Peripheral nerve entrapment


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Presentation of the aetiology and pathology associated with peripheral nerve entrapments.

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  • Some grade Neurotmesis into 3 levels
  • Amyloidosis systemic disease where proteins are deposited in specific bady tissues causing them to thinken Sarcoodosis systemic inflammatory disease causing thickening of certain tissues ie skin
  • Wartenberg’s sign positive as interossei do not oppose ext digiti minimi Froment’s positive 2ry to weak adductor pollicis
  • Agg factors leaning on elbows and repeated flex activities Elbow splint (towel round elbow)
  • Supination weak 2ry to involvement of supinator and brachioradialis Normal elbow ext as triceps innervation branches proximal to spiral groove Finger abd to be tested with hand flat on a table as appears weak in flex wrist position
  • Compression from # can occurs as direct result of the initial injury, while reducing # or as callous forms leading to conpression
  • Axilla compression from crutch walking PIN compression of radial nerve after it emerges from the supinator muscle Leads to weakness of Ext carpi uln therefore wrist radially deviates during ext as ECR spared
  • Advantage of US is that it may identify neural swelling earlier even prior to NCS changes Also lower cost, more accetpable to pt’s and can assess long sections of nerve rapidly. Surgery may remove nerve sheath tumour, lipoma or compressive fibrous tissue
  • Pt may be unaware as other muscles may compensate Pain as suprascap nerve has deep sensory fibres to the Ac Jt and GH jt. Pain worse with sh mvt particularly ext add ie increase AND Suprascap nerve is quite immobile compared to the very mobile scapular it is prone to irriation by repetative movements
  • Those that fail conservative should have good outcome if they go on to have surgery Arthroscopic surgery as effective as open decompression
  • Ankle inversion should be tested in df to prevent mistaken impression that tib post is weak
  • Squatting from gardening Thin pt’s because of lack of protection and superficial location Ankle inversion injury slow recovery/reinjury
  • Not good prognosis for those with axonal loss on EMG/NCS Decompression surgery can help upto a year after onset
  • AAA causes pain by compression upper lumbar plexus Surgeries such as hernia repair, THR, Renal transplant, Iliac crest graft, Gastric bypass surgery CABG
  • Symptoms may be prolonged in pt’s with DM William and trizl 1991, 277 pt’s conservative group and 24 surgery group
  • Rest pain thought to be 2ry to venostasis and fluid build up around nerve Pain can easy with walking where as may increase with plantar fascitis No loss sensation if plantar fascitis
  • SLR should only increase pain in neural entrapment as cadarvic studies have show no increase tension in plantar fascia US mainly tested in carpal tunnel so not validated in heel pain could identify neural swelling
  • Possibly related to mt hyperextension from congenital foot deformity or wearing high heels
  • After steroid injection 47% went on to have surgery Alcohol inj more successful up to 94% of pt’s improved Couldn’t find any papers that had long term outcomes following surgery
  • Peripheral nerve entrapment

    1. 1. By Sean Dadswell June 2011
    2. 2. AimsDiscuss physiology associated to PNEDiscuss general signs and symptoms of PNEIdentify: Case Study Clinical presentation Pathophysiology Differential diagnosis Diagnostic technique/tests Treatment of some of the more common PNE’s
    3. 3. Neural PhysiologyNee & Butler 2005, Prinz et al 2005  Basic structure as shown  Neurons have a cell body which contains nucleus, cytoplasm, mitochondria and other organelles.  Dendrites which collect information and transport it to the cell body  Axon which transport information away from the cell body  Synapse which transfers info to other cells  How long is a neuron?  How fast do they repair?  WHY?
    4. 4. Cell Transport (Prinz et al, The speed of this transport2005) is from 0.1mm-400mm dayAxoplasmic flow Axons can be 10000 timesProcess by which nerve longer than the cell body cells transport proteins, lipids and other materials essential for the maintenance and repair of the cell from the cell body along the axon.Also means of removing molecules responsible for axon degradationMolecules are transported down microtubules by specific proteins and enzymes
    5. 5. Nerve injury Nerve injury secondary to compression or traction depends on intensity and duration. Seddon has classified nerve injuries into 3 categories: First, neuropraxia, is a transient episode of motor paralysis with little or no sensory or autonomic dysfunction. No disruption of the nerve or its sheath occurs. With removal of the compressing force, recovery should be complete. Second, axonotmesis, is a more severe nerve injury with disruption of the axon but with maintenance of the Schwann sheath. Motor, sensory, and autonomic paralysis results. Recovery can occur if the compressing force is removed in a timely fashion and if the axon regenerates. Third, neurotmesis is the most serious injury. The nerve and its sheath are disrupted. Although recovery may occur, it is never complete, secondary to loss of nerve continuity.
