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Upper Extremity Nerves
Learning Objectives Upper Extremity Nerves
At the completion of the course, the learner will be able to 1. describe the neuroanatomy from brain to fingertip. 2. describe current concepts of peripheral nerve biology and healing. 3. collect a good history & exam for common peripheral nerve conditions. 4. educate patients regarding their condition and treatments. 5. participate more effectively in the patients’ care
Course Content Meets These AOTA Classification Codes for CE activities
Category 1: Domain of OT METHODS Areas of occupation: ADLs Performance skills: motor skills • 12 lectures Activity demands: required actions, body functions and • 2 question and answer sessions structures • networking Category 2: OT Process Develop intervention plan/approaches • some repetition between talks Implement intervention bad news: unavoidable because of multiple speakers Category 3: Professional Issues good news: repetition is a good learning tool OT education: teaching theory and methods Supervision: competence Contemporary issues/trends: professional development/continuing competence
Upper Extremity Nerves for OTs and PTs
For Your Questions during the Discussion Sessions: Write them on notecards as you think of them
Practical Matters Can everybody see? Hear? MACRO ANATOMY Room temperature? Cell phones, beepers From Brain to Fingertips Auditorium’s policy on food/beverage Restrooms Evaluation forms and certificates Naveed Nosrati, MD Ready, set, go……
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Motor Pathways: Major Elements Outline Central Nervous System • Motor pathways (cortex to finger tip) cerebral cortex • Sensory pathways (finger tip to cortex) brain stem • 6 major nerves spinal cord • Anatomic anomalies Peripheral Nervous System • Sympathetic nervous system root plexus branch/periph n. end organ
Motor Strip Sensory Strip Motor Impulses • Motor Impulses • travel through the internal capsule • originate in (white matter) parietal cortex gray matter • cross in the brainstem – each • originate in the side of the cortex “motor strip” controls the opposite side of the body
spinal cord (CNS) gives off nerve roots (PNS) brachial plexus is formed from: -inferior 4 cervical nerve roots (C5-C8) -superior thoracic nerve root (T1) Anterior: Dorsal: posterior anterior Motor Sensory Roots Roots
Cell bodies Cell bodies in anterior In dorsal horn of root ganglia spinal cord
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The Brachial Plexus Has 5 Anatomical Parts Bony Landmarks and the Parts of the Brachialroots Plexus
Randy Travis Drinks Cold Beer
Brachial Plexus Brachial Plexus and Axillary Artery • emerges And between anterior Muscles/Bones and medial scalene muscles Medial, lateral, • passes beneath and posterior clavicle cords • passes deep to •Closely pectoralis major associated with and minor AA •Named for their relationships to the AA
The brachial plexus is complicated…
Its major components can be learned and drawn as easy as 1,2,3 (x8)…
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dorsal scapular c5 suprascapular c5,6 C5 lateral pectoral c5,6,7 musculocutaneous c5,6,7 axillary C6 c5,6 median C7 c678t1 lower subscap c6,7 thoracodorsal c6,7,8 long upper radial c5,6,7,8 thoracic C8 subscap ulnar c8,t1 c5,6 c5,6,7 It is important to know the nerves, their routes medial antebrach cutan c8 through the brachial plexus, AND from which medial brachial cutan t1 T1 spinal roots they arise… medial pectoral c8,t1
How to begin making sense out of which muscles often get innervation from same nerve roots supply which muscles? root that supplies overlying skin 1. Know the sensory dermatomes Start with C6 it works for deltoid
Bang! C5 C5 C5 T1 T1 C6 C7 C8 C8
It works for biceps, brachialis How to begin making sense out of which and sort of for triceps nerve roots supply which muscles?
2. Make a “7” with your fingers, wrist and elbow C5 C5 C7: T1 C6 elbow extension C5,6 wrist flexion finger extension C7 C8
C7,8
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dorsal scapular c5 suprascapular c5,6 C5 lateral pectoral c5,6,7 Major components labeled musculocutaneous c5,6,7 IN OUT 1. Long Thoracic axillary C6 C5-8 c5,6 2. Musc Cut N. median T1 C7 3. Axillary N. c678t1 lower subscap c6,7 thoracodorsal c6,7,8 long 4. Median N. upper radial c5,6,7,8 thoracic C8 subscap 5. Radial N. ulnar c8,t1 c5,6 c5,6,7 medial antebrach cutan c8 6. Ulnar N. medial brachial cutan t1 T1 medial pectoral c8,t1
1) Long Thoracic Nerve 16 nerves exit the brachial plexus We will look at 6 major ones •courses (more detail to follow later today) inferiorly on anterior lateral 1) Long Thoracic chest wall 2) Axillary •innervates 3) Musculocutaneous SERRATUS 4) Radial ANTERIOR 5) Median 6) Ulnar •prevents scapular Quiz follows! winging
2) Axillary Nerve 3) Musculocutaneous Nerve posterior view •exits brachial plexus •Innervates the “BBC muscles” posteriorly • BICEPS • BRACIHALIS •courses through • CORACOBRACHIALIS “quadrilateral •Continues as the lateral space” antebrachial cutaneous nerve •innervates DELTOID.
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4) Radial Nerve 4) Radial Nerve •Leaves brachial plexus Lateral View posteriorly Posterior View Passes medial •Passes laterally behind the to lateral behind humerus the humerus •Crosses anterior to lateral epicondyle •Pierces supinator Passes •Passes along anteriorly over dorsolateral forearm lateral aspect of •Innervates triceps, wrist humerus and finger extensors posterior view
5) Median Nerve 6) Ulnar Nerve • arm: medial, with brachial artery • arm: medial; posterior to median nerve and brachial artery • elbow: central, medial to biceps tendon • elbow: posterior to medial epicondyle • forearm: central, beneath fds innervates fds, ½ fdp, fcr, • forearm: medial, beneath fcu pronator teres innervates fcu and ½ fdp • palm: central, through carpal • palm: Guyon’s canal; innervates tunnel innervates thenar hypothenars, interossei, add muscles, 2 lumbricals pollicis, 2 lumbricals
6) Ulnar Nerve QUIZ! Name that palsy!
Posterior Views • passes posterior to medial epicondyle of the humerus
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Motor Impulses Terminate at the Sensory Impulses Neuromuscular Junction Nerve • Motor impulses move distally away from CNS • Sensory impulses move proximally toward the CNS Muscle – share nerves with motor system, use different fibers • Sensory nerves innervate skin in the area of their motor counterpart – (i.e. axillary nerve transmits sensory information from the skin of the On to sensory nerves….. shoulder)
Sensation in the Hand Differences in Sensory Nerve Pathways
• S. nerves enter spinal cord thru Median: palmar aspect of lateral 3 ½ digits + dorsal roots nail beds of same • S. nerves cross to opposite side Ulnar: palmar/dorsal aspects of medial 1 ½ in brain stem or spinal cord fingers + hand continuous with same • Pass through the thalamus • Terminate in the sensory strip Radial: volar aspect of lateral 3 ½ digits and hand continuous with same (excluding nail beds).
The Sympathetic Nervous System Stellate in the Upper Extremity Ganglion = Inferior 2 parellel Cervical + chains of Superior GANGLIA Thoracic along sides of spinal cord. Ganglia
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References Sympathetic Fibers • Falconer, Spinner: Anatomic variations in the motor in the Upper Extremity and sensory supply of the thumb. Clin Orthop 1985;195:83-96. •pass through stellate ganglion • Russomano et al: Riche-Cannieu anastomosis with partial transection of the median nerve. Muscle •travel along arteries Nerve 1995;18:120-2. • Sachs, Raynor, Shefner: The all ulnar motor hand •control vessel without forearm anastomosis. Muscle Nerve constriction/relaxation; sweat; 1995;18:309-13. piloerection • Meals, R, Shaner: Variations in digital sensory patterns: a study of the ulnar nerve-median nerve •implicated in some chronic palmar communicating ramus. J Hand Surgery, regional pain syndromes 1983;8:411-414
Outline
Microanatomy Nerve Micro-Anatomy Biology and Biology Nerve Injuries Physiology Classification Adam Martin, MD UCLA Hand Fellow Nerve response to injury no relevant disclosures
Anatomy of Neuron
Cell body Dendrites Sensory neuron Receive incoming impulses Axon Conducts outgoing impulses Motor neuron Schwann Cells
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Anatomy of a Peripheral Nerve Nerve Fiber (Axon) Counts 1. Axon: basic subunit Electric lamp cord: ~60 copper strands . Nerve fiber = Digital nerve: ~1500 nerve fibers axon + Schwann cell + Median nerve: ~25,000 nerve fibers myelin Brachial plexus: ~145,000 nerve fibers 2. Fascicle: groups of axons 3. Peripheral nerve: groups of fascicles
Connective tissue layers Cross-section of peripheral nerve
Epineurium 1. Epineurium Cushions nerve 2. Perineurium Nerve gliding 3. Endoneurium Perineurium Surrounds fascicle Vascular supply Tight junctions Intrinsic + extrinsic Fascicle Mitchell adapted from www.CDNPA.com Endoneurium Surrounds axons
External epineurium Internal epineurium
Fascicle
Axon + Endoneurium
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Nerve Physiology Nerve Injury Axonal transport Mechanical injuries Secondary injury Protein synthesis in cell body Distance too long for diffusion Compression Infection Products motored along Traction Scarring microtubules Laceration Fracture callus Retrograde transport Combination Ischemia Returns waste products for (e.g. GSWs) recycling Transports growth factors to nucleus Implications with injury
Response to Injury Nerve Injury Classification Limited repertoire of responses to nerve Seddon H: Three types of nerve injury. Brain, injury 1943. 1. Mild injury 1. Neurapraxia schwann cells/myelin sheath 2. Axonotmesis Focal demyelination 3. Neurotmesis 2. Severe injury axons Axonal degeneration
Neurapraxia Neurapraxia
Conduction block More severe injury Demyelination All supporting layers entirely intact Disrupts impulse conduction Mild neurapraxia transient ischemia Axons are physically intact, physiologically out Impairs polarization of cell membrane Unable to conduct action potential
Focal Demyelination
axon axon
epineurium perineurium endoneurium epineurium perineurium endoneurium
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Neurapraxia Axonotmesis
Prognosis for recovery excellent Loss of axon continuity Axons remain intact no axonal degeneration Connective tissue envelope intact Mild cases: relief of temporary ischemia Degeneration of injured axons distally Severe cases: Schwann cells remyelinate damaged segment Restores conduction along axon Symptoms may last moments to months axon
epineurium perineurium endoneurium
Axonotmesis Axonal Injury: Wallerian Degeneration
Axonal transport interrupted Recovery requires axonal regeneration Survival of axonal segments prolonged recovery connected to cell body Prognosis for recovery good Distal segments endoneurial tubes are intact -> no Deprived of metabolic miswiring support Limiting factor is the distance of Degeneration of axons regeneration required beyond point of injury
Neurotmesis Neurotmesis- End Result Complete nerve transection Neuroma Degeneration of all axons distal to injury Separation of nerve ends spontaneous recovery will not occur Surgical problem
axon
epineurium perineurium endoneurium
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Physiology of Injury Chronic compression
Laceration Neurotmesis Ischemia + mechanical Smaller zone of injury compression Traction Axonotmesis At 30 mm Hg Axons most susceptible Decreased intra-neural Larger zone of injury blood flow Acute compression Neurapraxia Axonal transport disrupted o Local contusion with 2 circulatory Progressive axonal loss changes (axonotmesis) and fibrosis Inflammation scarring and further Damage often permanent compression
Nerve regeneration Axonal Regeneration
Wallerian degeneration Proximal effects Distal axon Loss of trophic support fragmentation Sometimes neuronal death Disintegration of myelin Survivors alter metabolic Macrophage invasion activity in preparation Clears endoneurial Axonal sprouting tubes of debris Growth cones Schwann cell proliferation Samples environment Pathway for later axonal Seeks sensory or motor regeneration pathways Guided by Schwann cells
Nerve Regeneration If gap exists, axonal sprouts migrate aimlessly Axons that find distal No distal targets are reached tubules are guided along (1mm/day) Neuroma formation Sprouts that reach distal connections mature Increase in axon and myelin thickness Sprouts which fail to make connections die back
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Neurotrophic Factors Nerve Regeneration: Molecular Level Promote survival and maintenance of neuron Axonal injury disruption of retrograde supply Neurotrophic factors (“fertilizer”) of growth factors Neurotropic factors (directional signals) Schwann cells provide trophic support Matrix substrates Proteins presented along regenerating pathway Metabolic factors for nourishment Picked up by axonal sprouts to sustain neuron Examples Nerve Growth Factor sensory neurons Brain-derived neurotrophic factor motor
Neurotropic factors Neurotropic factors Anti-neurotropic factors Promote extension and branching of negative or repulsive guidance cues axonal sprouts deflect axons from inappropriate targets Attract sprouting axons toward distal nerve segment 2 mechanisms: contact-guidance versus attraction at a distance Laminin and fibronectin: matrix-bound glycoproteins Soluble mediators Adapted from Carmeliet P, Nature Reviews Genetics 4:2003
Topographic Specificity Clinical Perspective Accuracy with which regenerating axons re- Axons regrow about ~1mm/day (1” / month) innervate appropriate Motor end plates degrade ~1%/week targets Need > 50% of motor endplates for function Dramatically affects Maximum distance to restore motor function is outcomes after nerve ~35 cm injury Sensory end-organs may survive much longer Axonotmesis >> Late nerve reconstruction can offer recovery of neurotmesis protective sensation Miswiring: axons wander into wrong tubules
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Clinical Perspective References Functional result following nerve injury 1. Regal S, Tang P. Surgical management of dependent on numerous factors neuromas in the hand and wrist. J Am 1. extent of neuron survival Acad Orthop Surg. 2018 Nov 13 2. rate and quality of axonal outgrowth 2. Eberlin KR, Treiser M. Anatomy and 3. topographic specificity of regenerating axons physiology of the peripheral nerve. ASSH 4. survival of end organs Surgical Anatomy: Nerve Reconstruction, 5. cortical reorganizational 2017 . Clinical recovery often incomplete 3. Dahlin LB. The nerve’s response to injury. ASSH Upper Extremity Nerve Repair Tips and Techniques: A Master Skills Publication, 2008
Burning Questions about Sensation
“You claim my nerve is recovering, why do I Diagnostic Testing for Nerves have pain every time I touch something?”
