basics of nerve conduction study

1. Nerve Conduction
Study
Dr Archana Verma
Guide: Dr Neha Rai

2. Overview
• History
• Introduction
• Basic anatomy and physiology
• NCS
• Motor
• Sensory
• Patterns
• Axonal loss
• Demyelination
• Conduction block
• Special conditions
• Late responses
• Blink reflex
• Repetitive nerve stimulation
• Anomalous innervations
• Artifacts and technical factors

3. History*
• 1771- Galvani *
• electrical stimulation of muscular tissue produces contraction and
force
• 1852- Herman von Helmholz #
• measured nerve conduction velocities in human subjects
• 1922- Gasser and Erlanger*
• cathode ray oscilloscope an recording equipment
• 1940- Weddell, Hodes, Dawson and Scott #
• Electromyography (EMG) and NCSs became a practical tool
with the publications of Weddell, Hodes, Dawson and Scott .
• * Mohamed Kazamel, History of Electromyography (EMG) and Nerve Conduction Studies (NCS): A Tribute to the
Founding Fathers (P05.259),Neurology February 12, 2013 vol. 80 no. 7 Supplement P05.259
• # Rossitza I, EMG and Nerve Conduction Studies in Clinical Practice,. January/February 2010 | Practical Neurology

4. Electrodiagnostic study
• An extension of clinical examination.
• It includes
• NCS
• EMG
• RNST
• Late responses
• Blink reflex

5. localization

6. Cardinal rules

7. Patient encounter
History
Examination
D/d
Formulate the
study
Explain to
patient
NCS

8. Anatomy

16. A 𝛼 = MNAP
A 𝛽 = CMAP, SNAP
A𝛿, B, C = Not recorded

17. Physiology
(What )
Saltatory conduction

18. Recording (How)
• Volume conduction
• Wave form morphology
• Near field and far field
potential

19. Nerve conduction study
V
CMAP
SNAP
MNAP

20. Motor conduction study (CMAP)
• Latency - reflects fastest
conducting motor fibers.
• Amplitude – reflects number of
depolarizing muscle fibers.
• Area - reflects number of
depolarizing muscle fibers.
• Duration- is a measure of
synchrony.
• Conduction velocity -reflects
fastest conducting motor fibers.
• Distance between proximal
and distal stimulation/ time
• Time= PL - DL

21. Sensory conduction study (SNAP)
Onset latency
Peak latency
Amplitude
Duration
Conduction velocity
Difference from CMAP
1. Two latencies
2. Distal stimulation only for conduction velocity calculation.

22. ONSET VS PEAK LATENCY
ONSET PEAK
Time for stimulus to
initial negative
deflection.
Stimulus to midpoint of
first negative peak.
Represents fastest
conducting fibers.
Population represented
not known.
Used in calculating
conduction velocity.
-
Inter examiner
variation.
No (normal values
exist)

23. MOTOR VS SENSORY CONDUCTION
• TABLE
1.Technically
2.Order
3.Amplitude
4. Gain
5.Duration
6. Current
Less
demanding
Performed first
Milli volt
2-5 milli volt
5-6 msec
20-50 mA
Electrical noise
important
Later
Micro volt
10-20 micro volt
1.5 msec
5-30mA
SNAP

24. MIXED CONDUCTION STUDY
(MNAP)
1. Sensory muscle afferent 1 a fibres
are recorded only in this study.
2. Done in median ,ulnar or distal
tibial nerve.
3. 1a fibres are earliest affected in
demyelinating and entrapment
neuropathies.
4. Settings used same as SNAP.

25. ANTIDROMIC VS ORTHODROMIC
1.Superior
2.Higher amplitude SNAP
3.For recording very small
potentials
4.Less subject to noise and
artifacts.
5.Followed by large volume
conducted motor potential
6.Misinterpretation error

26. LESIONS PROXIMAL TO DRG
RESULTS IN NORMAL SNAP
Lesions of sensory nerve
root/spinalcord/brain causes
normal SNAP. Because DRG
and peripheral nerve is
preserved.
Insensate limb with
normal SNAP
signifies lesions
proximal to DRG

27. TEMPORAL DISPERSION AND
PHASE CANCELLATION
Increase in duration and decrease in amplitude and area
More prominent with proximal stimulation in sensory studies.
Less prominent with motor studies.
In demyelinating lesions temporal dispersion and phase cancellation
become prominent for motor fibers.
.

