Dominic Stone
Denervated muscles are those that have been affected by nerve damage, which can be caused by a variety of factors, including trauma, infection, inflammation, and medical procedures. This can lead to muscle atrophy, degeneration, and a loss of function. The process of denervation involves the loss of nerve supply to a muscle, resulting in a decrease in muscle size and strength. Recovery from denervation can be achieved through muscle electrostimulation, which helps to counteract the effects of denervation and preserve muscle tissue. The time it takes to recover depends on the severity of nerve damage, age, and overall health. Denervation is a common issue, especially in older individuals, and can be managed with the right rehabilitation techniques.
| Characteristics | Values |
|---|---|
| Cause | Nerve damage, nerve supply disruption, trauma to the spine, peripheral nerve trauma, infection, inflammation, certain medical procedures, diseases affecting nerves (e.g., ALS, Guillain-Barré syndrome) |
| Symptoms | Muscle weakness, wasting/atrophy, fasciculations, edema, reduced contraction speed, decreased tension, twitch force, increased muscle excitability in chemical-induced electrical currents |
| Diagnosis | EMG/NCS, MRI, high-resolution ultrasonography, muscle biopsy |
| Treatment | Electrical stimulation, functional electrical stimulation, muscle plasticity, physical therapy, hyperbaric oxygen treatment |
| Complications | Insulin resistance, muscle degeneration, fibrosis, fatty infiltration, irreversible changes |
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What You'll Learn
Denervated muscle atrophy
Denervation is any loss of nerve supply and can result from injury, disorders, or surgical procedures. It can affect one or multiple muscles. In skeletal muscle denervation, there are two distinct diagnoses: entrapment and compressive neuropathies, or non-entrapment neuropathies. Following denervation, muscular atrophy and degeneration occur within the affected skeletal muscle tissue. This is characterised by a progressive loss of weight, a reduction in muscle fibre size and quantity, a slowing of contraction speed, a reduction of developed tension, and twitch force.
Muscular oedema is the earliest abnormality to appear in denervated muscles, and it is present in the acute and subacute phases. This can last up to a year. If normal innervation is not restored, chronic and permanent atrophy with fatty infiltration develops, indicating irreversible changes. The chronic appearance of muscle denervation is the fatty replacement of muscle and muscular atrophy.
Denervated muscles can be reinnervated either through the regrowth of injured nerve axons or by collateral sprouting of terminal axons from adjacent surviving motor units. Denervation-induced muscle atrophy can be reduced, and muscle function preserved, through hyperbaric oxygen treatment, which increases the level of antioxidants that mitigate the action of reactive oxygen species released after denervation.
Denervation atrophy is caused by peripheral neuropathies and motor neuron diseases. Myofibres that lose their innervation become angular and shrink, losing 80-90% of their mass within a few months. In chronic denervating processes, remaining healthy axons sprout and synapse with denervated fibres.
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Denervated muscle degeneration
The denervation process can be understood in three stages. The first stage is characterised by an immediate loss of voluntary function and rapid loss of muscle mass. This is followed by the second stage, where muscle atrophy becomes increasingly severe, along with the loss of sarcomeric organisation. The final stage is marked by muscle fibre degeneration and the replacement of muscle tissue with fibrous connective tissue and fat. This replacement of functioning muscle mass by connective tissue and fat was previously believed to be irreversible. However, recent studies have shown that denervated muscles possess the capability for active myogenesis and functional restoration, especially when stimulated by techniques such as functional electrical stimulation.
The progression of denervation-induced muscle atrophy and degeneration can be slowed or even improved through various interventions. One innovative approach is hyperbaric oxygen treatment, which has been found to increase antioxidant levels in rats, thereby mitigating the action of reactive oxygen species released after denervation. This treatment improved diaphragm-specific force production and attenuated muscle fibre atrophy, mitochondrial dysfunction, and ROS production. Additionally, electrical stimulation has been shown to assist in preserving muscle tissue quality during recovery, reducing long-term complications, and improving the trophic situation.
EMG examinations can be used to detect signs of denervation, such as fibrillation potentials and positive sharp waves, which indicate abnormal spontaneous activity in the muscle. Furthermore, MUAP configuration analysis during mild muscle contraction can provide evidence of reinnervation, as motor unit reinnervation results in prolonged durations, increased amplitudes, and polyphasic configurations of MUAPs.
While denervated muscle degeneration can have significant impacts, recent advancements in understanding its biology and innovative treatments offer promising avenues for mitigating atrophy and restoring muscle function.
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Denervated muscle reinnervation
The denervation process causes profound structural and functional changes within skeletal muscle. It leads to muscle atrophy, a decrease in muscle fiber size, and a reduction in contractile proteins. These changes can be observed through imaging techniques such as Magnetic Resonance Imaging (MRI) and high-resolution ultrasonography. One of the earliest abnormalities to appear in denervated muscles is muscular edema, which is characterised by uniform edema throughout the affected muscle and high signal intensity on fluid-sensitive images.
