3/5/2019
LEARNING OBJECTIVES
1. Describe the neuroanatomy from brain to fingertip. 2. Describe current concepts of peripheral nerve biology and healing. • Excellence in Education 3. Collect a good history & exam for common • for OTs and PTs peripheral nerve conditions. • Since 1990 4. Educate patients regarding their condition and treatments. 5. Participate more effectively in the patients’ care. • www.ddhands.com
METHODS Questions during the Discussion Sessions: ▪ Write them on note cards as you think of 1. 14 lectures them 2. Two question and answer sessions 3. Networking Practical Matters: 4. Some repetition between talks ▪ Can everybody see? Hear? ▪ Room temperature? a. Bad news: unavoidable because of ▪ Cell phones, beepers multiple speakers ▪ Auditorium’s policy on food/beverage b. Good news: repetition is a good ▪ Restrooms learning tool ▪ Evaluation forms and certificates ▪ Ready, set, go…
Organization of the Upper Limb
• Some anatomy • Some topology John Elfar Penn State Hershey, • Some embryology Center for Orthopaedic Research and Translational Science Department of Orthopaedics and Rehabilitation
Special thanks to: Robert S. Staron, Ph.D. • Goal is a framework for Summer Anatomy Immersion, Ohio University understanding anatomy in function.
1 3/5/2019
Gray’s Anatomy 37th ed Grant’s Atlas of Anatomy 8th ed Grant’s Atlas 8th ed Grant’s Atlas of Anatomy 8th ed
Antr division: flexor comp.
Postr division: ext comp.
Wikipedia open license (accessed 2019)
Netter’s Atlas of Human Embryology 2002
Muscle Anterior Grant’s Dissector 13th ed musculocutaneous n. Origin of Limb Compartments Humerus Muscles of the Upper Limb Dorsal muscle mass forms radial n. extensors and supinators in (including a portion Posterior upper limb, extensors and of the brachialis m.) Anterior abductors in lower limb. Ventral muscle mass forms median n. & ulnar n. flexors and pronators in Radius upper limb and flexors and Ulna adductors in lower limb. radial n. Posterior Morphogenesis guided by CT, (including ECRL & not myoblasts brachioradialis mm.) ulnar n. & median n. Anterior Split into individual muscles, 5th metacarpal cell death involved
Posterior Carlson l999 Human Embryology Larsen 1993
2 3/5/2019
Hollinshead’s Textbook of Anatomy 5th ed Grant’s Dissector 13th ed
21. Brachial Plexus
nd Rohen/Yokochi Color Atlas of Anatomy 2nd ed Netter’s Atlas 2 ed
Extrinsic shoulder mm. Intrinsic shoulder mm. 1) trapezius m. 1) infraspinatus m. 2) latissimus dorsi m. 2) supraspinatus m. 3) levator scapulae m. 3) subscapularis m. 4) rhomboideus major m. 4) teres minor m. 5) rhomboideus minor m. 5) teres major m. 6) serratus anterior m. 6) deltoid m. Anterior thorax mm. 1) pectoralis major and minor mm. 2) subclavius m. hand – forearm – arm – shoulder distal proximal Grant’s Atlas of Anatomy 8th ed
3 3/5/2019
Extrinsic shoulder mm. 1) trapezius m. (spinal accessory n. - CN XI + C3 & C4)
2) latissimus dorsi m. (thoracodorsal n. - C6, C7, C8)
3) levator scapulae m. (C3 & C4 + dorsal scapular n. - C5)
4) rhomboideus major m. (dorsal scapular n. - C5)
5) rhomboideus minor m. (dorsal scapular n. - C5)
6) serratus anterior m. (long thoracic n. - C5, C6, C7) Anterior thorax mm. med/lat
1) pectoralis major ( C5-T1) & minor (C6-C8) mm. pect nn. ed
2) subclavius m. (n. to subclavius m. - C5, C6) th
Grant’s Atlas 8 Grant’s Grant’s Atlas of Anatomy 8th ed
Netter’s Atlas 2nd ed
Netter’s Atlas of Human Anatomy 2nd ed
Intrinsic shoulder mm. 1) infraspinatus m. (suprascapular n. - C5, C6)
2) supraspinatus m. (suprascapular n. - C5, C6)
3) subscapularis m. (upper + lower subscapular nn. - C5, C6)
4) teres minor m. (axillary n. - C5, C6)
5) teres major m. (lower subscapular n. - C5, C6)
6) deltoid m. (axillary n. - C5, C6)
ed th
Grant’s Atlas 8 Grant’s Grant’s Atlas of Anatomy 8th ed
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rotator cuff musculature
Netter’s Atlas of Human Anatomy 2nd ed Netter’s Atlas 2nd ed
Anterior Grant’s Dissector 13th ed Grant’s Dissector 13th ed Muscle musculocutaneous n.
Compartments Humerus of the Upper Limb - arm radial n. (including a portion Posterior of the brachialis m.) Anterior
median n. & ulnar n. Radius Ulna
radial n. Posterior (including ECRL & brachioradialis mm.) ulnar n. & median n. Anterior
5th metacarpal
Posterior
brachium musculocutaneous n. (C5-C7) antr compartment postr compartment biceps brachii m. triceps brachii m. biceps brachii m. (C5, C6) long head lateral head brachialis m. (C5, C6) short head medial head brachialis m. long head coracobrachialis m. (C5-C7) coracobrachialis m. anconeus m.
Netter’s Atlas of Human Anatomy 2nd ed
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Grant’s Dissector 13th ed axillary n. (C5-C6) deltoid m. (C5, C6) teres minor m. (C5, C6)
radial n. (C5-T1) triceps brachii m. (C6-C8) anconeus m. (C7, C8)
(brachialis m. C5, C6)
Netter’s Atlas of Human Anatomy 2nd ed
Anterior Grant’s Dissector 13th ed Anterior Grant’s Dissector 13th ed Muscle musculocutaneous n. Muscle musculocutaneous n.
Compartments Humerus Compartments Humerus of the Upper of the Upper Limb - forearm Limb - forearm radial n. radial n. (including a portion Posterior (including a portion Posterior of the brachialis m.) Anterior of the brachialis m.) Anterior
median n. & ulnar n. median n. & ulnar n. (FCU & ulnar ½ Radius Radius FDP) Ulna Ulna
radial n. Posterior radial n. Posterior (including ECRL & (including ECRL & brachioradialis mm.) ulnar n. & median n. brachioradialis mm.) ulnar n. & median n. Anterior Anterior
5th metacarpal 5th metacarpal
Posterior Posterior
antebrachium antr compartment postr compartment pronator teres m. brachioradialis m. flex. carpi radialis m. ext. carpi radialis longus m. palmaris longus m. ext. carpi radialis brevis m. flex. carpi ulnaris m. ext. carpi ulnaris m. extensor digitorum m. flex. digit. superf. m. extensor digiti minimi m. flex. digit. profund. m. extensor indicis m. flex. pollicis longus m. abd pollicis longus m. pronator quadratus m. ext. pollicis longus/brevis m. supinator m.
Grant’s Dissector 13th ed
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antebrachium ulnar n. (C7-T1) antr compartment (median & ulnar nn.) pronator teres m. (C6, C7) flex carpi ulnaris m. flex. carpi radialis m. (C6, C7) medial ½ FDP palmaris longus m. (C7, C8)
flex. carpi ulnaris m. (C7, C8) flex. digit. superf. m. (C7, C8, T1) + 14 intrinsic hand flex. digit. profund. m. (C7, C8, T1) muscles
flex. pollicis longus m. (C8, T1)
pronator quadratus m. (C8, T1)
Netter’s Atlas of Human Anatomy 2nd ed
median n. (C5-T1) antebrachium postr compartment (radial n. C5-T1) brachioradialis m. (C5, C6) PT, FCR, PL, ext. carpi radialis longus m. (C6, C7) FDS, lat ½ FDP, ext. carpi radialis brevis m. (C6, C7 or C7, C8) FPL, PQ ext. carpi ulnaris m. (C7, C8) extensor digitorum m. (C7, C8) extensor digiti minimi m. (C7, C8) + 5 intrinsic hand extensor indicis m. (C7, C8) muscles abd pollicis longus m. (C7, C8) ext. pollicis longus/brevis m. (C7, C8) supinator m. (C5, C6)
Netter’s Atlas of Human Anatomy 2nd ed
Grant’s Atlas of Anatomy 11th ed radial n. (C5-T1) triceps brachii m., anconeus m. (brachialis m.)
BR, ECRL, ECRB, ED, EDM, supinator, ECU, EI, AbdPL, EPL, EPB
Netter’s Atlas of Human Anatomy 2nd ed
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Anterior Grant’s Dissector 13th ed Anterior Grant’s Dissector 13th ed Muscle musculocutaneous n. Muscle musculocutaneous n.
Compartments Humerus Compartments Humerus of the Upper of the Upper Limb - hand Limb - hand radial n. radial n. (including a portion Posterior (including a portion Posterior of the brachialis m.) Anterior of the brachialis m.) Anterior
median n. & ulnar n. median n. & ulnar n. (FCU & ulnar ½ (FCU & ulnar ½ Radius FDP) Radius FDP) Ulna Ulna
radial n. Posterior radial n. Posterior (including ECRL & (including ECRL & brachioradialis mm.) ulnar n. & median n. brachioradialis mm.) ulnar n. & median n. Anterior Anterior (thenar mm. & 1st, 2nd lumbricals) 5th metacarpal 5th metacarpal
Posterior Posterior
intrinsic hand muscles (C8, T1) intrinsic hand muscles (median & ulnar nn.)
7 interosseii mm. (4 dorsal/3 palmar) 7 interosseii mm. (4 dorsal/3 palmar) 4 lumbrical mm. (1, 2, 3, 4) 4 lumbrical mm. (1, 2, 3, 4) palmaris brevis m. palmaris brevis m. adductor pollicis m. adductor pollicis m. three thenar mm. (OP, abd.PB, FPB) three thenar mm. (OP, abd.PB, FPB) three hypothenar mm. (ODM, abd.DM, FDMB) three hypothenar mm. (ODM, abd.DM, FDMB)
upper limb - upper limb – cutaneous innervation dermatome pattern
Netter’s Atlas of Human Anatomy 2nd ed Netter’s Atlas of Human Anatomy 2nd ed
8 3/5/2019
Anatomy is a Journey
.The quicker you embark . What could be re-routed to the more of the journey serve another function? you will appreciate. . Which surgeries are .It is not only about rational? And which John Elfar memorizing what inserts surgeries are ill-advised? Penn State Hershey, Center for Orthopaedic Research and Translational Science where and which nerve . Knowledge of anatomy can Department of Orthopaedics and Rehabilitation innervates which muscle. give subtle insights into Special thanks to: Adam Martin, MD .We think not only of function and possible UCLA Hand Fellow what exists, but what rehabilitation. could exist. . Enjoy your journey.
