Electrodiagnostic Testing MAJ Min Ho Chang MD. Outline What is EDX? Anatomy & Physiology Nerve Injury Nerve Conduction Studies/Needle Exam Clinical Utility.

Electrodiagnostic Testing

MAJ Min Ho Chang MD

Outline

• What is EDX?• Anatomy & Physiology• Nerve Injury• Nerve Conduction Studies/Needle Exam• Clinical Utility

EMG and Nerve Conduction Studies

• An extension of the Physical Examination• Assess physiology of nerve and muscle• Quantitates nerve and/or muscle injury• Real time data• Provides Useful Data Regarding Nerve Injury– Diagnosis - Duration– Prognosis - Site– Treatment - Type– Further Testing - Severity

Anatomy & Physiology

• Motor Unit– Anterior Horn Cell– Axon– Terminal Branches– Neuromuscular Junction– Muscle Fibers

• Epineurium• Perineurium• Endoneurium• Myelin• Axons

Action Potential

Nerve Fiber ClassificatonFiber Type

Function Diameter Conduction Velocity

Aα Proprioception, somatomotor, touch

10-20 50-120

Aβ Touch, pressure, extrafusal 4-12 25-70Aγ Motor to muscle spindle 2-8 10-50Aδ Pain (esp cold) 1-5 3-30B Preganglionic autonomic 1-3 3-15C Pain/temp/postganglionic

autonomic/mechanoreceptor<1 <2

NMJ Anatomy

• Synaptic cleft• Acetylcholine• Motor end plate

Electrochemical Conduction

• Acetylcholine– In presynaptic vesicles

(Quanta=10000)– Exocytosis via Ca++

mediated pathway

Muscle Fibers

MUSCLE CONTRACTION

• Troponin-Tropomyosin complex

• Calcium Binding• Excitation-Contraction

Coupling

MUSCLE FIBER TYPES

• Type 1– “Slow Twitch”– Small Cell Body– Thinner axon

• Type 2– “Fast Twitch”– Larger Cell Body– Thicker Axon

MUSCLE FIBER TYPES

NERVE INJURY

• Seddon’s Classification– Neurapraxia (Conduction Block)– Axonotmesis– Neurotmesis

• Neurapraxia– Demyelination– Axon Intact– No Wallerian

Degeneration– Action Potential

slowed– Prognosis Good

Wallerian Degeneration

• Axonotmesis– Axon disrupted– Connective Tissue

(endoneurial/perineural) may or may not be intact.

– Wallerian Degeneration DOES occur

– Denervation– Prognosis depends

• Neurotmesis– Axon and connective tissue disrupted– Complete severance of nerve– Surgical Repair– Poor prognosis

• Mechanisms of Recovery– Remyelination– Collateral Sprouting– Regeneration

NERVE INJURY

Collateral Sprouting

REINNERVATION (FIBER TYPE GROUPING)REINNERVATION (FIBER TYPE GROUPING)

For Practical Purposes

• “Demyelinating Injury”– Neurapraxia (Conduction Block)– Diffuse Demyelination– Good prognosis

• “Axonal Injury”– Axonotmesis – Neurotmesis– Prognosis depends on length/severity

NCS/EMG

NCS EMG

INSTRUMENTATION

• Electrodes– Active (Recording)• “G1”, “E1”• Action Potential• Electrical “Noise”

– Reference• “G2”, “E2”• No Action Potential• Electrical “Noise”

– Ground• Excess Charge G2 G1 GROUND

NERVE CONDUCTION STUDIES

3 Main AP measured

• Compound Motor Action Potential (CMAP)• Sensory Nerve Action Potential (SNAP)• Compound Nerve Action Potential (CNAP)

NCS Parameters

• Latency– determined by conduction velocity of the

nerve, neuromuscular junction & muscle• Amplitude– determined by number of muscle fibers

activated• Conduction velocity– determined by conduction velocity of the

fastest fibers

Important Patterns

• Axonal Loss– Decreased amplitude– Maintain latency

• Demyelination– Prolonged latency

• Conduction Block– 50% drop in amplitude

(variable)

Important Patterns

• Proximal Lesions (Radiculopathy)– Sensory Nerve Root• Proximal to DRG• Peripheral Axon Intact