Reinnervation of denervated muscles can occur through two main mechanisms: the regrowth of injured nerve axons and collateral sprouting of terminal axons from adjacent surviving motor units. Prompt reinnervation with a sufficient number of motion-specific motor axons is crucial for optimal structural and functional recovery. The time required for chronic denervation changes to develop can vary from 3 to 6 months, depending on the distance between the site of nerve injury and the muscle.
The success of reinnervation can be assessed through electrophysiological evaluations, such as evaluating MUAP configuration during mild muscle contraction. As a result of motor unit reinnervation, MUAPs exhibit a prolonged duration, increased amplitude, and often a polyphasic configuration. Additionally, the disappearance of fibrillation potentials (Fib) is a positive indicator of reinnervation progress. Fib amplitude, muscle fiber conduction velocity, and muscle fiber diameter are all factors that reflect the severity and length of denervation, providing valuable information for surgical decision-making and predicting the outcomes of delayed nerve repair.
The literature suggests that if reinnervation is not achieved within 18 months, the potential for recovery significantly diminishes. Therefore, early intervention and effective treatment methods are crucial for optimising reinnervation outcomes and preventing irreversible muscle damage.
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Denervated muscle imaging
MRI examinations of denervated muscles reveal distinct signal intensity patterns that vary depending on the stage of muscle denervation. In the acute and subacute phases, denervated muscles exhibit a high signal intensity pattern on fluid-sensitive sequences, specifically T2-weighted images, and normal signal intensity on T1-weighted images. This phenomenon is attributed to muscular oedema, which is the earliest abnormality to manifest in denervated muscles.
In the subacute stage, MRI images typically show uniform oedema throughout the affected muscle, with high signal intensity on fluid-sensitive and inversion recovery imaging. This finding becomes more pronounced until approximately 2–4 weeks after denervation. If the muscle remains denervated for an extended period, it enters the chronic phase, characterised by irreversible changes such as muscle atrophy and fatty infiltration. In this phase, T1-weighted images demonstrate high signal changes associated with volume loss, while T2-weighted images show variable changes.
MRI is particularly useful for detecting acute and subacute changes in denervated muscles, while computed tomography (CT) scans are more effective at visualising chronic alterations. Advanced MRI techniques, such as diffusion-weighted imaging and dynamic susceptibility contrast MRI, enhance the evaluation of denervated muscles and facilitate the study of muscle physiology following spinal trauma. Sequential MR imaging also plays a role in understanding the correlation between denervation and reinnervation processes and their functional outcomes.
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Denervated muscle treatments
One innovative approach to reducing denervation-induced muscle atrophy and preserving muscle function involves hyperbaric oxygen treatment. This treatment increases the level of antioxidants, which mitigate the action of reactive oxygen species released after denervation. In rats, this treatment improved diaphragm-specific force production, attenuated muscle fibre atrophy, and reduced mitochondrial dysfunction and ROS production.
Another approach to treating denervation-induced muscle atrophy involves the use of natural compounds such as royal jelly produced by honeybees, geranylgeraniol, soy proteins, isoflavones, and vitamins C, D, and E. These compounds can be potentially used in humans as a safe adjuvant therapy to diminish skeletal muscle atrophy.
Reinnervation of denervated muscle fibres can occur either via the regrowth of injured nerve axons or by collateral sprouting of terminal axons from adjacent surviving motor units. Prompt reinnervation of a muscle with a sufficient number of motion-specific motor axons generally results in good structural and functional recovery. Nerve transfer has been highly efficacious in improving the clinical outcomes of patients with skeletal muscle denervation, especially in proximal limb nerve injuries.
Electrophysiological evidence of reinnervation can be seen during mild muscle contraction and evaluation of MUAP configuration. As a result of motor unit reinnervation, MUAPs develop a prolonged duration, increased amplitude, and often a polyphasic configuration.
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Frequently asked questions
Denervated muscles are those that have lost nerve supply, often due to nerve damage or injury. This can occur as a result of trauma, infection, inflammation, or certain medical procedures. Denervation can also be caused by diseases that affect the nerves, such as amyotrophic lateral sclerosis (ALS) or Guillain-Barré syndrome.
Denervated muscles may exhibit muscle weakness, wasting or atrophy, and fasciculations. During the acute and subacute stages, there is muscular oedema, which can be detected by T2W and STIR hyperintensity on imaging. In the chronic phase, there is fatty replacement of muscle and muscular atrophy, which can be seen on CT scans.
Denervated muscles can recover with time and appropriate rehabilitation. Electrical stimulation techniques, such as home-based functional electrical stimulation, have been shown to be effective in rescuing muscles affected by severe atrophy. In some cases, muscle plasticity may occur, where new nerve connections are formed and dormant muscle fibers are activated.
