Type: Local Anesthetic

MOA: Blocks nerve impluses by reversibly binding to the Na+ channel, inhibits norepinephrine uptake, local vasoconstrictor (last two unique to cocaine)

Clinical Utility: Topical anesthetic of upper respiratory tract

Side Effects: High Toxicity due to reduced catecholamine uptake, highly addictive and euphoric

Type: Local Anesthetic (intermediate duration)

MOA: Blocks nerve impluses by reversibly binding to the Na+ channel

Pharmacokinetics: Used in conjuction with vasoconstrictor, intermediate acting, alkylated by CYP

Clinical Utility: Used in almost any application where local anesthetic of intermediate duration is needed

Side Effects: Drowsiness, tinnitus, dysgeusia, dizziness, twitching, large doses can produce seizures, coma and respiratory and cardiovascular depression

Type: Local Anesthetic (long-acting duration)

MOA: Blocks nerve impluses by reversibly binding to the Na+ channel

Pharmacokinetics: Long-acting

Clinical Utility: More sensory than motor block and long-acting makes it popular for use during labor or post-operative period

Side Effects: More cardiotoxic than lidocaine, can cause ventricular arrythmia and myocardial depression

Drug Type: Spasmolytic (Benzodiazepine)

MOA: Enhances GABA transmission through the GABA-A receptor, works in the spinal cord to increase the effects of inhibitory interneurons via GABA-A receptors on the alpha-motor neurons, hyperpolarization of alpha-motor neurons

Clinical Uses: Primarily for orthopedic manipulations and spasticity associated w/other musculoskeletal disorders (eg. strains, sprains)

Side Effects: sedation (more than Baclofen, which is why not used in chronic spasticity), dizziness, blurred vision, muscle weakness, ataxia

Drug Type: Spasmolytic

MOA: Agonist at GABA-B receptors, inhibits presynaptic release of excitatory neurotransmitters, decreases glutamate release, decreases excitatory drive to alpha-motor neurons

Clinical Uses: Primarily for ALS, spinal cord trauma, MS, CP, intrathecal administration more commonly being used for chronic spasticity

Side Effects: sedation (less than Diazepam), dizziness, blurred vision, muscle weakness, ataxia, intrathecal could lead to CNS depression, increases seizure activity in epileptics or with sudden withdrawal

Drug Type: Spasmolytic

MOA: Centrally acting alpha-2 antagonist, short duration of action, increases pre-synaptic inhibition of motor neurons, works at both spinal and supraspinal levels, decreases both poly- and monosynaptic spinal reflexes, decreases muscle tone and frequency of spasms

Clinical Uses: Used mostly in treatment of MS or after stroke

Side Effects: Not as much muscle weakness or withdrawal problems as Baclofen, dry mouth, sedation, asthenia, dizziness, hypotension, bradycardia, visual hallucination

Type: Direct-Acting Cholinoceptor Stimulant (Choline Ester)

Absorption: Rapidly hydrolyzed by cholinesterase, large amounts must be infused by IV, works at both receptors (muscarinic and nicotinic)

Type: Direct-Acting Cholinoceptor Stimulant (Choline Ester)

Absorption: More resistant to hydrolysis by cholinesterase than acetylcholine, works at muscarinic receptors

Type: Direct-Acting Cholinoceptor Stimulant (Alkaloid)

Absorption:Can be absorbed across skin