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Anatomy II > EMG/NCS > Flashcards

EMG/NCS Flashcards

1
Q

Different names for clinical electrophysiology test

A
  • Electromyography (EMG)
  • Nerve conduction studies (NCS)
  • Nerve conduction velocity (NCV)
  • Electrodiagnostic tests
  • Electrophysiologic tests
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2
Q

Neurogenic Symptoms

A
  • Pain
  • Numbness
  • Paresthesias
  • Dysesthesias
  • Weakness
  • Cramping
  • Allodynia
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3
Q

Differential diagnoses that clinical electrophysiologic tests can detect?

A
  • Focal mononeuropathy
  • Cervical/Lumbar radiculopathy
  • Polyneuropathy
  • Brachial plexopathy
  • CNS disorder (exclusion bc it is not a good test for this)
  • Myopathy
  • Any combination of above
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4
Q

How Would You Evaluate the Results of a Radiologic Study?

A
  • Take a history and form a differential Dx
  • Perform your clinical examination and begin to narrow the differential Dx
  • You would look at the image (i.e. the data)
  • You would read the radiologist’s report
  • You would base your diagnosis on your evaluation of data from the history, your
    clinical tests & measures, your impression
    of the image and the radiologist’s report
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5
Q

Is electrophysiologic data alone sufficient for diagnosis?

A

no
gotta correlate the findings with other clinical evidence

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6
Q

Outcome of EPT is to classify/clarify….

A

– Nerve(s)
– Location
– Motor vs. sensory vs. both
– Axonal vs. demyelinating vs. both
– Timing (chronic, acute, etc)
– Re-innervation?
– What its not
– Recommendations

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7
Q

5 parts of The Clinical Electrophysiologic Examination

A
  • Patient history
  • Clarifying examination
  • Nerve conduction studies
  • Electromyography
  • Interpretation
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8
Q

5 salient features analyzed in nerve conduction studies

A

– Amplitude
– Latency
– Duration
– Conduction velocity
– Waveform shape

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9
Q

Parts of a motor nerve conduction study

A
  • Stimulating sites (anode and cathode)
  • ground electrode
  • active electrode
  • reference electrode
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10
Q

What is latency

A

Time between onset of stimulus and onset or peak of response

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11
Q

What does onset latency reflect?

A

the conduction of the induced impulse of the fastest and largest fibers

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12
Q

Amplitude

A
  • Baseline -to- peak (motor) or peak-to-trough (sensory) amplitudes
  • Compound Muscle or Sensory Nerve Action Potential (CMAP or SNAP)
  • Represents the total number of physiologically intact axons
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13
Q

What is duration

A

interval from first negative deflection to the return to baseline

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14
Q

How to calculate conduction velocity ?

A

distance/time OR
distance / (T2 - T1)

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15
Q

Can you calculate NCV from distal stimulation site to recording electrodes for motor study?

A
  • no
    1) terminal nerve starts to arborize, 2) conduction slows as diameter decreases, 3) distance of terminal branches not known, 4) time for neuromuscular transmission is unknown
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16
Q

Normal velocity for UE

A

> 50 m/sec

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17
Q

Orthodromic sensory nerve conduction study

A

normal direction
stimulating distally and recording proximal

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18
Q

antidromic sensory nerve conduction

A

stimulate at wrist and record at fingers

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19
Q

Axonal damage/dysfunction =

A

decreased amplitude proximal and distal

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20
Q

demyelination =

A

increased latency, decreased conduction velocity, decreased amplitude proximal to injury

21
Q

entrapment neuropathies:

A

mild cases = demyelination
severe cases = axonal loss and demyelination

22
Q

Does demyelination or axonal degeneration recover faster?

A

demyelination

23
Q

NCS benefits

A

– Excellent for identifying demyelination
– Entrapment neuropathies
– Only technique for sensory study
– +/- identifying axonal injury
– Limited use for radiculopathies or myopathies
– Not helpful for timing

24
Q

EMG Beenfits

A

– Gold standard to identify axonal injury
– Identifies radiculopathies and myopathies
– Helpful for classifying acuteness
– Not helpful to identify demyelination
– Only evaluates motor nerves or muscle

25
Q

4 conditions that electromyography records?

A

– with needle movement – insertional activity
– at rest – spontaneous potentials
– with minimal voluntary contraction – motor
unit size/shape
– with contraction increasing to maximum - recruitment

26
Q

What is insertional activity?

A
  • EMG parameter
  • Electrical activity due to insertion or movement of a needle in muscle
    – Normal, increased, decreased, or prolonged
27
Q

What is increased insertional activity associated with?

A

spontaneous potentials

28
Q

What does decreased insertional activity indicate?