Sensory, Motor, Electrical, Imaging “So if I have carpal tunnel syndrome, why aren’t my thenar muscles weak?”
Roy A. Meals, MD “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 & gland
The Anatomy of Fingertip Skin Meissner -
corpuscles epi
and dermis Specialized Sensory End Organs Merkel A-β cell C A-Δ
neurite dermis complex
A-β Pacinian fat digital nerve corpuscle
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Nerve Fiber Types Specialized Sensory End Organs Supplied by A-β Fibers Fiber Myelin Size in Function Meters type sheath? microns per sec Pacinian Meissner Merkel cell C No 1 Burning 2 corpuscle corpuscle neurite cplx pain Schematic A-Δ Yes 2-5 Sticking 20 & temp # of nerve 1 >1 <1 A-β Yes 10-15 Light 60 fibers/rcptr Important for normal sensation touch Recovery Poor Excellent Fair ? A-α Yes 15-20 Motor 60 after ? ? laceration ?
Specialized Sensory End Organs Supplied by A-beta Fibers What constitutes normal sensation? Pacinian Meissner Merkel cell 1. A multitude of A-beta fibers present, corpuscle corpuscle neurite cplx supplying various types of end organs Stimulus Response III II III II II I I I I Adaptation Quick Quick Slow Response to: Touch 2. Each nerve fiber functioning properly Constant Poor Poor Good Moving Good Good Poor Vibration 30 cycle 256 cycle No
What can go wrong? When something goes wrong, 1. A multitude of A-beta fibers present, inquiring minds want to know: supplying various types of end organs How many nerve fibers are present? •Laceration (physical disruption of axon and (more is better) entire sheath = neurotmesis) Innervation density •Marked compression/stretch (physical disruption of axon but continuity of sheath = How much energy does it take to stimulate a axonotmesis) nerve fiber? (less is better) Threshold 2. Each nerve fiber functioning properly •Compression (physiologic disruption, aka POP QUIZ! ischemia = neurapraxia)
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Two Point Discrimination (The Innervation Density Test) Matching: Maybe if I How wide do move along 1. Innervation I have to density test the finger I can A stretch to find find 2 fibers 2 functioning more easily. 2. Threshold test nerve fibers? I go wide when nerve fibers are missing, e.g., lacerations, B severe compressions
Monofilament Testing For Your
(The Threshold Test) Reference:
Mono Filament # Force in grams
Mono Filament # Force in grams I can’t go wide. I am 1.65 .01 4.56 4.2 looking for a single 2.36 .02 4.74 4.6 nerve fiber to stimulate 2.44 .04 4.93 5.2 but I can push only so 2.83 .08 5.07 7.4 hard. 3.22 .17 5.18 13 3.61 .22 5.46 21 If I can’t push hard 3.84 .45 5.88 47 enough to make the 4.08 .75 6.10 85 nerve fire, maybe my big 4.17 .98 6.45 164 brother can! 4.31 2.4 6.65 279
Final Exam: MFT vs. TPD Inquiring minds want to know:
1. What test is appropriate for testing nerve “You claim my nerve is recovering. Why do I regeneration after laceration and repair? have pain every time I touch something?” 2. What test is appropriate for testing sensory loss in early cubital tunnel Rephrased: Why is pain the first sensation syndrome? to return after nerve repair? 3. What test is appropriate in severe carpal tunnel syndrome when MFT is markedly The unsophisticated unmyelinated C fibers
abnormal? grow back the quickest. 1. TPD, 2. MFT, 3. TPD 3. MFT, 2. TPD, 1.
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Inquiring minds want to know: Inquiring minds want to know: “You tell me I am maximally recovered from “So if I have carpal tunnel syndrome, why my nerve laceration, why can’t I feel my aren’t my thenar muscles weak?” electric tooth brush is vibrating?”
Rephrased: Why does sensory loss occur Rephrased: Why does response to low before motor loss in carpal tunnel frequency vibration return poorly after syndrome? nerve repair? The motor fibers are larger and are more resistant to compression ischemia. Because the Pacinian corpuscles reinnervate poorly.
Scratch Collapse Test Muscle Testing for Carpal Tunnel and Cubital Tunnel Syndromes Quantitate where possible patient Grip and pinch meters Compare to opposite side (ideally without examiner in the middle)
examiner 1 2 3 See Ref 7
Muscle Testing, Reconsidered For Reference: Muscle Testing • McAvoy and Green: The well-known Medical Research Council – Cadaver study, elbow flexion 0-5 scale – Only 4% of normal force required to flex 0 = no function against gravity 1 = palpable contraction, no movement • MRC Grade 0 1 2 3 4 5 2 = movement with gravity neutalized % of normal 0 <4 <4 4 >4 100 3 = movement against gravity 4 = movement against some resistance 95% 5 = normal strength 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 Electromyography (EMG) • Affected by the room’s temperature, patient age, anomalous innervation patterns • Usually with surface electrodes Nerve conduction velocity (NCV) Stimulating Recording • Tests nerve Needle electrode exam (NEE) • Velocity = distance divided by time • Tests muscle >50 meters/sec for all upper extremity nerves
• Latency (time in milliseconds) substitutes for velocity when distance is uncertain
NCV in Neurapraxia • Ulnar nerve NCV in Axonmetsis and Neurotmesis – 54 meters/sec remains normal for 2-3 days – 42 meters/sec – Conclusion: cubital tunnel synd
• Median nerve – Sensory distal latency 4.0 millisec • (nl <3.6 millisec) – Motor distal latency 4.8 millisec • (nl <4.6 millisec) axon – Conclusion: carpal tunnel synd
Needle Electrode Nerve Imaging • Normal muscle Exam – Electrically silent at rest • Nerves not seen on x-ray or CT scan – Electrical activity proportionate to force • Nerves not seen well on conventional MRI – of active contraction (recruitment) – Magnetic Resonance Neurography (MRN)
• Denervated muscle Indian J Plast Surg. 2015 May-Aug; – Fibrillations and sharp waves at rest 48(2): 129–137 begin 2-3 weeks after injury – No change on active contraction effort • Reinnervating muscle – Fibrillations and sharp waves – Disorganized recruitment pattern—seen 1-2 months before clinical improvement noted
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MRN: Cervical Spine Magnetic Resonance Neurography: CTS
flat
C6 Compression Aagaard3 flat BP Injury Yoshikawa4 T.O.S. normal Filler5 Aagaard3
Neurofibromatosis 6 Filler5 Cudlip
References 5. Filler et al, MR neurography and muscle MR 1.Dellon, Evaluation of sensibility and re- imaging Neurol Clin 2004, 22:643-682 education of sensation in the hand. Williams and Wilkins, Baltimore, 1983. 6. Cudlip et al, Magnetic resonance 2.MacAvoy, Green: Critical reappraisal of neurography studies of the median nerve Medical Research Council muscle testing for before and after carpal tunnel elbow flexion. J Hand Surg, 2007; 32A:149- decompression. J Neurosurg 2002, 96:1046- 153. 1051 3.Aagaard, Maravilla, Kliot: Magnetic resonance imaging of peripheral nerves. Neuroimaging 7. Cheng, et al: Scratch collapse test for Clinics of North America, 2001; 8:131-146. evaluation of carpal and cutibal tunnel 4.Yoshikawa et al: Brachial plexus injury. syndrome. J Hand Surg 2008, 33A:1518- Radiographics, 2006; 26:S133-143 1524
Introduction
Pain and paraesthesias of the upper extremity
Nerve Pathology in the Proximal • Cervical radiculopathy Portion of the Upper Limb • Brachial plexopathy • Thoracic outlet syndrome Eugene Farng, MD Anatomy is key
Southern California Permanente Medical Group
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Cervical Spine Cervical Spine Cross Section
Dermatome Distribution Motor Innervation
• C5 Deltoid, Biceps • C6 Biceps, wrist extensor • C7 Triceps, wrist flexors, finger extensors • C8 Interossei, Finger flexors • T1 Interossei
Reflexes Anatomy
• Biceps – C5, C6 • Brachioradialis – C6 • Triceps – C7
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Pathomechanics of Cervical Symptoms of radiculopathy Radiculopathy • Compression of nerve root • Based on nerve root affected – Disc pathology or herniation • Radicular pain, numbness, or weakness – Arthritis • Neck and shoulder pain are common – Congenital stenosis • Pain, paraesthesias, weakness in – Trauma distribution of the affected nerve – Tumor • Anatomy is key
Diagnosis of radiculopathy X-ray
• History and physical – Spurling’s test: extension, ipsilateral rotation, and downward pressure • XR • MRI • Electrodiagnostics – Primarily to evaluate for other sites of compression
Treatment of Radiculopathy Brachial Plexus Injuries • Initial – pain control, anti-inflammatories and analgesics, +/- steroid injections – Traction and manipulation: controversial – Neck strengthening • Surgery – ACDF – Laminectomy – Foraminotomy
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Brachial Plexus Injuries Brachial Plexus Injuries
- Trauma - Upper trunk palsy - congenital - weakness in abduction and elbow - low energy flexion - stinger - radial sided hand numbness - high energy - Lower Trunk - motorcycle - lose hand function - penetrating trauma - ulnar sided hand numbness
