Nerve Conduction Velocity Definition .
Nerve conduction velocity (NCV) tests are used to determine the speed with which a peripheral motor or sensory nerve conducts an impulse. EMG and NCV are two important diagnostic procedures that can provide complete information about the extent of nerve injury or muscle disease. These data can be valuable for diagnosis of disease and determination of rehabilitation goals for patients with musculoskeletal and neuromuscular disorders.
Nerve conduction velocity can be tested for any superficial nerve that is superficial enough to be stimulated through the skin at two different points. Most commonly NCV test is performed on ulnar, median, peroneal and posterior tibial nerves and less commonly on radial, femoral and sciatic nerves.
Principles of Motor Nerve Conduction .
Motor nerve conduction velocity is calculated measuring the distance between two points of stimulation in mm which is divided by the latency difference in ms. The nerve conduction velocity is expressed as m/sec. Measurement of latency difference between the two points of stimulations eliminates the effect of residual latency.
Conduction Velocity = D / PL – DL
Where, D = distance between proximal and distal stimulation in mm
DL = distal latency in m-sec
PL = proximal latency in m-sec
The motor nerve is stimulated at least at two points along its course . The stimulating electrode is typically a two pronged bipolar electrode with the cathode and anode. Small surface electrodes are usually used to record the evoked potential from the test muscle, although needle electrodes may be used when responses are very weak. A ground electrode is placed between the stimulating and recording electrodes. The pulse is adjusted to record a compound muscle action potential. A biphasic action potential with the initial negativity is thus recorded.
For accurate motor nerve conduction velocity measurement, the distance between two points of stimulation should be at least 10 cm. This reduces the error due to faulty distance measurement. Stimulation at shorter segments of the nerve, however, is necessary in the evaluation of focal compressive neuropathies, e.g. carpal tunnel syndrome. In a diseased nerve, the excitability is reduced and the current requirement may be much higher than normal. The measurement for motor nerve conduction study includes the onset latency, duration and amplitude of compound muscle action potential (CMAP) and nerve conduction velocity.
The onset latency is the time in ms from the stimulus artifact to the first negative deflection of CMAP. The amplitude of CMAP is measured from baseline to the negative peak (base to peak) or between negative and positive peaks (peak to peak) . The duration of CMAP is measured from the onset to the negative or positive peak or the final return of waveform to the baseline .
Principles of Sensory Nerve Conduction .
The sensory conduction can be measured orthodromically or antidromically. In orthodromic conduction, a distal portion of the nerve, e.g. digital nerve is stimulated and sensory nerve action potential (SNAP) is recorded at a proximal point along the nerve . In antidromic sensory nerve conduction, the nerve is stimulated at a proximal point and nerve action potential is recorded distally. In antidromic sensory nerve conduction measurement, the action potential may be obscured by superimposed muscle action potential, which is elicited due to simultaneous stimulation of motor axon in the mixed nerve.
For orthodromic conduction, ring electrodes are preferred to stimulate the digital nerve; whereas surface stimulating electrodes are commonly used for antidromic stimulation. Recording is also done by surface electrodes; however, in difficult situations needle electrode may be tried. Similar to motor nerve conduction study, the sensory nerve conduction measurement includes onset latency, amplitude, duration of sensory nerve action potential (SNAP) and nerve conduction velocity.
The latency of orthodromic potential is measured from the stimulus artifact to the initial positive or subsequent negative peak. The latency following orthodromic stimulation is shorter compared to antidromic. In practice, however, both orthodromic and antidromic methods provide the desired information. The initial positive peak in sensory nerve action potential giving it a triphasic appearance is a feature of orthodromic potential. In antidromic potential, the initial positivity in sensory nerve action potential is lacking. The sensory nerve action potential amplitude is measured from baseline to negative peak or from positive to negative peak .
The sensory nerve action potential recorded with a surface electrode is of higher amplitude in antidromic recording compared to orthodromic; because nerves are closer to the recording electrode especially in digital nerves. The duration of sensory nerve action potential is measured from the initial positive peak to the intersection between the descending phase and the baseline or to the negative or subsequent positive peak or return to the baseline . The amplitude of sensory nerve action potential is variable not only in different normal subjects but also in the same individual on two sides.
Sensory nerve action potential unlike motor conduction velocity may be measured by stimulating at a single stimulation site; because the residual latency which comprises of neuromuscular transmission time and muscle propagation time is not applicable in sensory nerve conduction. Thus, the sensory conduction velocity is calculated by dividing the distance (mm) between stimulating and recording site by the latency (ms).
