Procedure EMG
The aim of electromyography (EMG) is to find out whether the clinical symptoms are due to To this end, electromyography (EMG) uses various characteristics of the action potential of motor units (MUAP) to enable a decided evaluation of the electromyography. The parameters to be evaluated include the wavelength (amplitude) of the MUAP, time to first peak, duration of the MUAP, and the number of phases. Furthermore, it can be discussed whether the number of MUAPs triggered per stimulation of the muscle is sufficient, increased or decreased.
The electromyographic examination of each muscle consists of four different test procedures, all of which are performed at different locations in the muscle. When the electrode is inserted, the muscle is briefly stimulated and a dissipative electrical potential is generated. If this electrical activity continues even significantly after the needle has been inserted into the muscle, this indicates a pre-existing damage to the muscle.
This can be the result of inflammation, pathological changes in the muscle (myotonia) or a lack of connection to the nerve (denervation) of the muscle. If there is no electrical activity whatsoever when the needle is inserted, this indicates either a significant muscle atrophy or a connective tissue remodelling of the muscle (fibrotic muscle).
- A damage of the nerve,
- From a damage of the muscle or
- From none of the above arises.
The second test procedure of electromyography (EMG) is to assess the spontaneous activity of the muscle at rest after insertion of the needle.
A normal muscle at rest sends no electrical impulses, except for small potentials near the motor end plate, at the transmission point of nerve and muscle. These potentials are very short at 0.5 – 2 ms and completely normal (physiological). In this case, one should try to reinsert the needle at another location where no motor end plates are stimulated, in order to remove this interference factor from the electrical conduction.
If an electrical potential is nevertheless detected in the muscle to be examined, this is called fibrillation. These usually occur when the muscle no longer has contact with its actual nerve and then permanently generates an electrical potential itself.Fibrillaton potentials usually last 1 to 4 milliseconds and can have a wavelength of several 100 microvolts. In addition, fibrillation potentials are strictly rhythmic and often occur two or three times directly after each other.
After nerve damage, it can take 10 to 14 days before fibrillations are visible in electromyography (EMG). In addition to disorders of innervation, however, inflammatory changes can also lead to increased electrical activity at rest, especially if these occur acutely and are associated with cell death (necrosis). In addition to fibrillations, fasciculations may occur at rest.
This fasciculation is caused by damage to the nerve that innervates the motor unit. The nerve is electrically discharged (depolarized) which leads to the formation of action potentials in the motor unit. This usually happens several times a minute and is a sign of nerve damage (neuropathy).
In addition to nerve damage, damage to the muscle itself can also be detected with the discharge at rest. The so-called myotonic discharges are action potentials that are triggered about 100 times per second and last a few seconds. They indicate damage to the ion channels in the muscle membrane.
In the third examination method, the electrical activity of the muscle is derived with minimal voluntary movement of the muscle. This method examines whether the muscles take a pause interval of 50 to 250 ms between contractions. If this time is significantly reduced (2 – 20 ms), this indicates increased excitability (hyperexcitatory) of the muscle.
This status can be caused, for example, by hyperventilation, tetanus or neuronal diseases such as amyotrophic lateral sclerosis (ALS). If no electrical potential is found during this phase of electromyography (EMG), it is assumed that the nerve fibers are completely separated from the muscle (total denervation). A renewed supply of nerve fibers to the muscle can take a very long time, since nerve fibers only grow at a rate of 1mm/day and this can take a correspondingly long time after the muscle has been removed from the injury site.
However, chronic partial denervation of the muscle fibers is much more common in everyday clinical practice. In this case, some motor units of the muscle are no longer supplied by the nerves assigned to them, for example as a result of an illness or accident. The body tries to repair this by branching out the remaining nerve fibers again to innervate muscle fibers that are no longer supplied by nerves.
In this way, individual nerve fibers can reach up to five times more muscle fibers than before. If, on the other hand, there is a loss of motor units, one often sees an enlargement (hypertrophy) of the remaining motor units. The fourth discipline of electromyography is used to detect MUAPs under increased voluntary muscle contraction up to maximum contraction.
This is also called interference pattern analysis. This approach can provide a first indication of whether the clinical signs are due to damage to the nerve or the muscle. If the cause of the symptoms is muscle damage, the MUAP has a lower amplitude; if the cause of the symptoms is nerve damage, the MUAP has a higher amplitude and the MUAP itself takes longer. However, none of the two findings alone is characteristic of either type of damage.
