on cross member and apposes thumb and index finger. This is more suitable when median N is also involved with ulnar N and it becomes necessary to correct thumb opposition also.

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Compression of Ulnar N at elbow Also called traumatic ulnar neuritis, tardy ulnar N palsy and ulnar neuropathy at elbow. Chronic repetitive blunt trauma : Ulnar N is superficial within post condylar groove between olecrenon and medial epicondyle. Here it is vulnerable to single, severe direct blow or to repeated external pressures, sustained under occupational conditions. Post # : Nerve is held firmly within groove by firm dense fascia. Roughening of bone due to # imposes frictional force against gliding nerve. Cubitus Valgus deformity : Nerve is supposedly stretched over medial prominence at elbow. Deformity may be congenital and associated with anterior dislocation of radial head, retarded growth of lateral portion of lower humeral epiphyses following trauma or infection, or mal union of #. Arthritis of joint : OA produces irregularities of post condylar groove or may compress nerve by prominent osteophyte or protruding ganglion. Rheumatoid synovium may penetrate the medial capsule and compress nerve. Recurrent subluxation or dislocation of nerve : When fascia covering nerve in groove is thin and lax, ulnar N moves out of its groove onto tip of medial epicondyle when elbow is completely flexed, returning to its normal location when elbow is extended. Repetitive subluxation normally occurs in 16% of population. Acute trauma, infection : Produce scarring which can incarcerate ulnar N. Muscle compression : By an accessory muscle, anconeus epitrochlearis, which bridges the groove. Idiopathic : Not unusual.

Pathophysiology

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2 cm distal to medial epicondyle, an aponeurotic arch passes

between 2 heads of origin of FCU, one firmly attached to medial epicondyle and other loosely attached to olecrenon, with aponeurotic arch forming roof of cubital tunnel. Floor of tunnel is formed by medial capsule of elbow. During flexion, space of tunnel is diminished by tightening of aponeurotic arch and by outward bulging of capsule. INP is 3 times when elbow is flexed with wrist extended; adding abduction and external rotation of arm as when placing hand behind head, INP is 6 times that of relaxed N, such pressures are capable of damaging nerves. Aponeurotic arch, is slack in extension. When this is divided, underlying N is often found flattened, and proximally it presents a fusiform swelling. Normally, ulnar N elongates by 5 mm during flexion and glides freely in groove. Encroachment on groove or cubital tunnel, produce friction, pressure and tension, which compromises IN vascularity and results in edema and scarring. Symptoms are highly variable, from subjective dysesthesias to combination of sensory and motor deficit. FCU and ulnar half of FDP are usually spared. Reason is, fibers to these muscles are deeply situated in nerve at elbow and are generally unaffected by external compression. Clinical Picture H/O Cubitus valgus deformity, severe direct trauma or repetitive trauma to ulnar groove. Symptoms are related to severity of involvement. Minimal nerve irritation causes subjective dysesthesias in ulnar distribution and sensation of clumsiness. Moderate involvement produces pronounced subjective pain and paraesthesia and IO weakness and atrophy. FCU & FDP to DP of little and ring fingers are rarely affected. Nerve may be tender and palpably enlarged at post condylar groove. Severe N lesions are rare. Interossei are very weak and atrophied. FCU & ulnar half of FDP are partially weakened. Sensory loss varies from marked hypoesthesia to anesthesia. Sweating in reduced, although hyperhydrosis is not infrequent. Cubital tunnel syndrome caused by compression of N by arcuate ligament is provoked by prolonged flexion attitudes of elbow, such as during sleep. Sometimes symptoms can be

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elicited by acutely flexing elbow for about 5 minutes (elbow flexion test). Recurrent ulnar N subluxation at elbow are usually asymptomatic, unless trauma is superimposed. Complete anterior displacement is exceptional. Condition is nearly always bilateral. Enlarged tender N can be felt to slip beneath examining finger during flexion and extension.

