Centrally acting muscle relaxants
They produce effects centrally in brain or spinal cord.
They are used to decrease the spasm and release spasticity as well as to reduce the pain.
Reasons for spasm
Spasm may be due to:
1. hyperactive stretch reflexes or
2. increased activation of alpha motor neurons or
3. imbalance between excitatory and inhibitory neurotransmitters.
- Multiple sclerosis
- Cerebral palsy
These drugs do not improve the power or functions of muscles; rather actually decrease the power of muscles.
Skeletal muscle relaxants
In patients of stroke, spasticity is important because it helps in walking, providing support. When skeletal muscle relaxants are given, they expose the weakness of limbs.
Mechanism of Action of centrally acting drugs
Decrease the hyperactivity of stretch reflex arc, as well as decrease the activation of alpha motor neurons.
This is achieved either by increasing the release of inhibitory neurotransmitters or decreasing the release of excitatory neurotransmitters. The pain encountered in these spasms is due to release of subs P, which is decreased by these drugs.
These drugs depress the pulse transmission in polysynaptic pathways.
Benzodiazepines are commonly used for relieving skeletal muscle spasms. They are safe as have fewer adverse effects.
Mechanism of Action
They produce their effects by GABAergic effect meaning that they potentiate the effects of GABA, without directly activating GABA receptors. They bind GABA A component of supramolecular complex.
They can be given orally or parentally. They can be given I/V for controlling the convulsions in status epilepticus, as well as in tetanus. They are metabolized by the liver.
Mainly affect CNS, evident in the form of sedation, drowsiness, ataxia, impaired judgment. Only in increased doses can cause depression of CVS and respiratory system.
Given in a dose of 5 mg, which may be increased to 60 mg.
Clonazepam and Nitrazepam have similar actions to that of diazepam, but have shorter duration of action.