1. Nerve
Conduction
Studies

2. Nerve Conduction Studies
Is the evaluation of the conducting efficiency of
peripheral n. added a new dimension to
electrodiagnostic testing.
Four determinations can be made with this test:
- Motor nerve conduction velocity.
- Motor latency.
- Sensory nerve conduction velocity.
- Sensory latency.

3. NCS have been used clinically to:
 Locate peripheral n. disease within single
nerves and along the length of nerves.
 Differentiate nerve lesions from diseases
of muscles or NMJ.
 Distinguish axonal degeneration from
segmental demyelination.

4. Conduction velocity:
It is the speed at which motor and
sensory impulses traverse a given
segment of nerve (meter/sec)
 Larger axons & proximal
segments conduct faster than smaller
ones & distal segments.
 New born infant's nerves have
slower velocities than adult.
 CV in UL is faster than in LL.
 In elderly there is slowing of
conduction.
 ↓ in local tissue temperature
slows CV.

5. latency
Latency:
 It is the time in msec. from the
application of the stimulus
artifact until the action potential
appears on the oscilloscope.
 Motor latency include several un
measurable events:
- Utilization time (time required
to produce rheobasic stim.).
- End plate potential.
 These events are eliminated
when 2 point stimulation Study is
used.

6. Latency:
 In some nerve segments where
only one site can be stimulated
for reasons of anatomical
inaccessibility, latency
measurement must replace CV.
 Latency varies directly with the
distance of stimulating electrode
from muscle.
latency

7. Motor nerve conduction:
• The nerve is stimulated
supramaximally by means of
surface electrode placed over the
nerve where it is relatively
superficial, with the cathode is
closer to recording electrode.
N.B: Needle stimulating electrode
is used in deep nerves as sciatic
nerve.

8. Motor nerve conduction:
• Recording from one muscle
supplied by this nerve distal to
site of stimulation using surface
electrodes:
- Active electrode over ms
belly.
- Reference electrode over ms
tendon.
 N.B.: Needle recording
electrodes used in deep muscles.

9. Motor nerve conduction:
• The directly evoked muscle action
potential recorded after stimulation at T1
of peripheral n. this AP called M
response.
• The same nerve is stimulated similarly
at a more distal point and this latency
(T2) is also recorded.
• The distance between 2 point of
stimulation is measured in cm.

10. DL (m/s) CV (msec) Amp(mV)
Wrist-APB 3.2 15.0
Elbow-Wrist 55 14.8
Velocity of conduction = Distance (cm) x 100
(Meter/sec) T1-T2 (millisecond)

11. Normal conduction values:
• Motor conduction velocity ↓↓ in lesions affecting the
axon of peripheral nerve esp. in diseases affecting
myelin sheath than those affecting axoplasm.
• Striking reduction occurs in infectious polyneuritis
and Charcot Marie-Tooth disease.
Sensory CVMotor CVSensory latencyMotor latencyNerve
50-70 m/sec.45-70 m/sec.<4 millisecond<4.5 millisecondMedian
50-70 m/sec.45-70 m/sec.
(elbow to wrist)
<3.5 millisecond
(at wrist)
<4 millisecond
(at wrist)
Ulnar

12. Compound motor action potential
(CMAP):
Stimulation of any peripheral nerve evoke
an electrical and mechanical response in
those muscles innervated by the nerve
distal to site of stimulation.
The electrical response is called CMAP or
M- wave and it is the summated electrical
activity of all muscle fibers in the region
of recording electrode that are innervated
by the nerve.
M wave is described by its latency,
amplitude and configuration.

13. Motor Latency is the time in
millisecond from application of
stimulus to initial deflection from
the baseline. It is the time required
for AP in the fast conducting fibers
to reach nerve terminals and
activate ms. fibers.

14. Amplitude of M wave is the
height in millivolts from baseline
to the peak of –ve deflection.
• Amplitude is normally ↓ with
proximal stim.
• Amplitude is normally
constant in size on repeated
stim.
• Amplitude is directly
proportional to no. of ms.
fibers depolarized.

15. Duration of M wave is the time in
milliseconds from onset to end of initial –
ve phase of the potential.
Duration reflect synchrony of discharge
of individual ms fibers i.e. when ms fibers
are discharged in near synchrony 
shorter duration of AP. If conduction
velocities vary widely among different
axons  some ms fibers are activated
earlier than others longer duration of
CMAP.
M wave duration
M wave amplitude

16. Duration normally ↑ with
proximal stimulation .. why?
Proximal stimulation
Distal stimulation

17. The normal configuration of CMAP:
1- G1 over end plate region of
stimulated ms. biphasic, negative
positive.
2- G1 not over end plate region of
stimulated ms. triphasic with initial
positivity.
Normally only minimal changes in
configuration at proximal sites of
stimulation.
G 1
G 2

18. FWAVE
Late CMAP evoked by supramaximal stim.
of motor nerve with stim. cathode proximal
to anode & recording from distal muscle.
Antidromic motor conduction  Activation
of AHC santidromically Discharge another
AP orthodromicaly
Along their axons  Recording second MP
after20-40msdelay
F wave has variable latency with repetitive
stimulation .
Although it represent a sampling of axons in
the nerves it can give an estimate of
conduction in central segments of motor
fibers
Used in detecting motor root compromise.

