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entrapment neuropathies at elbow

  1. 1. Dr. Mahima Agrawal MBBS, MD, DNB, MNAMS PMR Assistant Professor, Dept. of PMR, JLNMC, Ajmer
  2. 2. Definition Etiology Pathophysiology Diagnostic evaluation Differential diagnosis Management Specific Entrapment neuropathies
  3. 3.  It is a neuropathy due to a structural abnormality, such as compression, displacement, or traction of the nerve, or by an intrinsic abnormality of the nerve, such as nerve cell tumor  With these lesions, stretching and angulation of the nerve may be as important a source of injury as compression
  4. 4.  Trauma, direct pressure and space-occupying lesions at any level in the upper extremity  There are other situations that are not a direct cause of nerve compression, but may increase the risk and may predispose the nerve to be compressed specially when the soft tissues are swollen like synovitis, pregnancy, hypothyroidism, diabetes or alcoholism
  5. 5. Epineurium Fascicle Endoneurium Perineurium Artery and Vein within the perineurium Layers of nerve
  6. 6. Acute nerve compression  Pressures exceeding 20 mm Hg Reduced epineurial blood flow  Pressures exceeding 30 mm Hg Inhibits anterior and retrograde axonal transport  Pressures exceeding 80 mm Hg Cessation of intraneurial blood flow  These changes are transitory Reversible in short term  Example is Tourniquet palsy
  7. 7. Blood Nerve Barrier
  8. 8. Repetitive stress, prolonged compression Wallerian degeneration Localized demyelination Demyelination of nerve fibres
  9. 9.  A proximal level of nerve compression could cause more distal sites to be susceptible to compression  The summation of compression along the nerve would result in alterations of axoplasmic flow and subsequent pathology and symptomatology  The possibility of a distal site of compression making the more proximal nerve susceptible to secondary compression: A reverse double crush  Systemic diseases such as obesity, diabetes, thyroid disease, alcoholism, rheumatoid arthritis and neuropatthies lower the threshold for the occurrence of a nerve compression and alter axoplasmic transport rendering that nerve more susceptible to develop compression neuropathy and act as a ‘crush’
  10. 10.  DM is a significant predisposing factor for entrapment neuropathies TN-C(Tenascin-C) expression in the endoneurium is closely correlated with nerve function Metabolic and phenotypic abnormalities of endoneurial and perineurial fibroblasts lies behind the vulnerability of DM patients to entrapment neuropathy  In contrast to angiopathies, retinopathy, and nephropathy, three representative complications of DM, mast cells do not play significant roles in the onset or progression of the entrapment neuropathy associated with DM  Ref: Histol Histopathol (2008) 23: 157-166
  11. 11. Temporal sequence Irritative or inflammatory pain Paraesthesia (Tingling , Burning) Ablative Numbness Weakness and atrophy Dry, thin, hairless skin Ridged, thickened, cracked nails Recurrent skin ulcerations
  12. 12.  Clinical evaluation  History  Electro diagnosis: mainstay • Nerve Conduction studies(NCS) • Electromyography(EMG)  Electromyography (EMG)  EMG tests detect abnormal electrical activity in motor neuropathy and can help differentiate between muscle and nerve disorders
  13. 13. Sensory nerve conduction studies are the earliest to show abnormality of slowing (focal demyelination) in the nerve across the site of the entrapment Slow transmission rates and impulse blockage tend to indicate damage to the myelin sheath, while a reduction in the strength of impulses at normal speeds is a sign of axonal degeneration Motor conduction abnormalities generally present later with slowing across the site followed by loss of axons (both sensory and motor) if the entrapment is unrelieved Needle electromyography is used to detect axon loss which is chronic unless there is a super added acute external pressure on an existing entrapped nerve
  14. 14.  Nerve biopsy Although this test can provide valuable information about the degree of nerve damage, it is an invasive procedure that is difficult to perform and may itself cause neuropathic side effects  Skin biopsy (examine nerve fibre endings) This test offers some unique advantages over NCV tests and nerve biopsy. Unlike NCV, it can reveal damage present in smaller fibres; in contrast to conventional nerve biopsy, skin biopsy is less invasive, has fewer side effects, and is easier to perform
  15. 15.  Magnetic resonance imaging (MRI) can show muscle quality and size, detect fatty replacement of muscle tissue, and can help rule out tumors, herniated discs, or other abnormalities that may be causing the neuropathy  Ultrasound: The impact of sonography on clinical management has yet to be determined, even though upper extremity nerves are well-depicted Sonographically
  16. 16.  Myelopathy  Brachial plexopathy  Radiculopathy  Other central nervous system disorders, that can mimic peripheral nerve entrapment  Painful rheumatologic and orthopaedic disorders; and other psychological entities, such as somatoform and factitious disorders
  17. 17. Treat the underlying cause Infection Toxin exposure Medication related toxicity Vitamin deficiencies Hormonal deficiencies Autoimmune disease Management of systemic diseases Early management of injuries TREATMENT Healthy lifestyle Optimal weight Balanced diet Exercising Limiting alcohol consumption Correcting vitamin deficiencies
