PowerPoint Presentation - doctorsdemystify.com · 3/5/2019 1 • Excellence in Education • for...

3/5/2019

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• Excellence in Education

• for OTs and PTs

• Since 1990

• www.ddhands.com

LEARNING OBJECTIVES

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.

METHODS

1. 14 lectures2. Two question and answer sessions3. Networking4. Some repetition between talks

a. Bad news: unavoidable because of multiple speakers

b. Good news: repetition is a good learning tool

Questions during the Discussion Sessions: ▪ Write them on note cards as you think of them

Practical Matters:▪ Can everybody see? Hear?▪ Room temperature?▪ Cell phones, beepers▪ Auditorium’s policy on food/beverage▪ Restrooms▪ Evaluation forms and certificates▪ Ready, set, go…

John Elfar Penn State Hershey,

Center for Orthopaedic Research and Translational Science

Department of Orthopaedics and Rehabilitation

Special thanks to: Robert S. Staron, Ph.D.

Summer Anatomy Immersion, Ohio University

Organization of the Upper Limb

• Some anatomy

• Some topology

• Some embryology

• Goal is a framework for understanding anatomy in function.

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Grant’s Atlas of Anatomy 8th edGray’s Anatomy 37th ed Grant’s Atlas of Anatomy 8th edGrant’s Atlas 8th ed

Antr division:

flexor comp.

Postr division:

ext comp.

Netter’s Atlas of Human Embryology 2002

Wikipedia open license (accessed 2019)

Grant’s Dissector 13th edAnterior

musculocutaneous n.

Humerus

radial n.

UlnaRadius

median n. & ulnar n.

radial n.(including ECRL &

brachioradialis mm.)

5th metacarpal

ulnar n. & median n.

Anterior

Anterior

Posterior

Posterior

Posterior(including a portion

of the brachialis m.)

Muscle

Compartments

of the Upper

Limb

Origin of Limb

Muscles

Dorsal muscle mass forms

extensors and supinators in

upper limb, extensors and

abductors in lower limb.

Ventral muscle mass forms

flexors and pronators in

upper limb and flexors and

adductors in lower limb.

Morphogenesis guided by CT,

not myoblasts

Split into individual muscles,

cell death involved

Carlson l999 Human Embryology Larsen 1993

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Hollinshead’s Textbook of Anatomy 5th ed Grant’s Dissector 13th ed

21.

Rohen/Yokochi Color Atlas of Anatomy 2nd ed

Brachial Plexus

Netter’s Atlas 2nd ed

Grant’s Atlas of Anatomy 8th ed

hand – forearm – arm – shoulder

distal proximal

1) trapezius m.

2) latissimus dorsi m.

3) levator scapulae m.

4) rhomboideus major m.

5) rhomboideus minor m.

6) serratus anterior m.

1) infraspinatus m.

2) supraspinatus m.

3) subscapularis m.

4) teres minor m.

5) teres major m.

6) deltoid m.

Extrinsic shoulder mm. Intrinsic shoulder mm.

Anterior thorax mm.1) pectoralis major and minor mm.2) subclavius m.

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1) trapezius m. (spinal accessory n. - CN XI + C3 & C4)

2) latissimus dorsi m. (thoracodorsal n. - C6, C7, C8)

3) levator scapulae m. (C3 & C4 + dorsal scapular n. - C5)

4) rhomboideus major m. (dorsal scapular n. - C5)

5) rhomboideus minor m. (dorsal scapular n. - C5)

6) serratus anterior m. (long thoracic n. - C5, C6, C7)

Extrinsic shoulder mm.

Anterior thorax mm.

1) pectoralis major ( C5-T1) & minor (C6-C8) mm. 2) subclavius m. (n. to subclavius m. - C5, C6)

med/lat

pect nn.

Grant’s Atlas of Anatomy 8th edGra

nt’s

Atl

as 8

thed

Netter’s Atlas of Human Anatomy 2nd ed


1) infraspinatus m. (suprascapular n. - C5, C6)

2) supraspinatus m. (suprascapular n. - C5, C6)

3) subscapularis m. (upper + lower subscapular nn. - C5, C6)

4) teres minor m. (axillary n. - C5, C6)

5) teres major m. (lower subscapular n. - C5, C6)

6) deltoid m. (axillary n. - C5, C6)

Intrinsic shoulder mm.

Grant’s Atlas of Anatomy 8th edGra

nt’s

Atl

as 8

thed

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rotator cuff musculature



musculocutaneous n.

Humerus

radial n.

UlnaRadius




5th metacarpal


Anterior

Anterior

Posterior

Posterior



Muscle

Compartments

of the Upper

Limb - arm

Grant’s Dissector 13th ed

brachium

biceps brachii m.

long head

short head

brachialis m.

coracobrachialis m.

triceps brachii m.

lateral head

medial head

long head

anconeus m.

antr compartment postr compartment

musculocutaneous n.

(C5-C7)


biceps brachii m. (C5, C6)

brachialis m. (C5, C6)

coracobrachialis m. (C5-C7)

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axillary n. (C5-C6)

radial n. (C5-T1)


deltoid m. (C5, C6)

teres minor m. (C5, C6)

triceps brachii m. (C6-C8)

anconeus m. (C7, C8)

(brachialis m. C5, C6)



musculocutaneous n.

Humerus

radial n.

UlnaRadius




5th metacarpal


Anterior

Anterior

Posterior

Posterior



Muscle

Compartments

of the Upper

Limb - forearm


musculocutaneous n.

Humerus

radial n.

UlnaRadius




5th metacarpal


Anterior

Anterior

Posterior

Posterior



Muscle

Compartments

of the Upper

Limb - forearm

(FCU & ulnar ½

FDP)


antebrachium

pronator teres m.

flex. carpi radialis m.

palmaris longus m.

flex. carpi ulnaris m.

flex. digit. superf. m.

flex. digit. profund. m.

flex. pollicis longus m.

pronator quadratus m.

brachioradialis m.

ext. carpi radialis longus m.

ext. carpi radialis brevis m.

ext. carpi ulnaris m.

extensor digitorum m.

extensor digiti minimi m.

extensor indicis m.

abd pollicis longus m.

ext. pollicis longus/brevis m.

supinator m.

antr compartment postr compartment

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antebrachium

pronator teres m. (C6, C7)

flex. carpi radialis m. (C6, C7)

palmaris longus m. (C7, C8)

flex. carpi ulnaris m. (C7, C8)

flex. digit. superf. m. (C7, C8, T1)

flex. digit. profund. m. (C7, C8, T1)

flex. pollicis longus m. (C8, T1)

pronator quadratus m. (C8, T1)

antr compartment (median & ulnar nn.)

ulnar n. (C7-T1)


flex carpi ulnaris m.

medial ½ FDP

+ 14 intrinsic handmuscles

median n. (C5-T1)


PT, FCR, PL,

FDS, lat ½ FDP,

FPL, PQ

+ 5 intrinsic handmuscles

antebrachium

brachioradialis m. (C5, C6)

ext. carpi radialis longus m. (C6, C7)

ext. carpi radialis brevis m. (C6, C7 or C7, C8)

ext. carpi ulnaris m. (C7, C8)

extensor digitorum m. (C7, C8)

extensor digiti minimi m. (C7, C8)

extensor indicis m. (C7, C8)

abd pollicis longus m. (C7, C8)

ext. pollicis longus/brevis m. (C7, C8)

supinator m. (C5, C6)

postr compartment (radial n. C5-T1)

radial n. (C5-T1)


triceps brachii m.,

anconeus m.

(brachialis m.)

BR, ECRL, ECRB,

ED, EDM,

supinator, ECU,

EI, AbdPL, EPL,

EPB

Grant’s Atlas of Anatomy 11th ed

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musculocutaneous n.

Humerus

radial n.

UlnaRadius




5th metacarpal


Anterior

Anterior

Posterior

Posterior



Muscle

Compartments

of the Upper

Limb - hand

(FCU & ulnar ½

FDP)


musculocutaneous n.

Humerus

radial n.

UlnaRadius




5th metacarpal


Anterior

Anterior

Posterior

Posterior



Muscle

Compartments

of the Upper

Limb - hand

(FCU & ulnar ½

FDP)

(thenar mm. & 1st,

2nd lumbricals)

intrinsic hand muscles (C8, T1)

7 interosseii mm. (4 dorsal/3 palmar)

4 lumbrical mm. (1, 2, 3, 4)

palmaris brevis m.

adductor pollicis m.

three thenar mm. (OP, abd.PB, FPB)

three hypothenar mm. (ODM, abd.DM, FDMB)

intrinsic hand muscles (median & ulnar nn.)

7 interosseii mm. (4 dorsal/3 palmar)

4 lumbrical mm. (1, 2, 3, 4)

palmaris brevis m.

adductor pollicis m.

three thenar mm. (OP, abd.PB, FPB)

three hypothenar mm. (ODM, abd.DM, FDMB)

upper limb -

cutaneous innervation


upper limb –

dermatome pattern


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Anatomy is a Journey

The quicker you embark the more of the journey you will appreciate.

It is not only about memorizing what inserts where and which nerve innervates which muscle.

We think not only of what exists, but what could exist.

What could be re-routed to serve another function?

Which surgeries are rational? And which surgeries are ill-advised?

Knowledge of anatomy can give subtle insights into function and possible rehabilitation.

Enjoy your journey.

John Elfar Penn State Hershey,

Center for Orthopaedic Research and Translational Science

Department of Orthopaedics and Rehabilitation

Special thanks to: Adam Martin, MD

UCLA Hand Fellow

Outline

• Microanatomy

• Biology

• Nerve Injuries

– Physiology

– Classification

– Nerve response to injury

Anatomy of Neuron

Cell body

Dendrites

Receive incoming impulses

Axon

Conducts outgoing impulses

Schwann cells, produce

myelin sheath

Courtesy Roadnottaken

Wikimedia

Sensory neuron

Motor neuron

Anatomy of a Peripheral Nerve

1. Axon: basic subunit

Nerve fiber = axon + Schwann cell + myelin

2. Fascicle: groups of axons

3. Peripheral nerve: groups of fascicles

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How Many Fibers?