Brachial Plexus Treatment Pathomechanics of TOS
- depends on etiology and status of nerve • Poor posture and descent of shoulder - sharp laceration → direct repair girdle - nerve graft or transfer • Congenital anatomic variations – cervical - intercostal to musculocutaneous ribs, long transverse processes, congenital - spinal accessory to suprascapular bands - radial N (triceps) to axillary • Apical lung tumors (Pancoast tumors) - ulnar motor to musculocutaneous • Malunion or non-union of the clavicle, sternoclavicular dislocations
TOS Symptoms TOS Symptoms
• Arterial • Neurogenic TOS • Venous – Classic presentation with objective • Neurogenic physical evidence is rare – Hypothenar atrophy, decreased grip strength, sensory (C8/T1) deficits
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TOS Symptoms TOS Symptoms • Disputed Neurogenic TOS • Upper trunk involvement mimics cervical – Chronic, insidious onset pain of neck, radiculopathy or carpal tunnel syndrome upper chest, and shoulder girdle • Radiates into ulnar side of arm and • Left shoulder and chest pain mimics hand, and rarely into radial side angina or heart attack – Worse with elevation of arm during • Pain with overhead activity mimics cuff sleep/activity, driving, or heavy objects tears – Subtle findings may be confined to ulnar • Glenohumeral instability and global upper intrinsics of hand, mimic ulnar extremity symptoms neuropathy
Diagnosis of TOS Diagnosis of TOS
• History and physical • Evaluate posture and head position • Diagnosis of exclusion • Forward head position • Rule out distal sites of compression • Shoulder droop • C8-T1 cervical radiculopathy is rare but • Venous collaterals should still be excluded (usually with MRI) • Muscle bulk and tone • Arm swelling • Hand atrophy, intrinsic muscle testing • Sensory abnormalities
Diagnosis: Provocative Roos test – “stick up test” Testing for TOS • Look for reproduction of symptoms or loss • 90 degree abduction and external rotation of radial pulse test • Beware: many positions can cause • Pump hand for 3 diminution of radial pulse, and are not minutes diagnostic in isolation • Rapid fatigue or reproduction of • 64 volunteers symptoms – 17% with symptoms on questionnaire • Most sensitive and – 58% had one provocative test positive reproducible
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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 syndrome – Apical lung tumors – Useful to RULE OUT 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
TOS Treatment Treatment - Surgery
– Risk factors for failure of therapy • Vascular occlusion can be treated with • Obesity thrombolytics and long term • Poor cardiovascular condition anticoagulation, or surgical decompression • First rib resection – Obesity, chronic pain and associated • Claviculectomy for malunions or depression exacerbate poor posture • Antidepressants or psychotherapy can hypertrophic callus improve symptoms – Loss of strut → shoulder droop → worsening symptoms
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Complications of Surgery Prognosis
• Pneumothorax • Review of 10 studies of conservative treatment • Nerve injury – brachial plexus from traction, found no randomized trials, systematic reviews, long thoracic N on middle scalene, phrenic N or meta-analsyis. on anterior scalene • Unclear if conservative treatment better than no • Vascular injury – death from exsanguination has been reported. treatment, or what type of treatment is best • Persistent symptoms -- inadequate resection – Less than 20% of patients diagnosed vs incorrect diagnosis progress to surgery – When appropriately done, 75% good to excellent results in some series
Summary References
• ANATOMY IS KEY - Kuhn, JE, Lebus V, Bible JE. Thoracic • First line treatment is always conservative Outlet Syndrome. JAAOS, April 2015. 23(4) 222-32 • TOS is a diagnosis of exclusion with few reproducible objective tests or - Rhee JM, Yoon T, Riew KD. Cervical measurements. Treat with postural training Radiculopathy. JAAOS, Aug 2007. 15(8): 486 - 94 • Surgical decompression works well for cervical radiculopathy and for clear cases of TOS
Thank you Adson’s test
• Arm at the side, hyperextend neck, turn toward affected side, and inhale deeply
• Pulse diminishes • Symptoms reproduced
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Halsted Maneuver Wright’s hyperabduction test • Costoclavicular test/military brace test • External rotate and • Arms at side abduct arm 180 • Move shoulders down and degrees back with protruding chest • Inhale deeply • Clavicle closes on 1st rib • Downward compression of • Symptoms worsen clavicle with traction of affected extremity accentuates symptoms
TOS Treatment - Step 1
• Identify and treat myofascial trigger points, local spasm, tendonitis, bursitis – Use relaxants, mild narcotics, antidepressants, anti-inflammatories, TCA, tegratol, neurontin. – Modalities such as heat/ice, TENS, ultrasound are debatable (can promote 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
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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 ALI GHIASSI, MD • Orthotics for scapular retraction may help, but must be part of muscular strengthening plan
Median Nerve Compression Syndromes CARPAL TUNNEL SYNDROME • Epidemiology • Nerve Entrapment at the Wrist – Classically • Posttraumatic – Carpal tunnel syndrome • Female • Compressive Neuropathies in Proximal Forearm • Middle age – Pronator syndrome – More recently • Younger – Anterior interosseous syndrome • Industrial worker • Repetitive motions
RISK FACTORS RISK FACTORS
• Clear intrinsic risk • Occupational factors factors • Task repetition • Female • Posture • Mechanical stress • Pregnancy • Force • Diabetes • Vibration • Rheumatoid • Temperature arthritis (cold)
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CARPAL TUNNEL SYNDROME CARPAL TUNNEL SYNDROME • Median nerve entrapment in the • Nakamichi ‘98: carpal tunnel – Looked at the • Chronic inflammation? histology of 166 patients with CTS • Amyloid deposition? – 74% normal • Repeated mechanical histology of TCL stress? – 25% had mucoid, • Vascular sclerosis and amyloid deposits ischemia? – Concluded: No typical histological changes noted
CARPAL TUNNEL SYNDROME CARPAL TUNNEL SYNDROME
• Ikdea (06): • Szabo (‘89) – Increases in carpal • Increased carpal canal pressure tunnel pressures with – 10 mm distal to exercise in patients distal wrist crease with CTS – Pressures • Sustained and correlated with delayed recovery of nerve conduction normal pressures results after exercise in CTS
Carpal Tunnel Syndrome
• History & examination are most important tools in diagnosis – Szabo (JHS 99) • Night pain in median nerve distribution • Sensory changes in median nerve • Median nerve compression test • EMG/NCS not helpful in diagnosis
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Carpal Tunnel Syndrome CARPAL TUNNEL SYNDROME • X-rays, CT scan, MRI not useful • Pain • EMG/NCS are helpful • Along median in confirming nerve diagnosis • Parestehsias in – Double crush median nerve syndrome distribution – Diabetes • Normal thenar – Difficult exam sensation
CARPAL TUNNEL SYNDROME PHALEN’S MANUEVER • Symptoms worse at night (waking up) • Wrist flexion with elbow • Extreme wrist on table positions • Paresthesia in response • Talking on phone to position • Driving • Numbness and tingling • Dropping objects due in radial digits in 60 sec. to weakness or = pos. test altered sensibility • Cups, dishes • Probable CTS (sen.0.75, spec. 0.47)
TINEL’S SIGN CARPAL COMPRESSION TEST
• Tap on median nerve at • Direct compression of wrist median nerve • Site of irritable nerve due • Paresthesia in response to axonal injury to pressure • Tingeling and shooting • Paresthesia occur within pain in nerve dist. 30 sec. • Probable CTS (sen. 0.60, • Probable CTS (sen. 0.87, spec. 0.67) spec. 0.90)
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SENSORY TESTING EMG/NCS • Static two point • Monofilaments testing is • Its important to • Glowaki (JHS ‘96) discrimination >6 mm better • Value greater than .08 gm remember that CTS is – 30% Patient with = advanced nerve a CLINICAL diagnosis CTS and normal dysfunction or nerve (monofilament 2.83) in radial 3 digits • Electrodiagnostic NCS responded to laceration • Probable CTS (sen. 0.83) tests should NOT be surgery • Rarely useful in CTS used independently – Concluded: in making diagnosis EMG/NCS does not correlate with surgical outcome
CARPAL TUNNEL SYNDROME STEROID – Mild symptoms less INJECTIONS than 12 months – No weakness • Early – Intermittent sensory – changes Intermittent symptoms – Offer transient relief in – No weakness of thumb abduction 80% patients at 6 – No permanent numbness or paresthesias weeks – – Only 22% are No atrophy symptom free at 12 – Treatment = wrist splints, activity months modification, limb positioning 6–8 weeks
Wood et al, Gelberman et al, + Girlanda et al.