– Motor Nerve Root• Distal to Anterior Horn Cell• Axonal Degeneration Occurs

NERVE CONDUCTION STUDIES: Important Patterns

NEEDLE EMG

Needle EMG Parameter

• Spontaneous Muscle Membrane Electrical Activity• Motor Unit Configuration• Motor Unit Recruitment

• Spontaneous Activity:– Electrical Waveforms not under voluntary control– Healthy muscle is normally electrically silent at

rest

Abnormal Spontaneous Activity

• Fibrillation Potential (“Fib”)– Membrane

Instability• Denervation• Myopathy• Trauma

• Positive Sharp Wave (“PSW”)– Same significance as Fib

NEEDLE EMG: Spontaneous Activity

Motor Unit Analysis

• Morphology– Duration– Amplitude– Phases

• Stability• Recruitment

Common Patterns

• Axonal Loss– PSWs and Fibs present– Decreased Recruitment– MUAP changes

• Increased Duration• Polyphasia• Increased Amplitude

• Demyelinating Lesion– NO PSW’s and Fibs– No MUAP changes– Decreased Recruitment

• Myopathy

Common Patterns

• EMG and NCS changes evolve over time…..

– Wallerian Degeneration• 3-5 days for motor fibers• 6-10 days for sensory fibers

– Reinnervation

Evolution of NCS/EMG Changes

• Axonal Loss– <3 days old• No Wallerian

Degeneration• DISTAL NCS normal!!• No PSWs/Fibs• Normal MUAPs• Decreased

Recruitment

Evolution of NCS/EMG Changes

• Axonal Loss: 1-6 weeks old– NCS:• Decreased

Amplitude• Normal CV*• Normal Latency*

– EMG:• Fibs/PSWs present• Decreased

Recruitment• Normal MUAP

Evolution of NCS/EMG Changes

• Axonal Loss: Months-Years Later– NCS:• Decreased Amplitude• Normal CV*• Normal Latency*

– EMG:• No Fibs/PSWs• Decreased

Recruitment• MUAP

– Long Duration– High Amplitude– Polyphasic

Evolution of NCS/EMG Changes

• Demyelination– NCS• Decreased Conduction Velocity• Prolonged Latency• Variable changes in Amplitude

– Normal EMG!!

• Conduction Block– NCS• Decreased Amplitude• Prolonged Latency

– EMG• Decreased Recruitment• Normal MUAPs• No PSWs/Fibs

Clinical Use

Common Entrapment Syndrome

• Median at the Wrist (CTS)• Ulnar at the Elbow • Peroneal Palsy at the Fibular Head

Carpal Tunnel EDX Grading

• Simple Grading Scheme for median neuropathies at the wrist

  - Mild --> sensory latencies prolonged  - Moderate --> motor latencies prolonged  - Severe --> motor amplitude reduced and/or

evidence of EMG abnormalities on EMG.

CTS Clinical Pearl

• By 6 months post-surgery, the maximum improvement in latencies will have occurred

• 1/2 of patients post surgery do not return to normal latencies

• Must compare to post-operative latencies to pre-op latenciec to determine an unsuccessful surgery

• If no preoperative latencies, wait another 3-6 months and assess the interval change

Tarsal Tunnel

• EMG: Footwear and trauma cause low level of spontaneous activity in foot muscles

• Controversial

Radiculopathy

• Can confirm the presence of a radiculopathy with or without findings on imaging studies

• EMG is not needed in all radic patients• Most useful w/ multi-level pathology on MRI but

inconclusive PE– Can help determine location of radiculopathy

• Multi-level radics present in 12-30%• Excludes other possible diagnoses• Can determine time course or severity of

radiculopathy

• NCS usually WNL in radics; abnormalities are found on needle EMG– SNAP is normal in lesions prox to DRG, and nearly all radics damage nv

root proximal to DRG

• The NCS is done to r/o other conditions, specifically entrapment neuropathy and plexopathy

• False positive rates on MRI are 10% (cervical)• Radics can be seen without structural abnormalities on MRI• Sensitivity ranges from 55-84%

– Slightly lower compared to MRI– Sensitivity increases w/ neurologic abnormalities