Outline Anatomy of Neuron
• Microanatomy Cell body • Biology Dendrites • Nerve Injuries Receive incoming impulses – Physiology Axon – Classification Conducts outgoing impulses – Nerve response to injury Schwann cells, produce myelin sheath
Courtesy Roadnottaken Wikimedia
Anatomy of a Peripheral Nerve 1. Axon: basic subunit Sensory neuron . Nerve fiber = axon + Schwann cell + myelin 2. Fascicle: groups of axons 3. Peripheral nerve: Motor neuron groups of fascicles
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Connective tissue layers How Many Fibers? • Electric lamp cord: ~60 copper strands 1. Epineurium • Digital nerve: ~1500 nerve fibers 2. Perineurium • Median nerve: ~25,000 nerve fibers 3. Endoneurium • Brachial plexus: ~145,000 nerve fibers Vascular supply Intrinsic + extrinsic
Mitchell adapted from www.CDNPA.com
Cross-section of peripheral nerve External epineurium Epineurium Cushions nerve Internal epineurium Nerve gliding Fascicle Perineurium Surrounds fascicle Tight junctions Fascicle Endoneurium Surrounds axons Axon + Endoneurium
Nerve Physiology
• Axonal transport – Protein synthesis in cell body – Distance too long for diffusion – Products motored along microtubules • Retrograde transport – Returns waste products for recycling – Transports growth factors to nucleus • Implications with injury
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Response to Injury Nerve Injury Causes • Limited repertoire of • Mechanical injuries • Secondary injury responses to nerve – Compression – Infection injury – Traction – Scarring 1. Mild injury schwann – Laceration – Fracture callus cells/myelin sheath – Combination (e.g. – Ischemia – Focal demyelination gunshot wounds) 2. Severe injury axons – Axonal degeneration
Nerve Injury Classification Neurapraxia • Conduction block • All supporting layers entirely intact • Mild neurapraxia transient ischemia 1. Neurapraxia – Impairs polarization of cell membrane 2. Axonotmesis – Unable to conduct action potential 3. Neurotmesis axon
epineurium perineurium endoneurium
Neurapraxia Neurapraxia
• More severe injury Demyelination Prognosis for recovery excellent • Disrupts impulse conduction Axons remain intact no axonal degeneration • Axons are physically intact, physiologically out Mild cases: relief of temporary ischemia Focal Demyelination Severe cases: Schwann cells remyelinate damaged segment axon Restores conduction along axon Symptoms may last moments to months epineurium perineurium endoneurium
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Axonotmesis Axonal Injury: Wallerian Degeneration Axonal transport interrupted • Loss of axon continuity Survival of axonal segments • Connective tissue envelope intact connected to cell body • Degeneration of injured axons distally Distal segments Deprived of metabolic support Degeneration of axons beyond axon point of injury
epineurium perineurium endoneurium
Axonotmesis Neurotmesis • Recovery requires axonal regeneration • Complete nerve transection • prolonged recovery • Prognosis for recovery good • Degeneration of all axons distal to injury • endoneurial tubes are intact -> no miswiring • • Limiting factor is the distance of regeneration required Separation of nerve ends spontaneous recovery will not occur • Surgical problem
axon axon
epineurium perineurium endoneurium epineurium perineurium endoneurium
Physiology of Injury Neurotmesis- End Result Neuroma • Laceration Neurotmesis – Smaller zone of injury • Traction Axonotmesis – Axons most susceptible – Larger zone of injury • Acute compression Neurapraxia – Local contusion with 2o circulatory changes – Inflammation scarring and further compression
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Chronic compression Nerve regeneration Ischemia + mechanical • Wallerian degeneration compression – Distal axon fragmentation At 30 mm Hg – Disintegration of myelin Decreased intra-neural blood • Macrophage invasion flow – Clears endoneurial tubes of Axonal transport disrupted debris Progressive axonal loss • Schwann cell proliferation (axonotmesis) and fibrosis • Pathway for later axonal regeneration Damage often permanent
Axonal Regeneration Axons that find distal • Proximal effects tubules are guided along – Loss of trophic support (1mm/day) – Sometimes neuronal death Sprouts that reach distal – Survivors alter metabolic activity in connections mature preparation Increase in axon and myelin • Axonal sprouting thickness – Growth cones • Samples environment Sprouts which fail to make • Seeks sensory or motor pathways connections die back – Guided by Schwann cells
• If gap exists, axonal sprouts migrate aimlessly Nerve Regeneration: Molecular Level • No distal targets are reached • Neuroma formation • Neurotrophic factors (“fertilizer”) • Neurotropic factors (“traffic cops”) • Matrix substrates • Metabolic factors for nourishment
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Neurotrophic Factors Neurotropic factors Promote survival and maintenance of neuron • Promote extension and branching of axonal Axonal injury disruption of retrograde supply sprouts of growth factors • Attract sprouting axons toward distal nerve Schwann cells provide trophic support segment Proteins presented along regenerating pathway • 2 mechanisms: contact-guidance versus Picked up by axonal sprouts to sustain neuron attraction at a distance Examples – Laminin and fibronectin: matrix-bound Nerve Growth Factor sensory neurons glycoproteins Brain-derived neurotrophic factor motor – Soluble mediators
Neurotropic factors Topographic Specificity
• Anti-neurotropic factors • Accuracy with which – negative or repulsive guidance cues deflect axons regenerating axons re- from inappropriate targets innervate appropriate targets – Dramatically affects outcomes after nerve injury • Axonotmesis >> neurotmesis – Miswiring: axons wander into wrong tubules
Adapted from Carmeliet P, Nature Reviews Genetics 4:2003
Clinical Perspective Clinical Perspective
• Axons regrow about ~1mm/day (1” / month) • Functional result following nerve injury dependent on numerous factors • Motor end plates degrade ~1%/week 1.extent of neuron survival • Need > 50% of motor endplates for function 2.rate and quality of axonal outgrowth • Maximum distance to restore motor function is 3.topographic specificity of regenerating axons ~35 cm 4.survival of end organs • Sensory end-organs may survive much longer 5.cortical reorganizational . • Late nerve reconstruction can offer recovery of Clinical recovery often incomplete protective sensation
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References
1. Regal S, Tang P. Surgical management of neuromas in the hand and wrist. J Am Acad Orthop Surg. 2018 Nov 13 2. Eberlin KR, Treiser M. Anatomy and physiology of the peripheral nerve. ASSH Surgical Anatomy: Nerve Reconstruction, 2017 3. Dahlin LB. The nerve’s response to injury. ASSH Upper Extremity Diagnostic Testing for Nerves Nerve Repair Tips and Techniques: A Master Skills Publication, 2008 Sensory, Motor, Electrical, Imaging
Timothy Shane Johnson, MD Talk originally prepared by Roy A. Meals, MD
Burning Questions about Sensation The Anatomy of Fingertip Skin “You claim my nerve is recovering, why do I have pain and every time I touch something?” Specialized Sensory End Organs “So if I have carpal tunnel syndrome, why aren’t my thenar muscles weak?”
“You tell me I am maximally recovered from my nerve laceration, why can’t I feel my electric tooth brush vibrating?”
papillary ridges sweat pores sweat duct Nerve Fiber Types & gland Fiber Myelin Size in Function Meters
Meissner - type sheath? microns per sec
corpuscles epi dermis C No 1 Burning 2 pain Merkel A-β A-Δ Yes 2-5 Sticking 20 cell & temp C A-Δ A-β Yes 10-15 Light 60 neurite dermis complex Important for normal sensationtouch Pacinian A-α Yes 15-20 Motor 60 digital nerve corpuscle
A-β fat
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Specialized Sensory End Organs Specialized Sensory End Organs Supplied by A-β Fibers Supplied by A-beta Fibers Pacinian Meissner Merkel cell Pacinian Meissner Merkel cell corpuscle corpuscle neurite cplx corpuscle corpuscle neurite cplx
Stimulus Schematic Response III II III II II I I I I
Adaptation Quick Quick Slow # of nerve 1 >1 <1 Response to: fibers/rcptr Touch Constant Poor Poor Good Recovery Poor Excellent Fair Moving Good Good Poor after ? Vibration 30 cycle 256 cycle No laceration ? ? ?
What can go wrong? What constitutes normal sensation? 1. A multitude of A-beta fibers present, supplying various 1. A multitude of A-beta fibers present, supplying types of end organs various types of end organs •Laceration (physical disruption of axon and entire sheath = neurotmesis) •Marked compression/stretch (physical disruption of axon but continuity of sheath = axonotmesis) 2. Each nerve fiber functioning properly 2. Each nerve fiber functioning properly •Compression (physiologic disruption, aka ischemia = neurapraxia)
When something goes wrong, inquiring minds want to know: Matching: A How many nerve fibers are present? 1. Innervation (more is better) Innervation density density test
How much energy does it take to stimulate a nerve fiber? (less is better) 2. Threshold test Threshold B POP QUIZ!
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Two Point Discrimination Monofilament Testing (The Innervation Density Test) (The Threshold Test) Maybe if I move How wide do I along the finger I I can’t go wide. I am looking for have to stretch to can find 2 fibers a single nerve fiber to stimulate find 2 functioning more easily. but I can push only so hard. nerve fibers?
I go wide when nerve fibers are missing, e.g., lacerations, severe compressions If I can’t push hard enough to make the nerve fire, maybe my big brother can!
Final Exam: MFT vs. TPD
For Your
Mono Filament # in Force grams
Filament # in Force grams Reference: Mono 1. What test is appropriate for testing nerve 1.65 .01 4.56 4.2 2.36 .02 4.74 4.6 regeneration after laceration and repair? 2.44 .04 4.93 5.2 2. What test is appropriate for testing sensory loss in 2.83 .08 5.07 7.4 early cubital tunnel syndrome? 3.22 .17 5.18 13 3.61 .22 5.46 21 3. What test is appropriate in severe carpal tunnel 3.84 .45 5.88 47 syndrome when MFT is markedly abnormal? 4.08 .75 6.10 85
4.17 .98 6.45 164 4.31 2.4 6.65 279 TPD 3. MFT, 2. TPD, 1.
Inquiring minds want to know: Inquiring minds want to know:
“You claim my nerve is recovering. Why do I have “So if I have carpal tunnel syndrome, why aren’t pain every time I touch something?” my thenar muscles weak?”
Rephrased: Why is pain the first sensation to Rephrased: Why does sensory loss occur before return after nerve repair? motor loss in carpal tunnel syndrome?
The unsophisticated unmyelinated C fibers grow The motor fibers are larger and are more resistant to compression ischemia. back the quickest.
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Scratch Collapse Test Inquiring minds want to know: for Carpal Tunnel and Cubital Tunnel Syndromes (to be demonstrated during Q/A session) “You tell me I am maximally recovered from my patient nerve laceration, why can’t I feel my electric tooth brush is vibrating?”
Rephrased: Why does response to low frequency vibration return poorly after nerve repair?
Because the Pacinian corpuscles reinnervate 2 poorly. 1 3 examiner See Ref 7
Muscle Testing For Reference: Muscle Testing Quantitate where possible (Grip and pinch meters) Compare to opposite side (ideally without examiner in the middle) The well-known Medical Research Council 0-5 scale 0 = no function 1 = palpable contraction, no movement 2 = movement with gravity neutralized 3 = movement against gravity 4 = movement against some resistance 5 = normal strength
Muscle Testing, Reconsidered Electromyography (EMG) • McAvoy and Green: – Cadaver study, elbow flexion – Only 4% of normal force required to flex against gravity Nerve conduction velocity (NCV) • MRC Grade 0 1 2 3 4 5 • Tests nerve % of normal 0 <4 <4 4 >4 100 Needle electrode exam (NEE) • Tests muscle 95%
Grade 4 represents 95% of potential elbow flexion strength, therefore includes both weak and strong muscles. Better system needed!