    6. 6. Neural Injury Cascade Mechanical or chemical irritation Compromised intraneural circulation Reduced axoplasmic flowHypoxia and altered microvascular permeability Subperineurial oedema Intraneural fibrosis
    7. 7. How does this lead to pain?Endoneurial oedema Reduced axoplasmic flow increases sensitivity of =>Reduced myelin nocioceptors in the nervi thickness nervorum (nerves that Formation of Abnormal innervate the neural Impulse Generating Sites sheath of larger nerves) (AIGS)Intraneural fibrosis  As nerve injury leads to reduces extensibility of the altered gene expression nerves increasing and increases number of mechanical stimulation of ion channels along axon nervi nervorum (as ion channels can only form on unmyelinated parts of axon)  Ion channels increase sensitivity of neurons
    8. 8. AIGS sensitive to adrenaline and noradrenaline so neuropathic pain often sensitive to stressAfferent axons (ie those travelling from spinal cord outwards) can cause the release of pro-inflammatory chemicals into their target tissue (neurogenic inflammation) so can have a detrimental impact on the tissue it suppliesCentral sensitisation and altered descending pathway inhibition
    9. 9. Other symptomsPositive Symptoms Negative symptoms (abnormal level of (reduced impulse excitability of the conduction of neural nervous system) tissue) Pain (often deep) Hypoestesia/anesthesia Parasthesia weakness Dysesthesia  Hyperalgesia  Allodynia Spasm
    10. 10. Carpal Tunnel Syndrome (Shapiro & Preston 2009) Median nerve Most common entrapment sensory neuropathy distribution Median Median nerve compression by nerve the transverse carpal lig More women than men Often bilat but almost without exception more prominent in the dominant hand Paresthesia usually in median nerve distribution (thenar eminance spared as supplied by palmar cutaneous sensory branch which comes off proximal to the carpal tunnel Advanced cases may have thenar muscle Flexor weakness/wasting effecting Transverse tendons thumb opposition and ab carpal ligament
    11. 11. Causes of CTSOften idiopathic Persistent wrist flex ie duringRepeated stress to connective sleep tissueRepetitive hand useIndividuals with small carpal tunnelSystemic disorders (RA, hypothyroidism, DM, sarcoid, amyloidosisMass in wrist (ganglion cyst, neurofibroma, arteriovenous malformation) Thenar eminence wastingPregnancy
    12. 12. CTS contPhalan’s good specific (75- Differential diagnosis: 93%) and moderate  C6-7 radiculopathy sensitive (64-75%) for CTS  Bracial plexopathyTinel’s similar spec & sens  Proximal median (tetro et al, 1995 Bolland et neuropathy al, 2008) These can be identified byCarpal compression test pain in the neck, reduced more spec less sensitive reflexes, weakness outsideNCS and EMG can help median nerve confirm diagnosis and distribution, sensory loss in the thenar eminence. discount others (however can be normal in 25% of cases)
    13. 13. Treatments for CTSRemove causative factors Wrist stretchesSplints (night) Wrist mobsNSAIDs Median nerve mobsInjection (beware >3 may => tendon rupture) may be particularly helpful during pregnancy or other reversible condition i.e. HypothyroidismSurgical decompression (open safer than closed but longer recovery)
    14. 14.