  18. 18.  Symptom Management  1. Nonsteroidal anti-inflammatory drugs (NSAIDs) for mild pain  2. Antidepressants (tricyclic antidepressants such as amitriptyline or newer serotonin-norepinephrine reuptake inhibitors such as duloxetine hydrochloride or venlafaxine)  3. Anticonvulsants (tricyclic antidepressants such as amitriptyline or newer serotonin-norepinephrine reuptake inhibitors such as duloxetine hydrochloride or venlafaxine)  4. Antiarrythmics (Mexiletine)  5. Narcotic agents ( Tapentadol)
  19. 19.  6. Topically administered medications • Lidocaine • Capsaicin • Topical agents are generally most appropriate for localized chronic pain such as herpes zoster neuralgia (shingles) pain  7. TENS  8. Allied medicine (Acupuncture, massage etc.)  9. Orthosis  10. Surgery  11. Trans cranial magnetic stimulation
  20. 20.  Steroid injections (such as cortisone or prednisolone) shrink the swollen tissues and relieve pressure on the nerve  Corticosteroid injections are helpful for pregnant patients, as their symptoms often go away within 6 - 12 months after pregnancy  Most doctors limit steroid injections to about three per year, because they can cause complications, such as weakened or ruptured tendons, nerve irritation, or more widespread side effects  Low-Dose Oral Corticosteroids: A short course (1 - 2 weeks) of oral corticosteroid medicines may provide relief for some people, but the relief does not usually last. 
  21. 21.  USG guided percutaneous injection, hydrodissection, and fenestration • An extension of blind steroid injection with advantage of safety, accuracy of medication placement, effectiveness, non invasiveness, ease of performance and lower cost than open surgical release REF: Vol.10,No.3,2010,Journal of Applied research
  22. 22. CLASS AGENT(S) ACTION Neutrophic Factors and Chemoattractants Ciliary Neutrophic factor (CNTF) Nerve growth factor (NGF) Insulin-like growth factors (IGFs) Brain-derived Neutrophic factor (BDNF) NT-3 NT-4 Promote neuronal survival and regrowth Attract and guide axon Chemorepellent Factors Semaphorins Netrins Others Selectively repel some types of axons Inhibitors of Connective Tissue Formation Inhibitors of fibroblasts Collagenases Others Decrease fibrosis at the site of nerve injury to promote axonal regeneration
  23. 23. Nerve involved Site of entrapment Median N.(wrist) (Elbow) Ulnar N. (wrist) (Elbow) Lower trunk or medial cord of branchial plexus Suprascapular N Radial Nerve (Elbow) Carpal tunnel Between heads of Pronator teres Anterior Interosseous Nerve syndrome Guyon’s canal (Ulnar tunnel) Bicipital groove, Cubital tunnel Cervical rib or band at thoracic outlet Spinoglenoid notch Radial tunnel—at point of entrance into supinator muscle (arcade of Frohse) Posterior Interosseous Nerve syndrome
  24. 24. Median nerve in anterior elbow. Passing between two heads of Pronator teres muscle and into the forearm beneath the edge of the fibrous arch of flexor digitorum sublimis
  25. 25.  Possible areas for median nerve compression proximal to the carpal tunnel:  The ligament of Struthers  The bicipital bursa  Anomalous arteries, and anomalous muscles (such as Gantzer's muscle, an accessory FPL muscle)  Pronator syndrome  Anterior interosseous nerve syndrome  The last two remain the two most frequently referenced compression neuropathies of the median nerve in the forearm
  26. 26.  Compression of the median nerve as it passes between the two heads of the pronator teres muscle, Bicipital aponeurosis  Compression is due to hypertrophy and imbalance of regional tissues  Development of fibrous tissue due to inflammatory processes from repetitive stress, decreasing range of motion and increasing stresses
  27. 27.  Symptoms  Insidious onset  No history of trauma  Aching pain in the proximal, volar forearm  Paraesthesias radiating into the median innervated fingers  Worsened by repetitive pronosupination movements and wrist flexion  Carpenters, frequent computer users with a mouse, weight lifters, athletes especially yoga, golf and tennis PRONATOR SYNDROME
  28. 28.  Discriminating clinically between PS and CTS:  Loss of sensation over palmar cutaneous branch territory  No Tinel's on the wrist  No nocturnal disturbance  Pain on resisted pronation from a neutral position, especially as the elbow is extended  If resisted contraction of the FDS to the middle finger reproduces symptoms, median nerve compression at the level of the fibrous arch between the heads of the FDS might be suspected  If symptoms are elicited by resisted flexion of the forearm in full supination, compression at the more proximal level of the lacertus fibrosus might be considered
  29. 29.  Site of compression essentially same for both Pronator syndrome(PS) and AIN  PS:Vague volar forearm pain,Median nerve parasthesias,minimum motor findings  AIN:Pure motor palsy of any or all three 1.FPL,2.FDP of index and middle fingers,3.PQ.  Surgical indications for nerve decompression include persistent symptoms for >6 months in patients with PS or for a minimum of 12 months with no signs of motor improvement in those with AIN syndrome
  30. 30.  Pain may be present in the forearm along the course of the nerve  Inability to make an “OK” sign when asked by the examiner to flex his thumb interphalangeal joint and index finger distal interphalangeal joint  In patients with mild AIN compression, subtle weakness of these muscles may be the only clinical finding  Such weakness of the FPL and index finger FDP may be uncovered by asking the patient to pinch a sheet of paper between his thumb and index finger using only the fingertips and then trying to pull the paper away