The sensory nerve action potential amplitude shows a pronounced reduction on proximal recording in orthodromic nerve conduction studies. The sensory nerve action potential amplitude is also reduced in antidromic studies on proximal stimulation of nerve compared to distal. In contrast to this, the sensory nerve action potential amplitudes remain stable or there is minimal change on proximal stimulation in motor nerve conduction studies.
H-Reflex .
The H-reflex was described by Hoffman in 1918 and hence named as H-reflex. It is a useful diagnostic measure for radiculopathy and peripheral neuropathy. The H-reflex is a monosynaptic reflex elicited by submaximal stimulation of the tibial nerve and recorded from the calf muscle. In normal adults, it can also be recorded in other muscles of the limbs but not from the small muscles of hands and feet except in children below 2 years.
H-reflex can be enhanced by the maneuvers which increases motor neuron pool excitability such as muscle contraction. H-reflex has the advantage of evaluating the proximal sensory and motor pathways. It is therefore especially helpful in the evaluation of plexopathies and radiculopathies. In Guillain Barre syndrome, H-reflex may be absent, delayed or dispersed.
In S1 radiculopathy, the soleus H-reflex may be absent. Similarly, flexor carpi radialis H-reflex may be abnormal in C6–C7 radiculopathy. H-reflex is influenced by a number of spinal or supraspinal variables. The H-reflex studies, therefore, provides useful information which are helpful in understanding the pathophysiology of various central nervous system abnormalities.
F-Wave .
The F-wave was first described by Magladary and McDougal in 1950 in small muscles of the foot. The F-wave is a useful supplement to nerve conduction studies and electromyographic measures and is most helpful in the diagnosis of conditions where the most proximal portion of the axon is involved. It is elicited by the supramaximal stimulus of a peripheral nerve at a distal site, leading to both orthodromic and antidromic impulses.
While the orthodromic impulse travels to the distal muscle, the antidromic response travels to the anterior horn cell. The F-wave studies are valuable in the conditions like Guillain Barre Syndrome, thoracic outlet syndrome, brachial plexus injuries and radiculopathies.
Variables Affecting the Nerve Conduction Study .
A number of physiological and technical variables can influence the results of nerve conduction velocity. It is important to be aware of these factors and eliminate these as far as possible for reliable and reproducible results.
Physiological Variables .
1. Age .
The nerve conduction velocity in a full term infant is nearly half of the adult value. As the myelination progresses, the nerve conduction velocity attains the adult value by 3–5 years of age. The conduction velocity begins to decline after 30–40 years of age but the values normally change by less than 10 m/s at the sixth or even in the eight decades.
2. Upper versus lower limb .
The median and ulnar nerve conduction velocity is higher compared to tibial and peroneal. An inverse relationship between height and nerve conduction velocity suggests that the longer nerves conduct slower than the shorter nerves. These variables may also account for the faster conduction in the proximal nerves compared to distal.
3. Temperature .
Temperature significantly influences the conduction velocity and the amplitude compound muscle action potential. Low temperature results in slowing of nerve conduction velocity and increase the amplitude. For each degree Celsius fall in temperature, the latency increases by 0.3 ms. This is attributed to the effect of cooling on sodium channel.
On increasing the temperature, the velocity increase by 5% degree from 29 – 38ºC. The laboratory temperature, therefore, should be maintained between 21 – 23ºC. If skin temperature is below 34ºC, the limb should be warmed by infrared lamp, by warm water immersion or making appropriate correction of the results.
Technical Variables .
1. Stimulating system .
Failure of the stimulating system may result in unexpectedly small responses. The nerve may be stimulated submaximally or the applied current may not reach the intended target. An important source of failure of stimulating system is shunting of current between anode and cathode either by sweating or by the formation of a bridge by conducting jelly.
2. Recording system .
Faulty connection in the recording system may results in errors Inspite of optimal stimulation. The integrity of the recording system can be tested by asking the patient to contract the muscle with the electrode in position. The MUPs are displayed on the oscilloscope if the recording circuit is operational.
3. Inadvertent stimulation of unintended nerves .
Spread of stimulating current to an adjacent nerve or root not under study is frequent and failure to recognize, it results in errors in latency measurement. Needle electrodes are helpful in recording from restricted area of a muscle and are specially helpful in studying the innervation of individual motor branches or pattern of anomalies.
Neurogenic Disorders .