• Electric lamp cord: ~60 copper strands

• Digital nerve: ~1500 nerve fibers

• Median nerve: ~25,000 nerve fibers

• Brachial plexus: ~145,000 nerve fibers

Connective tissue layers

1. Epineurium

2. Perineurium

3. Endoneurium

Vascular supply

Intrinsic + extrinsic

Mitchell adapted from www.CDNPA.com

Cross-section of peripheral nerve Epineurium

Cushions nerve

Nerve gliding

Perineurium

Surrounds fascicle

Tight junctions

Fascicle

Endoneurium

Surrounds axons

External epineurium

Internal epineurium

Axon + Endoneurium

Fascicle

Nerve Physiology

• Axonal transport– Protein synthesis in cell body

– Distance too long for diffusion

– Products motored along microtubules

• Retrograde transport– Returns waste products for recycling

– Transports growth factors to nucleus

• Implications with injury

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• Mechanical injuries

– Compression

– Traction

– Laceration

– Combination (e.g. gunshot wounds)

• Secondary injury

– Infection

– Scarring

– Fracture callus

– Ischemia

Nerve Injury CausesResponse to Injury

• Limited repertoire of responses to nerve injury

1. Mild injury schwanncells/myelin sheath

– Focal demyelination

2. Severe injury axons

– Axonal degeneration

Nerve Injury Classification

1. Neurapraxia

2. Axonotmesis

3. Neurotmesis

Neurapraxia

• Conduction block• All supporting layers entirely intact• Mild neurapraxia transient ischemia

– Impairs polarization of cell membrane– Unable to conduct action potential

epineurium perineurium endoneurium

axon

Neurapraxia

• More severe injury Demyelination

• Disrupts impulse conduction

• Axons are physically intact, physiologically out


axon

Focal Demyelination

Neurapraxia

Prognosis for recovery excellent

Axons remain intact no axonal degeneration

Mild cases: relief of temporary ischemia

Severe cases: Schwann cells remyelinate damaged

segment

Restores conduction along axon

Symptoms may last moments to months

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Axonotmesis

• Loss of axon continuity

• Connective tissue envelope intact

• Degeneration of injured axons distally


axon

Axonal Injury: Wallerian Degeneration

Axonal transport interrupted

Survival of axonal segments

connected to cell body

Distal segments

Deprived of metabolic support

Degeneration of axons beyond

point of injury

Axonotmesis


axon

• Recovery requires axonal regeneration

• prolonged recovery

• Prognosis for recovery good

• endoneurial tubes are intact -> no miswiring

• Limiting factor is the distance of regeneration required

Neurotmesis

• Complete nerve transection

• Degeneration of all axons distal to injury

• Separation of nerve ends spontaneous recovery will not occur

• Surgical problem


axon

Neurotmesis- End Result

Neuroma

Physiology of Injury

• Laceration Neurotmesis– Smaller zone of injury

• Traction Axonotmesis – Axons most susceptible

– Larger zone of injury

• Acute compression Neurapraxia– Local contusion with 2o circulatory changes

– Inflammation scarring and further compression

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Chronic compression

Ischemia + mechanical

compression

At 30 mm Hg

Decreased intra-neural blood

flow

Axonal transport disrupted

Progressive axonal loss

(axonotmesis) and fibrosis

Damage often permanent

Nerve regeneration

• Wallerian degeneration– Distal axon fragmentation

– Disintegration of myelin

• Macrophage invasion– Clears endoneurial tubes of

debris

• Schwann cell proliferation

• Pathway for later axonal regeneration

Axonal Regeneration

• Proximal effects– Loss of trophic support

– Sometimes neuronal death

– Survivors alter metabolic activity in preparation

• Axonal sprouting – Growth cones

• Samples environment

• Seeks sensory or motor pathways

– Guided by Schwann cells

Axons that find distal

tubules are guided along

(1mm/day)

Sprouts that reach distal

connections mature

Increase in axon and myelin

thickness

Sprouts which fail to make

connections die back

• If gap exists, axonal sprouts migrate aimlessly

• No distal targets are reached

• Neuroma formation

Nerve Regeneration: Molecular Level

• Neurotrophic factors (“fertilizer”)

• Neurotropic factors (“traffic cops”)

• Matrix substrates

• Metabolic factors for nourishment

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Neurotrophic Factors

Promote survival and maintenance of neuron

Axonal injury disruption of retrograde supply

of growth factors

Schwann cells provide trophic support

Proteins presented along regenerating pathway

Picked up by axonal sprouts to sustain neuron

Examples

Nerve Growth Factor sensory neurons

Brain-derived neurotrophic factor motor

Neurotropic factors

• Promote extension and branching of axonal sprouts

• Attract sprouting axons toward distal nerve segment

• 2 mechanisms: contact-guidance versus attraction at a distance

– Laminin and fibronectin: matrix-bound glycoproteins

– Soluble mediators

• Anti-neurotropic factors – negative or repulsive guidance cues deflect axons

from inappropriate targets

Adapted from Carmeliet P, Nature Reviews Genetics 4:2003

Neurotropic factors Topographic Specificity

• Accuracy with which regenerating axons re-innervate appropriate targets

– Dramatically affects outcomes after nerve injury

• Axonotmesis >> neurotmesis

– Miswiring: axons wander into wrong tubules

Clinical Perspective

• Axons regrow about ~1mm/day (1” / month)

• Motor end plates degrade ~1%/week

• Need > 50% of motor endplates for function

• Maximum distance to restore motor function is

~35 cm

• Sensory end-organs may survive much longer

• Late nerve reconstruction can offer recovery of

protective sensation

Clinical Perspective

• Functional result following nerve injury dependent on numerous factors

1. extent of neuron survival

2. rate and quality of axonal outgrowth

3. topographic specificity of regenerating axons

4. survival of end organs

5. cortical reorganizational

Clinical recovery often incomplete

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References

1. Regal S, Tang P. Surgical management of neuromas in the hand and

wrist. J Am Acad Orthop Surg. 2018 Nov 13

2. Eberlin KR, Treiser M. Anatomy and physiology of the peripheral

nerve. ASSH Surgical Anatomy: Nerve Reconstruction, 2017

3. Dahlin LB. The nerve’s response to injury. ASSH Upper Extremity

Nerve Repair Tips and Techniques: A Master Skills Publication, 2008

Diagnostic Testing for Nerves

Sensory, Motor, Electrical, Imaging

Timothy Shane Johnson, MD

Talk originally prepared by Roy A. Meals, MD

Burning Questions about Sensation

“You claim my nerve is recovering, why do I have pain every time I touch something?”

“So if I have carpal tunnel syndrome, why aren’t my thenar muscles weak?”

“You tell me I am maximally recovered from my nerve laceration, why can’t I feel my electric tooth brush vibrating?”

The Anatomy of Fingertip Skinand

Specialized Sensory End Organs

epi-

derm

isderm

isfa

t

papillary ridges sweat pores sweat duct

& gland

Meissner

corpuscles

Pacinian

corpuscle

Merkel

cell

neurite

complex

digital nerve

C A-Δ

A-β

A-β

Fiber

type

Myelin

sheath?

Size in

microns

Function Meters

per sec

C No 1 Burning

pain

2

A-Δ Yes 2-5 Sticking

& temp

20

A-β Yes 10-15 Light

touch

60

A-α Yes 15-20 Motor 60

Nerve Fiber Types

Important for normal sensation

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Supplied by A-β Fibers Pacinian

corpuscle

Meissner

corpuscle

Merkel cell

neurite cplx

Schematic

# of nerve

fibers/rcptr

1 >1 <1

Recovery

after

laceration

Poor Excellent Fair

?

?? ?

Pacinian

corpuscle

Meissner

corpuscle

Merkel cell

neurite cplx

Stimulus

Response III II III II II I I I I

Adaptation Quick Quick Slow

Response to:

Touch

Constant

Moving

Vibration

Poor

Good

30 cycle

Poor

Good

256 cycle

Good

Poor

No


Supplied by A-beta Fibers

What constitutes normal sensation?

1. A multitude of A-beta fibers present, supplying various types of end organs

2. Each nerve fiber functioning properly

What can go wrong?

1. A multitude of A-beta fibers present, supplying various types of end organs

2. Each nerve fiber functioning properly

•Laceration (physical disruption of axon and entire

sheath = neurotmesis)

•Marked compression/stretch (physical disruption of

axon but continuity of sheath = axonotmesis)

•Compression (physiologic disruption, aka

ischemia = neurapraxia)

When something goes wrong, inquiring minds want to know:

How many nerve fibers are present?

(more is better)

How much energy does it take to stimulate a nerve fiber? (less is better)

Innervation density

Threshold

POP QUIZ!

Matching:

1. Innervation

density test

2. Threshold test

A

B

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Two Point Discrimination(The Innervation Density Test)

How wide do I

have to stretch to

find 2 functioning

nerve fibers?

Maybe if I move

along the finger I

can find 2 fibers

more easily.

I go wide when nerve fibers

are missing, e.g.,

lacerations, severe

compressions

Monofilament Testing(The Threshold Test)

I can’t go wide. I am looking for

a single nerve fiber to stimulate

but I can push only so hard.

If I can’t push hard enough to

make the nerve fire, maybe my

big brother can!

1.65 .01

2.36 .02

2.44 .04

2.83 .08

3.22 .17

3.61 .22

3.84 .45

4.08 .75

4.17 .98

4.31 2.4

Mono

Fila

ment

# Forc

e in

gra

ms

4.56 4.2

4.74 4.6

4.93 5.2

5.07 7.4

5.18 13

5.46 21

5.88 47

6.10 85

6.45 164

6.65 279

Mono

Fila

ment

# Forc

e in

gra

ms

For Your

Reference:

Final Exam: MFT vs. TPD

1. What test is appropriate for testing nerve regeneration after laceration and repair?

2. What test is appropriate for testing sensory loss in early cubital tunnel syndrome?

3. What test is appropriate in severe carpal tunnel syndrome when MFT is markedly abnormal?

1. TPD, 2. MFT, 3. TPD

Inquiring minds want to know:

“You claim my nerve is recovering. Why do I have pain every time I touch something?”

Rephrased: Why is pain the first sensation to

return after nerve repair?

The unsophisticated unmyelinated C fibers grow

back the quickest.


“So if I have carpal tunnel syndrome, why aren’t my thenar muscles weak?”

Rephrased: Why does sensory loss occur before motor loss in carpal tunnel syndrome?

The motor fibers are larger and are more resistant to compression ischemia.

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“You tell me I am maximally recovered from my nerve laceration, why can’t I feel my electric tooth brush is vibrating?”

Rephrased: Why does response to low frequency

vibration return poorly after nerve repair?

Because the Pacinian corpuscles reinnervate

poorly.

Scratch Collapse Testfor Carpal Tunnel and Cubital Tunnel Syndromes

(to be demonstrated during Q/A session)

patient

examiner1

2

See Ref 73

Muscle Testing

Quantitate where possible (Grip and pinch meters)

Compare to opposite side (ideally without examiner in the middle)

For Reference: Muscle Testing

The well-known Medical Research Council 0-5 scale

0 = no function

1 = palpable contraction, no movement

2 = movement with gravity neutralized

3 = movement against gravity

4 = movement against some resistance

5 = normal strength

Muscle Testing, Reconsidered

• McAvoy and Green:

– Cadaver study, elbow flexion

– Only 4% of normal force required to flex against gravity

• MRC Grade 0 1 2 3 4 5

% of normal 0 <4 <4 4 >4 100

95%

Grade 4 represents 95% of potential elbow flexion strength, therefore

includes both weak and strong muscles. Better system needed!

Electromyography (EMG)

Nerve conduction velocity (NCV)

• Tests nerve

Needle electrode exam (NEE)

• Tests muscle

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Nerve Conduction Velocity Parlance

• Affected by the room’s temperature, patient age, anomalous innervation patterns

• Usually with surface electrodes

Stimulating <- distance between -> Recording

• Velocity = distance divided by time

>50 meters/sec for all upper extremity nerves

• Latency (time in milliseconds) substitutes for velocity when distance is uncertain

NCV in Neurapraxia• Ulnar nerve

– 54 meters/sec

– 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)

– Conclusion: carpal tunnel synd

NCV in Axonmetsis and Neurotmesisremains normal for 2-3 days

axon

Needle Electrode Exam Parlance• Normal muscle

– Electrically silent at rest

– Electrical activity proportionate to force

– of active contraction (recruitment)

• Denervated muscle

– Fibrillations and sharp waves at rest begin 2-3 weeks after injury

– No change on active contraction effort

• Reinnervating muscle

– Disorganized recruitment pattern—seen 1-2 months before clinical improvement noted

Magnetic Resonance Neurography: CTS

Aagaard3

flat

Cudlip6

normal

flat

Nerves not seen at all on x-ray or CT scan

Nerves not seen well on conventional MRI

Magnetic Resonance Neurography (MRN): Under development

References

1. Dellon, Evaluation of sensibility and re-education of sensation in the hand. Williams and Wilkins, Baltimore, 1983.

2. MacAvoy, Green: Critical reappraisal of Medical Research Council muscle testing for elbow flexion. J Hand Surg, 2007; 32A:149-153.

