Central nervous system drugs muscle relaxants

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. 

Buspirone is as effective as the benzodiazepines in the treatment of general anxiety. However, the full anxiolytic effect of buspirone takes several weeks to develop, whereas the anxiolytic effect of the benzodiazepines is maximal after a few days of therapy. In therapeutic doses, buspirone has little or no sedative effect and lacks the muscle relaxant and anticonvulsant properties of the benzodiazepines. In addition, buspirone does not potentiate the central nervous system depression caused by sedative-hypnotic drugs or by alcohol, and it does not prevent the symptoms associated with benzodiazepine withdrawal. 

Although it is widely claimed that the benzodiazepine drugs have a specific calming or anxiolytic effect, their most prominent and easily quantifiable action is central nervous system depression. In very low therapeutic doses, this depression manifests as relief of anxiety that is often accompanied by a feeling of sluggishness or drowsiness. As the dose is increased, the degree of depression is intensified such that muscle relaxation, hyp-... 

Benzodiazepines have the capacity to depress polysynaptic reflexes and have been shown to decrease decerebrate rigidity in cats and spasticity in patients with cerebral palsy. What is not clear is whether they can, in humans, relax voluntary muscles in doses that do not cause considerable central nervous system depression. Nevertheless, benzodiazepines, such as diazepam, are often prescribed for patients who have muscle spasms and pain as a result of injury. In these circumstances, the sedative and anxiolytic properties of the drug also may promote relaxation and relieve tension associated with the condition. 

Katzung PHARMACOLOGY, 9e > Section V. Drugs That Act in the Central Nervous System > Chapter 27, Skeletal Muscle Relaxants > ... 

Because these drugs relax muscles, they can cause prolonged muscle weakness and motor coordination problems. Some of these drugs also act on the central nervous system and cause side effects such as confusion, dizziness, sedation, nausea, and dry mouth. Most muscle relaxants are prescribed... 

Virtually all effects of the benzodiazepines result from the action of these drugs on the central nervous system. The most prominent of these effects are sedation, hypnosis, decreased anxiety, muscle relaxation, anticonvulsant activity, and anterograde amnesia, in which individuals may experience a loss of memory for events that occurred while under the influence of the drug events occurring after the drug has worn off are remembered normally. 

Muscle relaxants may act either peripherally, that is directly on the muscle, or centrally, in the spinal cord. Most such drugs act centrally, though how they perform their task is not understood. These drugs do not act directly on the muscle to relax it, they do not interfere with conduction along the nerve fiber, they do not stop the neurotransmitter from being released or crossing the nerve-muscle junction, and they do not alter the ability of the muscle to respond to the neurotransmitter. Somehow they act centrally to depress the central nervous system and may have a sedative effect. 

Drugs that provide muscle relaxation by an action on the central nervous system or on the muscle itself are not useful for this purpose in surgery they are insufficiently selective and full relaxation, even if achievable, is accompanied by general cerebral depression. But there is a place for dmgs that reduce spasm of the voluntary muscles without impairing voluntary movement. Such drugs can be useful in spastic states, low back s5mdrome, and rheumatism with muscle spasm. 

For example, the nicotinic receptor for ACh (present in autonomic nervous system [ANS] ganglia, the skeletal myoneural junction, and the central nervous system [CNS]) is coupled to a Na+/K+ ion channel. The receptor is a target for many drugs, including nicotine, choline esters, ganglion blockers, and skeletal muscle relaxants. 

The skeletal muscle ma5 be relaxed by two different groups of drugs, namely first, by those exerting an aetion on the central nervous system (CNS) and used mainly for the relief of painful muscle spasms of spasticity taking place either in neuromuseular or musculoskeletal disorders secondly, those aflfeeting neuromuscular transmission that are employed as adjrmcts in anaesthesia in order to modify the musele relaxation ability. 

This drug substance enjoys the reputation to exert muscle relaxant aetivities having a central nervous system focus of action. It gets metabolised by eliminated via hepatic metabolism and its half-life is between 2 to 3 hours. It attains peak blood levels within a span of 2 hours, while the duration of action lasts from 4 to 6 hours. 

These drugs decrease pain, increase range of motion and have a sedative effect on the patient. Centrally acting muscle relaxants should not be taken concurrently with central nervous system depressants such as barbiturates, narcotics, and alcohol. 

Although it has been clinically available for a number of years, the United States Food and Drug Administration in early 1968 allowed labeling changes for diazepam (XXIV) to allow for new indications of use for the relief of muscle spasm and adjunctive use in convulsive disorders . It was reported that in cats the brain stem reticular system is the major locus of central nervous system depressant action of this centrally acting skeletal muscle relaxant. 

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