A

reduced number of healthy muscle fibers
- due to chronic denervation (fibrosis) or muscle necrosis = poor prognosis

29
Q

Abnormal Findings at rest

A

– Fibrillation Potentials (Fibs)
– Positive Sharp Waves (PSWs)
– Complex Repetitive Discharge (CRD)
– Myotonic Discharges
– Fasciculation Potentials

30
Q

What is myotonia

A

hereditary muscle disease that causes cramps

31
Q

What causes fibrillation potentials and positive sharp waves

A
  • due to either muscle fiber denervation or muscle fiber splitting (no longer receiving acetylcholine so they become extremely sensitive)
  • severity is graded from 1+ to 4+ to grossly reflect amount of denervation
32
Q

amplitude of fibrillation potentials and positive sharp waves

A

Acute = 600 mV (first 2 mo)
Chronic = 100 mV (1 year; muscle atrophy)

33
Q

Grading of fibrillation potentials and positive sharp waves

A

0: No PSWs or Fibs
1+ Persistent/unsustained single trains in at least two muscle regions
2+ Moderate numbers in 3 or more muscle
areas
3+ Many in all muscle regions
4+ Baseline obliterated with potentials in all
areas of muscle examined

34
Q

EMG Parameter: Complex Repetitive Discharge

A
  • Occur in a Wide Variety of Chronic,
    Progressive Neurogenic and Myopathic
    Disorders
    – To Include some Chronic Denervating
    Conditions
35
Q

Fasciculation Potential

A

discharge of entire motor unit
characterized in the company they keep

36
Q

Polyphasic or Large Amplitude Motor Units

A
  • Evidence of Motor Unit Reorganization;
    Reinnervation
  • Two Means of Reinnervation:
    – Collateral sprouting
    – Direct regeneration of the original nerve
    terminal
37
Q

Collateral Sprouting

A

Terminal branches of an intact axon sprout to reinnervate motor fibers of another degenerated axon/motor unit
– polyphasic motor unit potential with larger amplitude and duration (means at least subacute)

38
Q

Direct Reinnervation

A

Axons of a degenerated motor unit regenerate to directly reinnervate its own motor fibers
- polyphasic motor unit potential with smaller amplitude and short duration

39
Q

EMG Parameter: Neurogenic recruitment

A
  • Reduced Recruitment
    – Rate of Individual MUs Firing will be out of
    proportion to the total number that are firing
    – Smaller units drop out and the remaining ones increase their rate to increase force
    – Seen in disorders of axonal destruction/block – May be only sign in neurapraxi
40
Q

EMG Parameter: Myopathic recruitment

A
  • Rapid Recruitment
    – More motor units activated than expected for
    the force of contraction
    – Seen when the motor fibers can not generate
    normal force (i.e. in myopathic disorders)
    – Rate firing is normal but amplitude is small
41
Q

Abnormal EMG findings - Acute

A
  • increased insertional activity, positive sharp waves and fibrillation potentials
  • decreased recruitment
  • normal motor units
42
Q

Abnormal EMG findings - Subacute

A
  • increased insertional activity, positive sharp waves and fibrillation potentials
  • decreased recruitment
  • polyphasic motor unit or normal amplitude
43
Q

abnormal EMG findings - chronic

A
  • decreased insertional activity
  • non or very small amplitude PSWs and Fibs
  • decreased recruitment
  • large amplitude motor units
44
Q

Clinical Electrophysiologic Findings of Carpal Tunnel Syndrome

A
  • 1st neural defect in early CTS is demyelination of sensory fibers
  • increased median DSL (more important)
  • decreased median SNAP amplitude (less important)
  • increased median DML (less sensitive, appears later)
  • decreased median CMAP amplitude (less sensitive, appears later)
  • normal NCV forearm segment (usually but not always)
  • EMG abnormalities in hand intrinsic Mm. supplied by median N. (thenar Mm. & lumbricals I-II)
    – least sensitive, appear in advanced cases
    – PSWs, Fibs, increased insertional activity, decreased recruitment
45
Q

Mild Classification of CTS

A
  • prolonged DSL +/- decreased SNAP amplitude
46
Q

Moderate Classification of CTS

A

prolonged DSL +/- decreased SNAP amplitude plus prolonged DML

47
Q

Severe Classification of CTS

A

prolonged DSL, prolonged DML, decreased CMAP amplitude, EMG abnormalities

48
Q

Clinical Electrophysiologic findings of cubital tunnel syndrome

A

– decreased ulnar sensory and motor NCV across elbow
– absent DUC SNAP in moderate to severe lesions
– decreased ulnar SNAP amplitude (possibly)
– > 20% CMAP amp. decreased with stim. above elbow (conduction block)
– > 0.4 ms latency difference in sequential 1-cm “inching” technique
– EMG abnormalities all ulnar Mm. except FCU
* least sensitive, appear only in severe cases
* PSWs, Fibs, increased insertional activity, decreased recruitment

49
Q

Pitfalls of NCS/EMG

A
  • Anatomic variations *
    Reference values
  • Temperature: cold hand = increased latency, increased amplitude
  • Excessive stimulus intensity - increased NCV, volume conduction to adjacent nerve

Anatomy II (8 decks)

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