3. Aagaard, Maravilla, Kliot: Magnetic resonance imaging of peripheral nerves. Neuroimaging Clinics of North America, 2001; 8:131-146.

4. Yoshikawa et al: Brachial plexus injury. Radiographics, 2006; 26:S133-143

5. Filler et al, MR neurography and muscle MR imaging Neurol Clin 2004, 22:643-682

6. Cudlip et al, Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg 2002, 96:1046-1051

7. Cheng, et al: Scratch collapse test for evaluation of carpal and cutibal tunnel syndrome. J Hand Surg 2008, 33A:1518-1524

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Nerve Lacerations, Repair, Grafting, Transfers, Neurotization

Timothy Shane Johnson, MD

Talk originally prepared by Katherine Au, MD

Seddon Injury Classification

• Neuropraxia

– Temporary paralysis

• Axonotmesis

– Likely recovery

• Neurotmesis

– No recovery without repair

Basic Injury Types

Compression –

“Saturday night palsy”

Traction

Laceration

Mechanism of Injury

• Tidy wounds: knife, glass, surgical

• Untidy wounds:

– Open fracture

– Penetrating missile

• Avulsion

Nerve repair Indications for operative intervention

• Sensorimotor exam + mechanism

• Associated vascular/bony

Failure of nerve recovery

• Worsening of nerve injury

• Persistent pain

• Painful neuroma

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Reasons not to repair

• General condition of the patient

• Skill/availability of operating team and specialized equipment

• Uncertain viability or state of nerve trunks

• Local or systemic sepsis

• Tendon transfer or nerve transfer will give better results

Early exploration

Definitive repair if sharp laceration

Crush injury – zone of injury not apparent

Timing of Nerve Repairs Open Injuries

Timing of Repair Closed Injuries

• Expectant observation

– Expect complete recovery in 6 weeks

– If none

– 6 wks: baseline EMG/NCS

– 12 wks – clinical exam, repeat EMG/NCS

– 3 months – operative exploration

Classification of Nerve Repair

Primary repair (<1week)

Delayed primary repair (after 3-4 days)

Secondary repair (>1week)

Dvali & Mackinnon, Clin Plastic Surg (2003)

Principles of Repair

• Meticulous surgical technique

– (microscope preferred to loupes)

• Debride to healthy nerve ends

• Primary tension-free repair

Graft if tension-free repair not possible

• Fascicular matching (motor to motor, sensory to sensory)

Nerve Repair Technique

• Correct alignment/orientation of fascicles

• Use surface blood vessels for rotational alignment

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Group Fascicular Nerve Repair Epineural Nerve Repair

Factors in Outcomes

Age

Nerve gap

Delay to repair

Level of Injury

Condition of nerve ends

Management of Nerve Gaps

Nerve Grafts

• Graft: tissue that depends on recipient bed blood supply

• Indication: Cannot achieve tensionless direct repair

Nerve Grafts

Autografts (same person)

Allografts (same species, rendered immune

innert)

Pedicled nerve grafts (nerve flaps)

Vascularized nerve flaps

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Donor NervesDonor Length Deficit

Sural 30-40

cm

Lateral

foot

Lateral

antebrachial

cutaneous

5-8 cm Lateral

forearm

Medial

antebrachial

cutaneous

(ant. br.)

10-20

cm

Medial

arm and

elbow

Cable Nerve Grafting

Disadvantages of Autologous Grafting

• Prolonged operative time

• Limited supply of expendable donor nerve

• Donor site morbidity

• Axons must cross 2 suture lines

• Motor axons must growth through potentially inhibitory sensory nerve environment

Avance™

• AxoGen Inc.

• Human cadaveric nerve allograft

• 1.5, 3, 5, and 7 cm lengths

• 1-5mm diameters

Nerve Conduits• Provide safe passage for regenerating nerves

• Localizes neurotrophic factors

• Protection from scarring

• Natural, synthetic, non/absorbable

• Vein, polyglycolic acid (PGA), collagen

Porous flexible PGA mesh

GEM NeurotubeSemipermeable collagen

Integra

Nerve Conduits

• Require population by Schwann cells from neural stumps to guide axonal growth

• Short (<3cm) nerve defects

Thumb digital nerve Repair w/ neurotube

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Cho et al. JHS 2012 Cho et al. JHS 2012

What if proximal end of damaged nerve is far from either

neuromuscular junction (motor end plates)?

sensory distribution (sensory end organs)?

Transfer a healthy proximal donor nerve

(or nerve fascicle)

to

distal palsied nerve

Principles of Nerve Transfer

• Expendable donor

• Donor nerve with large number of motor or sensory axons

• Donor near motor end plates of muscle or skin area served by sensory nerve

• Innervates a muscle that is synergistic to the target muscle (preferred)

Nerve Transfers

• Historically used in brachial plexus injuries

– No viable proximal nerve (eg, root avulsion)

Oberlin TransferRestoration of elbow flexion

Ulnar nerve fascicle to musculocutaneous nerve

Ulnar n.

Biceps

Musculocutaneous n.

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Indications for Nerve Transfer

Brachial plexus avulsion injuries

Avoid dissection through scar

Major trauma with segmental nerve loss

Alternative to grafting in older patients

Proximal nerve injury (with anticipated poor

recovery)

Nerve TransfersConvert high (proximal) injury to low (distal) injury

Recruiting redundant or noncritical fascicles

~35cm/~14in ~12cm/~4.7 in

High Ulnar Nerve Injury

Missing:

intrinsic function

sensation to ulnar 1 ½ digits & ulnar

dorsal hand

Median to ulnar transfers - Motor

• AIN (anterior interosseous n.) motor branch ulnar nerve

Adapted from Dvali et al. Clin Plastic Surg 2003

Median to ulnar transfers - Sensory

Median n. to 3rd webspace ulnar sensory nerve

End to side

Adapted from Dvali et al. Clin Plastic Surg 2003

Cortical Reorganization

• Sensory denervation of the hand “black hole” in sensory cortex of brain

• Tactile input from the hand causes functional cortical reorganization

• Organization of the sensorimotor cortex is not fixed

• “Hand speaks a new language to the brain.”

J. Surg. Ortho Advances 2008; 17(3) 159-164.

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References

• Oberlin C, et. al. Nerve transfer to biceps muscle using a part of ulnar nerve for C5-C6 avulsion of the brachial plexus: anatomical study and report of four cases. J Hand Surg[Am]. Mar 1994;19(2):232-7.

• Dvali L, et. Al. Nerve repair, grafting and nerve transfers. Clin Plastic Surg 2003; 30:203-221.

• Cho MS, et al. Functional outcome following nerve repair in the upper extremity. J Hand Surg 2012; 2340-9.

• Weber RV, et. al. Bridging the Neural Gap. Clin Plastic Surg 2005; 605-616.

• Brown et. al. Nerve Transfers in the Forearm and Hand. Hand Clin 2008; 24:319-340.

• Chiu, DTW et. al. A Prospective Clinical Evaluation of Autogenous Vein Grafts Used as a Nerve Conduit for Distal Sensory Nerve Defects of 3 cm or Less. Plast Recon Surg 1990; 928-934.

• Young et al, A randomized prospective comparison of fascicular and epineural digital nerve repairs. Plast Recon Surg 1981.

Nerve Pathology in the Proximal Portion of the Upper Limb

Mike Darowish

Introduction

Proximal causes of pain and paraesthesias of the upper extremity

• Cervical radiculopathy

• Brachial plexus issues

• Thoracic outlet syndrome

Cervical Spine

Cervical Spine Cross Section Dermatome Distribution

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Motor Innervation

• C5 Deltoid

• C6 Biceps, wrist extensor

• C7 Triceps, wrist flexors

• C8 Interossei, Finger flexors

• T1 Interossei

Reflexes

• Biceps – C5, C6

• Brachioradialis – C6

• Triceps – C7

• Hoffmann’s reflex – upper motor neuron

Pathomechanics of Cervical Radiculopathy

• Compression of nerve root

– Disc pathology or herniation

– Arthritis

– Congenital stenosis

– Trauma

– Tumor

Symptoms of radiculopathy• Based on nerve root

affected

• Radicular pain, numbness, or weakness

• Neck and shoulder pain

are common

• Pain, paraesthesias,

weakness in distribution of

the affected nerve

• Anatomy is key

Diagnosis of radiculopathy

• History and physical

– Spurling’s test: extension,

ipsilateral rotation, and

downward pressure

• XR

• MRI

• Electrodiagnostics

X-ray

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Treatment of Radiculopathy

• Nonsurgical

– pain control, anti-inflammatories

– Neck strengthening

– Traction and manipulation: controversial

– +/- steroid injections

• Surgery

– Decompression

– Fusion

– Disc replacement

Brachial Plexus Injuries


- Trauma- Birth injury- low energy

- stinger

- high energy- Motorcycle, fall

- penetrating trauma


- Upper trunk- weakness in abduction and

elbow flexion- radial sided hand numbness

- Lower Trunk- lose hand function- ulnar sided hand numbness

Brachial Plexus Treatment

- Depends on etiology and status of nerve- Pre- vs. post-ganglionic

- Preganglionic worse, +Horner’s syndrome

- Sharp laceration → direct repair- Nerve graft - Nerve transfer- Tendon transfer- Osteotomy

Thoracic Outlet Syndrome

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Pathomechanics of TOS

• Compression of the brachial plexus or

vessels at the “thoracic outlet”

• Congenital anatomic variations – cervical

ribs, long transverse processes, congenital

bands

• Apical lung tumors (Pancoast tumors)

• Malunion or non-union of the clavicle,

sternoclavicular dislocations

TOS Types

• Vascular• Compression of subclavian artery or vein

• Neurogenic

– Classic presentation with objective physical

evidence is rare

– Hypothenar atrophy, decreased grip strength,

sensory (C8/T1) deficits

• Disputed (Non-specific)

TOS Symptoms

• Disputed Neurogenic TOS

– Chronic, insidious onset pain of neck, upper chest, and shoulder girdle

• Radiates into ulnar side of arm and hand, and rarely into radial side

– Worse with elevation of arm during sleep/activity, driving, or heavy objects

– Subtle findings may be confined to ulnar intrinsics of hand, mimic ulnar neuropathy

Differential Diagnosis• Upper trunk involvement mimics cervical

radiculopathy or carpal tunnel syndrome

• Lower trunk involvement mimics cubital tunnel

syndrome

• Left shoulder and chest pain mimics angina or

heart attack

• Pain with overhead activity mimics cuff tears

• Glenohumeral instability and global upper extremity symptoms

Diagnosis of TOS

• Diagnosis of exclusion

• History and physical

• Rule out other sites of compression

• Ulnar nerve

• C-spine

Diagnosis of TOS• Evaluate posture and head position

• Forward head position

• Shoulder droop

• Muscle bulk and tone

• Arm swelling

• Hand atrophy, intrinsic muscle testing

• Sensory abnormalities

• Peripheral nerve compression signs

• Vascular exam

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Diagnosis: Provocative Testing for TOS

