Peripheral Nerve Trauma: Electrodiagnostic Workup and Indications for Surgical Referral to Limit Pain and Disability Faren H Williams, MD, MS Edward Calkins,

Peripheral Nerve Trauma: Electrodiagnostic Workup and Indications

for Surgical Referral to Limit Pain and Disability

Faren H Williams, MD, MS

Edward Calkins, M.D.

Marci Jones, M.D.

Anthony Howley, OTR/L, CHT

U of Massachusetts Medical School

Peripheral nerve injuries:Electrodiagnostic Considerations

Faren H. Williams, M.D., M.S.Chief and Clinical Professor

Physical Medicine and RehabilitationDept of Orthopedics and Physical Rehabilitation

University of Massachusetts

Peripheral nerve injuries

• 1167 peripheral nerve injuries –

• 5.7% sports – 10% traumatic

• Trauma – Falls, MVA’s, GSW’s

• UPPER extremities – more mobile– 88% upper extremity

Normal Nerve

Faren H. Williams, M.D., M.S. 4

Nerve Structure


Nerve Physiology


Peripheral Nerve Injury


Electrodiagnostic Testing

• Information about Integrity of

Anterior Horn Cell

Dorsal (Sensory) Ganglion– NERVE– NEUROMUSCULAR JUNCTION– MUSCLE



Nerve AnatomyAxon swelling/ Node of Ranvier



Overview NCS/ EMG

• Sensory distal latency– Time required for nerve impulses to travel between

• The stimulation and recording electrodes

•Motor distal latency•Time required neuromuscular transmission•Initiation of Action Potential

Latency Changes over time

Timing s/p Injury

Motor and Sensory Latency Changes Over Time

0 2 4 6 8 10 12 14

Time After Injury (Days)

Dis

tal L

ate

nc

y

DSL

DML

NORMAL

ABSENT0 -

Myelinopathies

• Affects the myelin sheath

• Intussusception of myelin –occludes– Nodal Gap

• Latency slowing

• Profound loss of myelin –– Associated Axonal loss

Neural Intussesception

Nerve AnatomySingle nerve fiber



Overview NCS/ EMG

• AmplitudeMeasures of the number of nerve fibers conducting impulses from the stimulating to the recording points

Relative conduction rates along those fibers

Distance between muscle/nerve fibers and

recording electrodes


Overview NCS/ EMG

• Duration– Relative rates in conduction of fibers between

• Stimulating & recording points

– Prolonged vs. dispersed– Motor – duration of negative response

Early NCS’s

• First week s/p injury– Allows for precise localization of the injury– Distal stump continues to conduct– Impaired conduction across site of major injury

– Ability to localize lost after 1st week as• Distal stump ceases to conduct



Overview NCS/ EMG

• Conduction block– Amplitude distal to the focal lesion is higher

• % loss in amplitude – related to % of fibers/ axons lost– After 7-10 days – can’t localize

• Day 1-2 – can’t differentiate axonal loss from demyelination

– Latency is usually slowed across the lesion-• Secondary to demyelination

Amplitude changes over time

Timing s/p Injury

Motor and Sensory Amplitude Changes Over Time

0

20

40

60

80

100

0 2 4 6 8 10 12 14

Time After Injury (Days)

% A

mp

litu

de

S. Amp.

M. Amp.

Early NCSs

• Lesion – electrophysiologically – Incomplete (Neuropraxia) or Complete– Incomplete lesions – MUAPs voluntarily controlled– Number of MUAPs less with more severe injury– Single MUAP indicates lesion is incomplete– Nerve trunk not disrupted– Better Prognosis


Ulnar Motor Inching Study

Contralateral side

• NCS’s imperative to determine degree of

• AXONAL loss –

If distal amplitude is same side: side

Then lesion is neuropraxic

If distal amplitude on affected side is 50% less

then 50% axonal loss

50% conduction block – across lesion


Ulnar Inching

NEEDLE EMG

• RESTING MUSCLE

is ELECTRICALLY SILENT

• with Needle EMG



Overview NCS/ EMG

• Needle EMG– Insertional activity

• Injury potentials mechanically evoked by needle movement

• Decreased when muscle atrophied, fatty, or fibrotic

• Increased (muscle membrane activity >300ms)– Non-specific

– Can be seen associated with denervation

– No diagnosis made based on this finding alone

Abnormal potentials

• Proximal muscles after 10-14 days

• Distal muscles after 3-4 weeks


Abnormal Potentials


Needle EMG

• Assists in localization

• Allow sufficient time for Wallerian degeneration

• Prognosis– Follow changes over time

More sensitive for detecting motor loss than NCSs

Complete lesion – no MUAPs

Incomplete lesion – reduced recruitment (rapid firing)



NCS/ EMG Overview

Normal AVI


Needle EMG and NCSs

• BOTH NEEDED for INTERPRETATION– NCSs -50% axonal loss, 50% conduction block

• Need data from contralateral (normal) limb

– 4+ fibs/ positive waves and no MUAPs

Doesn’t correlate with percent of axonal loss

– Represents neuropraxia and axonotmesis– Not complete axonal lesion


Neurotmesis

• No motor or sensory potentials – over time

• Axons and epineurium disrupted

• MRI neurography – localization

• Intraoperative electrodiagnosis

• Surgical repair tenuous

Nerve Regeneration

• Depends on distance from nerve lesion to muscle

• Type of Nerve Injury

• Age of Patient

• General Health of Patient/ Co-morbities



Overview NCS/ EMG

• Motor Unit Analysis– Early reinnervation

• MUAP’s – Increased polyphasicity and duration– Temporal dispersion– Poor synchronization of muscle fiber discharges