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Nerve Conduction Velocity Parlance NCV in Neurapraxia • Ulnar nerve • Affected by the room’s temperature, patient age, – 54 meters/sec anomalous innervation patterns – 42 meters/sec • Usually with surface electrodes – Conclusion: cubital tunnel synd Stimulating <- distance between -> Recording • Median nerve • Velocity = distance divided by time – Sensory distal latency 4.0 millisec >50 meters/sec for all upper extremity nerves • (nl <3.6 millisec) – Motor distal latency 4.8 millisec • Latency (time in milliseconds) substitutes for velocity when • (nl <4.6 millisec) distance is uncertain – Conclusion: carpal tunnel synd
Needle Electrode NCV in Axonmetsis and Neurotmesis • Normal muscle Exam Parlance remains normal for 2-3 days – Electrically silent at rest – Electrical activity proportionate to force – of active contraction (recruitment) • Denervated muscle – Fibrillations and sharp waves at rest begin 2-3 weeks after injury – No change on active contraction effort • Reinnervating muscle – Disorganized recruitment pattern—seen 1-2 months before axon clinical improvement noted
Magnetic Resonance Neurography: CTS References Nerves not seen at all on x-ray or CT scan Nerves not seen well on conventional MRI 1. Dellon, Evaluation of sensibility and re-education of sensation in the hand. Magnetic Resonance Neurography (MRN): Under development Williams and Wilkins, Baltimore, 1983. 2. MacAvoy, Green: Critical reappraisal of Medical Research Council muscle testing flat for elbow flexion. J Hand Surg, 2007; 32A:149-153. 3. Aagaard, Maravilla, Kliot: Magnetic resonance imaging of peripheral nerves. Neuroimaging Clinics of North America, 2001; 8:131-146. 4. Yoshikawa et al: Brachial plexus injury. Radiographics, 2006; 26:S133-143 5. Filler et al, MR neurography and muscle MR imaging Neurol Clin 2004, 22:643- 682 flat 6. Cudlip et al, Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg 2002, 96:1046-1051 7. Cheng, et al: Scratch collapse test for evaluation of carpal and cutibal tunnel normal syndrome. J Hand Surg 2008, 33A:1518-1524 3 Aagaard Cudlip6
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Seddon Injury Classification
Nerve Lacerations, Repair, Grafting, • Neuropraxia – Temporary paralysis Transfers, Neurotization • Axonotmesis – Likely recovery
Timothy Shane Johnson, MD • Neurotmesis Talk originally prepared by Katherine Au, MD – No recovery without repair
Mechanism of Injury Basic Injury Types • Tidy wounds: knife, glass, surgical Compression – “Saturday night palsy” • Untidy wounds: – Open fracture Traction – Penetrating missile
• Avulsion Laceration
Nerve repair Indications for operative intervention • Sensorimotor exam + mechanism • Associated vascular/bony Failure of nerve recovery • Worsening of nerve injury • Persistent pain • Painful neuroma
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Reasons not to repair Timing of Nerve Repairs Open Injuries • General condition of the patient • Skill/availability of operating team and Early exploration specialized equipment • Uncertain viability or state of nerve trunks Definitive repair if sharp laceration • Local or systemic sepsis • Tendon transfer or nerve transfer will give Crush injury – zone of injury not apparent better results
Timing of Repair Classification of Nerve Repair Closed Injuries • Expectant observation Primary repair (<1week) – Expect complete recovery in 6 weeks – If none Delayed primary repair (after 3-4 days) – 6 wks: baseline EMG/NCS – 12 wks – clinical exam, repeat EMG/NCS Secondary repair (>1week) – 3 months – operative exploration
Dvali & Mackinnon, Clin Plastic Surg (2003)
Principles of Repair Nerve Repair Technique • Correct alignment/orientation of fascicles • Meticulous surgical technique • Use surface blood vessels for rotational – (microscope preferred to loupes) alignment • Debride to healthy nerve ends • Primary tension-free repair Graft if tension-free repair not possible • Fascicular matching (motor to motor, sensory to sensory)
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Group Fascicular Nerve Repair Epineural Nerve Repair
Factors in Outcomes
Age Nerve gap Management of Nerve Gaps Delay to repair Level of Injury Condition of nerve ends
Nerve Grafts Nerve Grafts Autografts (same person) • Graft: tissue that depends on recipient bed blood supply Allografts (same species, rendered immune innert) • Indication: Cannot achieve tensionless direct repair Pedicled nerve grafts (nerve flaps) Vascularized nerve flaps
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Donor Nerves Cable Nerve Grafting Donor Length Deficit Sural 30-40 Lateral cm foot Lateral 5-8 cm Lateral antebrachial forearm cutaneous Medial 10-20 Medial antebrachial cm arm and cutaneous elbow (ant. br.)
Disadvantages of Autologous Avance™ Grafting • Prolonged operative time • AxoGen Inc. • Limited supply of expendable donor nerve • Human cadaveric nerve allograft • Donor site morbidity • 1.5, 3, 5, and 7 cm lengths • Axons must cross 2 suture lines • 1-5mm diameters • Motor axons must growth through potentially inhibitory sensory nerve environment
Nerve Conduits Nerve Conduits • Provide safe passage for regenerating nerves • Require population by Schwann cells from neural • Localizes neurotrophic factors stumps to guide axonal growth • Protection from scarring • Short (<3cm) nerve defects • Natural, synthetic, non/absorbable • Vein, polyglycolic acid (PGA), collagen
Porous flexible PGA mesh Semipermeable collagen GEM Neurotube Integra Thumb digital nerve Repair w/ neurotube
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Cho et al. JHS 2012 Cho et al. JHS 2012
What if proximal end of damaged nerve is far from Principles of Nerve Transfer either neuromuscular junction (motor end plates)? • Expendable donor sensory distribution (sensory end organs)? • Donor nerve with large number of motor or sensory axons • Transfer a healthy proximal donor nerve Donor near motor end plates of muscle or skin area served by sensory nerve (or nerve fascicle) • Innervates a muscle that is synergistic to the target to muscle (preferred) distal palsied nerve
Nerve Transfers Oberlin Transfer Restoration of elbow flexion • Historically used in brachial plexus injuries Ulnar nerve fascicle to musculocutaneous nerve – No viable proximal nerve (eg, root avulsion)
Musculocutaneous n. Ulnar n.
Biceps
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Indications for Nerve Transfer Nerve Transfers Convert high (proximal) injury to low (distal) injury Brachial plexus avulsion injuries Recruiting redundant or noncritical fascicles Avoid dissection through scar Major trauma with segmental nerve loss Alternative to grafting in older patients Proximal nerve injury (with anticipated poor recovery)
~35cm/~14in ~12cm/~4.7 in
High Ulnar Nerve Injury Median to ulnar transfers - Motor
• AIN (anterior interosseous n.) motor branch ulnar nerve Missing: intrinsic function sensation to ulnar 1 ½ digits & ulnar dorsal hand
Adapted from Dvali et al. Clin Plastic Surg 2003
Median to ulnar transfers - Sensory Cortical Reorganization
Median n. to 3rd webspace ulnar sensory nerve • Sensory denervation of the hand “black hole” in End to side sensory cortex of brain • Tactile input from the hand causes functional cortical reorganization • Organization of the sensorimotor cortex is not fixed • “Hand speaks a new language to the brain.”
Adapted from Dvali et al. Clin Plastic Surg 2003 J. Surg. Ortho Advances 2008; 17(3) 159-164.
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References
• Oberlin C, et. al. Nerve transfer to biceps muscle using a part of ulnar nerve for C5-C6 avulsion of the brachial plexus: anatomical study and report of four cases. J Hand Surg [Am]. Mar 1994;19(2):232-7. • Dvali L, et. Al. Nerve repair, grafting and nerve transfers. Clin Plastic Surg 2003; 30:203- 221. Nerve Pathology in the Proximal • Cho MS, et al. Functional outcome following nerve repair in the upper extremity. J Hand Surg 2012; 2340-9. • Weber RV, et. al. Bridging the Neural Gap. Clin Plastic Surg 2005; 605-616. Portion of the Upper Limb • Brown et. al. Nerve Transfers in the Forearm and Hand. Hand Clin 2008; 24:319-340. • Chiu, DTW et. al. A Prospective Clinical Evaluation of Autogenous Vein Grafts Used as a Nerve Conduit for Distal Sensory Nerve Defects of 3 cm or Less. Plast Recon Surg 1990; Mike Darowish 928-934. • Young et al, A randomized prospective comparison of fascicular and epineural digital nerve repairs. Plast Recon Surg 1981.