• Look for reproduction of symptoms or loss

of radial pulse

• Beware: many positions can cause

diminution of radial pulse, and are not

diagnostic in isolation

• 64 volunteers

– 17% with symptoms on questionnaire

– 58% had one provocative test positive

Roos test – “stick up test”• 90 degree abduction

and external rotation test

• Pump hand for 3 minutes

• Rapid fatigue or reproduction of symptoms

• Most sensitive and reproducible

Diagnosis - Imaging

• C-spine and chest films

• Consider CT scan if suspicion high

– Adventitious ribs, long transverse

process, cervical ribs, malunited fracture

– Apical lung tumors

• MRI

Diagnosis - Electrodiagnostics

• Generally, EMG/NCS not useful in

diagnosing TOS

– Results do NOT predict thoracic outlet

syndrome

– Useful to evaluate for carpal tunnel or ulnar neuropathy at the elbow

TOS: Treatment

– Therapy: focus on postural abnormalities,

muscle imbalances, and neural mobility

– Nutritional counseling, diet, and exercise

program

TOS Treatment Overview

• Key is to correct postural abnormalities

• Generic instructions from physicians may lead to treatment with stretching, soft tissue massage, nerve mobilization, or cervical traction – this does not help and may aggravate symptoms

• Limitation of aggravating activities (heavy loads, overhead work, backpacks)

• Identification of weakened muscles and strengthening of shoulder girdle to improve posture is key

• Bring shoulder girdle back posteriorly

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TOS Treatmentrisk factors for failure

• Poor cardiovascular condition

• Obesity, chronic pain and associated depression exacerbate poor posture–Antidepressants or psychotherapy can improve symptoms

Treatment - Surgery• Vascular occlusion can be treated with

thrombolytics and long term

anticoagulation, or surgical decompression

• Scalene muscle resection

• First rib resection

• Claviculectomy for malunions or

hypertrophic callus

– Loss of strut → shoulder droop →

worsening symptoms

Complications of Surgery

• Pneumothorax

• Nerve injury – brachial plexus from traction, long thoracic N on middle scalene, phrenic N on anterior scalene

• Vascular injury – death from exsanguination has been reported.

• Persistent symptoms -- inadequate resection vs incorrect diagnosis

Prognosis

• Review of 10 studies of conservative treatment found

no randomized trials, systematic reviews, or meta-

analysis.

• Unclear if conservative treatment better than no

treatment, or what type of treatment is best

– Less than 20% of patients diagnosed progress to

surgery

– When appropriately done, 75% good to excellent

results in some series

Adson’s test

• Arm at the side, hyperextend neck, turn toward affected side, and inhale deeply

• Pulse diminishes

• Symptoms reproduced

Halsted Maneuver

• Costoclavicular test/military brace test

• Arms at side

• Move shoulders down and back with protruding chest

• Clavicle closes on 1st rib

• Downward compression of clavicle with traction of affected extremity accentuates symptoms

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Wright’s hyperabduction test

• External rotate and

abduct arm 180

degrees

• Inhale deeply

• Symptoms worsen

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

• Concurrent postural training

• Stretching, relaxation, and myofascial manipulation restore posture in C-spine, shoulder girdle

• Upper trapezius, levator scapulae, scalenes, sternocleidomastoid, pectoralis minor, and suboccipitals

• Weight loss and CV conditioning

• Avoid pathologic postures - head-forward posture leads to decreased flexibility,scapular abduction, with tightening of anterior groups and elongation of posterior groups.


• Muscle strengthening, increased endurance, and restoration to pre-symptomatic levels– Not started until patient has adequate

pain-free ROM– Aggressive therapy at this time may

exacerbate symptoms– Typically weak in middle and lower

trapezius, and serratus anterior


• Home program for maintenance followed by return to work-place

• Analysis of workplace and job site • Scalene stretching, cervical protraction

and retraction, diaphragmatic exercises, pectoralis stretching, and shoulder circumduction

• Orthotics for scapular retraction may help, but must be part of muscular strengthening plan

MEDIAN NERVE ENTRAPMENT

Mike Darowish

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Median Nerve Compression Syndromes

• Nerve Entrapment at the Wrist– Carpal tunnel syndrome

• Compressive Neuropathies in Proximal Forearm– Pronator syndrome– Anterior interosseous syndrome

CARPAL TUNNEL SYNDROME• Epidemiology

– Classically• Posttraumatic• Female• Middle age

– More recently• Younger • Industrial

worker• Repetitive

motions

RISK FACTORS

• Clear intrinsic risk factors

• Female• Pregnancy• Diabetes• Rheumatoid arthritis

RISK FACTORS

• Occupational factors• Task repetition• Mechanical stress• Force• Vibration• Temperature (cold)

• Typing/mousing - controversial

CARPAL TUNNEL SYNDROME

• Median nerve entrapment in the carpal tunnel

• Chronic inflammation?

• Amyloid deposition?• Repeated mechanical

stress? Ligament? Nerve?

• Vascular sclerosis and ischemia?


• Nakamichi ‘98:– Looked at the

histology of patients with CTS

– 74% normal histology of TCL

– 25% had mucoid, amyloid deposits

– Conclusion: No typical histological changes noted

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• Intracarpal tunnel pressure• Maximal at level of hook

of hamate (smallest diameter)

• Increased with wrist extension>flexion

• Increased with grip (1151 mmHg)

• patients with CTS have increased pressure, more sustained and delayed recovery of normal pressures after exercise

My explanation to patients• Pressure decreases blood

flow• Over time, decreased blood

flow thins the insulation around the wire (myelin)

• In very severe cases, the wire itself starts to be affected (axons)

Sustained compression can lead to permanent impairment

Carpal Tunnel Syndrome

• History & examination are most important tools in diagnosis

• Night pain in median nerve distribution–More proximal often does not have

nocturnal symptoms• Sensory changes in median nerve• Median nerve compression test

–Not everyone reads the textbook• Can have proximal symptoms


• Pain

• Paresthesias in median nerve distribution

• Normal thenarsensation


• Symptoms worse at night (waking up)

• Extreme wrist positions• Talking on phone*• Driving*• Typing/mousing

• Dropping objects• Weakness• Can’t feel them

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Carpal Tunnel Syndrome

• X-rays, CT scan, MRI not useful

• EMG/NCS are helpful

• Confirm diagnosis

• Double crush syndrome

• Polyneuropathy

• Difficult exam

• Severity

TINEL’S SIGN

• Tap on median nerve at wrist

• Site of irritable nerve due to axonal injury

• Tingeling and shooting pain in nerve dist.

• Probable CTS (sen. 0.60, spec. 0.67)

PHALEN’S MANUEVER• Wrist flexion with elbow

on table

• Paresthesia in response to position

• Numbness and tingling in radial digits in 60 sec. = pos. test

• Probable CTS (sen.0.75, spec. 0.47)

WRIST COMPRESSION-FLEXION TEST

• Combines Phalen’s and Durkin’s

• Direct compression of median nerve with wrist flexion

• Paresthesia in response to pressure

• Probable CTS (sen. 0.80, spec. 0.92)

the best test

SENSORY TESTING• Static two point

discrimination >6 mm = advanced nerve dysfunction or nerve laceration

• Rarely useful in CTS

• Monofilament testing is better

• Value greater than .08 gm (monofilament 2.83) in radial 3 digits

• Probable CTS (sen. 0.83)

EMG/NCS

• Its important to remember that CTS is a CLINICAL diagnosis

• Electrodiagnostic tests should NOT be used independently in making diagnosis

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• Early– Intermittent symptoms– No weakness of thumb abduction– No permanent numbness or paresthesias– No atrophy– Treatment = wrist splints, activity modification,

limb positioning 6–8 weeks


• Intermediate– Constant paresthesias,

numbness– No atrophy– +/- Muscle weakness of

thumb abduction– Pain with irritability of

nerve– Treatment = surgical

decompression


• Late– Sensory loss– Muscle atrophy– Weakness grasping

objects– +/- Pain– Treatment = surgical

decompression– Surgery will halt

progression & pain

STEROIDINJECTIONS

– Mild symptoms less than 12 months

– No weakness– Intermittent sensory

changes– Offer transient relief

in 80% patients at 6 weeks

– 75+% went on to surgery within 12 months.

Wood et al, Gelberman et al, + Girlanda et al.

From Pauda, et al. Lancet Neurol. 2016

SURGICAL TECHNIQUES

• The surgical treatment is to completely divide the transverse carpal ligament

• How is this accomplished?– Open release– Limited open release– Two incision release– Endoscopic release

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OPEN CARPAL TUNNEL RELEASE

• Under direct vision release all structures

• Explore median nerve and other carpal pathology

• Safe and efficient under local

• Larger incision• May have more

incisional irritation

ENDOSCOPIC RELEASE

• Smaller incision• May have improved

short term recovery(?)

• Avoids palmar incision• People who rely on

hands for weightbearing

• Regional or general anesthesia

• Less visualization• Increased risk of NV

damage• Higher complication

rate• No difference >6

weeks

OPEN VS. ENDOSCOPIC

• Cochrane Review 2006• No better alternative than standard open CTR• Earlier return to work with endoscopic:

conflicting results• No strong evidence to replace standard open

CTR

HAND THERAPY• Pomerance (JHS ‘07)

– Prospective randomized study

– Two week of post operative therapy vs. home therapy

– No change in outcome noted

– Therapy added $600-$900

• However, there is a role for patients with– Limited digital

motion– Edema– Incision tenderness

SPECIAL CIRCUMSTANCES

• WORKER’ S COMPENSATION PATIENTS

• ELDERLY PATIENTS

• DEPRESSION

WORKER’S COMPENSATION

• Higgs (JHS ‘94)– CTS outcome in

worker’s compensation patients

– Residual symptoms more common in WC patients

– 73% of WC patients changed jobs due to residual symptoms

– 2% non-WC changed jobs

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ELDERLY PATIENTS

• Townshend (JHS ‘94)– 83 CTR in patients

over 70 yrs– 80% with severe

changes– 94% satisfied at 1 year

• Weber (JHS ‘04)– 105 CTR in patients

over 65 yrs– 83% very satisfied

with results at 6 months

– Reduced paresthesia, night pain

– Improved strength & sensibility

ELDERLY PATIENTS

• Keep in mind that 5-10% not satisfied

• Important to discuss goals and recovery before surgery

• Pain relief is main goal

• Long term recovery to be expected in most patients

DEPRESSION

• Ring (JHS ‘07)– 82 Patients with CTR– Survey of outcome and

satisfaction– Dissatisfaction correlates

with depression and ineffective coping skills

– More than a peripheral nerve problem

Improvement in depression and anxiety levels post opSymptoms correlated with levels of depression and anxiety

American Academy of Orthopedic Surgery RecommendationsFollowing Literature Review

(from aaos.org)

• Recommend carpal tunnel release for CTS– Epineurotomy and skin preservation procedures

not recommended

• Hand therapy is not among the options used for CTS

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AAOS WebsiteTreatments not Specifically Addressed or Advocated

Acupuncture, Steroids, Cold laser, Diuretics, Exercise,

Yoga, Vitamin B6, Fitness, Iontophoresis, Laser,

Stretching, Massage, Magnets, Manipulation, Activity

modification , Medications (NSAIDS, etc.), Cognitive

behavioral therapy, Nutritional supplements,

Phonophoresis, Smoking cessation, Therapeutic

touch, Electrical stimulation, Weight Reduction

Is there better evidence?

http://www.cochrane.org/

• Looked at all randomized trails for CTS– 4 main studies– Concluded surgery relieves symptoms better than

splinting– Not conclusive for patients with mild symptoms– No comparison made to injections.