– Later• Axonal sprouts mature – polyphasicity reduced

– Late• High amplitude, long duration, occ polyphasic

Distal Wallerian DegenerationProximal Sprouting



Regenerating Sprouts MatureRe-myelination



Polyphasic MUAPs


Overview EMG/ NCS

• Polyphasicity – suggests reinnervation– MUAPs with >5 phases– Isolated finding – non-specific– Overreported, Overinterpreted– 20-30% polyphasic MUAPs - normal


Overview NCS/ EMG

• Recruitment – helpful for prognosis– Reduction in lower motor neuron pool

• Increased firing rate (fewer vs. more MUAPs)

– Poor central effort• Effort, Pain inhibition, CNS problem

• Non-diagnostic

Intrepretation/ Recommendations

• Diagnosis – type of nerve injury/ Localization– Demyelination, Axonopathy, or both (mixed)

Prognosis

Recommendations- therapeutic regimen, medications

Repeat study to follow/ monitor progress

Surgical referral/ intervention


Patient Informatiion

• History

• Dominant arm

• Motor, sensory, reflexes

• Mechanism of injury

• Timing s/p Injury


Peripheral nerve injury

• Physical Examination– Strength– Sensation – dermatomal, peripheral– Reflexes – UMN, LMN– Contralateral limb– Muscle atrophy– Deformities, i.e. Claw hand

Sensation – Ventral Arm

Sensation – Dorsal Arm

Case #1

• 25 y/o R HD male, with R humerus fx, s/p MVA

2 months prior to EDX study – brachial a. repair

PE – triceps 3/5, B-R 2-/5, ECRL 2-/5, FDP to

middle, ring and little fingers 2/5, FDP –index 0/5

FPL 0/5, APB ?tr, impaired sensation median n


R Median motor response, s/p MVA


Left median motor


Right radial motor


Left Radial Motor


Motor NCS’s

• Right median motor– DL – 4.7 ms, ampli – 0.4 K with dispersed waveform

Left median motor

DL – 3.9 ms, amplitude 7.8 K

Right radial motor


Left radial motor



Right median –radial sensory


Right radial sensory- snuff box


Sensory NCS’s

• Right Median – No responses

• Right Radial – no response from thumb

• 4.2 ms peak latency, and 14 uV from snuff box

• Left Median – 2.4 ms peak latency, 68 uV ampl

• Left Radial (from thumb) -2.6 ms lat, 7.9 uV ampl

• from snuff box 3.2 peak latency, 40 uV ampli.Faren H. Williams, M.D., M.S. 56

Needle EMG- Right

• Spontaneous activity– APB, EIP, Pronator Teres, Brachioradialis, ECRL

– No MUAPs – in APB, and Pronator Teres– Radial innervated muscles – decreased recruitment

• Discrete recruitment in more distal muscles, all + MUAPs


Interpretation

Median nerve injury - > 95% axonal loss, Motor & Sens

0 MUAPs in median innervated muscles

• Radial nerve injury – 75% axonal loss, motor–Reinnervation – proximal to distal

Prognosis- median recovery guarded, radial fair


f/u EDX, 9 mos post-op

• Right radial motor ampl – 50% greater than ’12

• Right median motor (s/p median n graft)– Amplitude 10x’s greater than Nov ‘12

Right median sensory – from thumb and index finger

3-5 uV amplitude –improved from no response in ‘12

Needle EMG – ongoing fibs/ positive waves R APB

but with MUAPs with reduced/ discrete recruitment

in median innervated muscles. Radial ones polyphasicFaren H. Williams, M.D., M.S. 59

Median motor, s/p Nerve Repair


R radial motor, 9 mos post-op


Case #2

• 24 y/o R HD female, c L distal humerus fx MVA

• EDX 3 months later – no ulnar motor or sensory

• Needle study with spontaneous activity

• in all ulnar innervated muscles, incl FCU

• 0 MUAPS in 1st DI and ADM,

• Recruitment reduced in FCU


EDX 5 mos s/p MVA

• Left ulnar motor not obtainable

• Left ulnar dorsal cutaneous not obtainable

• Left ulnar sensory from little finger not obtainable

• Needle study with more firing MUAPs in FCU

• FDP –ulnar, polyphasic MUAPS, reduced recruit

• 0 MUAPs in 1st DI and ADM


Polyphasic MUAPs –FDP, ulnar


L Ulnar Motor, 6 mos, s/p MVA


L Ulnar sensory, 6 mos, s/p MVA


Summary- EDX Prognosis

• Type of Nerve Injury

• Timing s/p Injury

• NCS’s in combination with needle EMG– Complete vs Incomplete Lesion

• Distance from Lesion to Muscles

• Clinical Correlation with EDX findings

• Serial Electrodiagnostic Studies


References Campbell, W., Evaluation and Management of Peripheral Nerve Injury, 2008.

Malikowski, T., Micklesen, P J, Robinson, L., Prognostic Values of Electrodiagnostic Studies, Muscle and Nerve, Sept 2007, p. 364- 367.

Robinson, L.R., Traumatic Injury to Peripheral Nerves. AAEM Minimonograph #28, p 863-873.

Sahin et al. Correlation of Neurodiagnostics with Recovery. Hand, 2014.


Peripheral Nerve Trauma: Electrodiagnostic Workup and Indications for Surgical Referral to Limit Pain and Disability Faren H Williams, MD, MS Edward Calkins,

Documents

time slide

demyelination slide

normal nerve faren

nerve structure faren

nerve physiology faren

peripheral nerve injury

axonal loss slide

upper extremity slide