STEROID INJECTIONS CARPAL TUNNEL SYNDROME • Intermediate Preoperative response – Constant paresthesias, to cortisone injection numbness – No atrophy • Diagnostic value – +/- Muscle weakness of • Prognostic value thumb abduction – Pain with irritability of nerve – Treatment = surgical decompression
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SURGICAL TECHNIQUES CARPAL TUNNEL SYNDROME • Late • What is the better surgical technique? – Sensory loss – Muscle atrophy – Open release – Weakness grasping – Limited open release objects – Two incision release – +/- Pain – Treatment = surgical – Endoscopic release decompression – Surgery will halt progression & pain
OPEN CARPAL TUNNEL RELEASE ENDOSCOPIC RELEASE
• Under direct vision • Larger incision • Smaller incision • Regional or general release all structures • May have more • May have improved anesthesia • Explore median incisional irritation short term recovery • Not able to visualize nerve and other • Avoid palmar incision median nerve or intercarpal pathology carpal pathology • Increased risk of NV • Safe and efficient damage under local
OPEN VS. ENDOSCOPIC OPEN VS. ENDOSCOPIC • MacDermit (JHS ‘02) • Endoscopic group – Randomized better short term • Cochrane Review 2006 blinded outcome • No better alternative than standard open prospective trail • Endoscopic group CTR – Short and long lower long term • Earlier return to work with endoscopic: term outcome conflicting results satisfaction (higher • No strong evidence to replace standard measures re-operation rate) open CTR • NO SUBSTANTIVE DIFFERENCE NOTED
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HAND THERAPY • Pomerance (JHS ‘07) – Prospective • However, there is a randomized study role for patients with – Two week of post – Limited digital operative therapy vs. motion Surgeons: Shared decision making home therapy Patients: Lead decision making – No change in outcome – Edema Non-Operative treatment =likely not to noted – Incision tenderness want an injection – Therapy added $600- Decision aid (evidence based medicine) $900 maybe helpful Both: Value in getting family support
SPECIAL CIRCUMSTANCES WORKER’S COMPENSTION
• WORKER’ S COMPENSATION PATIENTS • Higgs (JHS ‘94) – 73% of WC – • MORE MATURE PATIENTS CTS outcome in patients changed worker’s jobs due to • DEPRESSION compensation residual symptoms • RE-OPERATION patients – 2% non-WC – Residual symptoms changed jobs more common in WC patients
MATURE PATIENTS • Townshend (JHS ‘94) • Weber (JHS ‘04) – 83 CTR in patients – 105 CTR in patients over 70 yrs over 65 yrs – 80% with severe – 83% very satisfied changes with results at 6 – 94% satisfied at 1 months year – Reduced paresthesia, night pain – Improved strength & sensibility
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MATURE PATIENTS
• Keep in mind that 5- • Pain relief is main 10% not satisfied goal • Important to discuss • Long term recovery goals and recovery to be expected in One year post-op 87% improvement in NCS before surgery most patients NCS improvements correlated with clinical improvements
DEPRESSION • Ring (JHS ‘07) – 82 Patients with CTR – Survey of outcome and satisfaction – Dissatisfaction correlates Improvement in depression and anxiety levels post op with depression and Symptoms correlated with levels of depression and anxiety ineffective coping skills – More than a peripheral nerve problem
RE-OPERATION American Academy of Orthopedic Surgery Recommendations Following Literature Review • Cobb (JHS ‘96) – Risk factors for (from aaos.org) – 113 patient with failure CTR re-operation • Worker’s Comp • Recommend carpal tunnel release for CTS – 15 failed surgeries • Pain in ulnar – Epineurotomy and skin preservation needing 3rd nerve dist. procedures not recommended operation • Normal Nerve • Hand therapy is not among the options used studies for CTS • 20% dissatisfied with final result
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AAOS Website Treatments not Specifically Addressed or Advocated http://www.cochrane.org/
Acupuncture, Steroids, Cold laser, Diuretics, • Looked at all randomized trails for CTS Exercise, Yoga, Vitamin B6, Fitness, – 4 main studies Iontophoresis, Laser, Stretching, Massage, – Concluded surgery relieves symptoms better Magnets, Manipulation, Activity modification , than splinting Medications (NSAIDS, etc.), Cognitive – Not conclusive for patients with mild behavioral therapy, Nutritional supplements, symptoms Phonophoresis, Smoking cessation, – No comparison made to injections. Therapeutic touch, Electrical stimulation, Weight Reduction 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 AIN 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 12 incomplete with Complex Regional Pain Syndrome (CRPS), weakness Shingles, Parsonage-Turner Syndrome & Nerve Mobilization • FPL, FDP IF • Pinch causes IP hyperextension • Weak pronation with Nicholas E. Rose, MD elbow flexed Newport Beach, CA
NO VESTED INTEREST NO FDA OFF-LABEL USES PRESENTED
Complex Regional Pain Syndrome CRPS Background (CRPS) • Neurologist Silas Weir Mitchell: “Causalgia” • Chronic pain syndrome most often affecting seen after major nerve injuries in Civil War one arm or one leg vets at Philadelphia VA Hospital • Pain out of proportion to initial injury • Sudek, 1900: Localized bone atrophy on x-ray • Occurs after an injury, surgery, stroke or • Leriche, 1916: Noted similarities to ischemia, heart attack treated with sympathectomy • Incidence: 6-26/100,000 persons/year • Evans, 1946: Coined “reflex sympathetic dystrophy” (RSD) for syndrome w/o major • Females > Males at ratio of 3.4:1 nerve injury • UE > LE • Int’l Assn. Study of Pain (IASP), 1994: • Fracture = Most common precipitating event “CRPS” because “RSD” is not solely sympathetically-mediated pain
CRPS Overview CRPS • Type 1: No identifiable No single unifying explanation can account nerve injury for the diverse features. – Previously known as CRPS is probably a spectrum of disorders. RSD • Type 2: Identifiable CRPS II (causalgia) least common nerve injury – Previously known as causalgia when CRPS I (minor RSD) most common following major nerve injury
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CRPS Predisposing Factors CRPS Predisposing Factors
• Psychological factors? — Probably not • Elevated intra-cast pressure due to a tight • Menopause cast or extreme positions • History of migraines • Litigation • Osteoporosis • Genetic • Asthma – Siblings of CRPS patients under 50 years were at three times higher risk of developing the • ACE (Acetyl Choline Esterace)-inhibitor therapy condition – HLA-B62 and HLA-DQ8 alleles
The Perfect Storm for CRPS Features of CRPS Patient with wrist injury… • Pain out of proportion to the inciting cause Sling/tight bandage cause: • Non-dermatomal - Immobilization • Skin dry or overly moist - Ischemia • Skin color: Mottled or cyanotic - Edema • Skin temperature: Cool • Skin texture: Smooth, shiny, non-elastic • Edema • Soft tissue atrophy (especially fingertips) • Sweat: Excessive, reduced, absent
Features of CRPS • Not all CRPS is sympathetically-mediated • Hair changes: Loss, finer, longer • Not all sympathetically-mediated pain is • Nails: Ridged, curved, CRPS thin, brittle • Joints: Stiff Metabolic Neuropathies • Muscles: Wasted, Herpes zoster weak, tremor, spasms • Radiographs: SMP CRPS Osteoporosis Phantom Pain • Bone scan: Findings Neuralgias consistent with CRPS
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Useful Definitions and a Conundrum Budapest Diagnostic Criteria for CRPS The following FOUR criteria must be met: • Hyperalgesia: Increased pain response to a stimulus that is normally painful (1) Pain out of proportion to inciting event (2) Must report at least 1 symptom in 3 of the • Hyperesthesia: Abnormal increase in following 4 categories: sensitivity to stimuli of any of the senses (a) Sensory: Hyperesthesia and/or allodynia (b) Vasomotor: Temperature asymmetry and/or • Allodynia: Non-painful stimuli evoke pain skin color changes and/or skin color asymmetry (c) Sudomotor/edema: Edema and/or sweating changes and/or sweating asymmetry When does pain become abnormal? (d) Motor/trophic: Decreased ROM and/or motor Who says so? dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin)
Budapest Diagnostic Criteria for CRPS(Cont.): CRPS Pathophysiology (3) Must display at least 1 sign in 2 of the following categories: (a) Sensory: Hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint • Exaggerated inflammatory response movement) (b) Vasomotor: Temperature asymmetry and/or skin color • Altered cutaneous innervation changes and/or asymmetry (c) Sudomotor/edema: Edema and/or sweating changes • Central & peripheral sensitization and/or sweating asymmetry • Altered sympathetic nervous system fxn (d) Motor/trophic: Decreased ROM and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, • Circulating catecholamines nails, skin) • Autoimmunity (4) There is no other diagnosis that better explains the signs and • Distorted sensory representation of affected symptoms limb in brain
Causes of CRPS Type I CRPS, Type I • 50% follow trauma • Peripheral insult: Limb trauma/surgery, – Possibly trivial electric shock – Distal radius fracture • Peripheral and central insult: Herpes zoster, – Surgery: Including CTR, Dupuytren’s brachial plexus avulsion • Immobilization contributes • Central insult: Stroke, MS, spinal cord injury, – Self-induced and/or iatrogenic brain injury/tumor – Immobilization by itself causes stiffness, • Drugs: Isoniazid, phenobarbital clumsiness, atrophy of muscle, skin, fat • Heart/lung disorders: Myocardial infarction, • Tight bandage, cast, splint post-op cardiac surgery, lung disease • Was it the injury, the surgery, the bandage?
