skeletal muscle relaxants are indicated for the treatment of which sports medicine condition

What are skeletal muscle relaxants?

Mar 20, 2018 · Skeletal muscle relaxants are drugs that are used to relax and reduce tension in muscles. They are more simply referred to as muscle relaxants. Some work in the brain or spinal cord to block or dampen down excessively stimulated nerve pathways. These are called centrally acting muscle relaxants and examples include baclofen, methocarbamol, and tizanidine.

Which muscle relaxants are used in the treatment of low back pain?

Centrally acting muscle relaxantsare also prescribed for muscle spasms that are _________ to antiinflammatory medications, physical therapy, or other treatment modalities. Skeletal …

How common are muscle relaxants in the US?

Jun 15, 2016 · Although grouped under a single drug class, skeletal muscle relaxants are a heterogeneous group of structurally unrelated medications with variable pharmacologic and …

What is an example of a centrally acting muscle relaxant?

Skeletal muscle spasticity is a form of muscular hyperactivity that causes painful contractions of the muscles, resulting in limited mobility. Centrally acting muscle relaxants act on the spinal …

What are skeletal muscle relaxants used for?

What condition is treated with muscle relaxants?

Why are relaxants used in sports?

Which drug is a skeletal muscle relaxant?

What is Flexeril used for?

What are relaxants list five examples of relaxants?

When are muscle relaxers used?

When should muscle relaxers be used?

Can you play sports on muscle relaxers?

What Are Skeletal Muscle relaxants Used for?

Skeletal muscle relaxants are mainly used to treat: 1. spasticity, which is another term for stiff and rigid muscles caused by conditions such as c...

What Are The Differences Between Skeletal Muscle Relaxants?

Skeletal muscle relaxants differ in the way they work (centrally or peripherally as discussed above), their side effects, and their effectiveness f...

Are Skeletal Muscle relaxants Safe?

Evidence supporting the effectiveness of skeletal muscle relaxants for muscle spasm is sparse; most trials are old and not of good quality. Skeleta...

What Are The Side Effects of Skeletal Muscle Relaxants?

Drowsiness is common, particularly with centrally acting muscle relaxants; however, drowsiness can occur with some peripherally acting muscle relax...

What are the two main categories of muscle relaxants?

Skeletal muscle relaxants include a variety of structurally unrelated compounds that can be classified into two main categories: antispasticity and antispasmodic medications. These agents have different indications, mechanisms of action, and side-effect profiles. Understanding these differences can improve selection of an appropriate agent to optimize patient-specific therapy.

What is the purpose of antispasmodics?

Antispasmodics decrease muscle spasms through alterations of CNS conduction. They are divided into benzodiazepines, which inhibit transmission on the postsynaptic γ-aminobutyric acid (GABA) neurons, and nonbenzodiazepine agents, which act at the brain stem and spinal cord.1Benzodiazepines (e.g., diazepam) are used as sedatives, anxiolytics, and anticonvulsants, and have been shown to have efficacy in the acute management of low back pain.6Other antispasmodics commonly prescribed for the reduction of muscle spasms include: carisoprodol, cyclobenzaprine, metaxalone, and methocarbamol.

Is skeletal muscle relaxant safe for back pain?

A systematic review indicated that skeletal muscle relaxants were effective in the short-term relief of acute low back pain when compared with placebo.6However, these agents were associated with a 50% increased risk of adverse events (AEs) with a relative risk of 1.50 (95% CI, 1.14–1.98).6Specifically, central nervous system (CNS) adverse events had a stronger association with skeletal muscle relaxant use, with a relative risk of 2.04 (95% CI, 1.23–3.37).6In addition to sedation, patients may experience headaches, blurred vision, and dependency with the use of these agents.

Can muscle relaxants be used for back pain?