  31. 31.  A patient with AIN syndrome may be unable to hold on to the sheet of paper with just his fingertips and may compensate by using a more adaptive grip in which the interphalangeal joint of the thumb and distal interphalangeal joint of the index finger remain extended  Differential diagnosis  Brachial neuritis  Viral neuritis (Parsonage–Turner syndrome)  Rupture of the FPL tendon
  32. 32. Anterior view of radial nerve course. PIN entrapment occurs because of prominent radial recurrent artery(RRA), medial edge of ECRB, proximal edge of S (Arcade of frohse, RN (Radial nerve), SRN (Superficial Radial Nerve)
  33. 33.  Anatomy- Formed from posterior cord to emerge between long and lateral heads of triceps, spiral groove of humerus proceeding medially to laterally to emerge between brachialis and brachioradialis on lateral elbow to enter the radial tunnel  On exit from radial tunnel, the deep branch pierces the supinator and exits the posterior aspect to emerge as Posterior interosseous nerve
  34. 34.  Anatomically, there are five potential sites of compression of the Radial nerve in the area of the radial tunnel • Fibrous bands of tissue anterior to the radiocapitellar joint between the brachialis and brachioradialis • The recurrent radial vessels that fan out across the PIN at the level of the radial neck as the so-called leash of Henry • The leading (medial proximal) edge of the extensor carpi radialis brevis (ECRB) • The proximal edge of the superficial portion of the supinator, commonly referred to as the arcade of Fröhse • The distal edge of the supinator muscle
  35. 35.  Radial nerve compression can lead to either radial tunnel syndrome or posterior interosseous nerve syndrome (also called Supinator syndrome)
  36. 36.  PIN is a branch of the radial nerve, originating in the lateral intermuscular septum  Purely motor function  Innervates the supinator, extensor carpi ulnaris, extensor digitorum communis, extensor digiti minimi, abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis proprius muscles  Most common in racquet sports, bowlers, rowers, discus throwers, golfers, swimmers  All involve repetitive supination and pronation  May occur in synovitis, neoplasm etc
  37. 37.  Symptoms and signs:  Inability to extend fingers and thumb  ECRL function intact—the wrist extends and radially deviates  Whereas patients with PIN syndrome have a loss of motor function, patients with RTS typically, present with mobile wad and lateral forearm pain without motor involvement
  38. 38.  Symptoms and signs:  Pain distal to lateral epicondyle, tenderness over the radial tunnel along the path of PIN  Pain worsened by extending the elbow, pronating the forearm and flexing the wrist  Pain with resisted active supination or wrist extension  Pain with active supination against resistance  Pain with wrist extension against resistance  Pain with resisted middle finger extension at the metacarpophalangeal joint  No neurological deficit  Pain disappears after instilling local anaesthetic at the site of entry of PIN
  39. 39.  There is no motor weakness  Unlike a case of lateral epicondylitis the pain is not on the lateral epicondyle of the humerus but slightly distal to it  It is described as being in the area of the mobile wad and radial tunnel  Differential diagnosis:  Lateral epiconylitis  Osteoarthritis of the radial capitellar joint  Impingement of the articular branch of the radial nerve  Synovitis of the radiocapitellar joint  Muscle tear of the extensor carpi radialis brevis
  40. 40. Course of ulnar nerve from posterior view. It travels deep to the flexor carpi ulnaris muscle beneath the arcuate ligament
  41. 41.  Entrapment of the ulnar nerve is the second most common compression neuropathy in the upper extremity after CTS  The arcade of Struthers is a band of fascia that connects the medial head of the triceps with the intermuscular septum of the arm  The cubital tunnel is a fibroosseous channel formed by the olecranon process laterally, the posterior cortex of the medial epicondyle medially, the elbow joint capsule and posterior bundle of the medial collateral ligament anteriorly, and the ligament of Osborne (the cubital retinaculum) posteriorly
  42. 42. •Truck drivers who lean the flexed elbow against the open window of their truck •Constant cell-telephone users •Baseball pitchers are also at risk because of the valgus stress that is induced in the late cocking and early acceleration phases of throwing •Recurrent anterior dislocation of the ulnar nerve •Risk factors for ulnar nerve dislocation include cubitus varus deformity, an absent or lax ligament of Osborne, a hypertrophic medial head of the triceps, or an accessory head of the triceps and the dislocation may be associated with activities that involve resisted elbow extension, such as the early acceleration phase of throwing and bench press CUBITAL TUNNEL SYNDROME
  43. 43.  Entrapment neuropathies are far more common than thought  These syndromes are underdiagnosed  Early diagnosis can lead to faster and near complete recovery  Conservative management followed by surgery in non responsive cases gives good results
  44. 44. Theodore T. Miller, William R. Reinus. Nerve Entrapment Syndromes of the Elbow, Forearm, and Wrist Adam’s and Victor’s Principles of neurology Entrapment Neuropathies John D. England, MD
  45. 45. THANK YOU