19. Sensory nerve conduction (SNC):
SCV measurements differ from MNC in that the action
potential of the nerve itself rather than of a muscle
serves as the observable end point.
SNAP are of much smaller amplitude.
SNCS are more sensitive than MNCS in detecting
early and mild disorders.

20. Orthodromic method:
Stimulating electrode (supramax.)
over distal sensory branches of n.
Recording electrode over more
proximal point on n. trunk.
The nerve will conduct the impulse
orthodromically as normal from
distal to proximal.

21. Antidromic method
• Stimulating electrode over
proximal point on n. trunk.
• Recording electrode at distal
sensory branches of n.
 The nerve will conduct the
impulse antidromically opposite
to normal from proximal to
distal.
 Diabetic neuropathies striking
↓↓ in SNCV.

22. Motor and sensory latencies:
• Helpful in evaluation of distal portion of peripheral n.
• ↑↑ terminal latency in entrapment neuropathies
(CTS, TTS) and in peripheral neuropathies but to
lesser degree.
• Distortion of A.P (↑ duration and polyphasia) is also
seen in entrapment neuropathies due to temporal
dispersion.
• CNS help in:
- Determining type, extent, site of peripheral nerve
lesion.
- Follow up.

23. A- Neuropraxia
(temporal block of n. conduction due to
mild compression or traction):
1- Conduction study:
• Distal stimulation: (below site of block)
 normal response.
• Proximal stimulation:
 complete block  no response.
 partial block  ↓ amplitude of CMAP
 focal demyelination  prolonged
latency.
localized slowing of conduction along
compressed seg.
↓ amplitude, ↑ duration and split up of M
response.

24. 2- EMG at ms. innervated distal to lesion:
No spontaneous activity (as there is no
Wallerian deg.).
On voluntary contraction:
- complete block → loss of MU.
- partial block → few normal MU under
vol. control
→ reduced IP.

25. B- Axonotemsis & Neurotemesis
1- Conduction study:
In 1st 72 hr the distal segment conduct normally.
After that (4-7days), Wallerian deg. Of axons occur
no conduction of damaged fs ↓ amplitude of
M response (proportional to no. of fs not severely
damaged to undergo degeneration.
If complete cut of nerve no response.

26. B- Axonotemsis & Neurotemesis
2- EMG:
Complete denervated ms (complete n. cut):
immediately after injury  no MU under vol. control.
few days after  ↑ insertional activity.
12-16 days after injury  abnormal spontanous
activity earlier in muscles more proximal to nerve lesion.

27. Partial denervated ms (partial cut):
- Immediately after injury → ↓ no of MU under vol.
control → ↓ IP.
- 14-21 days after injury → spontaneous activity
fibrillation and
+ve sharp waves earlier in proximal ms.
As reinnervation occur: in axonotemesis only:
- ↓↓ spontaneous activity.
- Low amplitude polyphasic potentials (nascent potentials)
by time replaced by normal potentials.
- Recruitment pattern ↑ towards normal.
- Slow conduction in regeneration n. fibers.

28. C- Neuropathies:
2- Axonal neuropathies (drug induced
neuropathies):
CV normal if even only one fast conducting motor fiber is
spared, or slightly ↓ by loss of fast fibers and sparing slow
conducting fibers.
↓ amplitude of CMAP and SAP due to loss of some
conducting fibers.
Needle EMG → picture of chronic partial denervation is
distal muscles of limbs.

29. At rest: prolonged insertional activity.
Abnormal spont. Activity → fibrillations and +ve sharp waves.
At mild volition: ↑ duration of MUAPs.
Slight ↑ in amplitude of MUAP.
↑ % polyphasia.
At max. volition: ↓ IP (reduction is proportinal to no. of
degenerated n. fibrrs.
↑ firing rate of MU.

30. Demyelinative neuropathies (diabetic neuropathy):
 Latency measurements are lengthened.
 CV ↓ by > 40%.
 ↓ amplitude and ↑ duration of evoked potential and freq. split up.
 Orthodromic sensory cond. is most sensitive test for Diabetic
neuropathy.

31.  Needle EMG:
 Normal (no spont. activity, nomal MUAP parameters,
normal IP).
 If conduction block occur → ↓ IP.
 If conduction block + axonal deg. occur → ↓ IP + spont.
activity.
Mixed picture (infective polyneuropathy) denervation
potentials + ↓ CV.