In general, muscle relaxants are controversial alternatives that have efficacy in nonspecific back pain but carry risks of adverse effects and increased cost. Although they are not recommended as primary treatment, 35% of patients are prescribed muscle relaxants for nonspecific low back pain, and 18.5% receive initial muscle relaxant therapy.2,6,7Patients are often prescribed these agents for the treatment of acute back pain, and many experience relief within several weeks of starting therapy.8For example, patients receiving cyclobenzaprine were more likely to report symptomatic improvement at two weeks compared with placebo (number needed to treat = 3).8Given the frequency of use, the questionable role in the treatment of back pain, and the potential for misuse, it is imperative for clinicians to be aware of the facts regarding commonly used muscle relaxants in the United States.

What is the first line of treatment for low back pain?

The American Pain Society and the American College of Physicians published guidelines in 2007 for low back pain, recommending acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) as first-line treatment for most patients. This recommendation is primarily due to the favorable side-effect profile of these agents compared with other options as opposed to superior efficacy.1After failure of a first-line agent, skeletal muscle relaxants, benzodiazepines, and opioids may be initiated based on evidence of temporary additional pain relief.1

Can antispasmodics be used as muscle relaxants?

In general, antispasticity agents and antispasmodics are not interchangeable and should not be substituted for one another. However, some muscle relaxants, such as tizanadine and diazepam, carry indications approved by the Food and Drug Administration (FDA) for both conditions (Figure 1). Limited evidence exists for comparing one agent with another, so selecting an optimal agent relies on important patient-specific factors such as risks for side effects, potential drug interactions with concomitant therapies, and total cost.6

Is carisoprodol a controlled substance?

In an effort to investigate the potential shift in abuse or misuse of agents after carisoprodol was reclassified as a controlled substance, a search was conducted on skeletal muscle relaxant exposures reported to the Florida Poison Information Center Network from 2009 to 2012. Data extracted included intentional abuse or misuse of carisoprodol, cyclobenzaprine, and a combination of other muscle relaxants. The frequency of carisoprodol exposure in 2012 after its reclassification as a controlled substance was 75 cases, compared with an average of 132 cases annually between 2009 and 2011.16Interestingly, the frequency of cyclobenzaprine exposure decreased to 27 cases in 2012 compared with an average of 36 cases annually between 2009 and 2011.16Data on other muscle relaxant exposures showed variation among years without a clear increase in abuse or misuse after carisoprodol became a controlled substance.16Additional analysis must be done to assess the impact of the reclassification of carisoprodol on the frequency of misuse and abuse of other, noncontrolled skeletal muscle relaxants.

How many people are prescribed muscle relaxers?

Approximately 2 million Americans, including more than 300,000 people over 60 years of age , are prescribed muscle relaxants. 3. Spasticity and spasms are distinct etiologies, and each condition responds differently to certain medications.

Which system regulates skeletal muscle excitability?

Neuromuscular System. There are 2 pathways that regulate skeletal muscle excitability and contraction: the monosynaptic and polysynaptic reflex pathways. 8,10,13 In the monosynaptic reflex, afferent signals from muscle cells return to the spinal cord, resulting in negative feedback on motor movements.

How much gabapentin is safe for spasticity?

Gabapentin has been shown to have a dose-related efficacy in controlling spasticity at dosages of 1,200 mg to 3,600 mg/day. 33 Gabapentin has variable interindividual bioavailability, and exhibits saturable oral absorption; its bioavailability decreases as the dose increases. 2,36 Gabapentin also is available in extended-release formulations with improved absorption, a tablet (Gralise), 39 and a gastroretentive prodrug, gabapentin enacarbil (Horizant).40 Gralise is indicated for the management of postherpetic neuralgia, 39 whereas Horizant is approved for the treatment of postherpetic neuralgia and moderate-to-severe primary restless legs syndrome. 40

How does riluzole affect AUC?

Riluzole’s absorption is reduced by administration with high-fat meals, which results in a 20% reduction in AUC and a 45% reduction in peak plasma concentration. 41 Riluzole undergoes hepatic metabolism through CYP1A2 followed by glucuronidation, and is excreted as glucuronide metabolites in the urine (85%). 41

How long does it take for botulinum toxin to work?