Introduction Cervical Spine
Proximal causes of pain and paraesthesias of the upper extremity
• Cervical radiculopathy • Brachial plexus issues • Thoracic outlet syndrome
Cervical Spine Cross Section Dermatome Distribution
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Motor Innervation Reflexes
• C5 Deltoid • Biceps – C5, C6 • C6 Biceps, wrist extensor • Brachioradialis – C6 • C7 Triceps, wrist flexors • Triceps – C7 • C8 Interossei, Finger flexors • Hoffmann’s reflex – upper motor neuron • T1 Interossei
Pathomechanics of Cervical Symptoms of radiculopathy Radiculopathy • Based on nerve root • Compression of nerve root affected – Disc pathology or herniation • Radicular pain, numbness, or weakness – Arthritis • Neck and shoulder pain – Congenital stenosis are common – Trauma • Pain, paraesthesias, – Tumor weakness in distribution of the affected nerve • Anatomy is key
Diagnosis of radiculopathy X-ray
• History and physical – Spurling’s test: extension, ipsilateral rotation, and downward pressure • XR • MRI • Electrodiagnostics
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Treatment of Radiculopathy Brachial Plexus Injuries
• Nonsurgical – pain control, anti-inflammatories – Neck strengthening – Traction and manipulation: controversial – +/- steroid injections • Surgery – Decompression – Fusion – Disc replacement
Brachial Plexus Injuries Brachial Plexus Injuries
- Upper trunk - Trauma - weakness in abduction and - Birth injury elbow flexion - low energy - radial sided hand numbness - stinger - high energy - Motorcycle, fall - penetrating trauma - Lower Trunk - lose hand function - ulnar sided hand numbness
Brachial Plexus Treatment Thoracic Outlet Syndrome
- Depends on etiology and status of nerve - Pre- vs. post-ganglionic - Preganglionic worse, +Horner’s syndrome - Sharp laceration → direct repair - Nerve graft - Nerve transfer - Tendon transfer - Osteotomy
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Pathomechanics of TOS TOS Types • Compression of the brachial plexus or • Vascular vessels at the “thoracic outlet” • Compression of subclavian artery or vein • Congenital anatomic variations – cervical • Neurogenic ribs, long transverse processes, congenital – Classic presentation with objective physical bands evidence is rare • Apical lung tumors (Pancoast tumors) – Hypothenar atrophy, decreased grip strength, • Malunion or non-union of the clavicle, sensory (C8/T1) deficits sternoclavicular dislocations • Disputed (Non-specific)
TOS Symptoms Differential Diagnosis • Disputed Neurogenic TOS • Upper trunk involvement mimics cervical – Chronic, insidious onset pain of neck, upper radiculopathy or carpal tunnel syndrome chest, and shoulder girdle • Lower trunk involvement mimics cubital tunnel • Radiates into ulnar side of arm and hand, syndrome and rarely into radial side • Left shoulder and chest pain mimics angina or – Worse with elevation of arm during heart attack sleep/activity, driving, or heavy objects • Pain with overhead activity mimics cuff tears – Subtle findings may be confined to ulnar • Glenohumeral instability and global upper intrinsics of hand, mimic ulnar neuropathy extremity symptoms
Diagnosis of TOS Diagnosis of TOS • Evaluate posture and head position • Diagnosis of exclusion • Forward head position • History and physical • Shoulder droop • Rule out other sites of compression • Muscle bulk and tone • Ulnar nerve • Arm swelling • C-spine • Hand atrophy, intrinsic muscle testing • Sensory abnormalities • Peripheral nerve compression signs • Vascular exam
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Diagnosis: Provocative Roos test – “stick up test” Testing for TOS • 90 degree abduction • Look for reproduction of symptoms or loss and external rotation of radial pulse test • Pump hand for 3 • Beware: many positions can cause minutes diminution of radial pulse, and are not • Rapid fatigue or diagnostic in isolation reproduction of • 64 volunteers symptoms • Most sensitive and – 17% with symptoms on questionnaire reproducible – 58% had one provocative test positive
Diagnosis - Imaging Diagnosis - Electrodiagnostics
• C-spine and chest films • Generally, EMG/NCS not useful in • Consider CT scan if suspicion high diagnosing TOS – Adventitious ribs, long transverse – Results do NOT predict thoracic outlet process, cervical ribs, malunited fracture syndrome – Apical lung tumors – Useful to evaluate for carpal tunnel or • MRI ulnar neuropathy at the elbow
TOS: Treatment TOS Treatment Overview
– Therapy: focus on postural abnormalities, • Key is to correct postural abnormalities • Generic instructions from physicians may lead to muscle imbalances, and neural mobility treatment with stretching, soft tissue massage, – Nutritional counseling, diet, and exercise nerve mobilization, or cervical traction – this does not help and may aggravate symptoms program • Limitation of aggravating activities (heavy loads, overhead work, backpacks) • Identification of weakened muscles and strengthening of shoulder girdle to improve posture is key • Bring shoulder girdle back posteriorly
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TOS Treatment risk factors for failure Treatment - Surgery • Vascular occlusion can be treated with • Poor cardiovascular condition thrombolytics and long term anticoagulation, or surgical decompression • Obesity, chronic pain and associated • Scalene muscle resection depression exacerbate poor posture • First rib resection –Antidepressants or psychotherapy • Claviculectomy for malunions or can improve symptoms hypertrophic callus – Loss of strut → shoulder droop → worsening symptoms
Complications of Surgery Prognosis • Review of 10 studies of conservative treatment found • Pneumothorax no randomized trials, systematic reviews, or meta- • Nerve injury – brachial plexus from traction, long thoracic N on middle scalene, phrenic N on analysis. anterior scalene • Unclear if conservative treatment better than no • Vascular injury – death from exsanguination has treatment, or what type of treatment is best been reported. – Less than 20% of patients diagnosed progress to • Persistent symptoms -- inadequate resection vs incorrect diagnosis surgery – When appropriately done, 75% good to excellent results in some series
Adson’s test Halsted Maneuver • Costoclavicular test/military • Arm at the side, brace test hyperextend neck, • Arms at side turn toward • Move shoulders down and affected side, and back with protruding chest inhale deeply • Clavicle closes on 1st rib • Downward compression of • Pulse diminishes clavicle with traction of • Symptoms affected extremity reproduced accentuates symptoms
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Wright’s hyperabduction test TOS Treatment - Step 1
• External rotate and • Identify and treat myofascial trigger points, local spasm, tendonitis, bursitis abduct arm 180 – Use relaxants, mild narcotics, degrees antidepressants, anti-inflammatories, • Inhale deeply TCA, tegratol, neurontin. – Modalities such as heat/ice, TENS, ultrasound are debatable (can promote • Symptoms worsen dependence on therapy) – Trigger injections, botox injections, and epidural steroids
TOS Treatment – Step 2 TOS Treatment – Step 3 • Concurrent postural training • Stretching, relaxation, and myofascial manipulation • Muscle strengthening, increased restore posture in C-spine, shoulder girdle endurance, and restoration to pre- • Upper trapezius, levator scapulae, scalenes, symptomatic levels sternocleidomastoid, pectoralis minor, and – Not started until patient has adequate suboccipitals pain-free ROM • Weight loss and CV conditioning – Aggressive therapy at this time may • Avoid pathologic postures - head-forward posture exacerbate symptoms leads to decreased flexibility,scapular abduction, with tightening of anterior groups and elongation of – Typically weak in middle and lower posterior groups. trapezius, and serratus anterior
TOS Treatment – Step 4
• Home program for maintenance followed by return to work-place • Analysis of workplace and job site MEDIAN NERVE ENTRAPMENT • Scalene stretching, cervical protraction and retraction, diaphragmatic exercises, pectoralis stretching, and shoulder circumduction Mike Darowish • Orthotics for scapular retraction may help, but must be part of muscular strengthening plan
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Median Nerve Compression Syndromes CARPAL TUNNEL SYNDROME • Epidemiology • Nerve Entrapment at the Wrist – Classically – Carpal tunnel syndrome • Posttraumatic • Female • Compressive Neuropathies in Proximal Forearm • Middle age – Pronator syndrome – More recently – Anterior interosseous syndrome • Younger • Industrial worker • Repetitive motions
RISK FACTORS RISK FACTORS
• Clear intrinsic risk • Occupational factors factors • Task repetition • Female • Mechanical stress • Pregnancy • Force • Diabetes • Vibration • Rheumatoid arthritis • Temperature (cold) • Typing/mousing - controversial
CARPAL TUNNEL SYNDROME CARPAL TUNNEL SYNDROME • Median nerve entrapment in the • Nakamichi ‘98: carpal tunnel – Looked at the • Chronic histology of patients inflammation? with CTS • – 74% normal Amyloid deposition? histology of TCL • Repeated mechanical – 25% had mucoid, stress? Ligament? amyloid deposits Nerve? • Vascular sclerosis and – Conclusion: No ischemia? typical histological changes noted
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CARPAL TUNNEL SYNDROME My explanation to patients • Intracarpal tunnel • Pressure decreases blood pressure flow • Maximal at level of hook • Over time, decreased blood of hamate (smallest diameter) flow thins the insulation • Increased with wrist around the wire (myelin) extension>flexion • In very severe cases, the • Increased with grip wire itself starts to be (1151 mmHg) affected (axons) • patients with CTS have increased pressure, more sustained and delayed recovery of normal pressures after exercise
Sustained compression can lead to Carpal Tunnel Syndrome permanent impairment • History & examination are most important tools in diagnosis • Night pain in median nerve distribution –More proximal often does not have nocturnal symptoms • Sensory changes in median nerve • Median nerve compression test –Not everyone reads the textbook • Can have proximal symptoms
CARPAL TUNNEL SYNDROME CARPAL TUNNEL SYNDROME • Symptoms worse at • Pain night (waking up) • Paresthesias in • Extreme wrist median nerve positions • Talking on phone* distribution • Driving* • Normal thenar • Typing/mousing sensation • Dropping objects • Weakness • Can’t feel them
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Carpal Tunnel Syndrome TINEL’S SIGN
• X-rays, CT scan, MRI • Tap on median nerve at not useful wrist • EMG/NCS are helpful • Site of irritable nerve • Confirm diagnosis due to axonal injury • Double crush • Tingeling and shooting syndrome pain in nerve dist. • Polyneuropathy • Probable CTS (sen. 0.60, • Difficult exam spec. 0.67) • Severity
the best PHALEN’S MANUEVER test WRIST COMPRESSION-FLEXION TEST • Wrist flexion with elbow on table • Combines Phalen’s and Durkin’s • Paresthesia in response • Direct compression of to position median nerve with wrist • Numbness and tingling flexion in radial digits in 60 sec. • Paresthesia in response to = pos. test pressure • Probable CTS (sen.0.75, • Probable CTS (sen. 0.80, spec. 0.47) spec. 0.92)
SENSORY TESTING EMG/NCS • Static two point • Monofilament testing is discrimination >6 mm better • Its important to = advanced nerve • Value greater than .08 gm remember that CTS dysfunction or nerve (monofilament 2.83) in is a CLINICAL laceration radial 3 digits diagnosis • Rarely useful in CTS • Probable CTS (sen. 0.83) • Electrodiagnostic tests should NOT be used independently in making diagnosis
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CARPAL TUNNEL SYNDROME CARPAL TUNNEL SYNDROME • Intermediate • Early – Constant paresthesias, numbness – Intermittent symptoms – No atrophy – No weakness of thumb abduction – +/- Muscle weakness of – No permanent numbness or paresthesias thumb abduction – No atrophy – Pain with irritability of – Treatment = wrist splints, activity modification, nerve limb positioning 6–8 weeks – Treatment = surgical decompression
STEROID CARPAL TUNNEL SYNDROME INJECTIONS – Mild symptoms less • Late than 12 months – Sensory loss – No weakness – Muscle atrophy – Intermittent sensory – Weakness grasping changes objects – Offer transient relief – +/- Pain – Treatment = surgical in 80% patients at 6 decompression weeks – Surgery will halt – 75+% went on to progression & pain surgery within 12 months.
Wood et al, Gelberman et al, + Girlanda et al.
SURGICAL TECHNIQUES • The surgical treatment is to completely divide the transverse carpal ligament • How is this accomplished? – Open release – Limited open release – Two incision release – Endoscopic release
From Pauda, et al. Lancet Neurol. 2016
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OPEN CARPAL TUNNEL RELEASE ENDOSCOPIC RELEASE
• • • • Regional or general Under direct vision Larger incision Smaller incision anesthesia release all structures • May have more • May have improved • Less visualization • Explore median incisional irritation short term recovery • Increased risk of NV damage nerve and other (?) • • Higher complication carpal pathology Avoids palmar rate incision • No difference >6 • Safe and efficient • People who rely on weeks under local hands for weightbearing
OPEN VS. ENDOSCOPIC HAND THERAPY • Pomerance (JHS ‘07) – Prospective • However, there is a • Cochrane Review 2006 randomized study role for patients with – Two week of post • No better alternative than standard open CTR – Limited digital • Earlier return to work with endoscopic: operative therapy vs. conflicting results home therapy motion • No strong evidence to replace standard open – Edema CTR – No change in outcome noted – Incision tenderness – Therapy added $600- $900
SPECIAL CIRCUMSTANCES WORKER’S COMPENSATION
• Higgs (JHS ‘94) – 73% of WC – CTS outcome in patients changed • WORKER’ S COMPENSATION PATIENTS worker’s jobs due to • ELDERLY PATIENTS compensation residual symptoms patients – • DEPRESSION – Residual symptoms 2% non-WC more common in WC changed jobs patients
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ELDERLY PATIENTS • Townshend (JHS ‘94) • Weber (JHS ‘04) – 83 CTR in patients – 105 CTR in patients over 70 yrs over 65 yrs – 80% with severe – changes 83% very satisfied – with results at 6 94% satisfied at 1 year months – Reduced paresthesia, night pain – Improved strength & sensibility
ELDERLY PATIENTS DEPRESSION
• Ring (JHS ‘07) • Keep in mind that 5- • Pain relief is main – 82 Patients with CTR 10% not satisfied goal – Survey of outcome and • Important to discuss • Long term recovery satisfaction goals and recovery to be expected in – Dissatisfaction correlates before surgery most patients with depression and ineffective coping skills – More than a peripheral nerve problem
American Academy of Orthopedic Surgery Recommendations Following Literature Review (from aaos.org) • Recommend carpal tunnel release for CTS – Epineurotomy and skin preservation procedures not recommended Improvement in depression and anxiety levels post op Symptoms correlated with levels of depression and anxiety • Hand therapy is not among the options used for CTS
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AAOS Website Treatments not Specifically Addressed or Advocated http://www.cochrane.org/
Acupuncture, Steroids, Cold laser, Diuretics, Exercise, • Yoga, Vitamin B6, Fitness, Iontophoresis, Laser, Looked at all randomized trails for CTS – Stretching, Massage, Magnets, Manipulation, Activity 4 main studies – modification , Medications (NSAIDS, etc.), Cognitive Concluded surgery relieves symptoms better than behavioral therapy, Nutritional supplements, splinting – Phonophoresis, Smoking cessation, Therapeutic Not conclusive for patients with mild symptoms – touch, Electrical stimulation, Weight Reduction No comparison made to injections.