• Specificity ranges upto 90-95%– Slightly higher than MRI

EMG Caveats

• Time Course in Radiculopathy– Acute phase: decreased MUAP recruitment but NML

morphology– Day 10-14: + waves/fibs in paraspinals– Day 14-21: + waves/fibs in prox peripheral muscles– Day 21-28: + waves/fibs in distal peripheral muscles (up to

5-6 wks total time)– MUAP morphology is the same as denervation occurs, but

polyphasia (also paraspinalproxdistal muscles) heralds reinnervation (over the course of months, i.e. chronic radic)

Caveats• Limitations of Needle EMG– May have NML EMG in acute phase – If only demyelination is present, EMG can be NML (only

sig CB w/ weakness will give decreased MUAP recruitment (rare in radic))

– If sensory root is predominantly affected, EMG will be NML– Different fascicles may be more or less involved (i.e. some

muscles of a particular myotome may be involved while others spared)

Caveats

• The “double crush”– Cervical radic (C6-C7) plus median neuropathy at

the wrist – C8-T1 radic plus ulnar neuropathy at the elbow– Does not infer that radic predisposes to median

neuropathy at the wrist

Peripheral Neuropathy

Plexopathy

• Compression (CABG)• Inflammatory (Parsonage-Turner

Syndrome)• Radiation Injury (Radiotherapy)• Traumatic Injury (Traction, laceration, missile)• Ischemia (Diabetic amyotrophy)

Neurogenic Thoracic Outlet Syndrome

• Incidence 1:1,000,000• A partial lower trunk plexopathy or C8/T1 root

injury• Secondary to prominent C7 transverse process

or prominent cervical rib• Normal study focused on brachial plexus trunk

essentially rules out

Other Pearls

• Electrodiagnostic studies are a supplement to, and not a replacement, for the history and physical examination

• Electrodiagnostic results are often time-dependent

• Electrodiagnostic studies are not “standardized” investigations and may be modified by the practitioner to answer the diagnostic question

EDX Testing

When to order EDX testing

• Neck/arm pain, back/leg pain, suspected CTS, peripheral neuropathy, weakness, wasting, cramps.

• Sort out these problems, establish etiology, assess severity, provide objective/prognostic information.

• Accurate diagnosis leads to effective treatment.

Typical diagnosis for consideration on EDX consultation

• Mononeuropathy• Mononeuropathy Multiplex• Radiculopathy• Plexopathy (Brachial or Lumbosacral)• Anterior Horn Cell Disorders

• Diffuse neuropathies• Cranial neuropathies• Neuromuscular Junction Disorders• Myopathy • Traumatic nerve injury– Intervention vs wait– Assess improvement– 18 month time frame

When Not to order EDX• Central Nervous System Disorders (Stroke, TIA,

Encephalopathy, spinal cord injury)• Multiple Sclerosis• Total body fatigue, fibromyalgia• Joint pain• EDX consult is not a substitute for

PM&R/Neurology/Orthopedic etc…

Counseling Patients

• Inform the patient about the test and the reasons behind it.

• Give them heads up about what to expect.– Small gauge solid needle test portion– Electrical stimulation portion– Duration of test depends on findings but typically

about 60minutes.– Not the most comfortable but tolerable for just about

anyone.– Risks very small. Verbal consent only.

Reading EMG Reports• Tailored to referring provider

– Specific questions from ie Hand surgeon, spine surgeon– Fuzzier question, ie generalized weakness

• Two broad styles– Tabular or narrative– Most read final impression only

• Clinical Management usually deferred to referring provider• Clinical vs Electro diagnostic impression• An outline of the localization, severity, and acuity of the

process• Notation of other diagnoses that are detected/excluded• Explanation of any technical problems

Summary: Utility of EMG/NCS

• Highly sensitive indicator of early nerve injury• Detects dynamic and functional injury missed by MRI• Provides information regarding chronicity of nerve injury• Provides prognostic data• Highly localizing• Clarifies clinical scenarios when one disorder mimics another• Identifies combined multi-site injury, avoiding missed diagnoses• Identifies more global neuromuscular injury with focal onset• Provides longitudinal data for charting course, response to

therapy

QUESTIONS ?