• Looked at 21 trials– Alternative non-surgical treatment– Excluded cortisone injections– Short term benefit

• Oral steroids• Splinting• Ultrasound• Yoga

REFERENCES

• http://www.jhandsurg.org/• http://www.cochrane.org/• http://www.aaos.org/

Appendix for self-studyPRONATOR SYNDROME

• Entrapment of median nerve in proximal forearm

• Forearm pain along median nerve

• Sensory changes in median nerve distribution

• Rare if actually real

Anterior Interosseous Nerve Palsy

• AIN innervations– FPL– FDP IF (MF) – PQ – No sensory

component

http://www.jhandsurg.org/


http://www.aaos.org/

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AIN PALSY

• Complete palsy or incomplete with weakness

• FPL, FDP IF

• Pinch causes IP hyperextension

• Weak pronation with elbow flexed

Ulnar Nerve Compression

Talk originally prepared by David J. Slutsky

MD, FRCS(C)

Randy M. Hauck, MD, MS, FACS

Microcirculatory Effectsof Compression

• increased permeability / edema

• increased endoneurial fluid pressure

• sub-perineurial demyelination

• compressed nerves have a lower threshold to mechanical pressure

• provocative nerve tests reproduce paresthesias

Wall et al. J Bone Joint Surg (Br). 1992

Experimental Stretch Neuropathy

@ 6%, motor potential

amplitude decreases by

70%, but returns to

normal after 1 hour

@ 12% strain, conduction is blocked

and shows minimal recovery after 1 hourWatanabe et al. J Hand Surg 2001

• Continuous stretching of rat tibial nerve for 1 hour resulted in no histologic, electrical, or functional abnormality

• Same load applied cyclically 60-120 times/hr lead to abnormalities

• This suggests that a small strain applied repeatedly might lead to nerve dysfunction

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Lunborg G, Dahlin LB. Hand Clinics 1992

Traction Neuropathy: Pathophysiology

• Injury/scarring of mesoneurium -> nerve adherence to surrounding structures

• Subsequent movement -> traction on the nerve

Lunborg G, Dahlin LB. Hand Clinics 1992

Traction Neuropathy: Pathophysiology

• Stretching injuries -> micro-lesions -> epineural/intraneural fibrosis and permanent nerve entrapment

• Thickening of epineurium/perineurium interfere with interfere with blood flow -> dynamic ischemia

Proximal Ulnar Nerve Fascicular Topography

• Approximately 20 fascicles

• motor fibers to FCU, FDP are deep

• motor fibers to intrinsics, sensory fibers are superficial, hence more susceptible to early compression

CUBITAL TUNNEL SYNDROMESymptoms

• Aching discomfort Medial

aspect of elbow

• Pain, paresthesia's, numbness

Ulnar forearm Ulnar ½

ring finger Small finger

Ulnar dorsal ½ of the hand

• Hand clumsiness and weakness

Cubital Tunnel Syndrome

• Exacerbation by repetitive elbow flexion

– Sleeping position

– Holding a phone, reading a newspaper

– Driving

– Leaning on a flexed elbow

CUBITAL TUNNEL SYNDROMESigns

• 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

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TINEL’S SIGN ELBOW FLEXION TEST

IncorrectCorrect

STRENGTH TESTINGCUBITAL TUNNEL SYNDROME

Scratch Collapse Test

Cheng et al. JHS

2008, 33(9), 1518-

24.

Cubital Tunnel Syndrome

• Can be mild to severe

McGowan’s Scale

1: Purely subjective symptoms and mild hypaesthesia

2: Sensory loss and weakness of intrinsic hand muscles, with or without slight wasting

3: Severe sensorimotor deficit

Cubital Tunnel Syndrome• Severe neuropathy:

– Abnormal 2pd of ring and small fingers

– Weak intrinsics, clawing of ring, small

– Positive Froment’s sign

mailto:[email protected]

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• Avoidance of elbow flexion

• Avoid direct pressure on the elbow (arm rest in car,

desk chair)

• Ergonomic workstation modification

• Nighttime elbow extension splint

– Anterior elbow splint with elbow at 30° of flexion

CUBITAL TUNNEL SYNDROMEOperative Procedures

Simple Decompression Medial Epicondylectomy

Simple In-Situ

Decompression

Medial

Epicondylectomy

SUBCUTANEOUS TRANSPOSITION

INTRAMUSCULAR and SUBMUSCULAR TRANSPOSITION

Within or beneath the flexor pronator massTomaino et al. J Hand Surg 2001;26A:1077-81

Outcomes

• 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.

• Intrinsic wasting rarely recovers in an adult.

http://www.painreliever.com/pics/9/hely-weber/hely-weber-cubital-comfort-brace.3847.3._raw.jpg

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Ulnar Tunnel Syndrome

Etiology• Benign tumors (ganglion >> lipoma, giant cell tumor

of tendon sheath)

• Trauma (hook of hamate fracture, cycling, wheelchair athletes)

• Anomalous muscles, thickened pisohamate lig.

• Ulnar artery aneurysms, thrombosis

GanglionNeurilemmoma

• Paresthesias of ring and small fingers

• ↓ Semmes Weinstein of ring and small

• Tinel’s sign over Guyon’s canal

• Weakness of intrinsics and ADM

• Froment’s sign

• Normal FCU, FDP

• Normal Dorsal Cutaneous Br. of Ulnar N.

• NEGATIVE ELBOW FLEXION TEST

Roof volar carpal ligament

piso-hamate

ligament (motor branch)

Medial pisiform

Lateral hook of hamate

ULNAR TUNNEL SYNDROMEAnatomy of Guyon’s Canal

3 Zones:

• Type I:

-mixed motor and sensory

Type II:

-pure sensory

Type III:

-pure motor

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Indications for Surgical Treatment

• Clinical recovery in majority of patients treated for tumor or ganglion [Foucher, 1993]

• Motor recovery less predictable than sensoryrecovery, especially when compression caused by longstanding fibrotic hypothenar arch [Zoch, 1990]

Suggested Reading

• Slutsky, DJ. Techniques for Nerve Compression Syndromes. In Hand and Upper Extremity Reconstruction. Chung KC, ed. Elsevier, 2008

• Rayan GM. Proximal ulnar nerve compression: Cubital tunnel syndrome. Hand Clin 1992;8:325-336

• Gelberman RH. Ulnar tunnel syndrome. In: GelbermanRH,ed., Operative Nerve Repair and Reconstruction. Philadelphia, Lippincott, 1991:1131–43.

• Chung K. Treatment of ulnar nerve compression at the elbow. J Hand Surg 2008, 33A:1625-1627

Randy M. Hauck, MD, MS, FACS

Radial Nerve Compression

• Origin

– Derived primarily from C6, C7 and C8. T1 contribution in ~ 11% of population

– All three trunks (upper, middle, lower) contribute to posterior cord

– Posterior cord branches into radial and axillary nerves

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• Triceps

• Anconeus

• Brachioradialis

• ECRL

• ECRB

• Supinator

• Divides into PIN and

Superficial Branch

High Radial Neuropathy: Etiology

– humeral shaft fx, 14% incidence

– tourniquet palsy

– “Sat. night palsy”, crutch injuries

– anomalous muscle, rare

– penetration by an aberrant artery

– tumors

– strenuous muscle activity

– windmill pitching

High Radial Neuropathy: Clinical Features

– ± 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

– Spontaneous onset, no mass, nl imaging

• dynamic wrist splint, passive ROM exercises

• if no evidence of recovery at 3-6 months, surgical exploration

–Neurolysis

–If humeral nonunion, shorten humerus

High Radial Neuropathy: Management

• If neuropathy has lasted longer than 12-18 months, perform tendon transfers

– Common tendon transfers:

• pronator teres to ECRB - wrist extension

• FCR to EDC - finger extension

• palmaris longus to EPL – thumb extension

High Radial Neuropathy: ManagementHumerus 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

– Anatomic constraints

• Fibrous bands, crossing veins, ECRB

• Supinator, prox. edge (Arcade of Frohse)

–Distal edge

– Tumor

– Proximal 1/3 radius fx

– Radial head dislocation

– Surgical retraction• (especially from distal biceps reattachment)

Wasting, weakness

PIN Compression: Management

• Treat known compressor (eg mass, radial head)

• If new onset, not progressive, and images nl:

– 6-8 weeks long arm splint

– Digital extensor tenodesis splint

• If no improvement

- Surgical

decompression

Arcade of Frohse

– If progressive or open injury:

Surgical exploration

– If palsy for greater than 18 months, tendon transfers

Radial Tunnel Syndrome: Symptoms

Pain

• deep aching pain over lateral aspect of elbow and dorsal proximal forearm, commonly at night

• can radiate proximally or distally

• pain often aggravated by activity

Radial Tunnel Syndrome: Exam

– Tender over radial tunnel

– Provocative maneuvers

• Resisted supination

• Resisted middle finger extension

• Passive pronation and wrist flexion

– Weakness

• uncommon

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• Differential Diagnosis

– Lateral epicondylitis (may coexist in 5% of cases)

– Parsonage-Turner Syndrome

– Cervical radiculopathy

– Systemic disorders

– Chronic compartment syndrome

Radial Tunnel Syndrome: Management

• Initially, nonoperative

– NSAID, rest, avoid provocative activities

– Long arm splint with elbow in flexion and supination, wrist in extension

• Recalcitrant after 3 months

– Surgical exploration

– Results mixed

Wartenberg’s Syndrome• Also known as:

– Superficial radial nerve entrapment

– Radial sensory nerve entrapment

– Cheiralgia paresthetica

– Handcuff neuropathy

– Wristwatch neuropathy

Wartenberg’s Syndrome: Etiology

– entrapment between BR and ECRL, esp with repetitive movement

– anatomic anomalies

– compression over radial styloid (handcuffs, watch band)

– surgical injury

– tumors

– trauma- crush injuries, fractures, lacerations

– synovial rupture in RA

Wartenberg’s Syndrome: Clinical Features

Paresthesias or dysesthesias dorsoradial forearm, wrist and hand

– increased with wrist flexion, thumb flexion and ulnar deviation (false + Finkelstein test)

– decreased sensation first web space

– positive Tinel’s at BR tendon

– pain may lead to decreased grip strength, although no motor denervation

Wartenberg’s Syndrome: Differential Dx

– De Quervain’s extensor tenosynovitis

– Lateral antebrachial cutaneous nerve injury

– Cervical radiculopathy

– Scaphoid fracture

– OA of thumb CMC joint

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Wartenberg’s Syndrome: Management

• Initial treatment- nonoperative

– NSAIDS, rest, activity modification

– Thumb spica splint with wrist extended

– Eliminate external compression

• If persists greater than 3 months, surgical exploration

• 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.

