Dominic Stone
Muscle denervation is a condition that occurs due to nerve damage, often as a result of traumatic injuries, and can lead to atrophy and degeneration of the affected muscle tissue. It is characterised by an initial loss of function and rapid weight loss, followed by severe muscle atrophy and a decrease in contraction speed and tension. Denervation can affect one or multiple muscles and is commonly associated with various clinical settings, including diabetic neuropathy, degenerative disc disease, and viral infections such as polio. The molecular mechanisms underlying muscle denervation are complex and not yet fully understood, but it has been established that it induces an increase in Gadd45a mRNA, leading to muscle atrophy. Functional electrical stimulation has shown potential in rescuing muscles from atrophy and restoring movement.
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What You'll Learn
Muscle denervation is caused by nerve damage
In most neurogenic diseases, a muscle biopsy will show only a certain percentage of fibres denervated at one time. This partial denervation can be caused by the percentage of axons destroyed, the duration of the denervation process, and the number of muscle fibres reinnervated through axon regeneration or collateral sprouting. When a large number of axons are destroyed, there will be large numbers of denervated, atrophic fibres in the biopsy specimen, often found in small or larger groups.
Muscle denervation can also be caused by certain medical procedures or diseases that affect the nerves, such as amyotrophic lateral sclerosis (ALS), Guillain-Barré syndrome, or post-polio syndrome. Additionally, denervation can be intentional, as it is a valuable surgical technique for managing some medical conditions. For example, renal denervation is used in the treatment of uncontrolled hypertension. However, pathological denervation can have serious health consequences, including increased infection susceptibility and tissue dysfunction.
After denervation, muscle tissue experiences a rapid loss of mass, increasing atrophy, and muscle fibre degeneration. Recovery from denervation can take several weeks or months, depending on the severity of nerve damage and the individual's age and health. Techniques such as functional electrical stimulation can help restore muscle bulk and tissue quality in denervated muscles.
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It is associated with post-polio syndrome
Muscle denervation is caused by nerve damage and is a secondary sign of perineural spread. It is commonly observed in traumatic injuries and diabetic peripheral neuropathy. Denervation affects the muscle activation process and causes muscular atrophy and degeneration within the affected skeletal muscle tissue.
Denervation is strongly associated with post-polio syndrome (PPS). PPS is a neurologic disorder that occurs in survivors of paralytic polio after a period of functional stability, usually 15 years or more, and is characterised by new weakness or muscle fatigability, with or without general fatigue, muscle atrophy, or pain in muscles and/or joints. It is estimated that about 40% of polio survivors develop post-polio syndrome. PPS is caused by the deterioration of motor neurons, which leads to a loss of muscle strength and dysfunction. The poliovirus attacks specific neurons in the brainstem and the anterior horn cells of the spinal cord, resulting in the death of a substantial fraction of the motor neurons controlling skeletal muscles.
In individuals with post-polio syndrome, a continuous cycle of denervation and reinnervation occurs after acute poliomyelitis. Over time, this cycle leads to an increase in the size of motor units in skeletal muscle fibres. Eventually, the motor unit areas grow so large that reinnervation is no longer possible, resulting in uncompensated denervation of the motor units. This ultimately leads to muscle atrophy and myasthenia. Following an acute poliovirus infection, symptoms such as fatigue, asthenia, and pain are believed to be linked to muscle denervation.
The overuse and underuse of muscles may also contribute to muscle weakness in PPS patients. Diagnosis of PPS can be challenging due to the lack of specific tests and because symptoms are hard to separate from complications due to the original polio infection, and from the normal infirmities of aging.
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It can be treated with functional electrical stimulation
Muscle denervation is caused by nerve damage, which is often a secondary sign of perineural spread. It can also be caused by nerve damage resulting from traumatic injuries, such as sciatic nerve transection. Diabetic peripheral neuropathy is one of the most frequent causes of muscle denervation.
Following denervation, muscular atrophy and degeneration occur within the affected skeletal muscle tissue. This results in a progressive loss of weight, a reduction in muscle fibre size and quantity, a slowing of contraction speed, reduced tension, and twitch force.
Functional electrical stimulation (FES) has been shown to be an effective treatment for muscle denervation. FES involves electrically stimulating the nerves innervating the affected part of the body, using electrodes placed on the skin. This process can rescue muscles that have experienced severe atrophy due to denervation.