    15. 15. Ulnar Neuropathy at the Elbow(Robertson & Saratsiotis 2005)Second most common PNE in upper limbCaused by compression of ulnar nerve in the ulnar groove or cubital tunnelResults from repeated trauma,OA following #, ganglion/tumours/fibrous tissueManifests as progressive loss of grip and pinch strength and interosseus muscle functionClumsinessWasting of thenar and hypothenar eminence
    16. 16. Thenar and hypothenar eminence wasting in the left hand
    17. 17. Interosseous muscle wasting
    18. 18. Ulnar neuropathy contMay be minimal sensory loss reported but may be evident 4th and 5th finger on AxElbow pain common spreading to wristUlnar nerve may be palpable and tenderParesthesia provoked by tinel’s, ulnar nerve compression or elbow flexionMaking a fist may result in 4th and 5th finger not flexing (FDP innervated by UN)Thumb ab and opposition are spared
    19. 19. Ulnar neuropathy contSeveral classic hand postures may be present Benediction posture Wartenberg’s sign Froment’s sign
    20. 20. Differential diagnosis Ax C8-T1 radiculopathy All previously Brachial plexopathy mentioned findings UNE forearm or wrist NCS EMG There may be weakness in muscles not innervated by the ulnar nerve or loss of sensation extending up the forearm
    21. 21. Treatment for UNE Conservative treatment ie avoid aggrevating factors Jt protection Elbow splint Surgical options  Transportation  Decompression cubital tunnel  Medial epicondylectomy Many will recover spontaneously but surgery very effective (Padua et al 2002) 90% of pt’s with mild symptoms will recover with conservative Ulnar nerve transportation Rx (Robertson & Saratsiotis 2005)
    22. 22. Ulnar nerve compression at the wristSimilar manifestation with May require MRI or CT for weakness of the hand diagnosis as well as EMG intrinsics and thenar and and NCS hypothenar eminences Conservative treatmentExacerbated by activities usually successful but may such as riding bike or require decompression if manual labour that mass present repetitively compresses ulnar side of the wrist and Guyon’s canal#, trauma, ganglion cysts, ulnar artery thombus
    23. 23. Radial Neuropathy at the Spiral Groove(Shapiro & Preston 2009) Saturday night palsy Presents with complete wrist and finger drop Numbness in the lat dorsum of the hand Also weak supination and elbow flex Elbow ext normal Finger abd should be unaffected (must be tested in neutral) Triceps reflex normal Brachioradialis reflex reduced or absent
    24. 24. Radial nerve entrapment cause.Radial nerve lies in juxtaposed to spiral groove making it liable to compressionProlonged compression leads to demylinationCan result from # humerus, vasculitis or stenuous muscle effort
    25. 25. Differential diagnosis Radial nerve compression other  Will result in reduced elbow ext sites i.e. Axilla and numbness ext post forearm and upper arm Posterior interosseous  Radial dev during wrist ext neuropathy (PIN)  No loss of reflexes Posterior cord radial plexus  Weak lat dorsi and deltoid and lesion weak all Unusual C7 radiculopathy  Weak C7 innervated muscles including pronation and wrist flex  UMN S&S Central lesion
    26. 26. Diagnosis and TreatmentEMG and NCS should be Treatment usually done to define location conservative of entrapment Protection (properHigh resolution US crutch use) thought to be accurate Wrist splint (Lo et al, 2008; Bianchi, Recovery depends on 2008) demylination (several weeks) or axonal damage (several months to > 1 year) Surgery for ongoing symptoms
    27. 27. Suprascapular NeuropathyAldridge et al, 2001Presents insidious onset wasting over infra and suraspinatusInability to lat rot / abduct (Pt may be unaware)Pain post sh and on palpCommon in weight liftersNerve trapped in suprascapular notch beneath transverse scapular ligLess common entrapment at spiroglenoid notch
    28. 28. Causes Suprascap nerve entrapmentCertain activities which i.e. throwing, dancing, liftingGanglions, sarcoma, carcinomaSurgical positioningDirect trauma
    29. 29. Differential diagnosis DiagnosisC5-6 radiculopathy EMG and NCS Neck pain US to differentiate rot Reduced biceps and brachiorad reflex cuff injury Weakness other C5-6 innervated muscles Treatment Sensory changes Conservative i.e stopBrachial plexopathy offending activity As above no neck pain Surgery especially if massRotator cuff tear identified MOI Conservative and surgical treatment equally effective May be difficult to usually differentiate
    30. 30. Peroneal Neuropathy at the Fibular HeadUsually involves both deep and superficial peroneal nervesTherefore weakness in ankle df and eversionSensory loss over dorsum of the foot and lat calfMay be pain and Tinel’s over fib neckAnkle inversion spared as innervated by Tib nerve.