• 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

Axillary Nerve

• C5 and C6 -> posterior cord

• Gives braches to shoulder capsule

• Goes through quadrilateral space with posterior humeral circumflex artery

humerusteres minor

teres major

triceps (long head)

Quadrilateral Space Syndrome

• Occlusion of posterior humeral circumflex artery (and axillary nerve)

• occurs with arm in abduction, extension, and external rotation

• shoulder pain and distal paresthesias, worse with overhead activity

• MRI: atrophy of the teres minor• Arteriogram, Doppler studies• EMG• surgery

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Axillary Nerve Injury

• Weakness of abduction

• Weakness in external rotation (teres minor)

• Atrophy

• Anesthesia over lateral shoulder not reliable

• EMG

SuprascapularNerve Palsy: Anatomy

• Suprascapular notch

– suprascapular ligament or shoulder joint cyst -> paralysis of supraspinatus and infraspinatus

• Spinoglenoid notch palsy of infraspinatus

Suprascapular Nerve Palsy: Etiology

• Trauma

• Iatrogenic

• Activity (volleyball, stretching at spinoglenoid notch)

• Mass effect (ganglion)

• Pain and weakness (rotator cuff)

• Dull aching pain in post lateral aspect

• More common in males

• Worse with arm elevation and exercise

• Depending on site either supra/infra vs infraspinatus

• Atrophy (infraspinatus more superficial)

• Diagnosis of exclusion

• EMG

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Suprascapular Nerve Injury: Treatment

Nerve Tumors

Alexander Payatakes, MDAssociate Professor / Hand Surgery

No vested interests, No FDA off-label uses presented

Talk originally prepared by Kodi K. Azari, MD, FACS, Roy A. Meals and Gina Farias-Eisner, MD

CASE #1

HPI: 51-year-old female

2 cm laceration to the right index finger, repaired in the ED

2 months later:

Diminished sensation on radial aspect of finger

Electrical sensation at skin scar on direct contact

What is the diagnosis?

Neuroma

Neuroma:

A group of regenerating nerve fibers which fail to reach distal targets or end organs

Neuroma

= Group of regenerating nerve fibers which fail to reach distal targets or end organs

• Wallerian degeneration after injury

• Sprouts emerge from proximal stump of the axon to find distal end

Pathophysiology

Failure to find target Neuroma!

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Pathophysiology

Neuroma:

A group of regenerating nerve fibers which fail to reach distal targets or end organs

Neuroma-in-continuity

Physical Exam

Tinel sign

• Distalmost aspect of regenerating axonsproduces paresthesias when tapped

Treatment

• Surgical explorationResection to healthy fascicles

• Primary repairvs

Nerve grafting

• Bury neuroma in muscle/bonevs

Repair to alternate nerve target?

CASE #2

HPI: 42-year-old male

Painless mass in right small finger in line with ulnar neurovascular

bundle

Slowly enlarging over past year

Somewhat mobile side-to-side, but not proximal-to-distal

What is the most likely diagnosis?

Schwannoma(aka Neurilemmoma, Benign nerve sheath tumor)

• Most common benign nerve tumor of UE

• Arises from Schwann cells

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• MRICharacteristic “Egg on a string” appearance

Treatment

• Typically easy to shell outwithout damage to nerve function

• Very rare reports of malignant transformation

CASE#3

HPI: 20-year-old female

Multiple painful subcutaneous masses on hand and forearm

Lesions vary in size, firm, and tender

Faint café-au-lait skin changes and freckling in the axillary region


Neurofibromatosis type 1(aka von Recklinghausen’s disease)

Physical Exam

• Solitary lesions may be seen

• Multiple neurofibromas common in

Neurofibromatosis type 1 (von Recklinghausen’s disease)

• Café-au-lait macules

• Axillary freckling

• 60% spine deformities

Treatment

• Excision?Only large / symptomatic lesionsOR if unclear Dx

• Typically results in nerve deficit

• Often requires segmental nerve resection and reconstruction

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CASE #4

HPI: 45-year-old woman

Exquisitely painful area in digital pulp

She avoids use of digit to avoid pain

“This finger doesn’t like cold water”


Glomus Tumor

• Typically in pulp or nail bed

• Arises from neuromyoarterial shunting apparatus (thermoregulation)

• PhEx: May have subtle bluish tinge

• Cold sensitivity(tip: ethyl chloride!)

• MRI (T2):High signal intensity oval lesion

Diagnosis

• Surgical excision

• Beware satellite lesions “Recurrence”

Treatment

CASE #5

HPI: 22-year-old man

Gradually enlarging nontender thickening at wrist

Numbness and tingling in the median nerve distribution

What is the most likely diagnosis?

Lipofibromatous Hamartoma

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• Fibrofatty infiltration of nerve(diffuse)

• Consider if CTS + mass

• Especially in child with CTS

• Often intraoperative finding

Treatment

• Simple decompression

• Interfascicular resection?NOT possible and contraindicated!

• If deterioration of nerve function Resection and nerve grafting?

References

1. Watson J et al. Neuroma of the hand and upper extremity. J Hand Surg Am. 2010 Mar;35(3):499-510.

2. Netscher DT et al. Subungual glomus tumor. J Hand Surg Am. 2012 Apr;37(4):821-3;quiz 824.

3. Tahiri Y et al. Lipofibromatous hamartoma of the median nerve: a comprehensive review and systematic approach to evaluation, diagnosis, and treatment. J Hand Surg Am. 2013 Oct; 38(10):2055-76

4. Wolfe, S. Hotchkiss, R. Pederson, W. Kozin,S. (2011) Green’s Operative Hand Surgery 6th

Edition. Philadelphia: Elsevier/Churchill Livingstone.

Numbness

Alexander Payatakes, MDAssociate Professor / Hand Surgery

No vested interests, No FDA off-label uses presented

Talk originally prepared by Joshua Bales and Mark Morris, MD

Overview

Anatomy review

Definitions

Sensory testing

Patterns of sensory loss

Mononeuropathy, radiculopathy, polyneuropathy

Common and uncommon causes of numbness

Summary

Numbness aka Peripheral Neuropathy

• At any time 2-4% population affected

• Most common cause in USA is DM

• Hansen’s disease (leprosy) is most common in SE Asia

• Must determine: Distribution Symptoms Duration Course

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Definitions

Ability to perceive stimuli Sensitivity to stimuli

Hypesthesia Diminished Intact

Anesthesia Absent Intact

Hypalgesia Intact Diminished

Analgesia Intact No sensitivity

• Hyperpathia, hyperesthesia, allodynia

= Increased sensitivity to sensory stimuli

• NOTE:

In peripheral neuropathies:

Patients can vacillate between periods of hyperesthesia and hypesthesia

Sensory Exam

• Peripheral nervedistribution

Sensory Exam

• Dermatomedistribution

Sensory Exam

Sensory Exam

• A brain stem injury could have this pattern of paresthesia

• Whereas a central cord syndrome would present with this pattern

Sensory Exam

• Common axonal neuropathies present in a stocking-glove distribution Feet affected first!

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Sensory Testing

• Follow the patterns: Confined to distal aspect of limb Confined to discrete area of a limb Confined to the whole limb, side of body Involves reflexes Involves cognitive deficits

Clinical Pearls

• Distribution of peripheral nerve

think of pathology of that nerve

(e.g. Median nerve Carpal tunnel syndrome)

(though often atypical!)

• Distribution of a dermatome

think corresponding nerve root (e.g. C5 radiculopathy)

• Stocking-glove sensory loss

think axonal neuropathies - diabetes

Axonal Neuropathies

• Diabetes mellitus

• Alcohol

• Vitamin B12 deficiency

• HIV

• Lyme Disease

• Uremia

• Chemotherapy

• Leprosy

• Syphilis

• Vasculitis

• Amyloidosis

• Multiple sclerosis

• Idiopathic

• Paraneoplastic

neuropathy

• Syphilis

• Vasculitis

• Amyloidosis

• Multiple sclerosis

• Idiopathic

• Paraneoplastic neuropathy

Just to name a few…

• Neuropathy secondary to microvascular insult tovasa nervorum which supplies the nerves

• Occurs in 20% of DM patients

• Implicated in 50-75% of non-traumatic amputations

• Risk factors:

Duration of DM, tobacco use, age, HTN, HLD

Diabetic Neuropathy

Diabetic Neuropathy

• Clinical manifestations

Numbness Hypalgesia Erectile dysfunction Vision changes Dizziness Diarrhea

Diabetic Neuropathy

• Pearls to spot DM Classic triad

Polyuria, polydipsia, polyphagia(Increased urination, drinking, and eating)

Acanthosis nigricans

Stocking-glove distribution Loss of proprioception

Ketone (fruity/alcoholic) odor in breath

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• In DM & syphilis, patients may present with Neuropathic (Charcot) joint

• Due to insensate nature of joint, it gradually degenerates and deforms

• Uncommon in non-weight-bearing joints

Diabetic Neuropathy Alcohol

• 32% of heavy users peripheral neuropathy

• Confounded by nutritional deficiencies

• Risk factor for compression neuropathies

(“Saturday night palsies”)

Alcoholic Neuropathy

• Characterized as gradually progressive affecting sensory, motor, and autonomic nerves.

• Starts symmetrically and distally (feet first)

• Associated with loss of reflexes Loss of ankle jerk first

Alcohol Neuropathy Treatment

• Stop drinking!

• Thiamine supplementation

• Better nutrition

• Full recovery is uncommon

• Some medications can help

with burning dysesthesias

Multiple Sclerosis

• Idiopathic CNS inflammatory disease

• Demyelination and axonal degeneration

• Young adults

• = 2 : 1

• MRI diagnostic for lesion

• Differential diagnosis:

Spinal cord compression, vitamin deficiency, infection

• Clinical, radiographic lesions separated in time & space

Multiple Sclerosis

• Where is the neuropathy?

• MS may cause a constellation of symptoms,

all of which wax and wane

Depression

Fatigue

Numbness/pain

Urinary problems

Nystagmus

Diplopia / Red color perception

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Lyme Disease

• Emerging infectious disease

• Endemic in PA

• Caused by Borrelia burgdorferi

• 1% of tick bites

• Bacterial infection easily treated by antibiotics

• When untreated can cause a variety of joint, heart, and nervous system disease

Lyme Disease

• Incubation period 1-2 weeks

• Early:

Erythema chronicum migrans

Headache, fever, malaise

• Late persistent infection (mos)

Polyneuropathy

Lyme Disease

• Polyneuropathy symptoms:

Numbness Shooting pain Difficulty with concentration Depression Bell’s palsy

Peripheral neuropathy “Chemo fog”

Taxanes (Paclitaxel, Taxo) (breast CA) Burning paresthesias, loss of reflexes

Vincristine (leukemias) Both motor/sensory fibers, virtually all pts

Thalidomide (MM, ovarian CA) 75% sensory neuropathy, reversible with dosage adjustment

Chemotherapy Neuropathy

Methotrexate (for RA) Encephalopathy

Propylthiouracil (thyroid disease) (dose-dependent)

Other Drug-Induced Neuropathies Summary

• A numb finger is not always “carpal tunnel syndrome”

• Review distribution of altered sensation with patient

• What are the other symptoms?

• Look at the big picture– Past medical history, travel history, habits, diet

(See appendix for info on HIV, syphilis, Hansen’s disease)

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References

1. England et al. Peripheral Neuropathy. Lancet 2004: 363:2151-61

2. Robinson, LR. Role of Neurophysiologic Evaluation in Diagnosis. JAAOS. 2000 May;8(3): 190-199

3. Veves et al. Painful diabetic neuropathy: epidemiology, natural history, early diagnosis, and treatment options. Pain Med. 2008 Sept;9(6):660-74

4. Calabresi, PA. Diagnosis and Management of Multiple Sclerosis. Am Fam Physician. 2004 Nov 15;70(10):1935-44

5. Gonzalez-Duarte A, Cikurel K, Simpson DM. Managing HIV peripheral neuropathy. Current HIV/AIDS reports 2007 4 (3): 114–8

6. Scollard DM. The biology of nerve injury in leprosy. Lepr Rev. 2008 Setp;79(3)242-53

7. Hu LT. Lyme disease. Ann Intern Med. 2016; 164(9): ITC65-ITC80.

8. Ontaneda D, Thompson AJ, Fox RJ, Cohen JA. Progressive multiple sclerosis: prospects for disease therapy, repair, and restoration of function. Lancet 2017; 389(10076): 1357-1366.