Diagnosis Traumatic ulnar neuritis at elbow must be differentiated from ulnar N compression at wrist. Dorsal cutaneous branch of ulnar N leaves parent N beyond elbow. So sensory impairment in dorsal ulnar aspect of hand localizes lesion proximally. Contrariwise, absence of this finding does not necessarily implicate ulnar N lesion at wrist, because N may be only partially involved at elbow. Electro diagnostic studies will reveal slowing of conduction at elbow, and differentiate whether N is involved proximally (at thoracic outlet) or distally at wrist. Preoperatively it is important to determine compressive bone lesion about ulnar groove. In addition to routine x-rays, special view is taken to outline groove. The externally rotated arm is placed against cassette, while elbow is acutely flexed, and central x-ray beam is directed vertically. Prognosis Depends largely on degree of N involvement and time interval between onset of symptoms and surgical intervention. In minimal involvement, anterior transposition of N leads to immediate relief of local discomfort and peripheral paraesthesia. With moderate sensory and motor impairment, following surgery, hand becomes stronger, but variable weakness and sensory impairment persist in some. In advanced paralysis, surgery results in partial recovery of motor power in some but sensory recovery is better, normal function is never regained.

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After 1 year, only about 1/4th of patients will achieve satisfactory recovery after anterior transposition and improvement after simple aponeurotic release is poor. Muscle power continue to improve over 6 months to year. Long flexor muscles recover more completely than intrinsic. Variable sensory deficit often persists. Complete recovery is rarely attained if course exceeds 3 months and chances are poor when symptoms have existed for 1 year. Treatment Nerve must be transposed anteriorly. Sites of potential kinking should receive proper attention. MIMS extending proximally from epicondyle must be adequately resected. Aponeurotic band is released. N should not be laid in groove cut in muscle, because scarring and IMS become adherent to N. Origin of common flexor pronator tendon should be elevated, the N placed beneath the muscle mass, and tendon origin restored. Occasionally, it may be possible to remove local compressing lesion like ganglion or osteophyte without need for anterior transposition. Ulnar N compression at wrist Ulnar N courses through tunnel anterior to FR just lateral to pisiform, then divides into superficial (mainly sensory) and deep branch as it proceeds distally. Floor of narrow canal is formed by ligaments between pisiform, triquetrum and hamate. Because of limited diameter, it is vulnerable to lesions that encroach on canal (OA osteophyte, ganglion, rheumatoid pannus). When N is compressed proximal to point of bifurcation, both sensory and intrinsic muscle deficit results. As dorsal branch leaves ulnar N proximal to wrist, sensation to medial third of back of hand and entire dorsal surface of little and ulnar half of ring finger as far as MP is preserved. When N compression is within tunnel distal to bifurcation, only deep branch is affected, hypothenars are often spared, and intrinsic muscles denervated. FDP to little and ring fingers and FCU is unaffected. Ulnar N compression at wrist-Anatomy Ulnar A and N enter hand through triangular space (Guyon’s canal), which is bordered medially and proximally by FCU and

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pisiform, anteriorly by thin VCL blended with tendinous insertion of FCU and posteriorly by TCL overlying pisotriquetral joint. Distal to Guyon’s canal, under cover of PB muscle, nerve divides into superficial and deep branches. Superficial branch supplies overlying muscle and passes through fat pad, courses distally and SC to provide sensory innervations to ulnar side of palm. Deep branch passes lateral to pisiform, then medial to hook of hamate, where it makes an abrupt turn as it dips between origins of ADM & FDM. It enters narrow fibro-osseous tunnel that is bounded proximally by pisohamate ligament. Before it passes into this extremely narrow tunnel, deep palmar branch supplies motor N to hypothenar muscles; then passes through opponens and turns laterally under cover of deep flexor tendons along line of deep palmar arch and supplies branches to interossei, 3rd & 4th lumbricals, adductor pollicis and deep part of FPB. As deep branch passes across palm, it lies in close relationship to proximal end of MC, providing hard surface against which nerve may be compressed. Within Guyon’s canal, ulnar N lies medially and ulnar A lies laterally, and remainder of space is occupied by fat globules. Beyond narrow rigid fibro-osseous canal as nerve courses deep in palm, nerve is most often damaged by penetrating injury. Motor fibers are posterior and sensory fibers are anterior. Theoretically, if N is compressed posteriorly, motor weakness should prevail over sensory loss. However, this is not the clinical situation, because both motor and sensory deficits develop concomitantly. Because dorsal cutaneous branch leaves main N 6 to 8 cm proximal to wrist, an injury beyond this level spares the dorsal ulnar distribution. Pathology Ganglion produce largest number of compressive lesions at wrist. Often H/O blunt trauma over hypothenar area by single severe blow from using hand as hammer or by fall on outstretched hand or repetitive trauma. Pisiform appear to sustain the brunt of injury, and OA changes develop at pisotriquetral joint.

