Nerve Conduction Studies

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.

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.

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.

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.

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

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.

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.

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. T1

T2

DL (m/s) CV (msec) Amp(mV)Wrist-APB 3.2 15.0Elbow-Wrist 55 14.8

Velocity of conduction = Distance (cm) x 100(Meter/sec) T1-T2 (millisecond)

T1

T2

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 CV Motor CV Sensory latency Motor latency Nerve

50-70 m/sec. 45-70 m/sec. <4 millisecond <4.5 millisecond Median

50-70 m/sec. 45-70 m/sec.(elbow to wrist)

<3.5 millisecond (at wrist)

<4 millisecond (at wrist)

Ulnar

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.

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.

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.

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

Duration normally ↑ with proximal stimulation .. why?

Proximal stimulation

Distal stimulation

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

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 orthodromicalyAlong 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 fibersUsed in detecting motor root compromise.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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