9. Vinik AI, Nevoret ML, Caselini C, Parson H. Diabetic Neuropathy. Endocrinol Metab North Am 2013; 42(4): 747-787.

10. White C, Franco-Paredes C. Leprosy in the 21st century. Clin Microbiol Rev. 2015; 28(1): 80-94.

• Hypothesized to be secondary to dorsal root ganglion damage by the virus

• Occurs in 30% of HIV/AIDS pts

• Late - Typically presents in the feet

Death

HIV Neuropathy

HIV Neuropathy

• Main complaints Bizarre burning Hyperalgesia Allodynia

• Risk factors DM Nutritional deficiencies HIV Medications

Syphilis

• Caused by Treponema pallidum

• “Great imitator”

• Primary syphilis Skin lesion (chancre)

(21 d after exposure)

Secondary Syphilis

• Secondary syphilis 6-8 wks after exposure Rash in palms and hands Most contagious

Tertiary Syphilis

• Occurs 1-10 yrs after initial infection

• Changes in personality

• Tabes dorsalis Dorsal column disease causing a shuffling gait

• Neuropathic/Charcot joint disease Loss of proprioception

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Hansen’s Disease (Leprosy)

• Leprosy = Greek for scales on a fish

• Caused by Mycobacterium leprae

• Granulomas of the nerves, respiratory tract, skin, and eyes

• Since 600 BC

• Still leper colonies today

• Not actually highly contagious

Hansen’s Disease (Leprosy)

• Incubates for few weeks – up to 30 yrs (average 3-5 yrs)

• Affects 3 million/year (30% get neuropathy)

• Loss of sensation

Repeated injuries, infection due to unnoticed wounds Loss of body parts/deformity

• Affects Schwann cells• Causes inflammation/edema• Unmyelinated fibers are also affected (how?)

Weakness/Spasticity

Kenneth Taylor, MD

No conflicts of interest to report

Talk originally prepared by Lucie Krenek, MD

Stroke

• Leading cause of hemiplegia in adults• Immediate flaccid paralysis• Spasticity over several weeks (UMN)

◦ Spinal cord mediated reflexes intact• Associated perceptual/cognitive/visual

losses • Most recovery in first 6 months• Functional recovery can continue over time • Upper extremity < lower extremity recovery

◦ UE function more dependent on fine motor control

Stroke - Treatment

• Goals: ↑hygiene, ↓pain, ↑function • Contractures

◦ Cause pain and lead to joint subluxation(further pain)

• Acute – Prevention of contractures◦ Brachial pexus and distal nerve blocks◦ Botulinum (Botox)

• Chronic – Treatment of contractures◦ Antispasmodic medication◦ Surgery – after plateau ( ~6 months)

Stroke - Contractures

• Synergistic pattern of spasticity/contracture favors stronger muscles◦ Shoulder - adduction/internal rotation◦ Elbow - flexion ◦ Forearm - pronation◦ Wrist – flexion◦ Fingers - flexion

• Surgery after spasticity stabilizes◦ Lengthen if functionsl◦ Tenotomy if nonfunctional

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Other Neurologic Conditions Causing Weakness/Spasticity

• Uncommon

• Have general awareness ◦ Patient queries◦ Broad understanding of nerve

pathologies

Charcot-Marie-Tooth (CMT) Disease

• aka◦ Peroneal Muscular Atrophy◦ Hereditary Motor-Sensory Neuropathy

• Most common hereditary neuromuscular disorder (Usually autosomal dominant)

• Chronic, symmetric distal sensory/motor neuropathy

• Onset: late childhood/adolescence• Normal life expectancy

CMT Signs

• Lower extremity – begins first◦ Gait problems◦ Distal weakness – legs, feet◦ Inability to heel walk◦ Foot drop; ankle instability◦ Pes cavus; hammer toes

• Upper extremity – milder than LE◦ Difficulty with fine motor and strength◦ Rarely extends above elbow◦ Atrophy of hands/forearms◦ Intrinsic-minus hand deformity

CMT Treatment

• Stabilization of ankles – orthoses, tendon transfers, fusion

• Moderate aerobic exercise• Muscle stretching/strengthening• Excessive weight training not recommended

CMT Treatment

• Intrinsic minus hand most debilitating◦ MP extension block splint◦ Volar MP joint capsulodesis◦ Surgical: FDS rerouted to proximal

phalanges

Amyotrophic Lateral Sclerosis (ALS)(Lou Gherig’s Disease)

Lou Gherig Steven Hawking

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ALS

• Loss of upper and lower motor neurons◦ Lesion – motor neurons in spinal cord,

brainstem and motor cortex◦ Lateral corticospinal tract◦ Denervation atrophy/weakness of muscle◦ Tongue fasciculations pathognomonic

• No sensory or autonomic involvement• Etiology unknown

◦ Risk factors: pesticides, smoking, military, familial

ALS - Treatment

• Controversy regarding exercise• Strengthening and moderate endurance

exercise may result in better function• Little can be done to improve quality of

life, fatigue, or muscle strength• Ventilatory support when respiratory

muscles become affected

Guillain-Barre Syndrome (GBS)

• Acute autoimmune polyradiculopathy◦ 70% preceded by acute infection

∙ Usualy respiratory/gastrointestinal∙ Fue shot or other vaccines

• Demyelination of peripheral nerves• Plateau by 4 weeks• Recovery occurs with remyelination

GBS – Signs/Symptoms

• Rapid onset ascending motor paralysis• May have sensory/automonic symptoms• Generalized weakness - lower extremities

procedes to upper extremities• Neck, shoulder, back pain• Later – muscle atrophy, potential for

contractures with lack of motion• Severity of weakness highly variable

GBS – Treatment

• Acute phase◦ Maintain range of motion◦ Prevention of contractures

• Recovery phase◦ Retraining of many ADLs (grooming,

gait)◦ Muscle strengthening◦ Supervised exercise programs help

overcome fatigue and improve function

GBS – Prognosis

• Most need hospitalization• Up to 30% require ventilatory support• <5% mortality (usually due to pulmonary

complications• 85% full recovery by 1 year• Poorer prognosis for older patients, late

treatment, severe attacks

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Polio

• Viral infectious disease• Fecal-oral transmission• Usually infects children under 5 years old• Lower moton neuron lesion• Decreased reflexes and muscle wasting• Proximal muscles affected• Sensory loss rare

Polio

• Rare in developed countries• Afghanistan, Nigeria, Pakistan, India• <2,000 cases per year• 95% infected asymptomatic• 0.5% irreversible paralysis, usually legs• Of those with paralysis – 5-10% die due

to involvement of respiratory muscles

Polio

• Acute phase: all anterior horn cells affected

• Subacute phase: the ~50% of anterior horn cells that survived begin to recover

• After 16-24 months: extent of damage realized; rehabilitation begins

Polio - Treatment

• Acute ◦

• Subacute

• After 16-24 months: extent of damage realized; rehabilitation begins

Polio - Treatment

• Acute phase◦ Range of motion, splinting

• Subacute phase◦ Prevent deformity, preserve function◦ Splinting/bracing to maintain joint position and supplement function

• Residual phase◦ Surgical intervention if needed

Post Polio Syndrome

• Occurs years after acute illness• Muscle pain, severe fatigue, cramping,

fasciculations• Overuse of muscles originally affected• Slowly progressive weakness in already

weak muscles• Treatment – limited exercise with

frequent rest

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References

1. Adams and Victor’s Neurology, AH Ropper, RH Brown. 8th Edition2. Current Orthopedics, AE Keenan, S Mehta 3. Dillin L, Hoaglund FT, Scheck M. Brachial Neuritis. J Bone Joint Surg Am.

1985 Jul;67(6):878-80 4. Harrison’s Principles of Internal Medicine, 17th Edition. Fauci AS et al, eds.5. Hughes RA, et al. Supportive care for patients with Guillain-Barre

syndrome. Arch Neurol. 2005 Aug;62(8):1194-86. Hussey AJ, O’Brien CP, Regan PJ. Parsonage Turner Syndrome – Case

Report and Literature Review. Hand. 2007;2:218-221. 7. Pitetti KH, Barrett PJ, Abbas D. Endurance exercise training in Guillan-

Barre syndrome. Arch Phys Med Rehabil. 1993; 74: 761-765. 8. Tuckey J, Greenwood R. Rehabilitation after severe Guillain-Barre

syndrome: the use of partial body weight support. Physiother Res Int. 2004;9(2):96-103.

9. Tafti MA, Cramer SC, Gupta R. Orthopedic Management of the Upper Extremity of Stroke Patients. J Am Acad Orthop Surg. 2008;16:462-470.

Chronic Regional Pain Syndrome

Kenneth Taylor, MD

No conflicts of interest to report

Talk originally prepared by Nicholas Rose, MD

Chronic Regional Pain Syndrome (CRPS)

• Mitchell (1864): Described “Causalgia” in veterans sustaining nerve injury after gunshot wounds during American Civil War

• Sudek (1900): Noted bone atrophy on x-ray

• Leriche (1916): Noted similarities to ischemia. Treated with sympathectomies

• Evans (1946): Coined “Reflex Sympathetic Dystrophy” (RSD) for syndrome without major nerve injury

• Int’l Assn. Study of Pain (IASP) (1994): CRPS because “RSD” is not solely sympathetically-mediated

CRPS

• No single unifying explanation to account for diverse features

• Likely a spectrum of disorders• Type 1 (previously RSD)

◦ No identifiable nerve injury◦ More common

• Type 2 (previously Causalgia)◦ Following major nerve injury◦ Less common

CRPS – Predisposing Factors

• Identification of potential risk factors remains elusive◦ Heterogeneous studies◦ Mixed quality/relevance◦ Low prevalence with lack of gold standard

CRPS – Predisposing Factors

• Strong weight against bias◦ Post-menopausal female◦ Distal radius fracture, ankle dislocation, other

intra-articular fracture◦ Reports of higher pain in early phase after

trauma• Weaker weight against bias

◦ Immobilization◦ Psychological barriers◦ Positive diagnostic bone scan

Pons T. Anesthesiol Res Pract. 2015

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CRPS – The Perfect Storm

• Patient with wrist injury◦ Sling/tight bandage◦ Dependent position and

immobilization∙ Ischemia∙ Edema

CRPS – Features

• Pain out of proportion• Non-dermatomal• Skin dry or overly moist• Skin mottled or cyanotic• Skin temp - cool• Skin texture - smooth, shiny, non-elastic• Edema• Atrophy (especially fingertips)

CRPS – Chronic Features

• Hair – loss, finer, longer• Nails – ridged, curved, thin

brittle• Joints - stiff• Muscles – atrophy, weak,

tremor, spasm• Radiographs - osteopenia• Bone scan – inc. regional

isotopic uptake

• Not all CRPS is sympathetically-mediated

• Not all sympathetically-mediated pain (SMP) is CRPS

SMP CRPS

Herpes zoster

Neuralgias

Metabolic

Neuropathies

Phantom Pain

CRPS – Definitions and a Conundrum

• Hyperalgesia – Increased pain response to a stimulus that is normally painful

• Hyperesthesia – Abnormal increase in sensitivity to stimuli of any of the senses

• Alodynia – Non-painful stimuli evoke pain

• When does pain become abnormal?• Who decides?