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CRPS: Management CRPS: Management Overview • A. Drugs • Prevent it! • B. Interruption of sympathetic supply – No slings for hand and wrist problems • C. Implanted nerve stimulators, pain pumps – Mobilize all joints possible • D. Psychological approaches • Minimally restraining bandages, • E. Physical forms of treatment splints, casts • Encourage functional use Treatment is clearly multidisciplinary with – Elevate, elevate, elevate! treatment by hand surgeon, pain management specialist, therapist and psychologist – Loosen/replace tight bandages/casts
A: Drugs for CRPS B: Interrupt the Sympathetic Supply • Anti-inflammatory (NSAIDS, steroids) • Stellate ganglion block(s) • Vitamin C (preventative) • Topical antioxidants (DMSO) • Anti-convulsants (eg. Gabapentin) • Surgical sympathectomy • Ketamine • Peripheral blockade • Antidepressants (Nortriptyline, Cymbalta) – Local anesthetics • Narcotics – Guanethidine • Calcitonin • Intravenous immunoglobulin (IVIG) These treatments won’t work when the pain is not sympathetically mediated
C: Implanted Nerve Stimulators D: Psychological Approaches and Pain Pumps • Active self-management and participation • Spinal cord stimulation in a care plan • Peripheral nerve stimulation • Assess & treat patients for concomitant axis I disorders (depression, anxiety, • Spinal medication pumps PTSD) • Deep brain stimulation • Cognitive behavioral therapy • Biofeedback • Learning relaxation skills
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E: Therapy E: Therapy
• First line of treatment • Overcome kinesophobia • Active movement, resume ADLs • Massage • Passive motion, splinting after pain is controlled • Contrast baths • Posture normalization • Graded motor imagery (GMI) ** • Edema reduction • Transcutaneous electrical nerve stimulation • Desensitization • Isometric strengthening exercises • Stress loading • Encourage use of affected limb in ADLs – Scrubbing • Mirror box therapy ** – Carrying • Specialized garments or wrappings • Aerobic conditioning
Surgery During/After CRPS CRPS: Prognosis • Relief of CTS, cubital tunnel syndrome may help treat CRPS >> Don’t delay • Within first year, 70% improved (Bean et al) • Secondary surgery after CRPS is controlled, – 25% still met Budapest Criteria eg, distal ulna excision after distal radius fx – Only 5% without complaints – 47% recurrence rate • Patients with higher levels of anxiety and pain- – Make sure pain manager and therapist are related fear at beginning of therapy have in town to start treatment at earliest sign of worse long-term outcomes recurrent CRPS • CRPS present for >1 year rarely – Pain manager often recommends peri- spontaneously resolves operative stellate ganglion block • Prognosis poorer in smokers
CRPS References Shingles Resurgence of virus that causes • Tajerian M et al: New concepts in complex chickenpox in immunocompromised patient regional pain syndrome. Hand Clinics; February 2016; 32:1: 41-9. 0.5% > Age 60, 1% > Age 70 • Pain and rash follow a dermatome • Goh EL et al: Complex regional pain – Face > Trunk > Limb Courtesy Masryyy, Wikimedia syndrome: a recent update. Burns Trauma. • Pain (post-herpetic neuropathy) can last Jan 19, 2017; 5:2. for years, treated with meds • Marinus J et al: Clinical features and • Immunization now available, advised for pathophysiology of complex regional pain > 60 syndrome. The Lancet. July 2011; 10:7: 637- • Mueller, NH et al: Varicella zoster virus infection: 48 Clinical features, molecular pathogenesis of disease, and latency. Neurologic Clinics 2008; 26:675-697
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Parsonage Turner Syndrome Nerve Mobilization • Not published, discussed or understood in • Idiopathic brachial plexopathy hand surgery circles • Etiology unclear • Recent review by Mark Walsh, PT, MS, CHT, • Abrupt onset of shoulder pain (usually ACT (J Hand Therapy 2005, 18:241-258): unilateral) followed by a progressive – “Neural mobilization…is based on an neurologic deficits of motor weakness, eclectic compilation of theoretical concepts. dysesthesias and numbness There is a paucity of reported clinical • Pain may extend to trapezius, upper arm, studies using neural mobilization for the forearm and hand treatment of neuropathic pain” • Pain usually worse at night • Pain usually lasts 1-2 weeks ie: Doctors Demystify can’t help you much here
Targeted Muscle Reinnervation Walsh:
• Novel approach to post-amputation “The clinical technique for the application of neuroma pain neural mobilizationTHANK as a treatmentYOU approach is • Provides distal target and vascularized based on an eclectic compilation of theoretical scaffold to guide sprouting nerve axons concepts based on scientific and empirical • Improve functional prosthesis control experience. There is a paucity of reported clinical studies using neural mobilization for • Residual nerves from the amputated limb are transferred to reinnervate new muscle the treatment of neuropathic pain.” targets that have otherwise lost their function ie, Doctors Demystify can’t help you much here! • 0/26 patients developed neuroma pain after TMR (Souza et al, 2014)
Seddon Injury Classification Nerve Lacerations, Repair, Grafting, Neuropraxia Transfers, Neurotization – Temporary paralysis
Axonotmesis – Likely recovery
Neurotmesis Edward Kobraie, MD – No recovery Talk originally prepared by Katherine Au, MD without repair
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Mechanism of Injury Basic Injury Types Tidy wounds: knife, glass, surgical Compression – “Saturday night palsy” Untidy wounds: – Open fracture Traction – Penetrating missile
Avulsion Laceration
Indications for operative Nerve repair intervention Sensorimotor exam + mechanism Associated vascular/bony Failure of nerve recovery Worsening of nerve injury Persistent pain Painful neuroma
Timing of Nerve Repairs Reasons not to repair Open Injuries General condition of the patient Early exploration Skill/availability of operating team and specialized equipment Definitive repair if sharp laceration Uncertain viability or state of nerve trunks Local or systemic sepsis Crush injury – zone of injury not apparent Tendon transfer or nerve transfer will give better results
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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
Meticulous surgical technique Correct alignment/orientation of fascicles – (microscope preferred to loupes) Use external markings Debride to healthy nerve ends Primary tension-free repair Graft if tension-free repair not possible Match motor and sensory fascicles
Group Fascicular Nerve Repair Epineural Nerve Repair
Superficial radial nerve
Median nerve @ elbow
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Factors in Outcomes
Age Nerve gap Management of Nerve Gaps Delay to repair Level of Injury Condition of nerve ends
Nerve Grafts Nerve Grafts
Graft: tissue that depends on recipient bed Autografts (same person) blood supply Allografts (same species, rendered Indication: Cannot achieve tensionless immune innert) direct repair Pedicled nerve grafts (nerve flaps) Vascularized nerve flaps
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.)
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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 Localizes neurotrophic factors Require population by Schwann cells from Protection from scarring neural stumps to guide axonal growth Natural, synthetic, non/absorbable Short (<3cm) nerve defects Vein, polyglycolic acid (PGA), collagen
Porous flexible PGA mesh Semipermeable collagen GEM Neurotube Integra
Thumb digital nerve Repair w/ neurotube
Cho et al. JHS 2012 Cho et al. JHS 2012
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Principles of Nerve Transfer
What if there is no proximal nerve end that Expendable donor can be used in a repair? Donor with large number of pure axons Donor near motor end plates of muscle or Nerve Transfer target sensory nerve Healthy proximal donor distal palsied Innervates a muscle that is synergistic to nerve the target muscle (preferred)
Nerve Transfers Oberlin Transfer
Historically used in brachial plexus injuries Restoration of elbow flexion – No viable proximal nerve Ulnar nerve fascicle to musculocutaneous nerve
Musculocutaneous n.
biceps Ulnar n.
Indications for Nerve Transfer Nerve Transfers
Brachial plexus avulsion injuries Convert high injury to low injury Avoid dissection through scar Recruiting redundant or unimportant Major trauma with segmental nerve loss fascicles Alternative to grafting in older patients Proximal nerve injury
~35cm/~14in ~12cm/~4.7 in
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High Ulnar Nerve Injury Median to ulnar transfers - Motor
Missing: AIN (anterior interosseous n.) motor branch ulnar nerve 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 Sensory denervation of the hand ulnar sensory nerve “black hole” in sensory cortex of brain End to side 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.
References References
Oberlin C, et. al. Nerve transfer to biceps Cho MS, et al. Functional outcome muscle using a part of ulnar nerve for C5- following nerve repair in the upper C6 avulsion of the brachial plexus: extremity. J Hand Surg 2012; 2340-9. anatomical study and report of four Weber RV, et. al. Bridging the Neural Gap. cases. J Hand Surg Clin Plastic Surg 2005; 605-616. [Am]. Mar 1994;19(2):232-7. Brown et. al. Nerve Transfers in the Dvali L, et. Al. Nerve repair, grafting and Forearm and Hand. Hand Clin 2008; nerve transfers. Clin Plastic Surg 2003; 24:319-340. 30:203-221.
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References Chiu, DTW et. al. A Prospective Clinical 07 Ulnar Nerve Evaluation of Autogenous Vein Grafts Used as a Nerve Conduit for Distal Compression Syndromes Sensory Nerve Defects of 3 cm or Less. Plast Recon Surg 1990; 928-934. PROSPER BENHAIM, MD Young et al, A randomized prospective UCLA Department of Orthopaedic Surgery comparison of fascicular and epineural digital nerve repairs. Plast Recon Surg 1981. Talk originally prepared by David J. Slutsky MD, FRCS(C)
Microcirculatory Effects Nerve Gliding of Compression Ulnar nerve –above elbow: 8-10 mm increased permeability / edema –below elbow: 3-6 mm increased endoneurial fluid –localized scarring tethers the nerve pressure .joint motion & muscle pull results in traction injury proximal and sub-perineurial demyelination distal to site
Nerve Compression Experimental Clinical Implications Stretch Neuropathy @ 6%, motor compressed nerves have a lower potential amplitude threshold to mechanical pressure decreases by 70%, but returns to normal provocative nerve tests reproduce after 1 hour paresthesias @ 12% strain, conduction is blocked and shows minimal recovery after 1 hour
Wall et al. J Bone Joint Surg (Br). 1992
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Experimental Stretch Traction Neuropathy: Neuropathy Pathophysiology Continuous stretching (2N) of rat tibial nerve for 1 hour resulted in no histologic, EDX, or functional abnormality Injury/scarring of mesoneurium -> nerve adherence to surrounding 2N load applied cyclically 60-120 times/hr structures lead to abnormalities Subsequent movement -> traction on This suggests that a small strain applied repeatedly might lead to nerve dysfunction the nerve
Watanabe et al. J Hand Surg 2001 Lunborg G, Dahlin LB. Hand Clinics 1992
Traction Neuropathy: Pathophysiology Proximal Ulnar Nerve Fascicular Topography
Stretching injuries -> micro-lesions -> epineural/intraneural fibrosis and Approximately 20 fascicles permanent nerve entrapment motor fibers to FCU, FDP are deep Thickening of epineurium/perineurium motor fibers to intrinsics, sensory interfere with blood flow -> dynamic ischemia. fibers are superficial, hence more susceptible to early compression
Lunborg G, Dahlin LB. Hand Clinics 1992
CUBITAL TUNNEL SYNDROME Cubital Tunnel Syndrome Symptoms Exacerbation by repetitive elbow flexion Aching discomfort Medial aspect of elbow – Sleeping position
Pain, paresthesias, numbness – Holding a phone, reading a newspaper Ulnar forearm – Driving Ulnar ½ ring finger Small finger – Leaning on a flexed elbow Ulnar dorsal ½ of the hand
Hand clumsiness and weakness
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CUBITAL TUNNEL SYNDROME Signs TINEL’S SIGN
Tinel’s sign over ulnar nerve
Elbow flexion test
Decreased sensation in ulnar nerve distribution
Weakness of 1st dorsal interosseous muscle and FDP to RF & SF
Atrophy of intrinsic muscles and clawing
FIRST DORSAL ELBOW FLEXION TEST INTEROSSEOUS STRENGTH Correct Incorrect
LIGHT TOUCH SENSATION CUBITAL TUNNEL SYNDROME TESTING Scratch Collapse Test
Cheng et al. JHS 2008, 33(9), 1518- 24.
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Cubital Tunnel Syndrome Cubital Tunnel Syndrome
Severe neuropathy: – Abnormal 2pd of ring and small fingers Mild neuropathy: – Weak intrinsics, clawing of ring, small – Positive elbow flexion test – Positive Froment’s sign . (10% false positive) – ± Positive Tinel’s sign over cubital tunnel – ± Scratch collapse test
CUBITAL TUNNEL SYNDROME Nonoperative Treatment Operative Procedures Avoidance of elbow flexion In situ release (open vs. endoscopic) Avoid direct pressure on the elbow
NSAIDs (cortisone ineffective) Medial epicondylectomy
Ergonomic workstation modification Anterior transposition of ulnar nerve from Nighttime elbow extension splint behind the medial epicondyle: – Anterior elbow splint with elbow at 30° of subcutaneous flexion intramuscular submuscular
CUBITAL TUNNEL RELEASE ± MEDIAL EPICONDYLECTOMY SUBCUTANEOUS TRANSPOSITION
Simple In-Situ Medial Decompression Epicondylectomy
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Outcomes SUBMUSCULAR 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.
Beneath the flexor-pronator muscle mass Intrinsic wasting rarely recovers in an adult. Above the brachialis muscle Tomaino et al. J Hand Surg 2001;26A:1077-81
Etiology Benign tumors (ganglion >> lipoma, GCT 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
Clinical Presentation ULNAR TUNNEL SYNDROME Paresthesias of ring and small fingers Anatomy of Guyon’s Canal ↓ Semmes Weinstein of ring and small Roof volar carpal ligament Tinel’s sign over Guyon’s canal piso-hamate ligament (motor branch) Weakness of intrinsics and ADM Medial pisiform Froment’s sign Lateral hook of hamate Normal FCU, FDP Normal Dorsal Cutaneous Br. of Ulnar N.