Is there better evidence?
http://www.cochrane.org/ REFERENCES
• Looked at 21 trials • http://www.jhandsurg.org/ – Alternative non-surgical treatment • http://www.cochrane.org/ – Excluded cortisone injections • http://www.aaos.org/ – Short term benefit • Oral steroids • Splinting • Ultrasound • Yoga
Appendix for self-study Anterior Interosseous Nerve Palsy PRONATOR SYNDROME • Entrapment of • AIN innervations median nerve in – FPL proximal forearm – FDP IF (MF) • Forearm pain along – PQ median nerve – No sensory • Sensory changes in component median nerve distribution • Rare if actually real
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AIN PALSY
• Complete palsy or Ulnar Nerve Compression incomplete with weakness • FPL, FDP IF Randy M. Hauck, MD, MS, FACS • Pinch causes IP hyperextension Talk originally prepared by David J. Slutsky • Weak pronation with MD, FRCS(C) elbow flexed
Microcirculatory Effects of Compression • compressed nerves have a lower • increased permeability / edema threshold to mechanical pressure • increased endoneurial fluid pressure • provocative nerve tests reproduce • sub-perineurial demyelination paresthesias
Experimental Stretch Neuropathy
@ 6%, motor potential • Continuous stretching of rat tibial nerve for 1 hour amplitude decreases by resulted in no histologic, electrical, or functional abnormality 70%, but returns to normal after 1 hour • Same load applied cyclically 60-120 times/hr lead to abnormalities • This suggests that a small strain applied repeatedly @ 12% strain, conduction is blocked might lead to nerve dysfunction and shows minimal recovery after 1 hour Wall et al. J Bone Joint Surg (Br). 1992 Watanabe et al. J Hand Surg 2001
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Traction Neuropathy: Pathophysiology Traction Neuropathy: Pathophysiology
• Stretching injuries -> micro-lesions -> • Injury/scarring of mesoneurium -> nerve epineural/intraneural fibrosis and permanent nerve adherence to surrounding structures entrapment • Thickening of epineurium/perineurium interfere with • Subsequent movement -> traction on interfere with blood flow the nerve -> dynamic ischemia Lunborg G, Dahlin LB. Hand Clinics 1992
Lunborg G, Dahlin LB. Hand Clinics 1992
Proximal Ulnar Nerve CUBITAL TUNNEL SYNDROME Fascicular Topography Symptoms • Approximately 20 fascicles • Aching discomfort Medial aspect of elbow • motor fibers to FCU, FDP are deep • Pain, paresthesia's, numbness Ulnar forearm Ulnar ½ • motor fibers to intrinsics, sensory ring finger Small finger fibers are superficial, hence more Ulnar dorsal ½ of the hand susceptible to early compression • Hand clumsiness and weakness
Cubital Tunnel Syndrome CUBITAL TUNNEL SYNDROME • Exacerbation by repetitive elbow flexion Signs – Sleeping position • Tinel’s sign over ulnar nerve – Holding a phone, reading a newspaper • + Elbow flexion test – Driving • Decreased sensation in ulnar nerve distribution – Leaning on a flexed elbow • Weakness of 1st dorsal interosseous muscle and FDP to RF & SF • Atrophy of intrinsic muscles and clawing
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TINEL’S SIGN ELBOW FLEXION TEST Correct Incorrect
CUBITAL TUNNEL SYNDROME STRENGTH TESTING Scratch Collapse Test
Cheng et al. JHS 2008, 33(9), 1518- 24.
Cubital Tunnel Syndrome Cubital Tunnel Syndrome • Severe neuropathy: • Can be mild to severe – Abnormal 2pd of ring and small fingers McGowan’s Scale – Weak intrinsics, clawing of ring, small 1: Purely subjective symptoms and mild – Positive Froment’s sign hypaesthesia 2: Sensory loss and weakness of intrinsic hand muscles, with or without slight wasting 3: Severe sensorimotor deficit
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CUBITAL TUNNEL SYNDROME • Avoidance of elbow flexion Operative Procedures
• Avoid direct pressure on the elbow (arm rest in car, desk chair) • Ergonomic workstation modification • Nighttime elbow extension splint – Anterior elbow splint with elbow at 30° of flexion
Simple Decompression Medial Epicondylectomy
SUBCUTANEOUS TRANSPOSITION
Simple In-Situ Medial Decompression Epicondylectomy
INTRAMUSCULAR and SUBMUSCULAR Outcomes TRANSPOSITION • Good results for in-situ release in 17/18 patients with McGowan stage I (paresthesias only with normal motor and sensory exam). • When there are constant symptoms, demyelination is present and recovery may take 6-8 months. • Residual sensory complaints are common.
Within or beneath the flexor pronator mass • Intrinsic wasting rarely recovers in an adult. Tomaino et al. J Hand Surg 2001;26A:1077-81
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Etiology • Benign tumors (ganglion >> lipoma, giant cell tumor of tendon sheath) • Trauma (hook of hamate fracture, cycling, Ulnar Tunnel Syndrome wheelchair athletes) • Anomalous muscles, thickened pisohamate lig. • Ulnar artery aneurysms, thrombosis
Ganglion Neurilemmoma
ULNAR TUNNEL SYNDROME • Paresthesias of ring and small fingers • ↓ Semmes Weinstein of ring and small Anatomy of Guyon’s Canal
• Tinel’s sign over Guyon’s canal Roof volar carpal ligament piso-hamate • Weakness of intrinsics and ADM ligament (motor branch)
• Froment’s sign Medial pisiform
• Normal FCU, FDP Lateral hook of hamate • Normal Dorsal Cutaneous Br. of Ulnar N. • NEGATIVE ELBOW FLEXION TEST
3 Zones:
• Type I: -mixed motor and sensory Type II: -pure sensory Type III: -pure motor
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Indications for Surgical Treatment
• Clinical recovery in majority of patients treated for tumor or ganglion [Foucher, 1993]
• Motor recovery less predictable than sensory recovery, especially when compression caused by longstanding fibrotic hypothenar arch [Zoch, 1990]
Suggested Reading • Slutsky, DJ. Techniques for Nerve Compression Syndromes. In Hand and Upper Extremity Reconstruction. Chung KC, ed. Elsevier, 2008 Radial Nerve Compression • Rayan GM. Proximal ulnar nerve compression: Cubital tunnel syndrome. Hand Clin 1992;8:325-336 • Gelberman RH. Ulnar tunnel syndrome. In: Gelberman RH,ed., Operative Nerve Repair and Reconstruction. Randy M. Hauck, MD, MS, FACS Philadelphia, Lippincott, 1991:1131–43. • Chung K. Treatment of ulnar nerve compression at the elbow. J Hand Surg 2008, 33A:1625-1627
• Origin – Derived primarily from C6, C7 and C8. T1 contribution in ~ 11% of population – All three trunks (upper, middle, lower) contribute to posterior cord – Posterior cord branches into radial and axillary nerves
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High Radial Neuropathy: Etiology • Triceps – humeral shaft fx, 14% incidence • Anconeus – tourniquet palsy • Brachioradialis – “Sat. night palsy”, crutch injuries • ECRL – anomalous muscle, rare • ECRB – penetration by an aberrant artery • Supinator – tumors • Divides into PIN and – strenuous muscle activity Superficial Branch – windmill pitching
High Radial Neuropathy: Clinical Features High Radial Neuropathy: Management – ± triceps dysfunction depending on level of – Spontaneous onset, no mass, nl imaging lesion • dynamic wrist splint, passive ROM exercises – Wrist drop with inability to extend fingers or thumb • if no evidence of recovery at 3-6 months, surgical exploration – Decreased sensation SRN distribution –Neurolysis – ± decreased sensation posterolateral aspect arm and forearm –If humeral nonunion, shorten humerus
High Radial Neuropathy: Management High Radial Neuropathy: Management • If neuropathy has lasted longer than 12-18 months, Humerus Shaft Fracture perform tendon transfers • Somewhat controversial – Common tendon transfers: • Usually injury due to contusion or • pronator teres to ECRB - wrist extension mild stretch • FCR to EDC - finger extension • Most advocate non-operative • palmaris longus to EPL – thumb extension management with exploration at 4 months if persists • Exceptions: open fracture; loss of function after closed manipulation
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PIN Compression Syndrome: Etiology PIN Compression: Management – Anatomic constraints • Treat known compressor (eg mass, radial head) • Fibrous bands, crossing veins, ECRB • If new onset, not progressive, and images nl: • Supinator, prox. edge (Arcade of Frohse) – 6-8 weeks long arm splint –Distal edge – Digital extensor tenodesis splint – Tumor – Proximal 1/3 radius fx • If no improvement – Radial head dislocation - Surgical – Surgical retraction Wasting, weakness decompression • (especially from distal biceps reattachment)
Arcade of Frohse
– If progressive or open injury: Surgical exploration
– If palsy for greater than 18 months, tendon transfers
Radial Tunnel Syndrome: Symptoms Radial Tunnel Syndrome: Exam
– Tender over radial tunnel Pain – Provocative maneuvers • deep aching pain over lateral aspect of elbow and dorsal proximal forearm, • Resisted supination commonly at night • Resisted middle finger extension • can radiate proximally or distally • Passive pronation and wrist flexion • pain often aggravated by activity – Weakness • uncommon
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Radial Tunnel Syndrome: Management • Initially, nonoperative • Differential Diagnosis – NSAID, rest, avoid provocative activities – Lateral epicondylitis (may coexist in 5% of cases) – Long arm splint with elbow in flexion and supination, wrist in extension – Parsonage-Turner Syndrome • Recalcitrant after 3 months – Cervical radiculopathy – Surgical exploration – Systemic disorders – Results mixed – Chronic compartment syndrome
Wartenberg’s Syndrome Wartenberg’s Syndrome: Etiology – entrapment between BR and ECRL, esp with repetitive • Also known as: movement – Superficial radial nerve – anatomic anomalies entrapment – compression over radial styloid (handcuffs, watch band) – Radial sensory nerve – surgical injury entrapment – tumors – Cheiralgia paresthetica – trauma- crush injuries, fractures, lacerations – Handcuff neuropathy – synovial rupture in RA – Wristwatch neuropathy
Wartenberg’s Syndrome: Clinical Features Wartenberg’s Syndrome: Differential Dx
Paresthesias or dysesthesias dorsoradial forearm, wrist and – De Quervain’s extensor tenosynovitis hand – Lateral antebrachial cutaneous nerve injury – increased with wrist flexion, thumb flexion and ulnar – deviation (false + Finkelstein test) Cervical radiculopathy – decreased sensation first web space – Scaphoid fracture – positive Tinel’s at BR tendon – OA of thumb CMC joint – pain may lead to decreased grip strength, although no motor denervation
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Wartenberg’s Syndrome: Management
• J Hand Surg Am. 2009 Dec;34(10):1906-14. • Initial treatment- nonoperative Unusual compression neuropathies of the forearm, part I: radial nerve. Dang AC1, Rodner CM. – NSAIDS, rest, activity modification • J Am Acad Orthop Surg. 1998 Nov-Dec;6(6):378-86. – Thumb spica splint with wrist extended Uncommon nerve compression syndromes of the upper extremity. Lubahn JD1, Cermak MB. – Eliminate external compression • J Am Acad Orthop Surg. 2009 Nov;17(11):665-76. Review. • If persists greater than 3 months, surgical Suprascapular neuropathy. exploration Piasecki DP, Romeo AA, Bach BR Jr, Nicholson GP. • J Shoulder Elbow Surg. 2018 May;27(5):950-956. Quadrilateral space syndrome: a review. Flynn LS1, Wright TW1, King JJ2
Axillary Nerve Quadrilateral Space Syndrome • C5 and C6 -> posterior cord • Occlusion of posterior humeral circumflex • Gives braches to shoulder capsule artery (and axillary nerve) • Goes through quadrilateral space with • occurs with arm in abduction, extension, and posterior humeral circumflex artery external rotation • shoulder pain and distal paresthesias, worse with overhead activity humerus teres minor • MRI: atrophy of the teres minor teres major • Arteriogram, Doppler studies triceps (long head) • EMG • surgery
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Axillary Nerve Injury • Weakness of abduction • Weakness in external rotation (teres minor) • Atrophy • Anesthesia over lateral shoulder not reliable • EMG
Suprascapular Nerve Palsy: Anatomy
• Suprascapular notch – suprascapular ligament or shoulder joint cyst -> paralysis of supraspinatus and infraspinatus • Spinoglenoid notch palsy of infraspinatus
Suprascapular Nerve Palsy: Etiology
• Trauma • Pain and weakness (rotator cuff) • Iatrogenic • Dull aching pain in post lateral aspect • Activity (volleyball, • More common in males stretching at • Worse with arm elevation and exercise spinoglenoid notch) • Depending on site either supra/infra vs infraspinatus • Atrophy (infraspinatus more superficial) • Mass effect (ganglion) • Diagnosis of exclusion • EMG
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Suprascapular Nerve Injury: Treatment Nerve Tumors
Alexander Payatakes, MD Associate Professor / Hand Surgery
No vested interests, No FDA off-label uses presented Talk originally prepared by Kodi K. Azari, MD, FACS, Roy A. Meals and Gina Farias-Eisner, MD
CASE #1 Neuroma
HPI: 51-year-old female 2 cm laceration to the right index finger, repaired in the ED
2 months later: Diminished sensation on radial aspect of finger Electrical sensation at skin scar on direct contact
What is the diagnosis?