Budapest Diagnostic CriteriaThe following four criteria must be met

1) Pain out of proportion to inciting event

2) Must report @ least 1 symptom in 3 of 4 categoriesa) Sensory – hyperesthesia and/or allodyniab) Vasomotor – temperature asymmetry, skin

color changes, ± skin color asymmetryc) Sudomotor/Edema – edema, sweating

changes, and/or sweating asymmetryd) Motor/Trophic – decreased ROM, motor

dysfunction (weakness, tremor, dystonia), ±trophic changes (hair, nail, skin)

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Budapest Criteria Continued

3) Display @ least 1 sign in 2 of the followinga) Sensory – hyperalgesia (to pinprick) ± allodynia (to

light touch, deep somatic pressure ± joint movement)b) Vasomotor – temperature asymmetry, skin color

changes ± asymmetryc) Sudomotor/Edema – edema, sweating changes, ±

sweating asymmetryd) Motor/Trophic – decreased ROM, motor

dysfunction (weakness, tremor, dystonia), ± trophic changes (hair, nails, skin)

4) There is no other diagnosis that better explains the signs and symptoms

CRPS Pathophysiology

• Exaggerated inflammatory response• Altered cutaneous innervation• Central and peripheral sensitization• Altered sympathetic nervous system

function• Circulating catecholamines• Distorted sensory representation of

affected limb in brain

Bruehl S. Anesthesiology. 2010

CRPS Management

• Prevent it!◦ No slings for hand and wrist problems◦ Mobilize all joints possible

∙ Minimally restraining bandages, splints, casts∙ Encourage functional use

◦ Elevate the extremity◦ Loosen or replace tight bandages/casts

CRPS Management Overview

• Physical• Pharmacological• Implanted devises• Psychological approaches

• Treatment is multidisciplinary◦ Hand therapist◦ Hand Surgeon◦ Pain management specialist◦ Psychologist

Therapy

• First line of treatment• Active movement, resume ADLs• Passive motion, splinting after pain

controlled• Posture normalization• Edema reduction• Desensitization• Stress loading

◦ Scrubbing◦ Carrying

• Aerobic conditioning

Therapy

• Overcome kinesophobia• Massage• Contrast baths• Graded motor imagery*• Transcutaneous electrical

nerve stimulation• Isometric strengthening• Encourage use of affected limb in ADLs• Mirror box therapy*• Specialized garments/wrappings

* Topics for further discussion

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Medications Used for CRPS

• Anti-inflammatory – NSAID, steroids• Vitamin C – preventative?• Topical antioxidants (DMSO)• Anti-convulsants (Gabepentin)

• Ketamine• Antidepressants (Nortriptyline, Cymbalta)

• Narcotics• Calcitonin• Intravenous immunoglobulin (IVIG)

Interrupt the Sympathetic Supply

• Stellate ganglion block(s)• Surgical sympathectomy• Peripheral blockade

with Bier block

• These will not work unless pain is sympathetically-mediated

Implanted Nerve Stimulators and Pain Pumps

• Spinal cord stimulation• Peripheral nerve stimulation• Spinal medication pumps• Deep brain stimulation

Psychological Approaches

• Active self-management and participation in a care plan

• Assess/treat patients for concomitant Axis I disorders (depression, anxirty, PTDS)

• Cognitive behavioral therapy• Biofeedback• Learning relaxation skills

Surgery During/After CRPS

• Relief of carpal/cubital tunnel syndrome may help treat CRPS – don’t delay

• Secondary surgery after CRPS is controlled(e.g. distal ulna excision after dist rad fx)◦ 47% recurrence rate◦ Make sure to coordinate with pain team◦ Perioperative stellate ganglion block

often recommended

CRPS - Prognosis

• Within first year◦ 70% improved◦ 25% still met Budapest criteria◦ Only 5% without complaints

• Worse prognosis - Patients with higher levels of anxiety and pain-related fear at beginning of therapy

• Symptoms present >1 year rarely spontaneously resolve

• Smokers have worse prognosis

Bean D. J Pain. 2014

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Supplemental Material for Self-Study

• Shingles• Parsonage-Turner Syndrome• Post-traumatic Neuromas

Shingles

• Resurgence of virus that causes chickenpox in immunocompromised patient

• Incidence – 0.5% > age 60; 1% > age 70• Pain/rash follow dermatomal distribution

◦ Face > Trunk > Limb• Pain (post-herpetic neuropathy) can last for

years. Treated with meds.• Immunization available

◦ Recommended for > 60

Mueller N. Neurol Clin. 2008

Parsonage Turner Syndrome

• Idiopathic brachial plexopathy• Abrupt onset shoulder pain (usually

unilateral) followed by progressive motor weakness, dysesthesia, and numbness

• Pain may extend to trapezius, upper arm, forearm and hand

• Pain usually worse at night• Pain usually lasts 1-2 weeks


• Usually healthy individual or related to◦ Injection – vaccine, antibiotic, heroin◦ Childbirth◦ Surgical procedures◦ Infection

• Onset – intense pain/burning at shoulder/neck

• Early – inc pain with movement/palpation• Later – weakness and muscle wasting

◦ Diminished reflexes◦ Sensory loss◦ Fasciculations


• Signs◦ Proximal upper limb paralysis occurs (deltoid,

serratus anterior, rotator cuff, biceps, triceps)◦ May be bilateral by EMG though clinically

appears unilateral• Therapy when pain controlled

◦ Maintain range of motion◦ Strengthen rotator cuff and scapular stabilizers

• Recovery – weeks to year• 10% have residual weakness• 10% have recurrence

Post-traumatic Neuromas

• Targeted Muscle Reinnervation (TMR)• Nerve Mobilization

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Targeted Muscle Reinnervation

• Novel approach to post-amputation neuroma pain

• Provides distal target and vascularized scaffold to guide sprouting nerve axons

• Improves functional prosthesis control• Residual nerves from the amputated limb

are transferred to reinnervate new muscle targets tht have otherwise lost their function

• 0/26 patients developed neuroma pain after TMR (Souza J. Clin Orthop. 2014)

Nerve Mobilization

• Not published, discussed or understood in hand surgery circles

• Recent review by Mark Walsh, PT, MS, CHT, ACT (J Hand Ther. 2005, 18:241-258)◦ “Neural mobilization…is based on an eclectic

compilation of theoretical concepts. There is a paucity of reported clinical studies using neural mobilization for the treatment of neuropathic pain”

Quiz and Closing Comments

Reinforcement Quiz

Caution: The order of the questions and the order of the answer possibilities on website will be different than seen here.

So remember the right answers, not that the answer to question 16 here is F, for example.

Reinforcement Quiz

1. The cell bodies of peripheral sensory nerves are in the

A. anterior horn of spinal cordB. dorsal root gangliaC. white matter of brainD. gray matter of brain E. white matter of spinal cord

Reinforcement Quiz

2. What is the correct relationship of nerve injury severity?

A. axonotmesis > neuropraxia > neurogenesis B. neurotmesis > axonotmesis > neuropraxiaC. neuropraxia > neurotmesis > axonotmesisD. sensory > motor > autonomicE. men > women > children

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71

Reinforcement Quiz

3. In a patient with recent onset of mild carpal tunnel syndrome symptoms

A. two-point discrimination will be alteredB. monofilament testing may be normalC. thenar muscle wasting will precede monofilament

changesD. Meissner corpuscles will be atrophicE. loss of vibratory sensation to 256 cycles/second will

be present

Reinforcement Quiz

4. A successful nerve transfer requires

A. a healthy proximal donor nerve and a palsied distal recipient nerve

B. a distal palsied donor and a healthy recipient nerve C. complete absence of donor muscles for tendon

transfersD. more rehab than comparable tendon transfersE. more post-op immobilization than comparable

tendon transfers

Reinforcement Quiz

5. The Roos “stick up test” for thoracic outlet syndrome consists of

A. shoulder abduction and internal rotationB. turning head away from the side being testedC. externally rotating and abducting shoulder 180

degreesD. checking for radial pulse with patient seatedE. shoulder abduction to 90 degrees and external

rotation

Reinforcement Quiz

6. Which diagnostic test for carpal tunnel syndrome has the highest sensitivity and specificity?

A. Phalen testB. Tinel testC. Adson maneuverD. median nerve compression testE. Allen test

Reinforcement Quiz

7. In cubital tunnel syndrome, why do sensory changes and intrinsic wasting occur before forearm muscle weakness?

A. some nerve fibers have more myelin coveringB. the intrinsic muscles are smaller than the flexor carpi

ulnarisC. the sensory and motor fibers to hand are superficial

in the ulnar nerve at the elbowD. the sensory and motor fibers to hand are superficial

in the ulnar nerve at the wristE. the fibers affected early originate solely from the C8

nerve root

Reinforcement Quiz

8. Which nerve is most likely to be injured with a humeral shaft fracture?

A. median nerveB. ulnar nerveC. suprascapular nerveD. radial nerveE. medial pectoral nerve

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72

Reinforcement Quiz

9. A nerve sheath tumor (Schwannoma) in a digital nerve

A. will move more medially laterally than proximally distally

B. will move more proximally distally than medially laterally

C. is far less common than a neurofibromaD. will cause sensory loss if excisedE. will cause motor loss if excised

Reinforcement Quiz

10. Neuropathy occurs in what percent of patients with diabetes?

A. 1B. 5C. 20D. 50E. 95

Reinforcement Quiz

11. “Upper motor neuron” disorders include conditions such as

A. stroke, spinal cord injuryB. brachial plexus palsyC. Parsonage-Turner syndromeD.ShinglesE. proximal median nerve lacerations

Reinforcement Quiz

12. Chronic regional pain syndrome is

A. Usually preceded by a viral infectionB. Managed best by the patient’s personal physicianC. Probably a spectrum of disordersD.Fully responsive to stellate ganglion blocksE. Relieved by tight serial casting

To obtain continuing education credit for today’s course

All registrants:Complete the quiz at www.ddhands.comYou will be able to access your certificate

OTsThe AOTA recognizes DD as an Approved Provider of Continuing Education.Your certificate indicates this.

PTsApply for CE credit individually through your state board/associationThey 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.

Learn from the 22 On-line Self-Study Programs

72 hours of CE credit available:

AnatomyClinical Conditions

Journal Article ReviewsBooks

http://www.ddhands.com/

http://www.ddhands.com/

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73

DD Current Science for Hand TherapistsAugust 2-4, 2019

University of DenverDenver, Colorado

Update your understanding of the science that underpins hand therapy

• Learn hands-on in a resort setting

• Earn 20 continuing education hours

• Enjoy the area during long afternoon

breaks

Comments From Previous Sessions

• This was easily the most exciting,

innovative, motivating class I’ve been to.

• I came to the course with high

expectations. They were exceeded.

Register early! www.doctorsdemystify.com

2020Saturdays in Multiple Cities

MUSCLES and TENDONS

anatomy, physiology/healing, biomechanics,

injury/repair/rehab/tenolysis, inflammation

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Satisfaction guaranteed or your money back.

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