NEGATIVE ELBOW FLEXION TEST
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3 Zones:
Type I: -mixed motor and sensory Type II: -pure sensory Type III: -pure motor Green’s Operative Hand Surgery
Nonoperative Treatment Surgical Treatment Required
Activity modification Intrinisic wasting and/or sensory loss
Bicyclists: avoid riding with hands low on Space-occupying lesion handlebars Ulnar artery thrombosis/aneurysm -> Avoid repetitive percussion on ulnar ulnar artery repair or ligation. border of palm
Wrist splinting/cortisone injections
OUTCOMES Type IV: pure motor Clinical recovery in majority of patients treated with sparing of for a space-occupying lesion. [Foucher, 1993] hypothenars – motor branch Motor recovery less predictable than sensory distal to ADM IV v recovery, especially when compression caused by longstanding fibrotic hypothenar arch [Zoch, Type V: distal motor 1990] – just proximal to FDI and Add. Pollicus
Wu,Morris,Hogan. Arch Phys Med; Vol 66,Apr 1985
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Suggested Reading
Slutsky, DJ. Techniques for Nerve Compression Syndromes. In Hand and Upper Extremity Reconstruction. Chung KC, ed. Elsevier, 2008
Rayan GM. Proximal ulnar nerve compression: Cubital Radial, Axillary and tunnel syndrome. Hand Clin 1992;8:325-336 Suprascapular Nerve Palsies Gelberman RH. Ulnar tunnel syndrome. In: Gelberman RH,ed., Operative Nerve Repair and Reconstruction. Philadelphia, Lippincott, 1991:1131– Adil N Esmail, MD Chief of Service 43. Permanente Medical Group Panorama City Chung K. Treatment of ulnar nerve compression at Assistant Clinical Voluntary Professor the elbow. J Hand Surg 2008, 33A:1625-1627 UCLA, Department of Orthopaedic Surgery
Radial Nerve Anatomy • Origin • High – Derived primarily from C6, C7 and C8. T1 contribution in ~ 11% of population • Elbow Radial Tunnel and PIN – All three trunks (upper, middle, lower) contribute to posterior cord • Wrist Superficial radial nerve (SRN) – Posterior branches into radial and axillary entrapment (Wartenberg’s Syndrome) nerves
Anatomy High Radial Neuropathy: Etiology – humeral shaft fx, 14% incidence • Triceps – tourniquet palsy • Anconeus – “Sat. night palsy”, crutch injuries • Brachioradialis – anomalous muscle, rare • ECRL – penetration by an aberrant artery • ECRB • Supinator – tumors – strenuous muscle activity • Divides into PIN and Superficial Branch – windmill pitching
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High Radial Neuropathy: Clinical Features High Radial Neuropathy – ± triceps dysfunction depending on level of lesion – Wrist drop with inability to extend fingers or thumb – Decreased sensation SRN distribution – ± decreased sensation posterolateral aspect arm and forearm
High Radial Neuropathy: Management High Radial Neuropathy: Management
– Spontaneous onset, no mass, nl imaging • If neuropathy has lasted longer than 12-18 • dynamic wrist splint, passive ROM months, tendon transfer indicated exercises • if no evidence of recovery at 3-6 months, – Common tendon transfers: surgical exploration • palmaris longus to EPL –Neurolysis • pronator teres to ECRB –If humeral nonunion, shorten humerus • FCR to EDC
High Radial Neuropathy: Management Tendons Transfers Humerus Shaft Fracture
• Somewhat controversial • Usually injury due to contusion or mild stretch • Most advocate non-operative 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 extnsr tenodesis splint – Tumor – Proximal 1/3 radius fx • If no improvement – Radial head dislocation - Surgical decompression – Surgical retraction
PIN Compression: Management Radial Tunnel Syndrome: Etiology
– Same as PIN compression syndrome – If progressive or open injury: • Surgical exploration – Tumors less common
– If palsy for greater than 18 months, tendon transfers – Most commonly due to musculotendinous structures
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 Radial Tunnel Syndrome: Management • Initially, conservative • Differential Diagnosis – NSAID, rest, avoid provocative activities – Lateral epicondylitis (may coexist in about – Long arm splint with elbow in flexion and 5% of cases) supination, wrist in extension – Parsonage-Turner Syndrome – Treat lateral epicondylitis as needed – Cervical radiculopathy • Recalcitrant after 3 months – Systemic disorders – Surgical exploration – Chronic compartment syndrome – Results mixed
Wartenberg’s Syndrome Wartenberg’s Syndrome: Etiology • Also known as: – entrapment between BR and ECRL, esp with – Superficial radial nerve repetitive movement entrapment – anatomic anomalies (eg conjoined BR/ECRL) – Radial sensory nerve – compression over radial styloid entrapment – surgical injury – Cheiralgia paresthetica – tumors – Handcuff neuropathy – trauma- crush injuries, fractures, lacerations – Wristwatch neuropathy – synovial rupture in RA
Wartenberg’s Syndrome: Clinical Features Wartenberg’s Syndrome: Differential Dx
Paresthesias or dysesthesias dorsoradial forearm, wrist and hand – De Quervain’s extensor tenosynovitis – increased with wrist flexion, thumb flexion – Lateral antebrachial cutaneous nerve injury 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 Axillary Nerve • C5 and C6 -> posterior cord • Gives braches to shoulder capsule • Initial treatment- conservative • Goes through quadrilateral space with – NSAIDS, rest, activity modification posterior humeral circumflex artery – Thumb spica splint with wrist extended – Eliminate external compression humerus • If persists greater than 3 months, surgical teres minor exploration teres major triceps (long head)
Axillary Nerve Quadrilateral Space Syndrome after the quadrilateral space • Occlusion of posterior humeral circumflex • Posterior division– teres minor, posterior artery (and axillary nerve) deltoid and terminates superior lateral • occurs with arm in abduction, extension, cutaneous nerve and external rotation • shoulder pain and distal paresthesias, worse with overhead activity • Anterior division– middle and anterior • MRI: atrophy of the teres minor deltoid • Arteriogram, Doppler studies • EMG • Average 6cm lateral edge of acromion • surgery (can be as little 3.1cm)
Axillary Nerve Injury Axillary Nerve Injury • Weakness of abduction • Fracture (greater tuberosity) • Weakness in external rotation (teres minor) • Atrophy • Dislocations (5-33%) • Anesthesia over lateral shoulder not reliable • EMG • Iatrogenic
• Blunt trauma
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Suprascapular Nerve Axillary Nerve Injury: Treatment Entrapment • Conservative if not transection (can wait 6- • Motor and sensory nerve 12 months) • Upper trunk • Nerve grafting • Dull aching pain in post lateral aspect • Tendon transfers (latissimus, trapezius) • Sports, weight lifting, volleyball, baseball • Masses, ganglion • Iatrogenic, mobilizing large rotator cuff tears
Suprascapular Suprascapular Nerve Palsy: Etiology Nerve Palsy: Anatomy • Trauma • Suprascapular notch • Iatrogenic – suprascapular • Activity (volleyball, ligament or shoulder stretching at joint cyst -> paralysis spinoglenoid notch) of supraspinatus and infraspinatus • Mass effect (ganglion) • Spinoglenoid notch palsy of infraspinatus
Suprascapular Nerve Injury: Suprascapular Nerve Injury: Treatment Clinical Findings • Pain and weakness (RC) • Conservative • Dull aching pain in post lateral aspect • If no improvement in 2 months consider • More common in males decompression • Worse with arm elevation and exercise • Good results with early decompression • Depending on site either supra/infra vs • Need to know where compression is and infraspinatus decompress there • Atrophy (infraspinatus more superficial) • Diagnosis of exclusion • EMG
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References
• J Hand Surg Am. 2009 Dec;34(10):1906-14. Unusual compression neuropathies of the forearm, part I: radial nerve. Dang AC1, Rodner CM.
• J Am Acad Orthop Surg. 1998 Nov-Dec;6(6):378-86. Uncommon nerve compression syndromes of the upper extremity. Lubahn JD1, Cermak MB. THANK YOU • J Am Acad Orthop Surg. 2009 Nov;17(11):665-76. Review. Suprascapular neuropathy. 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
CLINIC PATIENT #1
HPI: 51 year old LHD female incurs a 2 cm laceration to the right index finger. Nerve Tumors The laceration is repaired in the ED. The patient notices loss of sensation in the radial digital nerve distribution of the index finger. Weeks later she notices Gina Farias-Eisner, MD severe electrical pain with pinch. No vested interests, No FDA off-label uses presented
Talk originally prepared by Kodi K. Azari, MD, FACS and Roy A. Meals, MD 360
CLINIC PATIENT #1 CASE #1: NEUROMA
HPI: 51 year old LHD female incurs a 2 cm laceration to the right index finger. The laceration is repaired in the ED. The patient notices loss of sensation in the radial digital nerve distribution of the index finger. Weeks later she notices severe electrical pain with pinch.
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A group of regenerating nerve fibers which fail What is a neuroma? to reach distal targets or end organs.
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Pathophysiology Physical Exam
• Wallerian degeneration after injury • The growing point of regenerating axons can produce paresthesias when tapped • Sprouts emerge from proximal stump of the axon to find the • Tinel sign distal end
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Treatment CLINIC PATIENT #2
• Surgical Exploration HPI: 42 year old RHD male presents with a painless mass along the flexor • Serial section until healthy fascicles surface of his right small finger that has been growing increasingly larger over • Primary repair the past year. On exam, the lesion is mobile transversely but not longitudinally.
• Nerve grafting
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CLINIC PATIENT #2 CASE #2: Schwannoma
HPI: 42 year old RHD male presents with a painless mass along the flexor surface of his right small finger that has been growing increasingly larger over the past year. On exam, the lesion is mobile transversely but not longitudinally.
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• Most common benign nerve tumor of the UE
What is a Schwannoma? • Arises from Schwann cells
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Treatment CLINIC PATIENT #3
• May be “shelled out” microsurgically HPI: 20 year old RHD female presents with multiple painful subcutaneous masses located on the volar and dorsal aspect of the right hand and forearm. On • Very rare reports of malignant transformation exam, the lesions were varying in size, firm, and tender. The patient had faint café au lait macules and freckling in the axillary region.
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CLINIC PATIENT #3 CASE #3: Neurofibroma
HPI: 20 year old RHD female presents with multiple painful subcutaneous masses located on the volar and dorsal aspect of the right hand and forearm. On exam, the lesions were varying in size, firm, and tender. The patient had faint café au lait macules and freckling in the axillary region.
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• Benign nerve tumors that What is a Neurofibroma? arise within nerve fasciculi
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Physical Exam Treatment
• Solitary lesions may be seen • Multiple neurofibromas common in Excision likely to require segmental nerve Neurofibromatosis (Von Recklinghausen’s resection and reconstruction disease) • Median Nerve • Café au lait macule • Axillary freckling • Ulnar Nerve • Lisch Nodules
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CLINIC PATIENT #4 CLINIC PATIENT #4
HPI: 22 year old RHD male presents with gradually enlarging nontender lesion HPI: 22 year old RHD male presents with gradually enlarging nontender lesion and complaints of numbness and tingling along the median nerve distribution of of the distal forearm and complaints of numbness and tingling along the median the thumb, index and middle fingers nerve distribution of the thumb, index and middle fingers
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CASE #4: Lipofibromatous Hamartoma
What is a Lipofibromatous Hamartoma ?