Pathophysiology
NeuromaNeuroma: = AGroup group of regeneratingof regenerating nerve nerve fibers • Wallerian degeneration after injury fiberswhich which fail failto reach to reach distal targets or end organs distal targets or end organs • Sprouts emerge from proximal stump of the axon to find distal end
Failure to find target Neuroma!
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Pathophysiology
Neuroma: A group of regenerating nerve fibers which fail to reach distal targets or end organs
Neuroma-in-continuity
Physical Exam Treatment
• Surgical exploration Resection to healthy fascicles
Tinel sign • Primary repair vs • Distalmost aspect of regenerating axons Nerve grafting produces paresthesias when tapped
• Bury neuroma in muscle/bone vs Repair to alternate nerve target?
CASE #2 Schwannoma (aka Neurilemmoma, Benign nerve sheath tumor)
HPI: 42-year-old male Painless mass in right small finger in line with ulnar neurovascular bundle Slowly enlarging over past year • Most common benign nerve tumor of UE Somewhat mobile side-to-side, but not proximal-to-distal • Arises from Schwann cells
What is the most likely diagnosis?
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Treatment
• Typically easy to shell out without damage to nerve function
• MRI Characteristic “Egg on a string” appearance • Very rare reports of malignant transformation
CASE#3 Neurofibromatosis type 1 (aka von Recklinghausen’s disease)
HPI: 20-year-old female Multiple painful subcutaneous masses on hand and forearm Lesions vary in size, firm, and tender Faint café-au-lait skin changes and freckling in the axillary region
What is the diagnosis?
Physical Exam Treatment
• Solitary lesions may be seen • Excision? • Multiple neurofibromas common in Only large / symptomatic lesions OR if unclear Dx Neurofibromatosis type 1 (von Recklinghausen’s disease)
• Café-au-lait macules • Typically results in nerve deficit • Axillary freckling • Often requires segmental nerve resection • 60% spine deformities and reconstruction
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CASE #4 Glomus Tumor
HPI: 45-year-old woman Exquisitely painful area in digital pulp She avoids use of digit to avoid pain “This finger doesn’t like cold water”
What is the diagnosis? • Typically in pulp or nail bed • Arises from neuromyoarterial shunting apparatus (thermoregulation)
Diagnosis Treatment
• PhEx: May have subtle bluish tinge
• Cold sensitivity (tip: ethyl chloride!) • Surgical excision
• Beware satellite lesions “Recurrence” • MRI (T2): High signal intensity oval lesion
CASE #5 Lipofibromatous Hamartoma
HPI: 22-year-old man Gradually enlarging nontender thickening at wrist Numbness and tingling in the median nerve distribution
What is the most likely diagnosis?
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Treatment
• Simple decompression • Fibrofatty infiltration of nerve (diffuse) • Interfascicular resection? NOT possible and contraindicated! • Consider if CTS + mass
• Especially in child with CTS • If deterioration of nerve function Resection and nerve grafting? • Often intraoperative finding
References Numbness
1. Watson J et al. Neuroma of the hand and upper extremity. J Hand Surg Am. 2010 Mar;35(3):499-510. Alexander Payatakes, MD 2. Netscher DT et al. Subungual glomus tumor. J Hand Surg Am. 2012 Apr;37(4):821-3;quiz 824. Associate Professor / Hand Surgery
3. Tahiri Y et al. Lipofibromatous hamartoma of the median nerve: a comprehensive review and systematic approach to evaluation, diagnosis, and treatment. J Hand Surg Am. 2013 Oct; 38(10):2055-76
4. Wolfe, S. Hotchkiss, R. Pederson, W. Kozin,S. (2011) Green’s Operative Hand Surgery 6th Edition. Philadelphia: Elsevier/Churchill Livingstone. No vested interests, No FDA off-label uses presented Talk originally prepared by Joshua Bales and Mark Morris, MD
Overview Numbness aka Peripheral Neuropathy
Anatomy review • At any time 2-4% population affected Definitions Sensory testing • Most common cause in USA is DM • Hansen’s disease (leprosy) is most common in SE Asia Patterns of sensory loss Mononeuropathy, radiculopathy, polyneuropathy • Must determine: Common and uncommon causes of numbness . Distribution . Symptoms Summary . Duration . Course
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Definitions Sensory Exam
Ability to perceive stimuli Sensitivity to stimuli Hypesthesia Diminished Intact Anesthesia Absent Intact Hypalgesia Intact Diminished Analgesia Intact No sensitivity • Peripheral nerve distribution • Hyperpathia, hyperesthesia, allodynia = Increased sensitivity to sensory stimuli
• NOTE: In peripheral neuropathies: Patients can vacillate between periods of hyperesthesia and hypesthesia
Sensory Exam Sensory Exam
• Dermatome distribution
Sensory Exam Sensory Exam
• A brain stem injury could have this pattern • Common axonal of paresthesia neuropathies present in a stocking-glove distribution . Feet affected first!
• Whereas a central cord syndrome would present with this pattern
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Sensory Testing Clinical Pearls
• Distribution of peripheral nerve think of pathology of that nerve (e.g. Median nerve Carpal tunnel syndrome) (though often atypical!) • Follow the patterns: . Confined to distal aspect of limb • Distribution of a dermatome . Confined to discrete area of a limb think corresponding nerve root (e.g. C5 radiculopathy) . Confined to the whole limb, side of body . Involves reflexes • Stocking-glove sensory loss . Involves cognitive deficits think axonal neuropathies - diabetes
Axonal Neuropathies Diabetic Neuropathy
• Diabetes mellitus • Syphilis • Alcohol • Vasculitis• Syphilis • Neuropathy secondary to microvascular insult to • Vitamin B12 deficiency vasa nervorum which supplies the nerves • Amyloidosis• Vasculitis • HIV • Multiple sclerosis • Lyme Disease • Idiopathic• Amyloidosis • Uremia • Paraneoplastic• Multiple sclerosis neuropathy • Chemotherapy • Occurs in 20% of DM patients • Leprosy • Idiopathic • Implicated in 50-75% of non-traumatic amputations • Paraneoplastic • Risk factors: Just to name a few… neuropathy Duration of DM, tobacco use, age, HTN, HLD
Diabetic Neuropathy Diabetic Neuropathy
• Clinical manifestations • Pearls to spot DM . Numbness . Classic triad . Hypalgesia . Polyuria, polydipsia, polyphagia (Increased urination, drinking, and eating) . Erectile dysfunction . Vision changes . Acanthosis nigricans . Dizziness . Diarrhea . Stocking-glove distribution . Loss of proprioception
. Ketone (fruity/alcoholic) odor in breath
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Diabetic Neuropathy Alcohol
• In DM & syphilis, patients may present with Neuropathic (Charcot) joint • Due to insensate nature of joint, it gradually degenerates and deforms • 32% of heavy users peripheral neuropathy
• Uncommon in non-weight-bearing joints • Confounded by nutritional deficiencies
• Risk factor for compression neuropathies (“Saturday night palsies”)
Alcoholic Neuropathy Alcohol Neuropathy Treatment
• Characterized as gradually • Stop drinking! progressive affecting sensory, motor, and autonomic nerves. • Thiamine supplementation • Better nutrition • Starts symmetrically and distally (feet first) • Full recovery is uncommon • Associated with loss of reflexes . Loss of ankle jerk first • Some medications can help with burning dysesthesias
Multiple Sclerosis Multiple Sclerosis
• Where is the neuropathy? • Idiopathic CNS inflammatory disease
• Demyelination and axonal degeneration • MS may cause a constellation of symptoms, • Young adults all of which wax and wane • = 2 : 1 . Depression . Fatigue • MRI diagnostic for lesion . Numbness/pain • Differential diagnosis: . Urinary problems Spinal cord compression, vitamin deficiency, infection . Nystagmus • Clinical, radiographic lesions separated in time & space . Diplopia / Red color perception
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Lyme Disease Lyme Disease
• Emerging infectious disease • Incubation period 1-2 weeks • Endemic in PA • Early: • Caused by Borrelia burgdorferi Erythema chronicum migrans • 1% of tick bites Headache, fever, malaise
• Bacterial infection easily treated by antibiotics • Late persistent infection (mos) Polyneuropathy • When untreated can cause a variety of joint, heart, and nervous system disease
Lyme Disease Chemotherapy Neuropathy
• Polyneuropathy symptoms: Peripheral neuropathy “Chemo fog” . Numbness . Shooting pain . Taxanes (Paclitaxel, Taxo) (breast CA) . Difficulty with concentration Burning paresthesias, loss of reflexes . Depression . Bell’s palsy . Vincristine (leukemias) Both motor/sensory fibers, virtually all pts
. Thalidomide (MM, ovarian CA) 75% sensory neuropathy, reversible with dosage adjustment
Other Drug-Induced Neuropathies Summary
• A numb finger is not always “carpal tunnel syndrome” • Review distribution of altered sensation with patient • What are the other symptoms? . Methotrexate (for RA) • Look at the big picture Encephalopathy – Past medical history, travel history, habits, diet
. Propylthiouracil (thyroid disease) (dose-dependent)
(See appendix for info on HIV, syphilis, Hansen’s disease)
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References HIV Neuropathy
1. England et al. Peripheral Neuropathy. Lancet 2004: 363:2151-61 • Hypothesized to be secondary to dorsal root ganglion 2. Robinson, LR. Role of Neurophysiologic Evaluation in Diagnosis. JAAOS. 2000 May;8(3): 190- damage by the virus 199 3. Veves et al. Painful diabetic neuropathy: epidemiology, natural history, early diagnosis, and • Occurs in 30% of HIV/AIDS pts treatment options. Pain Med. 2008 Sept;9(6):660-74 4. Calabresi, PA. Diagnosis and Management of Multiple Sclerosis. Am Fam Physician. 2004 Nov • Late - Typically presents in the feet 15;70(10):1935-44 5. Gonzalez-Duarte A, Cikurel K, Simpson DM. Managing HIV peripheral neuropathy. Current HIV/AIDS reports 2007 4 (3): 114–8 6. Scollard DM. The biology of nerve injury in leprosy. Lepr Rev. 2008 Setp;79(3)242-53 7. Hu LT. Lyme disease. Ann Intern Med. 2016; 164(9): ITC65-ITC80. Death 8. Ontaneda D, Thompson AJ, Fox RJ, Cohen JA. Progressive multiple sclerosis: prospects for disease therapy, repair, and restoration of function. Lancet 2017; 389(10076): 1357-1366. 9. Vinik AI, Nevoret ML, Caselini C, Parson H. Diabetic Neuropathy. Endocrinol Metab North Am 2013; 42(4): 747-787. 10. White C, Franco-Paredes C. Leprosy in the 21st century. Clin Microbiol Rev. 2015; 28(1): 80-94.