Botulinum toxin (BTX) is produced from Clostridium botulinum and is injected locally to inhibit presynaptic release of Ach in the neuromuscular junction, resulting in paralysis of the muscle. 49,50 The onset of effect varies depending on the indication but is typically 14 days for spasticity and cervical dystonia—the effect typically lasts approximately 3 months. 50 The effect diminishes when motor neurons develop new nerve terminals that start releasing Ach. 51 Resistance to the paralytic effect could develop with repeated injections due to development of antibodies against the toxin.52,53 Adverse effects include rash and muscle weakness at the injection site, flu-like symptoms, and headache.

What are the two distinct reactions to motor neurons that require unique and sometimes complementary therapies?

Spasticity and spasm: 2 distinct reactions to motor neurons that require unique and sometimes complementary therapies.

What is a spasticity?

Spasticity. Spasticity is defined as a velocity-dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex. 4 Clinical manifestations include muscle stiffness, co-contraction of flexors and extensors, and increased resistance to muscle stretching.

What is muscle relaxant?

Muscle relaxants are medications used to relieve muscular spasms and the pain associated with these spasms. Muscle spasms may be attributed to traumatic injuries or chronic debilitating diseases (e.g., MS, CVA, cerebral palsy, or head or spinal cord injuries). Spasticity can result from either increased muscle tone caused by increased CNS stimulation from cerebral neurons or from a lack of inhibition in the spinal cord or the skeletal muscles. Muscle relaxants depress neuronal action in the spinal cord or brain and may even augment neuronal inhibition in the skeletal muscles.

What is the name of the muscle relaxant that acts on the spinal muscles?

Skeletal muscle spasticity is a form of muscular hyperactivity that causes painful contractions of the muscles, resulting in limited mobility. Centrally acting muscle relaxants act on the spinal muscles. Baclofen, dantrolene, and tizanidine are all examples of centrally acting muscle relaxants used to treat spasticity. Diazepam, a benzodiazepine, has also been successfully used to treat muscle spasticity.

What is the most commonly used drug for muscle spasms?

Cyclobenzaprine is the most commonly used drug in this class, and is often prescribed to reduce spasms caused by musculoskeletal injuries. It is not effective against muscle spasms caused by central nervous system disorders.

What is the mechanism of action of muscle relaxants?

The actual mechanism of action of muscle relaxants is not entirely known. Centrally acting muscle relaxants are prescribed in cases of spasticity to repress hyperactive reflexes. They are also prescribed for muscle spasms that are resistant to antiinflammatory medications, physical therapy, or other treatment modalities.

What are the side effects of muscle relaxers?

The main adverse effects of muscle relaxants result from their effects on the CNS and skeletal muscles. Feelings of euphoria, lightheadedness, dizziness, drowsiness, fatigue, confusion, and muscle weakness may be experienced early in treatment. Many of these adverse side effects are transient and will subside as patients grow tolerant to the medications and their side effects over time.

What medications increase sedation?

Alcohol, barbiturates, tricyclic antidepressants, sedative-hypnotics, and other CNS depressants will increase sedation .

Why is cyclobenzaprine taught?

Patient teaching regarding cyclobenzaprine helps ensure patient safety and prevent adverse effects from this medication.

What is a central-acting muscle relaxant?

Central-acting muscle relaxants depress the neuron activity in the spinal cord or brain, or enhance the neuronal inhibition on the skeletal muscles. Click again to see term 👆. Tap again to see term 👆. Nice work!

What happens when you sedate a patient?

Sedate the patient the spasms and spasticity are decreased.

Should muscle relaxants be tapered?

Muscle relaxants should be tapered, rather than stopped abruptly, to avoid rebound spasms.

Can muscle relaxers make you drowsy?

Muscle relaxants have a sedative effect and can cause drowsiness. Patients taking muscle relaxants should avoid driving or participating in activities that require mental alertness.

Does cyclobenzaprine affect the CNS?

Concomitant use of cyclobenzaprine and alcohol and other CNS depressants may intensify CNS depressant effects of the drug.

When a skeletal muscle is injured, are satellite cells activated?

When a skeletal muscle is injured, satellite cells are activated by a variety of growth factors within 18 hours of injury, as a result of a response to a chemical stimulus [5, 36, 37]. At the same time, inflammatory cells migrate to the injury site from healthy areas of the muscle.