28. PRINCIPLES OF
STIMULATION
• 1. USE SUPRA MAXIMAL
STIMULATION
• OPTIMISE STIMULATION

29. Important basic patterns
V
• NEUROPATHIC
• AXONAL LOSS
• DEMYELINATION
• CONDUCTION BLOCK
• MYOPATHIC
• NMJ

30. Axonal loss
DEFINITION
decrease in amplitude
normal or decreased CV (never < 75% of lower normal )
normal or prolonged distal latency.(never > 130% of upper normal)
EXCEPTION
Hyperacute axonal loss (nerve transection/nerve infarction)

31. Demyelination
DEFINITION
marked slowing of CV (< 75% of lower normal)
marked prolongation of DL(> 130% of upper normal)
or both.
Any M/S/Mixed CV < 35m/s in upper limb or < 30m/s in lower limb
EXCEPTION
regenerating nerve fibers after complete axonal injury

32. Conduction block
A feature of acquired demyelinating disease
DEFINITION
1.> 50% drop in area/amplitude between proximal and distal stimulation
sites.
EXCEPTION
tibial nerve up to 50% drop may be normal with popliteal fossa stimulation
Demyelination associated with amplitude decrease is suggestive of
1.Axonal loss
2.Conduction block

33. Abnormal temporal dispersion
DEFINITION
1.drop in CMAP amplitude or area > 20% and < 50%
2.or increase in CMAP duration > 15%.
3. in axilla / erb’s point > 40% (amplitude/area) and > 30% (duration )
4. At proximal stimulation site.

34. Conduction block at non entrapment sites differentiate between acquired and
inherited demyelinating conditions.
1.inherited- uniform slowing of CV
2.acquired – conduction blocks ,
abnormal temporal dispersion
decreased CV

35. Late responses
V
F response
H reflex
Axon reflex

36. Late responses
To study more proximal Nerve segments
F response H reflex
Axon reflex

37. F response
F = Foot
Not a true reflex (no synapse)
Represents a small CMAP
Normal in conditions affecting
sensory nerves only.
Orthodromic motor response
Antidromic F response
F Response
Afferent Motor
Efferent Motor
Synapse No
Nerves studied All
Stimulation Supramaximal
Configuration
Usually polyphasic
Amplitude 1–5% CMAP
Varies with each simulation

38. F response
Minimal F wave
latency- most reliable
and most useful
Chrono dispersion
Persistence
F estimate
F Response
Major uses
Early Guillain–Barré
syndrome
C8–T1, L5–S1
radiculopathy
Polyneuropathy
Internal control
(entrapment neuropathy)
Normal values
≤32 ms median/ulnar*
≤56 ms peroneal/tibial*
Compare to F estimate
Compare symptomatic to
asymptomatic side
Chronodispersion
<4 ms (median/ulnar)
<6 ms (peroneal/tibial)
Persistence >50%
F estimate= 2D/CV X 10 +1 +DL

39. F response
Limitations
1.F responses may be absent in sleeping or sedated patients
2.F responses may be absent with low-amplitude distal CMAPs
3. Picks up C8-T1 and L5-S1 radiculopathies mainly.
4. Can’t pick up sensory radiculopathy.
May be enhanced by Jendrassik maneuver

40. H reflex
H Reflex
Afferent Sensory (Ia muscle spindle)
Efferent Motor
Synapse Yes
Nerves
studied
Tibial–soleus (median-FCR, femoral-
quads)
Stimulation Submaximal, long duration pulse (1 ms)
Configuration
Triphasic and stable
At low stimulation intensity, H is present
without M
As stimulation is increased, H and M
increase
At high stimulation, H decreases and M
increases
H = Hoffman,1918
True reflex

41. H Reflex
Major uses
Early polyneuropathy
S1 radiculopathy
Early Guillain–Barré syndrome
Tibial and sciatic neuropathy, sacral
plexopathy
Normal values
≤34 ms*
Leg length nomogram
Height nomogram
≤1.5 ms difference side to side
H/M ratio ≤50%
Miscellaneous
Electrical correlate of the ankle jerk
Must be present if ankle jerk is present
May be present even if ankle jerk is
absent
May be enhanced by Jendrassik
maneuver
H Reflex
Measurements
Minimal latency
H/M ratio
(maximal
H/maximal M
amplitude)

42. H reflex

43. Axon reflex
 Not a true reflex
 Seen in reinnervated muscle with submaximal
stimulation
 Suggestive of ephaptic spread of stimulus
 Found in
1.reinnervation following axon loss
2.GBS

44. Blink reflex
Electrical correlate of clinical corneal reflex
True reflex
Detects lesions of 5th , 7th ,pons , medulla.
R1= disynaptic= V1 Vm 7th nucleus with ipsilateral 7th
R2= multisynaptic= V1 Vs ipsi & contra 7th nucleus and nerve

45. Blink reflex
A: Normal pattern
B: Incomplete right trigeminal lesion
C: Complete right trigeminal lesion.
D: Incomplete right facial lesion.
E: Complete right facial lesion.
F: Right mid-pontine lesion
G: Right medullary lesion
H: Demyelinating peripheral polyneuropathy.

46. Anomalous innervation
V
Martin gruber anastomosis
Accessory peroneal nerve
Riche Cannieu anastomosis

47. Martin gruber anastomosis
1.Ulnar study: pseudo conduction block between wrist and BE
2.Ulnar study: pseudo conduction block between BE and AE

48. Martin gruber anastomosis
3.Ulnar study: pseudo conduction block between wrist and BE recording FDI
4.Median study: increased CMAP proximally

49. Martin gruber anastomosis
5.MGA & CTS : Positive proximal deflection and factitiously fast CV
6. Needle EMG and MGA

50. Accessory Peroneal Nerve

51. Artifacts and technical factors