    31. 31. CausesHabitual leg crossingRepetitive stretch from squattingThin pt’sGanglions etcAssociated to ankle inversion injury including # fib Traction to nerve Prolonged immobilisation (especially sedated pt’s)
    32. 32. Differential Diagnosis DiagnosisSciatic neuropathy EMG and NCSL5 radiculopathy MRI’s in slowly progressing to check forBoth identifiable by masses sensory changes lat knee and/or under/lat footWeak inversionReduce reflexesCRPS
    33. 33. Treatment (Shapiro&Preston 2009; Williams&Robinson 2009)Can be injectedAFOStretches to prevent contracturesGait rehabProprioceptive workEliminate offending activities ie leg crossingSurgery rarely needed except where extensive nerve damage or mass present
    34. 34. Meralgia Paresthetica (Williams and Trizl, 1991; Grossman etal, 2001) Classic presentation of lateral femoral cutaneous neuropathy is burning and numbness lat thigh with no reduction in reflexes or motor power Lat fem cutaneous nerve purely sensory From L2-3 passes under inguinal lig My also be hypersensitive Symptoms may be exacerbated by walking/standing and relieved by hip flex Positive tenderness or Tinel’s at Inguinal lig
    35. 35. Causes Differential DiagnosisIdiopathic Femoral neuropathyObesity Lumbar plexopathyTight underwear, Lumbar radiculopathy wearing tool beltDM Usually numbess lessAbdominal aortic well defined aneurysm Reduce reflexTumours WeaknessPregnancy Diagnosis usuallyPost surgery clinical as EMG not goodRarely caused by trauma for these pt’s. MRI if mass suspected
    36. 36. TreatmentUsually time limited Tricyclic, anticonvulsants,Reduce causitive factor anti depressants (tight clothes) Surgery decompression orLose weight transectionHave baby Conservative treatmentLocal steroid inj successful in 91% casesNSAID’s Surgical treatmentProlonged symptoms may successful in 95% cases require anaesthetic creams/patches
    37. 37. Tarsal Tunnel Syndrome and Plantar Heel/Footpain (Alishami et al, 2008) Compression of the tibial nerve branches under the flexor retinaculum Pain medial ankle, burning, numbness, tingling under foot More common women than men Worst with weight bearing Possible wasting of intrinsics in foot Tinel’s positive in tarsal tunnel Reduced light touch on soles of foot
    38. 38. CausesIrritation to medial or lateral plantar nerve or medial calcaneal nerveIdiopathicAnkle sprain/#RA/Degenerative jt diseaseDMHypothyroidismVV => compressionGanglionRepetitive jogging/wt bearing
    39. 39. PresentationAlways pain abductor hallucisPain after rest particularly morningPain may radiate distally with palp of nerve (should not in plantar fascitis)Pain may easy with walkingReduce d sensation over medial sole
    40. 40. Differential DiagnosisPlantar Fascitis Proximal nerve lesion DF with eversion then Check Lsp SLR Tibial nerve Tinel’s not +ve in pf entrapment in popliteal EMG/NCS fossa High resolution USFat pad atrophy More pain over fat pad Visible loss of fat pad
    41. 41. TreatmentGood evidence very Surgery to decompress limited is a last option andRest should only beNSAID’s considered ifSteroid Injections conservative treatment has failed for 6-12Heel pads monthsOrthosesStretching exercises for PF and calfAND techniques
    42. 42. Interdigital neuropathyMorton’s Neuroma(Cochranes review, 2011; Williams & Robinson, 2009)) Compression of the Plantar digital nerves in the space between the metatarsal headsUsually 3rd space followed by 2nd and rarely 1st or 4th spaceCan give pain which is debilitating as mobility severely limitedPain often relieved by removing tight footwearMay be accompanied by numbness of toes adjacent to pain
    43. 43. Cause Differential DiagnosisMost likely etiology is TTS repetitive compression Can be very difficult to of common plantar differentiate digital nerve between Plantar fascitis MT heads and the TMT OA transverse metatarsal lig. Both of these will have no neurological S&S Also compression of the MT heads should not be exquisitely painful
    44. 44. Diagnosis TreatmentEMG/NCS may help No good evidence exclude other peripheral Conservative treatment nerve or Nerve root helps 50% problems InsolesMRI may be of more Stop offending activities benefit but can often Steroid inj pick up none clinically Alcohol inj x4 relevant lesions Physio (not specified)US good for predicting size of neuroma (92% Surgery Sens 100% Spec) neurectomy/neurolysis (variable outcomes)
    45. 45. SummaryLots of nerve root entrapmentsLocation of entrapment very important in symptomsDifferentiation relies on multiple symptomsConsider could neuropathy be adding to symptoms/preventing/slowing recoveryQuestions?THE END