Treatment
• Fibro fatty • Simple decompression infiltration of nerve • Interfascicular resection is not possible and contraindicated • Part of DDx in child • Can have gradual deterioration of with CTS nerve function
• Resection and nerve grafting
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CLINIC PATIENT #5 CLINIC PATIENT #5
HPI: 45 year old RHD female presents with painful subungal nodule of the left HPI: 45 year old RHD female presents with painful subungal nodule of the left middle finger. The patient complains of cold hypersensitivity, intermittent middle finger. The patient complains of cold hypersensitivity, intermittent severe pain, point tenderness. severe pain, point tenderness.
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CASE #5: Glomus Tumor
What is a Glomus Tumor?
Imaging
• A rare benign neoplasm • MRI • High signal intensity oval • Arising from shaped lesion neuromyoarterial apparatus • Plain Film • Scalloped osteolytic defect
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Treatment
• Surgical Excision Thank You!
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References
• Watson J et al. Neuroma of the hand and upper extremity. J Hand Surg Am. 2010 Mar;35(3):499-510.
• Netscher DT et al. Subungual glomus tumor. J Hand Surg Am. 2012 Apr;37(4):821-3;quiz 824.
• 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
• Wolfe, S. Hotchkiss, R. Pederson, W. Kozin,S. (2011) Green’s Operative Hand Surgery 6th Edition. Numbness Philadelphia: Elsevier/Churchill Livingstone.
Mark Morris, MD 395 Hand Surgery Fellow, USC
Talk originally prepared by Joshua Bales, MD
Overview Numbness AKA Peripheral Neuropathy
• Anatomy review • At any time 2-4% population affected • Definitions • Most common cause in USA is DM • Sensory testing • Hanson’s disease (Leprosy) is most • Patterns of sensory loss common in Southeast Asia • Mononeuropathy, radiculopathy, • Must determine polyneuropathy – Distribution • Common and uncommon causes of – Symptoms numbness – Duration – Course • Summary
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Definitions Definitions cont
Ability to Sensitivity to • Hyperpathia, hyperesthesia, and allodynia perceive stimuli stimuli all refer to increased sensitivity to sensory Hypesthesia Diminished Intact stimuli • In peripheral neuropathies, patients can Anesthesia Absent Intact vacillate between periods of hyperesthesia and hypesthesia – Don’t be fooled Hypalgesia Intact Diminished
Analgesia Intact No sensitivity
Sensory Exam Sensory Exam
• Peripheral Nerve • Dermatome like Distribution distribution
Sensory exam Sensory exam
• Complete spinal • Instead, a brain cord injury, stem injury could appears easy to have this pattern diagnose; of paresthesia however this • Whereas a central cord presentation is syndrome would rare present with this pattern
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Sensory exam Sensory testing
• Common in axonal • Follow the patterns neuropathies – Confined to distal aspect present in a of limb stocking glove – Confined to discrete area distribution of a limb – Feet affected – Confined to the whole first! limb, side of body – Involves reflexes – Involves cognitive deficits
Clinical Pearls Axonal Neuropathies
• Distribution of peripheral nerve; think of • Diabetes mellitus • Syphilis that nerve – Carpal tunnel, median nerve • Alcohol • Vasculitis • Vitamin B12 deficiency • Distribution of a dermatome; think of the • Amyloidosis corresponding nerve root – C5 • HIV • Multiple sclerosis radiculopathy • Lyme Disease • Idiopathic • Stocking-glove sensory loss; think axonal • Uremia neuropathies - diabetes • Chemotherapy • Paraneoplastic • Leprosy neuropathy
Diabetes Diabetic Neuropathy • Neuropathy secondary to microvascular injury to the vasa • Clinical manifestations nervorum which supplies the – Numbness nerves Mitchell adapted from – Hypalgesia www.CDNPA.com • Occurs in 20% of DM patients – Diarrhea – Erectile dysfunction • Implicated in 50-75% of – Dizziness nontraumatic amputations – Vision changes • Durations of DM, tobacco use, age, HTN and hyperlipidemia are also risk factors
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Diabetic Neuropathy Diabetic Neuropathy • In both diabetes and syphilis, patients may • Pearls to spot DM present with a Neuropathic or Charcot joint – Classic Triad • Due to the insensate nature of the joint, it • Polyuria, polydipsia, polyphagia gradually degenerates and deforms • Increased urination, drinking, and eating • This is uncommon in nonweightbearing joints – Acanthosis nigricans – Loss of proprioception – Stocking glove distribution – Ketone (Fruity/Alcoholic) odor in breath
Alcoholic Neuropathy Alcohol
• Characterized as gradually • 32% of heavy users have progressive affecting peripheral neuropathy sensory, motor, and • Confounded by nutritional autonomic nerves. deficiency, as well as being • Starts symmetrically and distally (feet first) a risk factor for compression neuropathies • Associated with loss of reflexes • Associated with “Saturday – Loss of ankle jerk first night palsies”
HIV Neuropathy Alcohol Neuropathy Treatment • Hypothesized to be secondary to dorsal root ganglion damage by the virus • Stop drinking • Thiamine • Occurs in 30% of HIV/AIDS pts supplementation • Normally occurs in the feet • Better nutrition • Complete recovery is HIV Death uncommon Viral • Some medications can Load help with burning Neuropathy dysesthesias Infection Weeks Years
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HIV Neuropathy Multiple Sclerosis
• Main complaints • Idiopathic CNS inflammatory disease – Bizarre burning • Demyelination and axonal degeneration – Hyperalgesia • Young adults – Allodynia • 2 Women: 1 Man • Risk factors • MRI diagnostic for lesion – DM • Differential includes spinal cord – Nutritional deficiencies compression, vitamin deficiency, infection – HIV Medications • Clinical and radiographic lesions separated in time and space
Multiple Sclerosis Multiple Sclerosis • Where is the neuropathy? MS is a constellation of symptoms; -Depression -Fatigue -Numbness/pain Schwann cell Photomicrograph of -Urinary problems gradient -Nystagmus Of healthy and -Red color perception diseased myelin -All of which wax and wane
Multiple Sclerosis Syphilis • “Great imitator” • First outbreak in 1494 – French besieging Naples Moderate • Primary syphilis Probable High Risk – Skin lesion 21 days High after exposure – Risk Risk chancre – Caused by Treponema Low pallidum (bacteria) Risk
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Secondary Syphilis Tertiary Syphilis
• Secondary syphilis • Occurs 1-10 years after initial – 6-8 weeks after infection exposure • Changes in personality – Rash in palms • Tabes dorsalis and hands – Dorsal column disease causing – Most contagious a shuffling gait • Neuropathic/Charcot joint disease – Loss of proprioception
Lyme Disease Lyme Disease
• Emerging infectious • Incubation period 1-2 disease caused by tick weeks bites – 1% of bites • Initial erythema • Bacterial infection easily chronicum migrans treated by antibiotics • Then, headache, fever, • When untreated can malaise cause a variety of joint, • Late persistent infection heart, and nervous system after months - disease polyneuropathy
Lyme Disease Chemotherapy Neuropathy • Polyneuropathy symptoms include –Numbness • Chemotherapeutic Culprits –Shooting pain – Methotrexate (encephalopathy) –Difficulty with • Rheumatoid Arthritis concentration – Taxanes, ie Paclitaxel or Taxol (burning –Depression paresthesias and loss of reflexes) –Bell’s palsy • Breast Cancer
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Chemotherapy Hansen’s Disease (Leprosy)
– Vincristine (both motor/sensory fibers, • Leprosy – Greek for scales virtually all patients) on a fish • Leukemias • Caused by Mycobacterium – Propylthiouracil (dose dependent) leprae • Thyroid disease • Granulomas of the nerves, respiratory tract, skin, and – Thalidomide (75% get sensory eyes neuropathy but reversible with dosage • Since 600 BC adjustment) • Still leper colonies today • Myeloma, Ovarian • Not actually highly contagious
Hansen’s Disease Summary • Incubates either for weeks or as long as 30 • A numb finger is not always carpal tunnel years (average 3-5 years) • Review the distribution of altered sensation • Affects 3 million/year (30% get neuropathy) with patient • Loss of sensation —> repeated injuries, infection due to unnoticed wounds —> loss of • What are the other symptoms body parts/deformity • Look at the big picture • Affects Schwann cell – Past medical history, travel history, – Causes inflammation/edema – Yet scientists do not understand how habits, diet of patient unmyelinated fibers are affected Be a patient advocate, early diagnosis is always key
References References
• England et al. Peripheral Neuropathy. • Calabresi, PA. Diagnosis and Management Lancet 2004: 363:2151-61 of Multiple Sclerosis. Am Fam Physician. • Robinson, LR. Role of Neurophysiologic 2004 Nov 15;70(10):1935-44 Evaluation in Diagnosis. JAAOS. 2000 • Gonzalez-Duarte A, Cikurel K, Simpson DM. May;8(3): 190-199 Managing HIV peripheral neuropathy. • Veves et al. Painful diabetic neuropathy: Current HIV/AIDS reports 2007 4 (3): 114–8 epidemiology, natural history, early diagnosis, and treatment options. Pain • Scollard DM. The biology of nerve injury in Med. 2008 Sept;9(6):660-74 leprosy. Lepr Rev. 2008 Setp;79(3)242-53
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References
• Hu LT. Lyme disease. Ann Intern Med. 2016; 164(9): ITC65-ITC80. • Ontaneda D, Thompson AJ, Fox RJ, Cohen JA. 11 Weakness/Spasticity Progressive multiple sclerosis: prospects for disease therapy, repair, and restoration of function. Lancet 2017; 389(10076): 1357-1366. Roy A. Meals, MD • Vinik AI, Nevoret ML, Caselini C, Parson H. Diabetic Neuropathy. Endocrinol Metab North Am 2013; 42(4): 747-787. no conflicts, no off-label FDA treatments • White C, Franco-Paredes C. Leprosy in the 21st century. Clin Microbiol Rev. 2015; 28(1): 80-94.