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Scarring may develop weeks to months after an injury about hypothenar eminence, enveloping both ulnar N and ulnar A within Guyon’s canal. At surgery, edematous fibrous tissue and thrombosed vessels are found. They appear to constrict the nerve, and provided that collateral circulation is adequate, resection of scar tissue and affected segment of ulnar A and freeing the nerve will relieve neurological symptoms. Ulnar A because of superficial location is vulnerable to injury. Single or repetitive blunt trauma may damage intimae, resulting in thrombosis. Trauma also disrupts elastic fibers resulting in progressively enlarging true aneurysm, or penetrating injury may partially tear A, producing localized hemorrhagic mass whose interior becomes reanalyzed, developing a cystic, bulbous false aneurysm. Regardless of cause, ulnar neuritis occurs, and majority of cases produce paraesthesia and objective sensory loss. Clinical Picture Dependant on site and degree of injury. 2 anatomical patterns; lesion proximal to pisohamate ligament that causes both sensory and motor involvement and lesion deep in palm distal to pisohamate ligament that affects interossei and ulnar lumbricals but spares hypothenar muscles and ulnar volar sensations. Compression at level of Guyon’s canal presents following features :Compressive tissue (ganglion, RA pannus, bone fragment) is sometimes palpable. Sensory loss over volar ulnar distribution but spares dorsal area except over DP. Motor involvement affects hypothenar, ulnar 2 lumbricals and interossei. Clawing of little and ring fingers. Compressive lesions that exerts pressure only on deep branch produces purely motor weakness of interossei but spares hypothenar muscles. Abducted attitude of little finger results from unopposed action of ADM. Clawing of little and ring finger

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is seen sometimes. In general development and effects take place silently i.e. without pain. Penetrating injury within palm leads to involvement of motor structures beyond the point of nerve interruption. OA of pisotriquetral joint causes pain and tenderness over pisiform, crepts and pain elicited by passively moving pisiform bone from side to side. Active ulnar deviation and flexion of wrist against resistance reproduce pain. Rarely, superficial branch may sustain direct injury, leading to pain over ulnar side of palm and ring and little fingers, where sensory loss may be detected with no sensory loss over proximal portion of dorsal aspect of these fingers. Positive Tinel’s sign. X-ray evidence of bone fragment. Intrinsic muscles are not affected. Diagnosis Muscle weakness and wasting are seen but is common to whole lot of neurological and myopathic conditions. When symptoms suggest distal ulnar N involvement, inquire about injury such as laceration, despite a time lapse. Detailed sensory examination to distinguish between nerve compression at elbow from injury to distal portion. When sensation is lost over volar ulnar area, but intact over dorsal ulnar area, injury is localized distal to point of origin of dorsal sensory branch (6 to 8 cm above wrist). Muscle examination must be detailed. EMG studies of 1st dorsal interossei may show fibrillation potentials S/O involvement of deep branch. NCV studies between wrist and 1st DI or adductor pollicis, is highly diagnostic and any delay must be clearly demonstrated before surgical intervention. When fibrillation potentials are already present on EMG studies, denervation is far advanced. X-rays of wrist and hand, including special carpal tunnel and pisiform views are necessary to determine presence of OA, # and neoplasm. Treatment Immediate decompression of ulnar N is mandatory. Nerve is isolated adjacent to FCU tendon in distal forearm and then

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freed progressively by cutting volar carpal ligament and then fascial roof overlying interval between pisiform and hook of hamate. Any compressive lesion is identified and removed. When OA of pisotriquetral joint is present or pisiform is dislocated, bone may be removed without impairing power of wrist flexion. When possibility of severance of deep palmar branch by penetrating injury exists, nerve should be explored beneath the flexor tendons in palm and repair carried out. Thrombotic occlusion of ulnar A at wrist requires segmental arterial resection. Aneurysm of A requires excision of aneurysmal sac. If collateral circulation is insufficient, restoration of arterial continuity by end to end anastomosis or a vein graft is necessary.