7.13
Centrally Acting Muscle Relaxants: Therapeutic Uses
Centrally acting muscle relaxants reduce muscle tone and tension by interfering with the postsynaptic reflexes in the central nervous system.
Centrall…
Centrally acting muscle relaxants act on different receptors of pre and postsynaptic neurons in the central nervous system to reduce muscle tone and tension.
Based on their therapeutic use, centrally acting muscle relaxants are classified into spasmolytic and antispasmodic drugs.
Spasmolytic drugs inhibit spinal motor neurons and decrease muscle tone. Some spasmolytics like baclofen and diazepam, are γ-aminobutyric acid agonists, whereas tizanidine is an ɑ-2-adrenoceptor agonist.
These drugs treat severe and chronic muscle spasms caused by stroke, cerebral palsy, spinal cord and muscle injuries, and multiple sclerosis. If withdrawn abruptly, these drugs can have side effects like sedation, weakness, and return of spasticity.
In contrast, antispasmodic drugs such as cyclobenzaprine, methocarbamol, and orphenadrine primarily act on the brain stem and reduce hyperactive muscle reflexes.
They treat acute muscle spasms caused by local muscle injury, trauma and inflammation. Their side effects include visual hallucinations, constipation and urinary retention.
View the full transcript and gain access to JoVE Core videos
Q1: How do centrally acting muscle relaxants reduce muscle tone?
Centrally acting muscle relaxants reduce muscle tone by acting on pre- and postsynaptic receptors in the central nervous system to interfere with postsynaptic reflexes. They work by targeting different receptor types to decrease muscle tension and spasticity. These drugs are classified into spasmolytic and antispasmodic categories based on their therapeutic mechanisms and clinical applications.
Q2: What is the difference between spasmolytic and antispasmodic drugs?
Spasmolytic drugs like baclofen and diazepam inhibit spinal motor neurons to treat severe, chronic muscle spasms from stroke, cerebral palsy, and spinal cord injuries. Antispasmodic drugs such as cyclobenzaprine and methocarbamol act on the brain stem to reduce hyperactive muscle reflexes and treat acute spasms from local muscle injury and trauma. Each class targets different nervous system sites for distinct clinical conditions.
Q3: What receptor mechanisms do spasmolytic drugs use?
Spasmolytic drugs work through two main receptor mechanisms: baclofen and diazepam function as gamma-aminobutyric acid agonists, while tizanidine acts as an alpha-2-adrenoceptor agonist. Both mechanisms inhibit spinal motor neurons and decrease muscle tone. These different receptor pathways allow flexibility in treating severe and chronic muscle spasms.
Q4: What conditions do antispasmodic drugs treat?
Antispasmodic drugs treat acute muscle spasms caused by local muscle injury, trauma, and inflammation. Drugs like cyclobenzaprine, methocarbamol, and orphenadrine reduce hyperactive muscle reflexes by acting on the brain stem. They are administered orally and provide relief for short-term muscle tension related to musculoskeletal injuries.
Q5: What are the side effects of spasmolytic drug withdrawal?
Abrupt withdrawal of spasmolytic drugs can cause serious side effects including sedation, weakness, hypotension, and return of spasticity. These withdrawal effects occur because the drugs have been managing chronic muscle tone through continuous receptor agonism. Gradual tapering is recommended to avoid these adverse reactions in patients on long-term spasmolytic therapy.
Q6: What antimuscarinic side effects occur with antispasmodic drugs?
Antispasmodic drugs produce strong antimuscarinic side effects including constipation, bradycardia, and urinary retention. These effects result from the drugs' action on the brain stem and their anticholinergic properties. Visual hallucinations may also occur, making monitoring important during acute spasm treatment with these medications.
Q7: How do centrally acting muscle relaxants compare to other muscle relaxant classes?
Centrally acting muscle relaxants work through the central nervous system on pre- and postsynaptic receptors, unlike directly acting muscle relaxants that target peripheral sites. Understanding peripherally and centrally acting muscle relaxants comparison helps clinicians select appropriate agents based on whether spasticity is central or peripheral in origin. Each class offers distinct pharmacological advantages for specific clinical scenarios.