What are the Muscle Relaxers Medications ? I leave here an interesting video.
If you are new to this topic, you should start informing about different medications and ask the question:
What are the Muscle Relaxers Medications ?
The speaker is Dr. Robert Fenell.
Muscle relaxers, or relaxants, are a certain type of medicine used to ease the pain of muscle spasms by working through the central nervous system. Here’s a brief guide to muscle relaxers.
For more information I leave the definition of muscle relaxants in WikiPedia developed in response to the question What are the Muscle Relaxers Medications ?
From Wikipedia, the free encyclopedia
This article refers to skeletal muscle relaxants. For information on smooth muscle relaxants, see Antispasmodic.
A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term “muscle relaxant” is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause paralysis. Spasmolytics, also known as “centrally-acting” muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only.
Detailed view of a neuromuscular junction:
1. Presynaptic terminal
3. Synaptic vesicle
4. Nicotinic acetylcholine receptor
Main article: Neuromuscular-blocking drugs
Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the central nervous system, myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function by blocking transmission at the end plate of the neuromuscular junction. Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions which causes the exocytosis of synaptic vesicles containing acetylcholine. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by Acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na+ and Ca2+ ions to enter the cell and K+ ions to leave the cell causing a depolarization of the end plate, resulting in muscle contraction. Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase.
Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents like tubocurarine block the agonist, acetylcholine, from binding nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents such as succinylcholine are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction. These neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in pancuronium.
Spasmolytics like carisoprodol, cyclobenzaprine, metaxalone, and methocarbamol are commonly prescribed for low back pain or neck pain, fibromyalgia, tension headaches and myofascial pain syndrome. However, they are not recommended as first-line agents; in acute low back pain, they are not more effective than paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs), and in fibromyalgia they are not more effective than antidepressants. Nevertheless, there is some (low quality) evidence suggesting that muscle relaxants can add benefit to treatment with NSAIDs. In general, there is no high quality evidence to support their use. No drug has been shown to be better than another, and all of them have adverse effects, particularly dizziness and drowsiness. Concerns about possible abuse and interaction with other drugs, especially if increased sedation is a risk, further limit their use. A muscle relaxant is chosen based on its adverse-effect profile, tolerability, and cost.
Muscle relaxants (According to one study) were not advised for orthopedic conditions, but rather for neurological conditions such as spasticity in cerebral palsy and multiple sclerosis. Dantrolene, although thought of primarily as a peripherally acting agent, is associated with CNS effects, whereas baclofen activity is strictly associated with the CNS.
Muscle relaxants are thought to be useful in painful disorders based on the theory that pain induces spasm and spasm causes pain. However, there is considerable evidence to contradict this theory.
In general, muscle relaxers are not approved by FDA for long term use. However, rheumatologists often prescribe cyclobenzaprine nightly on a daily basis in order to increase stage 4 sleep. By increasing this sleep stage patients feel more refreshed in the morning. Improving sleep is also beneficial for patients who have fibromyalgia.
Muscle relaxants such as tizanidine are prescribed in the treatment of tension headaches.
Diazepam and carisoprodol are not recommended for older adults, pregnant women, or people who suffer depression or for those with a history of drug or alcohol addiction.
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