Long pulse width stimulation (LPWS) is a technique used to stimulate denervated muscles. It has been proven to restore the functional use of muscles post-denervation. LPWS has been shown to increase muscle cross-sectional area, the size of muscle fibres, and improve muscle function.
Human studies have shown that LPWS is an effective strategy for increasing muscle cross-sectional area, improving muscle function, and increasing the size of muscle fibres. This makes it a promising future stimulation intervention.
Triangular pulses are used to selectively stimulate denervated muscles without stimulating neighbouring innervated muscles. The duration and polarity of these pulses can be manipulated to achieve the desired stimulation intensity.
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It is linked to muscle atrophy and degeneration
Muscle denervation is a condition that can be caused by nerve damage, traumatic injuries, or diseases such as diabetic peripheral neuropathy. It is linked to muscle atrophy and degeneration, which occurs within the affected skeletal muscle tissue.
Following denervation, there is an immediate loss of voluntary function and rapid loss of muscle mass. This is followed by increasing atrophy and a loss of sarcomeric organisation, with a slowing of contraction speed and a reduction in developed tension and twitch force. The muscle fibres become angular and shrink, losing 80-90% of their mass within a few months. Eventually, the muscle is replaced by fibrous connective tissue and fat, with only a scattering of extremely attenuated muscle fibres remaining. This process can be visualised using magnetic resonance imaging (MRI) and high-resolution ultrasonography (US).
The molecular mechanisms underlying muscle atrophy due to denervation are not yet fully understood. However, studies have shown that denervation increases the level of Gadd45a mRNA in skeletal muscle fibres, which in turn increases the level of Gadd45a protein. This protein alters skeletal muscle gene expression in a way that stimulates protein breakdown, reduces protein synthesis, decreases mitochondria, inhibits anabolic signalling, and ultimately causes muscle fibre atrophy. Inhibition of Gadd45a expression has been shown to decrease denervation-induced muscle atrophy.
Functional electrical stimulation (FES) has been investigated as a potential treatment for muscle denervation. FES involves electrically stimulating the nerves innervating the affected part of the body, using electrodes placed on the skin. It has been shown to rescue muscles that have experienced severe atrophy due to denervation and may play a role in restoring movement to the limbs of paralysed patients. However, the effectiveness of FES may depend on the duration of denervation, as the spatial disorder of the excitation-contraction coupling apparatus may explain the poor excitability of long-term denervated muscles.
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It is observed in traumatic injuries
Muscle denervation is commonly observed in traumatic injuries. It is caused by nerve damage and is a secondary sign of perineural spread. In the acute and subacute stages, there is contrast enhancement and T2W and STIR hyperintensity secondary to muscular oedema. This can last up to a year and can be detected by CT scans and MRIs.
Muscular oedema is the earliest abnormality to appear in denervated muscles. It is present in the acute and subacute phases and affects the whole muscular body. It has been observed a few days after trauma in experimental studies. The intensity and duration of the oedema are related to the severity of the neuropathy.
In traumatic nerve injuries, the newly formed motor units during early reinnervation may be composed of only a few muscle fibres and are termed nascent. Reinnervation of denervated muscle fibres can occur through the regrowth of injured nerve axons or by collateral sprouting of intramuscular nerve fibres. This process can be accelerated by electrical stimulation of the nerves innervating the affected area.
Following denervation, muscular atrophy and degeneration occur within the affected skeletal muscle tissue. This leads to a progressive loss of weight, a reduction in muscle fibre size and quantity, a slowing of contraction speed, and a reduction in developed tension and twitch force. These changes can be observed through clinical imaging examinations such as MRI and high-resolution ultrasonography.
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Frequently asked questions
Muscle denervation is the loss of nerve supply to the muscles, which can be caused by nerve damage.
Muscle denervation can be caused by a variety of factors including trauma, diabetic neuropathy, degenerative disc disease, alcoholic neuropathy, pernicious anemia, and viral infections such as polio.
Symptoms of muscle denervation include fatigue, asthenia, pain, and muscle atrophy. The affected muscle may also show a decrease in contraction speed, reduction in tension, and twitch force.
Muscle denervation can be treated using functional electrical stimulation (FES), which involves electrically stimulating the nerves innervating the affected muscles. Magnetic resonance imaging (MRI) and high-resolution ultrasonography (US) are also used to diagnose and monitor the progression of muscle denervation.
Long-term muscle denervation can lead to severe muscle atrophy and degeneration, with a significant loss of muscle mass and contractile force. It can also result in fibrosis and fat substitution, causing irreversible changes to the muscle tissue.
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