Nerve Conduction Studies / EMG

Pathological Processes

 

Two possible types of injury

1.  Axonal

2.  Myelin sheath

 

Myelin Sheath Damage

 

Causes

 

Commonly seen in compression

- i.e. CTD, ulna nerve at elbow

- area of focal demyelination

 

Can progress to a conduction block

- some or all axons simply stop working

- decreases the amplitudes

 

Effect

 

1.  Usually affects sensory fibres first

- affects motor fibres later

 

2.  Results in slowing of conduction velocity

 

3.  Prolonged distal latency

- i.e. long time for stimulation to reach recording electrodes

 

4.  Effect is focal

- slowed conduction velocity above block

- normal below

- can isolate level of entrapment

 

5.  If progresses to conduction block

- decreased amplitude

 

Axonal Damage

 

Cause

 

Due to severe damage to the axon

- laceration / avulsion / severe contusion i.e. Sunderland type 3 and 4

 

Effect

 

1.  Decreased amplitude - related to number of axons affected

2.  Normal latency and conduction velocity

3.  In contrast to demyelination, cannot get normal result by stimulating below level of lesion

 

SNAP

 

Definition

 

Sensory nerve action potentials

 

Technique

 

Stimulate a sensory nerve and measure the action potential distally

 

Median nerve

- two stimulations over median nerve in forearm (S)

- ring type recording (R) electrodes on index and middle finger (sensory nerves only)

 

Ulna nerve

- stimulation over ulna nerve at elbow or wrist

- record over little finger

 

Measure

 

Latency

- time to reach distal electrodes

 

Conduction velocity

- simply measure distance between electrodes

- computer calculates velocity

 

Amplitude

- number of axons being stimulated

- also need all the axons transmitting at a similar velocity or get a wide, shorter velocity

 

NCS Sensory

 

Uses

 

Diagnosis of carpal tunnel syndrome

- measure conduction velocity

- in upper limb is usually > 50 m/s

- compare to ulna nerve / standard charts

- median nerve is slower than ulna, but difference should be < 0.2 ms

- usually use 0.3 ms as cut off

 

Ulna nerve compression

 

CPN compression

 

Radial nerve

 

Sciatic nerve

 

CMAP

 

Definition

 

Combined motor action potential

- called this because is difficult to stimulate just one muscle

- i.e. on thenar eminence want to stimulate just APB, but would get FPB also

 

Technique

 

Stimulate a nerve and record from a muscle that it innervates

 

Measure

 

1.  Distal latency

 

2.  Conduction velocity

- stimulate at 2 points and measure difference between times

- 50 m/s UL

- 40 m/s LL

 

3.  Amplitude

 

NCS Motor

 

Uses

 

Same as for SNAP

- entrapments

- slowing of conduction velocity and latency with demyelination

- +/- decreased amplitude if any axonal damage (severe entrapment, traumatic contusions, lacerations)

 

MNAP

 

Principle

Combine sensory and motor

- measuring electrodes simply in palm in median nerve distribution

- measure sensory and motor components

- see in delayed latency or conduction velocity

- very simple for CTD

- can move onto more specific SNAP and CMAP if needed

 

Responses

 

Amplitude

 

Proportional to number of functional axons

- loss of axons causes decrease in response amplitude

- amplitude is a measure of the total number of functioning axons in the nerve

 

Conduction Velocity

 

Calculated fro

m the latency values

- reflects only the function of the fastest conducting fibres

- fortunately most compressive or traumatic disorders affect the largest fibres

 

Calculated by

- dividing the latency by the distance between the stimulating and recording electrodes

 

Problem in CMAP

- the response is measured over the muscle

- the delay at the motor end plate must be considered

- conduction slowed by the small, unmyelinated terminal branches of the motor axon

- and by the time taken for release of Ach

- typically ~1 mS

- because the delay is fairly constant the terminal latency can be compared with the range of normal values

 

The Late Responses

 

Uses

 

Nerve root or proximal nerve lesions 

- cannot use simple NCS

- stimulate a peripheral nerve and recording over a muscle

- wait for a delayed signal

-  has travelled up the nerve to the anterior horn cell then returned to the muscle

 

F Response

 

Technique

 

Supramaximal stimulus is applied to a nerve

- motor nerves are directly depolarised

- like all axons they conduct equally well in all directions

 

2 impulses

Orthodromic 

- which travels to the muscle and produces the typical M response

 