HIV Neuropathy Syphilis
• Main complaints • Caused by Treponema pallidum . Bizarre burning . Hyperalgesia . Allodynia • “Great imitator”
• Risk factors • Primary syphilis . DM . Skin lesion (chancre) . Nutritional deficiencies (21 d after exposure) . HIV Medications
Secondary Syphilis Tertiary Syphilis
• Occurs 1-10 yrs after initial infection • Secondary syphilis • Changes in personality . 6-8 wks after exposure • Tabes dorsalis . Rash in palms and hands . Dorsal column disease causing a shuffling gait . Most contagious • Neuropathic/Charcot joint disease . Loss of proprioception
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Hansen’s Disease (Leprosy) Hansen’s Disease (Leprosy)
• Incubates for few weeks – up to 30 yrs (average 3-5 yrs) • Leprosy = Greek for scales on a fish • Affects 3 million/year (30% get neuropathy) • Caused by Mycobacterium leprae
• Granulomas of the nerves, • Loss of sensation respiratory tract, skin, and eyes Repeated injuries, infection due to unnoticed wounds Loss of body parts/deformity • Since 600 BC • Still leper colonies today • Affects Schwann cells • Not actually highly contagious • Causes inflammation/edema • Unmyelinated fibers are also affected (how?)
Stroke
• Leading cause of hemiplegia in adults • Immediate flaccid paralysis Weakness/Spasticity • Spasticity over several weeks (UMN) ◦ Spinal cord mediated reflexes intact • Associated perceptual/cognitive/visual Kenneth Taylor, MD losses • Most recovery in first 6 months No conflicts of interest to report • Functional recovery can continue over time Talk originally prepared by Lucie Krenek, MD • Upper extremity < lower extremity recovery ◦ UE function more dependent on fine motor control
Stroke - Treatment Stroke - Contractures
• Goals: ↑hygiene, ↓pain, ↑function • Synergistic pattern of spasticity/contracture • Contractures favors stronger muscles ◦ Cause pain and lead to joint subluxation ◦ Shoulder - adduction/internal rotation (further pain) ◦ Elbow - flexion • Acute – Prevention of contractures ◦ Forearm - pronation ◦ Brachial pexus and distal nerve blocks ◦ Wrist – flexion ◦ Botulinum (Botox) ◦ Fingers - flexion • Chronic – Treatment of contractures ◦ Antispasmodic medication • Surgery after spasticity stabilizes ◦ Surgery – after plateau ( ~6 months) ◦ Lengthen if functionsl ◦ Tenotomy if nonfunctional
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Other Neurologic Conditions Causing Charcot-Marie-Tooth (CMT) Disease Weakness/Spasticity • aka • Uncommon ◦ Peroneal Muscular Atrophy ◦ Hereditary Motor-Sensory Neuropathy • Have general awareness • Most common hereditary neuromuscular ◦ Patient queries disorder (Usually autosomal dominant) ◦ Broad understanding of nerve • Chronic, symmetric distal sensory/motor pathologies neuropathy • Onset: late childhood/adolescence • Normal life expectancy
CMT Signs CMT Treatment
• Lower extremity – begins first • Stabilization of ankles – orthoses, tendon ◦ Gait problems transfers, fusion ◦ Distal weakness – legs, feet • Moderate aerobic exercise ◦ Inability to heel walk • Muscle stretching/strengthening ◦ Foot drop; ankle instability • Excessive weight training not recommended ◦ Pes cavus; hammer toes • Upper extremity – milder than LE ◦ Difficulty with fine motor and strength ◦ Rarely extends above elbow ◦ Atrophy of hands/forearms ◦ Intrinsic-minus hand deformity
CMT Treatment Amyotrophic Lateral Sclerosis (ALS) (Lou Gherig’s Disease) • Intrinsic minus hand most debilitating ◦ MP extension block splint ◦ Volar MP joint capsulodesis ◦ Surgical: FDS rerouted to proximal phalanges
Lou Gherig Steven Hawking
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ALS ALS - Treatment
• Loss of upper and lower motor neurons • Controversy regarding exercise ◦ Lesion – motor neurons in spinal cord, • Strengthening and moderate endurance brainstem and motor cortex exercise may result in better function ◦ Lateral corticospinal tract • Little can be done to improve quality of ◦ Denervation atrophy/weakness of muscle life, fatigue, or muscle strength ◦ Tongue fasciculations pathognomonic • Ventilatory support when respiratory • No sensory or autonomic involvement muscles become affected • Etiology unknown ◦ Risk factors: pesticides, smoking, military, familial
Guillain-Barre Syndrome (GBS) GBS – Signs/Symptoms
• Acute autoimmune polyradiculopathy • Rapid onset ascending motor paralysis ◦ 70% preceded by acute infection • May have sensory/automonic symptoms ∙ Usualy respiratory/gastrointestinal • Generalized weakness - lower extremities ∙ Fue shot or other vaccines procedes to upper extremities • Demyelination of peripheral nerves • Neck, shoulder, back pain • Plateau by 4 weeks • Later – muscle atrophy, potential for • Recovery occurs with remyelination contractures with lack of motion • Severity of weakness highly variable
GBS – Treatment GBS – Prognosis
• Acute phase • Most need hospitalization ◦ Maintain range of motion • Up to 30% require ventilatory support ◦ Prevention of contractures • <5% mortality (usually due to pulmonary • Recovery phase complications ◦ Retraining of many ADLs (grooming, • 85% full recovery by 1 year gait) • Poorer prognosis for older patients, late ◦ Muscle strengthening treatment, severe attacks ◦ Supervised exercise programs help overcome fatigue and improve function
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Polio Polio
• Viral infectious disease • Rare in developed countries • Fecal-oral transmission • Afghanistan, Nigeria, Pakistan, India • Usually infects children under 5 years old • <2,000 cases per year • Lower moton neuron lesion • 95% infected asymptomatic • Decreased reflexes and muscle wasting • 0.5% irreversible paralysis, usually legs • Proximal muscles affected • Of those with paralysis – 5-10% die due • Sensory loss rare to involvement of respiratory muscles
Polio Polio - Treatment
• Acute phase: all anterior horn cells • Acute affected ◦ • Subacute phase: the ~50% of anterior • Subacute horn cells that survived begin to recover • After 16-24 months: extent of damage • After 16-24 months: extent of damage realized; rehabilitation begins realized; rehabilitation begins
Polio - Treatment Post Polio Syndrome
• Acute phase • Occurs years after acute illness ◦ Range of motion, splinting • Muscle pain, severe fatigue, cramping, • Subacute phase fasciculations ◦ Prevent deformity, preserve function • Overuse of muscles originally affected ◦ Splinting/bracing to maintain joint • Slowly progressive weakness in already position and supplement function weak muscles • Residual phase • Treatment – limited exercise with ◦ Surgical intervention if needed frequent rest
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References
1. Adams and Victor’s Neurology, AH Ropper, RH Brown. 8th Edition 2. Current Orthopedics, AE Keenan, S Mehta 3. Dillin L, Hoaglund FT, Scheck M. Brachial Neuritis. J Bone Joint Surg Am. 1985 Jul;67(6):878-80 Chronic Regional Pain 4. Harrison’s Principles of Internal Medicine, 17th Edition. Fauci AS et al, eds. 5. Hughes RA, et al. Supportive care for patients with Guillain-Barre Syndrome syndrome. Arch Neurol. 2005 Aug;62(8):1194-8 6. Hussey AJ, O’Brien CP, Regan PJ. Parsonage Turner Syndrome – Case Report and Literature Review. Hand. 2007;2:218-221. 7. Pitetti KH, Barrett PJ, Abbas D. Endurance exercise training in Guillan- Barre syndrome. Arch Phys Med Rehabil. 1993; 74: 761-765. Kenneth Taylor, MD 8. Tuckey J, Greenwood R. Rehabilitation after severe Guillain-Barre syndrome: the use of partial body weight support. Physiother Res Int. 2004;9(2):96-103. No conflicts of interest to report 9. Tafti MA, Cramer SC, Gupta R. Orthopedic Management of the Upper Extremity of Stroke Patients. J Am Acad Orthop Surg. 2008;16:462-470. Talk originally prepared by Nicholas Rose, MD
Chronic Regional Pain Syndrome (CRPS) CRPS • Mitchell (1864): Described “Causalgia” in veterans sustaining nerve injury after gunshot • No single unifying explanation to account for wounds during American Civil War diverse features • Sudek (1900): Noted bone atrophy on x-ray • Likely a spectrum of disorders • Leriche (1916): Noted similarities to ischemia. • Type 1 (previously RSD) Treated with sympathectomies ◦ No identifiable nerve injury • Evans (1946): Coined “Reflex Sympathetic ◦ More common Dystrophy” (RSD) for syndrome without major • Type 2 (previously Causalgia) nerve injury ◦ Following major nerve injury • Int’l Assn. Study of Pain (IASP) (1994): CRPS ◦ Less common because “RSD” is not solely sympathetically- mediated
CRPS – Predisposing Factors CRPS – Predisposing Factors
• Identification of potential risk factors • Strong weight against bias remains elusive ◦ Post-menopausal female ◦ Heterogeneous studies ◦ Distal radius fracture, ankle dislocation, other ◦ Mixed quality/relevance intra-articular fracture ◦ Low prevalence with lack of gold standard ◦ Reports of higher pain in early phase after trauma • Weaker weight against bias ◦ Immobilization ◦ Psychological barriers ◦ Positive diagnostic bone scan
Pons T. Anesthesiol Res Pract. 2015
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CRPS – The Perfect Storm CRPS – Features
• Patient with wrist injury • Pain out of proportion ◦ Sling/tight bandage • Non-dermatomal ◦ Dependent position and • Skin dry or overly moist immobilization • Skin mottled or cyanotic ∙ Ischemia ∙ Edema • Skin temp - cool • Skin texture - smooth, shiny, non-elastic • Edema • Atrophy (especially fingertips)
CRPS – Chronic Features • Not all CRPS is sympathetically-mediated • Not all sympathetically-mediated pain (SMP) is • Hair – loss, finer, longer CRPS • Nails – ridged, curved, thin brittle • Joints - stiff Metabolic Neuropathies • Muscles – atrophy, weak, Herpes zoster tremor, spasm • Radiographs - osteopenia SMP CRPS • Bone scan – inc. regional Phantom Pain isotopic uptake Neuralgias