Editor's Notes

  • Nerves have both axial (e.g. the median artery) and segmental vasculature (e.g. the Superior Ulnar colateral artery) all along its course
  • The histopathology of chronic nerve compression follows a continuum that parallels patient sensory complaints, which progress from intermittent paraesthesia to constant numbness. Motor complaints progress from aching to weakness to atrophy

    HISTOLOGY: ‘neuromatous’ enlargement just above the retinaculum with an abrupt reduction in size in the tunnel, distal to which the nerve regained its normal dimensions. The nerve bundles beneath the retinaculum were thinned with an increase in the endoneurium which had destroyed the ‘myelin sheaths’

    The swelling showed a considerable increase in both the epineurial and intrafunicular connective tissue though the great bulk of the swelling was due to the former
    Complete recovery of function after surgical decompression reflects remyelination of the injured nerve
    Incomplete recovery in more chronic and severe cases of entrapment is due to Wallerian degeneration of the axons and permanent fibrotic changes in the neuromuscular junction that may prevent full reinnervation and restoration of function

  • Blood–Nerve barrier
    The inner layers of the perineurium and the endothelial cells of the endoneurial microvessels create the blood–nerve barrier
    These cells have tight junctions that are impermeable to many substances
    Thus, the blood–nerve barrier provides a privileged environment within the endoneurial space
    There are no lymphatic vessels within the endoneurial or perineurial spaces
  • As the duration of compression increases beyond several hours, more diffuse demyelination will appear, being the last event in injury to the axons themselves
    This process begins at the distal end of compression or injury, a process termed wallerian degeneration. These neural changes may not appear at a uniform fashion among the whole neural sheath depending on the distribution of the compressive forces, causing mixed demyelinating and axonal injury resulting from a combination of mechanical distortion of the nerve, ischemic injury, and impaired axonal flow
  • Multiple and double crush syndrome
    They noted a high incidence of carpal and cubital tunnel syndrome with associated cervical root injuries

    This concept of double or multiple crush is important clinically in patients who demonstrate multiple levels of nerve compression, as failure to diagnose and treat these multiple levels of injury will result in failure to relieve patients’ symptoms. Systemic conditions such as obesity, diabetes, thyroid disease, alcoholism, rheumatoid arthritis and other neuropathies will similarly render a given individual more susceptible to the development of CTS and other compressions.