Talk originally prepared by Lucie Krenek MD
Stroke Stroke – Treatment • Goal - hygiene, pain, function • Leading cause of hemiplegia in adults • Acute • Most recovery in first 6 months – Prevention of contractures • Functional recovery can continue – Brachial plexus and phenol nerve blocks • Upper extremity < lower extremity recovery – Botulinum (Botox) • Flaccid paralysis immediately • Chronic treatment of contracture • Spasticity over several weeks – Antispasmodic medication • Associated perceptual/cognitive/visual losses – Surgery +/- after 6 months
Stroke - Shoulder Adduction/IR Contracture Stroke - Elbow • Spastic subscapularis, pectoralis major, • Flexion contracture latissimus dorsi, teres major – Biceps, brachialis, brachioradialis • Release pectoralis major and subscapularis, spasticity or all in nonfunctional extremity – Release some or all elbow flexors • Pain depending on severity – Complex regional pain syndrome – Severe contracture may require serial – Spasticity postoperative casting – Inferior subluxation
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Stroke - Forearm Stroke – Wrist and Fingers
• Pronation contracture • Flexion contractures – Pronator teres spasticity • FCR, FCU, PL spasticity – Proximal pronator teres advancement – With functional hand – cut PL, lentehen FCU and FCR – Tendon lengthening in nonfunctional – Nonfuctional hand – lengthen/cut long upper extremity digital flexors
Stroke - Thumb Stroke - Weakness
• Thumb-in-palm deformity • Wrist extension – Adductor pollicis/first dorsal – FCU transfer to ECRB interosseous/thenar spasticity • Intrinsic muscle imbalance/spasticity – Release muscle origins – Intrinsic plus deformity can occur if only hand extrinsics are lengthened
CMT • Most common hereditary neuromuscular disorder Charcot-Marie-Tooth (CMT) Disease • Usually autosomal dominant • Chronic distal sensory and motor neuropathy aka • Symmetric involvement Peroneal Muscular Atrophy • Parasthesias and cramps Hereditary Motor-Sensory Neuropathy • Onset: late childhood or adolescence • Normal life expectancy • Different types, affecting either axon or myelin
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CMT – Symptoms CMT – Symptoms • Lower extremity – begins first – gait problems • Upper extremity – Distal weakness legs and feet – Involvement milder than lower extremity – Inability to heel walk – Rarely extends above elbow – Foot drop, ankle instability – Pes cavus deformity, hammer toes – Atrophy of hand and forearm muscles – Reduction in distal tendon reflexes – Intrinsic-minus hand deformity – Difficulty with fine motor function and strength
Wikimedia
CMT – Treatment CMT – Treatment • Intrinsic minus hand most debilitating – MP extension block splint • Stabilization of ankles with orthoses, – Volar MP joint capsulodesis tendon transfers, fusion – Surgical – FDSR -> proximal phalanges • Moderate aerobic exercise • Muscle stretching/strengthening • Excessive weight training not recommended
Amyotrophic Lateral Sclerosis Amyotrophic Lateral Sclerosis
Lou Gherig’s Disease • Loss of upper and lower motor neurons • No sensory or autonomic involvement • Prevalence 3-5 per 100,000 • Etiology unknown – Increased risk - pesticides, smoking, military, familial
Lou Gherig Steven Hawking
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Guillain-Barre Syndrome (GBS) ALS – Treatment • Acute autoimmune polyradiculopathy • Controversy regarding exercise • Demyelination of peripheral nerves • Strengthening and moderate endurance • Recovery occurs with remyelination exercise may result in better function • Little can be done to improve quality of • 70% preceded by acute infection life, fatigue, or muscle strength – usually respiratory or gastrointestinal • Ventilatory support when respiratory – Flu shot/other vaccines muscles become affected • Plateau by 4 weeks •
GBS - Symptoms GBS – Treatment
• Rapid onset ascending motor paralysis • Acute phase • May have sensory/autonomic symptoms – Gentle strengthening • Generalized muscle weakness in lower – Maintenance of range of motion extremities, progresses to upper extremities • Back, shoulder and neck pain – Prevention of contractures • Later: muscle atrophy, and potential for • Medical treatment crucial - IV contractures due to lack of motion immunoglobulin • Severity of weakness highly variable
GBS - Treatment GBS - Prognosis
• Recovery phase • Most patients need hospitalization – Retraining necessary for many daily • Up to 30% require ventilatory support activities, ie grooming, gait • <5% mortality, usually due to pulmonary – Muscle strengthening complications • 85% achieve full recovery by 1 year – Supervised exercise programs help overcome fatigue and improve • Poorer prognosis for older patients, late treatment, severe attacks function
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Acute Flaccid Myositis (AFM) Acute Flaccid Myositis (AFM)
• On CDC’s radar since 2014 10 patients: • Sudden arm/leg weakness 4-35 day hospitalization – May also affect eye/face/throat/sphincters one on ventilator • Mostly affects young children no deaths • Incidence 1-2/million 7 received OT/PT (4 inpt, 3 outpt) • Cause: viral? 90% preceded by mild 6-12 weeks later: 5/9 normal, 3/9 residual respiratory illness/fever weakness, 1/9 ambulation with assistance – Not polio Free full text Morb Mortal Wkly Rep. 2017 Aug 11; 66(31): 826–829.
References References • Adams and Victor’s Neurology, AH Ropper, RH • Hussey AJ, O’Brien CP, Regan PJ. Parsonage Brown. 8th Edition Turner Syndrome – Case Report and Literature • Current Orthopedics, AE Keenan, S Mehta Review. Hand. 2007;2:218-221. • Pitetti KH, Barrett PJ, Abbas D. Endurance • Dillin L, Hoaglund FT, Scheck M. Brachial exercise training in Guillan-Barre syndrome. Neuritis. J Bone Joint Surg Am. 1985 Arch Phys Med Rehabil. 1993; 74: 761-765. Jul;67(6):878-80 • Tuckey J, Greenwood R. Rehabilitation after • Harrison’s Principles of Internal Medicine, 17th severe Guillain-Barre syndrome: the use of partial body weight support. Physiother Res Int. Edition. Fauci AS et al, eds. 2004;9(2):96-103. • Hughes RA, et al. Supportive care for patients • Tafti MA, Cramer SC, Gupta R. Orthopedic with Guillain-Barre syndrome. Arch Neurol. Management of the Upper Extremity of Stroke 2005 Aug;62(8):1194-8. Patients. J Am Acad Orthop Surg. 2008;16:462- 470.
Supplementary Material • http://www.ninds.nih.gov/disorders/char Polio cot_marie_tooth/detail_charcot_marie_t • Lower motor neuron lesion ooth.htm • Decreased reflexes and muscle wasting • http://www.who.int/mediacentre/factshe ets/fs114/en/index.html • Proximal muscles affected • Increase in Acute Flaccid Myelitis - • Sensory loss rare United States, 2018. Morb Mortal Wkly • Viral infectious disease Rep. 2018 Nov 16;67(45):1273-1275 • Fecal-oral transmission • Usually infects children under 5 years
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Polio Polio • Rare in developed countries • In acute phase, all anterior horn cells • Afghanistan, Nigeria, Pakistan, India affected • Less than 2000 cases per year • In subacute phase, the approximately 50% of anterior horn cells that survived begin to • 95% of infected patients asymptomatic recover • 0.5% irreversible paralysis, usually legs • After 16-24 months, extent of damage can • Of those with paralysis, 5-10% die due to be seen, and rehabilitation begins involvement of respiratory muscles
Post Polio Syndrome Polio – Treatment • Acute • Muscle pain, severe fatigue, cramping, fasciculations – Range of motion/splinting • Occurs years after acute illness • Subacute • Overuse of muscles that were originally – Prevent deformity and preserve function affected – Splinting/bracing to maintain joint position • Slowly progressive weakness in already and supplement function weak muscles • Residual stage • Treatment - limited exercise with frequent – Surgical intervention if needed rest
Upper Extremity Nerves, Reinforcement Quiz Reinforcement Quiz 1. The cell bodies of peripheral sensory nerves Caution: The order are in the of the questions and A. anterior horn of spinal cord the order of the answer possibilities B. dorsal root ganglia on website will be C. white matter of brain different than seen 4. A successful nerve transfer requires D. gray matter of brain here. So remember A. a healthy proximal donor nerve and a palsied distal recipient nerve E. white matter of spinal cord the right answers, B. a distal palsied donor and a healthy recipient nerve not that the answer C. complete absence of donor muscles for tendon transfers 2. What is the correct relationship of nerve injury severity? to question 16 here D. more rehab than comparable tendon transfers A. axonotmesis > neuropraxia > neurogenesis is F, for example. E. more post-op immobilization than comparable tendon transfers B. neurotmesis > axonotmesis > neuropraxia C. neuropraxia > neurotmesis > axonotmesis D. sensory > motor > autonomic 5. The Roos “stick up test” for thoracic outlet syndrome consists of E. men > women > children A. shoulder abduction and internal rotation B. turning head away from the side being tested 3. In a patient with recent onset of mild carpal tunnel syndrome symptoms C. externally rotating and abducting shoulder 180 degrees A. two-point discrimination will be altered D. checking for radial pulse with patient seated B. monofilament testing may be normal E. shoulder abduction to 90 degrees and external rotation C. thenar muscle wasting will precede monofilament changes D. Meissner corpuscles will be atrophic E. loss of vibratory sensation to 256 cycles/second will be present
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Reinforcement Quiz Reinforcement Quiz
6. Which diagnostic test for carpal tunnel syndrome has the highest sensitivity and specificity? 9. A nerve sheath tumor (Schwannoma) in a digital nerve A. Phalen test A. will move more medially laterally than proximally distally B. Tinel test B. will move more proximally distally than medially laterally C. Adson maneuver C. is far less common than a neurofibroma D. median nerve compression test D. will cause sensory loss if excised E. Allen test E. will cause motor loss if excised
7. In cubital tunnel syndrome, why do sensory changes and intrinsic wasting occur 10. Neuropathy occurs in what percent of patients with diabetes? before forearm muscle weakness? A. 1 A. some nerve fibers have more myelin covering B. 5 B. the intrinsic muscles are smaller than the flexor carpi ulnaris C. 20 C. the sensory and motor fibers to hand are superficial in the ulnar nerve at the elbow D. 50 D. the sensory and motor fibers to hand are superficial in the ulnar nerve at the wrist E. 95 E. the fibers affected early originate solely from the C8 nerve root
11. “Upper motor neuron” disorders include conditions such as 8. Which nerve is most likely to be injured with a humeral shaft fracture? A. stroke, spinal cord injury A. median nerve B. brachial plexus palsy B. ulnar nerve C. suprascapular nerve C. Parsonage-Turner syndrome D. radial nerve D. Shingles E. medial pectoral nerve E. proximal median nerve lacerations
Reinforcement Quiz
12. Chronic regional pain syndrome is A. Usually preceded by a viral infection B. Managed best by the patient’s personal physician How to obtain continuing education credit for today’s course C. Probably a spectrum of disorders D. Fully responsive to stellate ganglion blocks All registrants E. Relieved by tight serial casting Complete the quiz at www.ddhands.com You will be able to access your certificate
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PTs Apply for CE credit individually through your state board/association They will want Course Objectives and Schedule (available at www.ddhands.com) CVs of Dr. Meals and your local host (available on line) Copy of your certificate
DD Current Science for Hand Therapists August 2-4, 2019 Learn from the 22 On-line Self-Study Programs University of Denver Denver, Colorado
72 hours of CE credit available: Update your understanding of the science that underpins hand therapy Anatomy Clinical Conditions • Learn hands-on in a resort setting Journal Article Reviews • Earn 20 continuing education hours Books • Enjoy the area during long afternoon breaks
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2020 Details on all courses and self-study programs are at Saturdays in Multiple Cities www.doctorsdemystify.com MUSCLES and TENDONS Satisfaction guaranteed or your money back.
anatomy, physiology/healing, biomechanics, Thanks for participating. injury/repair/rehab/tenolysis, inflammation Please pick up around you.
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