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Last reviewed: 23.04.2024
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Fasciculations — contractions of one or several motor units (a separate motor neuron and a group of muscle fibers supplied to them) result in a rapid, visible to the eye, contraction of muscle bundles (fasciotic twitches or fasciculations). On EMG, fasciculations look like broad biphasic or multiphase action potentials. Simultaneous or sequential contraction of multiple motor units causes a wave-like contraction of the muscles, known as myokimiya.
Causes of the fasciculations
- Diseases of the motor neuron (ALS, progressive spinal amyotrophy, less often - other diseases)
- Benign fasciculations
- Painful muscle fasciculation syndrome
- Damage or compression of the spine or peripheral nerve
- Facial myokimiya (multiple sclerosis, brain tumor, syringobulbia, less often - other reasons)
- Neuromyotonia (Isaacs syndrome)
- Facial hemispasm (some forms)
- Post paralytic contracture of facial muscles
- Iatrogenic fasciculations.
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Diseases of the motor neuron
Fasciculations are typical of motor neuron diseases (ALS, progressive spinal amyotrophy). However, the presence of some fasciculations with no signs of denervation is insufficient for the diagnosis of motor neuron disease. In case of amyotrophic lateral sclerosis, EMG reveals widespread dysfunction of the anterior horn cells, including in clinically preserved muscles, and there are also symptoms of lesions of the upper motor neuron (pyramidal signs) and a progressive course of the disease. The characteristic picture of “asymmetric amyotrophy with hyperreflexia and progressive course” is revealed.
Progressive spinal amyotrophies are caused by the degeneration of anterior horn cells and are manifested only by symptoms of damage to the lower motor neuron (neuronopathy), there are no signs of damage to the upper motor neuron. Amyotrophies are more symmetrical. Fasciculations are detected, but not always. The disease has a more favorable course and prognosis. In the diagnosis of motor neuron diseases, EMG research is crucial.
Other lesions of the motor neuron (brain stem and spinal cord tumors, syringobulbia, OPCA, Machado-Joseph disease, late manifestations of poliomyelitis) can sometimes include fasciculations (usually more or less localized, for example, in trapezoidal muscles and sore muscles, among other manifestations). Perioral muscles, in the muscles of the arms or legs).
Benign fasciculations
Separate isolated fasciculations in the muscles of the leg or the circular muscles of the eye (sometimes they last up to several days) are found in perfectly healthy people. Sometimes benign fasciculations become more generalized and can be observed for several months or even years. But at the same time, the reflexes do not change, there are no violations of sensitivity, the speed of excitation along the nerve does not decrease, and there are no other deviations from the norm on EMG except fasciculation. Unlike ALS, benign fasciculations have more constant localization, they are more rhythmic and, possibly, more frequent. Sometimes this syndrome is called "benign disease of the motor neuron."
Painful muscle fasciculation syndrome
Painful fasciculation syndrome is an unstable term intended to refer to the rare syndrome of fasciculation, cramping, myalgia and poor exercise tolerance in the case of degeneration of the distal axonal peripheral nerves (peripheral neuropathy). Sometimes this term is used to refer to the previous syndrome, if it is accompanied by frequent painful cramps.
Damage or compression of the spine or peripheral nerve
These lesions can cause fasciculations, myokimia or krumpy in those muscles that are innervated by the root or nerve. These symptoms may persist after surgical treatment of compression radiculopathy.
[15], [16], [17], [18], [19], [20]
Facial Miokimia
Facial myokimiya is a rare neurological symptom and is often the only finding in neurological status. Facial myokimiya is of great diagnostic value, as it always indicates an organic lesion of the brain stem. Its beginning is usually sudden, and the duration is different - from several hours (for example, in multiple sclerosis) to several months and even years. Arbitrary mental activity, reflex automatisms, sleep, and other exogenous and endogenous factors have little or no effect on the course of myokinia. It is manifested by small wavelike (wormlike) contractions of muscles on one half of the face and most often develops on the background of multiple sclerosis or glioma of the brainstem. Less commonly, facial myokimia occurs in Guillain-Barré syndrome (may be bilateral), syringobulbia, facial nerve neuropathy, ALS, and other diseases. EMG detects spontaneous rhythmic activity in the form of single, double or group discharges with a relatively stable frequency.
Clinically, facial myokimia is usually easy to distinguish from other facial hyperkinesis.
The differential diagnosis of facial myokimia is carried out with facial hemispasm, miorhythmia, Jackson epileptic seizure, benign fasciculations.
Neiromyotonia
Neuromyotonia (Isaacs syndrome, a syndrome of constant muscle fiber activity) is found in both children and adults and is characterized by gradually increasing stiffness, muscle tension (stiffness) and small muscle contractions (myochemia and fascioculations). These symptoms begin to appear in the distal extremities, gradually spreading proximally. They persist during sleep. Pains are rarely observed, although the discomfort in the muscles is quite typical. Hands and feet take the position of constant flexion or extension of the fingers. The body also loses its natural plasticity and posture, the gait becomes strained (stiff) and constrained.
Causes: The syndrome is described as an idiopathic (autoimmune) disease (hereditary or sporadic), as well as in combination with peripheral neuropathy. In particular, Isaacs syndrome is sometimes observed with hereditary motor and sensory neuropathies, with CIDP, toxic neuropathies and neuropathies of unknown origin, in combination with a malignant neoplasm without neuropathy, in combination with myasthenia.
[25], [26], [27], [28], [29], [30], [31], [32]
Facial hemispasm
Fasciculations and myocomia, along with myoclonias, constitute the main clinical core in the manifestations of facial hemispasm. Clinically, fasciculations are not always easily visible, as they are overlapped by more massive muscle contractions.
Post paralytic contracture of facial muscles
The same can be said with regard to post-paralytic contracture of facial muscles (“facial hemispasm syndrome after neuropathy VII nerve”), which can manifest not only persistent contracture of muscles of varying severity, but also myoclonic local hyperkinesis, as well as fasciculations in the affected area branches of the facial nerve.
[38], [39], [40], [41], [42], [43], [44]
Iatrogenic fasciculations
Iatrogenic fasciculations have been described with penicillin and an overdose of anticholinergics.
Fasciculations can sometimes appear in hyperthyroidism, which, in combination with muscle atrophy and weakness, can mimic amyotrophic lateral sclerosis.
The bites of a rattlesnake, a scorpion, a black widow spider, and some stinging insects can cause cramps, myalgias, and fasciculations.
Symptoms of the fasciculations
Normally, a relaxed muscle is not accompanied by bioelectric activity. If fasciculations are the only symptom, that is, they are not accompanied by muscle atrophy and changes of reflexes, their clinical significance is small. With more severe motor neuron dysfunction, all muscle fibers that receive innervation from it are affected, which leads to muscle atrophy (denervation atrophy), decreased reflexes and is accompanied by fibrillation potentials, positive waves, fasciculations and changes in the potentials of motor units.
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Treatment of the fasciculations
The treatment is to change the diet, which is to increase the intake of magnesium from foods such as nuts (especially almonds), bananas and spinach. Medications containing magnesium can be recommended.