  • In a major mixed nerve (both sensory and motor), such as the sciatic or median nerves, signs of sympathetically mediated features may be prominent in chronic cases These changes manifest as the following

    Dry, thin, hairless skin
    Ridged, thickened, cracked nails
    Recurrent skin ulcerations

    Deep branch of the ulnar nerve at Guyon canal and PIN (both predominantly motor) and the lateral femoral cutaneous nerve (LFCN; pure sensory) near the anterior superior iliac spine (ASIS)

  • The electromyography detects the voluntary or spontaneous generated electrical activity. The registry of this activity is made through the needle insertion, at rest and during muscular activity to assess duration, amplitude, configuration and recruitment after injury. Recruitment will be affected if demyelination occurs, but will not result in abnormal spontaneous activity. Meanwhile, axonal injury will result in both recruitment and abnormal spontaneous activity, which will not be seen on needle electromyography until 2 weeks after the initial insult
  • Nerve conduction assesses for both sensory and motor nerves. This study consists in applying a voltage simulator to the skin over different points of the nerve in order to record the muscular action potential, analyzing the amplitude, duration, area, latency and conduction velocity. The amplitude indicates the number of available nerve fibers. Some authors consider diminished amplitude below 50% to be suggestive of compression. In such cases, we will find a normal response to distal stimulation but no response proximal to the site of entrapment. If the compression progresses, our results will be compatible with axonal degeneration with diminished amplitude of the response with relative preservation of the conduction velocity and distal latency until the remaining axons are completely damaged
  • Exercise can reduce cramps, improve muscle strength, and prevent muscle wasting

    Inflammatory and autoimmune conditions leading to neuropathy can be controlled in several ways
    Immunosuppressive drugs such as prednisone, cyclosporine, or azathioprine may be beneficial. Plasmapheresis — a procedure in which blood is removed, cleansed of immune system cells and antibodies, and then returned to the body — can help reduce inflammation or suppress immune system activity. Large intravenously administered doses of immunoglobulins (antibodies that alter the immune system, and agents such as rituximab that target specific inflammatory cells) also can suppress abnormal immune system activity.

  • Neuropathic pain, or pain caused by the injury to a nerve or nerves, is often difficult to control. . The antidepressant and anticonvulsant medications modulate pain through their mechanism of action on the peripheral nerves, spinal cord, or brain and tend to be the most effective types of medications to control neuropathic pain. Tapentadol, a drug with both opioid activity and norepinephrine-reuptake inhibition activity of an antidepressant.
  • Surgical intervention can be considered for some types of neuropathies. Injuries to a single nerve caused by focal compression such as at the carpal tunnel of the wrist, or other entrapment neuropathies, may respond well to surgery that releases the nerve from the tissues compressing it. Some surgical procedures reduce pain by destroying the nerve; this approach is appropriate only for pain caused by a single nerve and when other forms of treatment have failed to provide relief. Peripheral neuropathies that involve more diffuse nerve damage, such as diabetic neuropathy, are not amenable to surgical intervention. Neutrophic factors
  • The AIN innervates the deep muscles of the forearm (FPL, FDP to the index and middle fingers, and pronator quadratus), a patient with a complete AIN palsy would present with
    Absent motor function to all three of these muscles.
  • AIN comes out radially from the median nerve while most other branches come out Ulnarward
  • Anatomy
    The nerve begins posterior to the axillary artery and travels through the triangular space and then continues along the spiral groove of the humerus. The branches to the triceps are given off before this transition. All branches (sensory or motor) beyond the spiral groove pertain to the hand and forearm (Anconeus is the exception). The nerve travels from the posterior compartment of the arm into the anterior compartment as it penetrates the lateral intermuscular septum approximately 10–12 cm proximal to the elbow. The radial nerve continues to travel distally and ultimately bifurcates into deep (PIN) and superficial (SRN) branches approximately 6.0–10.5 cm distal to the lateral intermuscular septum and 3–4 cm proximal to the leading edge of the supinator.[35,36] The PIN is a motor nerve that courses deep beneath the supinator muscle; the SRN is a sensory nerve that travels anteriorly on the undersurface of the brachioradialis and, in the distal one-third of the forearm, travels subcutaneously to provide sensation to the dorsoradial hand

  • The PIN travels through the radial tunnel. Distally innervating the ECRB, supinator, ECU, EDC, EDM, APL, EPL, EPB, and EIP. It does not innervate the extensor carpi radialis longus (ECRL). The radial tunnel[34] is a potential space 3–4 finger breadths long, lying along the anterior aspect of the proximal radius through which the PIN travels. The floor of the radial tunnel is created by the capsule of the radiocapitellar joint, which continues as the deep head of the supinator muscle.