How long after a muscle injury can paracetamol be used?

In the 2 days after the injury, paracetamol can be used for analgesia. Prolonged use of NSAIDs (over 7 days) is not recommended as it would delay muscle regeneration by inactivating the proliferation and differentiation of satellite cells and inhibiting the production of growth factors [18, 19].

What are the cells that are involved in a muscle injury?

When a muscle is injured, the myofibers rupture and necrotize . A haematoma is formed. At the same time during this first phase, the inflammatory cells can freely invade the injury site because the blood vessels are torn. The most abundant inflammatory cells are the polymorphonuclear leukocytes. These are replaced by monocytes, a few hours after the injury. These cells eventually transform into macrophages. Macrophages have 2 functions. Firstly, they remove the necrotic myofibers by phagocytosis. Secondly, they produce, together with fibroblasts, chemotactic signals such as growth factors, cytokines, and chemokines. The extracellular matrix (ECM) also contains growth factors that become active when tissue is damaged. Some of these growth factors, such as FGF (fibroblast growth factor), IGF-1 (insulin-like growth factor-1), IGF-2 (insulin-like growth factor-2), TGF-β(transforming growth factor-β), HGF (hepatocyte growth factor), TNF-α(tumor necrosis factor-α), and IL-6 (interleukin-6) can activate myogenic precursors, called the satellite cell [3, 6, 7].

Why did Menetrey and al. use a muscle laceration model?

used a muscle laceration model developed in mice to investigate whether surgery is a better technique to accelerate recovery of a muscle injury than immobilization. At 2 days after the laceration, the mice that had surgery only had a superficially located minor haematoma, while the immobilized mice had a larger and deeper haematoma. At the end, the immobilized mice had more and deeper scar tissue than the sutured mice. The functional results of surgery were also superior to those of immobilization [35].

Why are NSAIDs used?

NSAIDs are primarily used for their analgesic, anti-inflammatory, and antipyretic properties [16]. Inflammatory cells play an important role in the healing process of an injured muscle. Therefore, the use of drugs that inhibit these cells, such as NSAIDs, is questioned nowadays. Experimental studies in which NSAIDs were given immediately after the injury, have shown conflicting results. NSAIDs would not have a greater effect on the pain of a muscle injury than paracetamol, but they have more side effects including asthma exacerbations, gastrointestinal and renal side effects, hypertension, and other. However, NSAIDs also have beneficial effects. The inflammatory process can be excessive and cause edema, resulting in anoxia and further cell death. This can be prevented by the administration of low-dose NSAIDs [17].

How long after muscle injury can you take NSAIDs?

Rahusen et al. reviewed earlier reports on the use of NSAIDs to clarify recommendations for their use [18]. Basically, NSAIDs should be given no sooner than 48 hours following exercise-induced muscle injuries to provide analgesia and to reduce the early inflammatory response. Earlier use can interfere with the cell chemotaxis that is necessary for the repair and remodeling of regenerating muscle. In the 2 days after the injury, paracetamol can be used for analgesia. Prolonged use of NSAIDs (over 7 days) is not recommended as it would delay muscle regeneration by inactivating the proliferation and differentiation of satellite cells and inhibiting the production of growth factors [18, 19].

What are the three stages of skeletal muscle injury?

Most types of muscle injuries would follow three stages: the acute inflammatory and degenerative phase, the repair phase and the remodeling phase. Present conservative treatment includes RICE (rest, ice, compression, elevation), nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy. However, if use improper, NSAIDs may suppress an essential inflammatory phase in the healing of injured skeletal muscle. Furthermore, it remains controversial whether or not they have adverse effects on the healing process or on the tensile strength. However, several growth factors might promote the regeneration of injured skeletal muscle, many novel treatments have involved on enhancing complete functional recovery. Exogenous growth factors have been shown to regulate satellite cell proliferation, differentiation and fusion in myotubes in vivo and in vitro, TGF-β1 antagonists behave as inhibitors of TGF-β1. They prevent collagen deposition and block formation of muscle fibrosis, so that a complete functional recovery can be achieved.