CRPS – Definitions and a Conundrum Budapest Diagnostic Criteria The following four criteria must be met • Hyperalgesia – Increased pain response to a 1) Pain out of proportion to inciting event stimulus that is normally painful • Hyperesthesia – Abnormal increase in 2) Must report @ least 1 symptom in 3 of 4 sensitivity to stimuli of any of the senses categories • Alodynia – Non-painful stimuli evoke pain a) Sensory – hyperesthesia and/or allodynia b) Vasomotor – temperature asymmetry, skin color changes, ± skin color asymmetry • When does pain become abnormal? c) Sudomotor/Edema – edema, sweating • Who decides? changes, and/or sweating asymmetry d) Motor/Trophic – decreased ROM, motor dysfunction (weakness, tremor, dystonia), ± trophic changes (hair, nail, skin)
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Budapest Criteria Continued CRPS Pathophysiology 3) Display @ least 1 sign in 2 of the following • Exaggerated inflammatory response a) Sensory – hyperalgesia (to pinprick) ± allodynia (to • Altered cutaneous innervation light touch, deep somatic pressure ± joint movement) • Central and peripheral sensitization b) Vasomotor – temperature asymmetry, skin color changes ± asymmetry • Altered sympathetic nervous system c) Sudomotor/Edema – edema, sweating changes, ± function sweating asymmetry • Circulating catecholamines d) Motor/Trophic – decreased ROM, motor • Distorted sensory representation of dysfunction (weakness, tremor, dystonia), ± trophic changes (hair, nails, skin) affected limb in brain
4) There is no other diagnosis that better explains the signs and symptoms Bruehl S. Anesthesiology. 2010
CRPS Management CRPS Management Overview • Prevent it! • Physical ◦ No slings for hand and wrist problems • Pharmacological ◦ Mobilize all joints possible • Implanted devises ∙ Minimally restraining bandages, splints, casts • Psychological approaches ∙ Encourage functional use ◦ Elevate the extremity ◦ Loosen or replace tight bandages/casts • Treatment is multidisciplinary ◦ Hand therapist ◦ Hand Surgeon ◦ Pain management specialist ◦ Psychologist
Therapy Therapy • First line of treatment • Overcome kinesophobia • Active movement, resume ADLs • Massage • Passive motion, splinting after pain • Contrast baths controlled • Graded motor imagery* • Posture normalization • Transcutaneous electrical • Edema reduction nerve stimulation • Desensitization • Isometric strengthening • Stress loading • Encourage use of affected limb in ADLs ◦ Scrubbing • Mirror box therapy* ◦ Carrying • Specialized garments/wrappings • Aerobic conditioning * Topics for further discussion
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Medications Used for CRPS Interrupt the Sympathetic Supply • Anti-inflammatory – NSAID, steroids • Stellate ganglion block(s) • Vitamin C – preventative? • Surgical sympathectomy • Topical antioxidants (DMSO) • Peripheral blockade • Anti-convulsants (Gabepentin) with Bier block • Ketamine • Antidepressants (Nortriptyline, Cymbalta) • These will not work unless • Narcotics pain is sympathetically-mediated • Calcitonin • Intravenous immunoglobulin (IVIG)
Implanted Nerve Stimulators and Psychological Approaches Pain Pumps • Active self-management and participation • Spinal cord stimulation in a care plan • Peripheral nerve stimulation • Assess/treat patients for concomitant Axis I • Spinal medication pumps disorders (depression, anxirty, PTDS) • Deep brain stimulation • Cognitive behavioral therapy • Biofeedback • Learning relaxation skills
Surgery During/After CRPS CRPS - Prognosis
• Relief of carpal/cubital tunnel syndrome • Within first year may help treat CRPS – don’t delay ◦ 70% improved • Secondary surgery after CRPS is controlled ◦ 25% still met Budapest criteria (e.g. distal ulna excision after dist rad fx) ◦ Only 5% without complaints ◦ 47% recurrence rate • Worse prognosis - Patients with higher ◦ Make sure to coordinate with pain team levels of anxiety and pain-related fear at ◦ Perioperative stellate ganglion block beginning of therapy often recommended • Symptoms present >1 year rarely spontaneously resolve • Smokers have worse prognosis
Bean D. J Pain. 2014
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Supplemental Material for Self-Study Shingles
• Shingles • Resurgence of virus that causes chickenpox • Parsonage-Turner Syndrome in immunocompromised patient • Post-traumatic Neuromas • Incidence – 0.5% > age 60; 1% > age 70 • Pain/rash follow dermatomal distribution ◦ Face > Trunk > Limb • Pain (post-herpetic neuropathy) can last for years. Treated with meds. • Immunization available ◦ Recommended for > 60
Mueller N. Neurol Clin. 2008
Parsonage Turner Syndrome Parsonage Turner Syndrome • Usually healthy individual or related to • Idiopathic brachial plexopathy • Abrupt onset shoulder pain (usually ◦ Injection – vaccine, antibiotic, heroin ◦ Childbirth unilateral) followed by progressive motor ◦ Surgical procedures weakness, dysesthesia, and numbness ◦ Infection • Pain may extend to trapezius, upper arm, • Onset – intense pain/burning at forearm and hand shoulder/neck • Pain usually worse at night • Early – inc pain with movement/palpation • Pain usually lasts 1-2 weeks • Later – weakness and muscle wasting ◦ Diminished reflexes ◦ Sensory loss ◦ Fasciculations
Parsonage Turner Syndrome Post-traumatic Neuromas • Signs • Targeted Muscle Reinnervation (TMR) ◦ Proximal upper limb paralysis occurs (deltoid, • Nerve Mobilization serratus anterior, rotator cuff, biceps, triceps) ◦ May be bilateral by EMG though clinically appears unilateral • Therapy when pain controlled ◦ Maintain range of motion ◦ Strengthen rotator cuff and scapular stabilizers • Recovery – weeks to year • 10% have residual weakness • 10% have recurrence
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Targeted Muscle Reinnervation Nerve Mobilization
• Novel approach to post-amputation • Not published, discussed or understood in neuroma pain hand surgery circles • Provides distal target and vascularized • Recent review by Mark Walsh, PT, MS, CHT, scaffold to guide sprouting nerve axons ACT (J Hand Ther. 2005, 18:241-258) • Improves functional prosthesis control ◦ “Neural mobilization…is based on an eclectic • Residual nerves from the amputated limb compilation of theoretical concepts. There is a are transferred to reinnervate new muscle paucity of reported clinical studies using neural mobilization for the treatment of targets tht have otherwise lost their neuropathic pain” function • 0/26 patients developed neuroma pain after TMR (Souza J. Clin Orthop. 2014)
Reinforcement Quiz
Caution: The order of the questions and the order of the answer possibilities on website will Quiz and Closing Comments be different than seen here.
So remember the right answers, not that the answer to question 16 here is F, for example.
Reinforcement Quiz Reinforcement Quiz
1. The cell bodies of peripheral sensory nerves are in 2. What is the correct relationship of nerve injury the severity?
A. anterior horn of spinal cord A. axonotmesis > neuropraxia > neurogenesis B. dorsal root ganglia B. neurotmesis > axonotmesis > neuropraxia C. white matter of brain C. neuropraxia > neurotmesis > axonotmesis D. gray matter of brain D. sensory > motor > autonomic E. white matter of spinal cord E. men > women > children
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Reinforcement Quiz Reinforcement Quiz
3. In a patient with recent onset of mild carpal tunnel 4. A successful nerve transfer requires syndrome symptoms A. a healthy proximal donor nerve and a palsied distal A. two-point discrimination will be altered recipient nerve B. monofilament testing may be normal B. a distal palsied donor and a healthy recipient nerve C. thenar muscle wasting will precede monofilament C. complete absence of donor muscles for tendon changes transfers D. Meissner corpuscles will be atrophic D. more rehab than comparable tendon transfers E. loss of vibratory sensation to 256 cycles/second will E. more post-op immobilization than comparable be present tendon transfers
Reinforcement Quiz Reinforcement Quiz
5. The Roos “stick up test” for thoracic outlet syndrome 6. Which diagnostic test for carpal tunnel syndrome consists of has the highest sensitivity and specificity?
A. shoulder abduction and internal rotation A. Phalen test B. turning head away from the side being tested B. Tinel test C. externally rotating and abducting shoulder 180 C. Adson maneuver degrees D. median nerve compression test D. checking for radial pulse with patient seated E. Allen test E. shoulder abduction to 90 degrees and external rotation
Reinforcement Quiz Reinforcement Quiz
7. In cubital tunnel syndrome, why do sensory changes and 8. Which nerve is most likely to be injured with a intrinsic wasting occur before forearm muscle weakness? humeral shaft fracture?
A. some nerve fibers have more myelin covering A. median nerve B. the intrinsic muscles are smaller than the flexor carpi B. ulnar nerve ulnaris C. suprascapular nerve C. the sensory and motor fibers to hand are superficial D. radial nerve in the ulnar nerve at the elbow D. the sensory and motor fibers to hand are superficial E. medial pectoral nerve in the ulnar nerve at the wrist E. the fibers affected early originate solely from the C8 nerve root
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Reinforcement Quiz Reinforcement Quiz
9. A nerve sheath tumor (Schwannoma) in a digital 10. Neuropathy occurs in what percent of patients with nerve diabetes?
A. will move more medially laterally than proximally A. 1 distally B. 5 B. will move more proximally distally than medially C. 20 laterally D. 50 C. is far less common than a neurofibroma E. 95 D. will cause sensory loss if excised E. will cause motor loss if excised
Reinforcement Quiz Reinforcement Quiz
11. “Upper motor neuron” disorders include conditions 12. Chronic regional pain syndrome is such as A. Usually preceded by a viral infection A. stroke, spinal cord injury B. Managed best by the patient’s personal physician B. brachial plexus palsy C. Probably a spectrum of disorders C. Parsonage-Turner syndrome D.Fully responsive to stellate ganglion blocks D.Shingles E. Relieved by tight serial casting E. proximal median nerve lacerations
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DD Current Science for Hand Therapists 2020 August 2-4, 2019 Saturdays in Multiple Cities University of Denver MUSCLES and TENDONS Denver, Colorado
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