1. Disorders of the peripheral nerves .
The electromyographic findings are valuable in the disorders of the peripheral nerves especially in cases of axonal degeneration. In the disorders of the peripheral nerves the lesions are of three types:
a. Neuropraxia .
b. Axonotmesis .
c. Neurotmesis.
They may be due to traumatic injury or due to entrapment. These disorders typically cause weakness and atrophy of the muscles innervated distal to the lesion.
a. Neuropraxia .
Neuropraxia involves some form of local block which slows or stops nerve conduction. Conduction above or below the block is usually normal. Bell’s palsy, Saturday night palsy, carpal tunnel syndrome, etc. are the common causes of conduction block. Nerve conduction measurement shows increased latency across the blockage but normal above and below the blockage.
b. Axonotmesis .
In axonotmesis, the neural tube is intact with axonal damage. On electromyography testing there will be fibrillation potential and positive sharp waves in two to three weeks following degeneration depending on the axon from the cell body.
c. Neurotmesis .
In neurotmesis, there is disruption of neural tube along with axonal damage. A nerve conduction velocity test cannot be performed because no evoked response can be obtained. In electromyography spontaneous potential will appear with the muscle at rest and no activity is produced with the attempted voluntary contraction.
2. Polyneuropathies .
In polyneuropathy, there is axonal damage or demyelination of axons. Polyneuropathies typically results in sensory changes with distal weakness and diminished reflexes. The common neuropathic conditions are:
a. Diabetic neuropathy .
b. Alcoholic neuropathy .
c. Neuropathy related with renal disease or carcinoma .
d. Uraemic neuropathy .
e. Nutritional neuropathies like Vitamin B12 deficiency neuropathy or Vitamin E deficiency neuropathy .
f. Neuropathy due to infections like leprosy or Guillain Barre’ syndrome .
g. Toxic neuropathies.
With axonal damage, recruitment will be severely affected. Partial interference pattern may be observed with maximal effort. The motor unit duration and amplitude may be decreased. There are typical fibrillation potentials, positive sharp waves and fasciculations.
3. Motor neuron disorders .
Motor neuron disorders most commonly involve degenerative diseases of the anterior horn cells. These include:
a. Poliomyelitis .
b. Syringomyelia .
Diseases that are characterized by degeneration of both upper and lower motor neuron such as:
a. Amyotrophic lateral sclerosis .
b. Progressive muscular atrophy .
c. Progressive bulbar palsy .
d. Spinal muscular atrophy.
Diseases of the anterior horn cell are classically indicated by fibrillation potentials and positive sharp waves at rest. They also present by reduced recruitment with voluntary contraction due to the loss of motor neurons. Polyphasic motor unit potentials of increased amplitude and duration are often seen later in the course of motor neuron disease due to reinnervation and collateral sprouting. This is a typical finding in post-polio paralysis and amyotrophic lateral sclerosis where enlarged motor units are found in partially denervated muscles.
Myogenic Disorders .
The electromyographic findings provide information regarding the electrical activity of muscle that supplements the clinical, biochemical and histological investigations in the diagnosis of the muscle disease. The electromyography not only supplements the other laboratory investigations of muscle disease but also provides information which cannot be obtained by other means such as neuromuscular transmission abnormalities, myotonic disorders and periodic paralysis. The common myogenic disorders are:
Inflammatory muscle diseases
Inflammatory muscle diseases include
- Polymyositis .
- Dermatomyositis .
- Inclusion body myositis .
- Viral myositis and parasitic myositis.
The classical triad of EMG findings in Inflammatory muscle diseases includes:
1. Increased insertional activity with complex repetitive discharges .
2. Fibrillations and positive sharp waves .
3. Small polyphasic short duration motor unit potential recruited rapidly in relation to the strength of contraction.
Muscular dystrophy .
The common types of muscular dystrophies include Duchenne muscular dystrophy, Becker muscular dystrophy, Facioscapulohumeral muscular dystrophy, limb girdle muscular dystrophy, Oculopharyngeal muscular dystrophy and myotonic dystrophy.
Myopathies .
Congenital myopathies, metabolic myopathies, endocrine myopathies, etc. In primary muscle disease such as the dystrophies or polymyositis, the motor unit remains intact but degeneration of muscle fibres is evident.
The typical findings are a decrease in duration and amplitude of motor unit potential, full recruitment pattern during full effort in spite of weakness and wasting. These changes may occur with or without spontaneous electrical activity.
Thanks for Visiting us .