Antidromic 

- which travels back to the anterior horn cell and depolarizes the cell body

- to be detected, the second muscle contraction has to occur after the first has subsided

- only muscles in which the round trip takes over 15 - 20 mS can be used

 

Problem

 

Does not measure sensory nerves

 

Uses

 

Brachial plexus injury

- want to know if nerve roots intact

- look in muscles relevant for each nerve root

- i.e. stimulate median nerve, look in thenar eminence (T1)

- look to see if F wave intact, delayed or absent

- problem is most muscles supplied by more than one nerve root

 

Now

- use MRI to see if nerve root avulsion

 

H Reflex

 

This is the electrical equivalent of the deep tendon reflex

A mixed peripheral nerve is sub maximally stimulated

- stimulates the large myelinated sensory nerves that convey muscle stretch

- they are the most easily depolarised of the axons

- following a relatively weak stimulus these sensory fibres are selectively depolarised

- a signal ascends to the dorsal root ganglion and then through the monosynaptic reflex arc

- depolarises the anterior horn cells 

- causes a secondary signal in the motor axons with a subsequent muscle contraction

 

Characterised by having a consistent latency 

- is elicited by a stimulus so small that it does not cause a direct muscle contraction.

 

Unfortunately it can only be elicited in the tibial nerve (and recorded over the gastrocnemius)

 

Electromyography (EMG)

 

Technique

 

Needle placed in relevant muscle

- record electrical potential

- at rest and voluntary contraction

 

NCS Motor

 

NCS Waveform

 

Neuropathy

 

Denervation

- takes 3/52 to see

- amount of time for wallerian degeneration to occur

- if do earlier will get a false negative

- normal muscle electrically silent at rest

 

Findings

- spontaneous depolarisation in muscle

- fibrillations

- positive sharp waves

 

Reinnervation

- takes 3/12 to see

- due to surviving motor axons branching out and recruiting other motor units

 

Findings

- see large polyphasic motor unit potentials

 

Myopathy

 

Muscle problems

- specific patterns of EMG
- Duchenne's muscular dystrophy /myotonica dystrophy

 

Shortfalls of EMG

 

It is only a sampling technique

- normal areas in an abnormal muscle may have normal potentials

 

Specific uses of NCS / EMG

 

Conduction blocks

 

SNAP / CMAP

- median nerve, ulna nerve

- confirm entrapment

- evaluate site of entrapment

 

Axonal / Nerve damage

 

1.  Radial nerve palsy with humeral fractures 

 

Question

- is nerve in continuum or lacerated?

 

NCS / EMG cannot tell you that

- similar findings for Stage 4 and 5 Sunderland

 

Can give information regarding severity of injury

- denervation potentials at 3/52

- indicates Sunderland grade 3 or greater

 

Can give idea of prognosis

- i.e. is there any chance of recovery?

- reinnervation on EMG at 3/12

 

2.  CPN injury at knee, sciatic nerve injury following THR

 

Can give you idea of prognosis

- i.e. SNAP intact at 3/12

- neuropraxia

 

Neuropraxia

 

Minimal axonal damage

- demyelinating / conduction block only

- no Wallerian degeneration

 

Findings

 

3/52

- some SNAP and CMAP still seen

- minimal denervation signs i.e. fibrillation

- means nerve is not too badly injured

- prognosis good

- should be just a neuropraxia

 

Laceration / Neurotmesis

 

Both conditions will lead to Wallerian degeneration

- severity dependant on number of axons injured

 

3/52

- no SNAP / CMAP

- may be reduced or no amplitudes depending on number of axons injured

- see fibrillations in muscle in EMG due to denervation

 

3/12

- looking for reinnervation

- hoping to see large polyphasic AP due to surviving motor axons branching out and recruiting

- if this is not seen, is a poor sign as means no surviving axons

- can repeat later hoping some axons have sprouted down intact tube

 

Problems with NCS

 

1.  Obese patient

2.  Oedema

3.  Electrical inteference

- 50 MHz from fluorescent lights

- need to do in Faraday room

- difficult to do in ICU

4.  Must remove oils / moisturiser

5.  Sweat

 

Spinal Cord Monitoring

 

Used to assess spinal cord integrity during spinal instrumentation

 

Technique

 

Posterior tibial nerve stimulated

- scalp SEP used to monitor for surgical induced changes

- signal monitored is in the posterior column

- relatively immune to compromise of the anterior spinal artery

- motor control is located anteriorly in the descending corticospinal tracts