Centrally acting muscle relaxant; GABA-mimetic

Use: Pts with chronic spasticity (decreases spasticity W/O SEDATION)

Mechanism: binds GABAb receptor (ONLY GABAb out there!): post synaptic decreases cAMP, opens K channels ->hyperpolarization; Presynaptic inhibition of Ca influx decreases NT release

Chronic spasticity use: decreases spasticity w/o much sedation at normal doses; 

Route: Intrathecal route allows better control of pain and spasticity than other routes; effects stay localized

Anticonvulsant

Uses: DOC for status epilepticus; Spasms from local muscle trauma (sedating effect); adjunct for chronic muscle spasticity

Use as muscle relaxant: acts at GABAa receptors in spinal cord to reduce spasticity

Tox: Preg Cat D

Other drugs: Lorazepam (Ativan)

Clonazepam (Klonopin) - Preg Cat D

Centrally acting muscle relaxant

Mechanism: Alpha 2 receptor agonist; inhibits pain transmission in dorsal horn; reinforces pre adn post synaptic inhibition in the psinal cord

Uses: reduce chronic muscle spasticity due to spinal cord injury; acute muscle spasms

Major Side effects: sedation, hyptension, dry mouth, muscle weakness (elderly)

Centrally acting muscle relaxant; Sedative

Mechanism: antimuscarinic effect, acts as sedative at the level of the brain stem; 

Uses: acute muscle spasms caused by trauma or sprain

Side effects: causes sedation, confusion is common

Others: Chlorzoxazone (Paraflex^®) 

Metaxalone (Skelaxin^®); Methacarbamol (Robaxin); Orphenadrine (Norflex)

Centrally acting muscle relaxant; Sedative

Use: muscle relaxant through sedation (not very good but popular); drug of abuse

Side effects: induces hepatic enzymes (chronic use); caution (probably just don't) in recovering addicts/alcoholics

Others: Chlorzoxazone (Paraflex^®) 

Metaxalone (Skelaxin^®); Methacarbamol (Robaxin); Orphenadrine (Norflex)

Muscle relaxant (no CNS, at the muscle)

Uses: neuroleptic malignant syndrom, malignant hyperthermia (caused by general anesthesia of NMJ blocking agents)

Mechanism: interferes with excitation-contraction coupling in muscle fiber; decreases Ca release from SR; SM more than smooth M; DOES NOT WORK THROUGH CNS, works at the muscle

Side effect: weakness, sedation

Centrally acting muscle relaxant

Use: Locally controls muscle spasms following stroke or neurological injury, strabismus in the eye; dystonias, muscle spasms, sweating in palms, remove wrinkles and smile lines

Mechanism: inhibits ACh release from nerve, degrades fusion proteins

Side Effects: Aberrant nerve regeneration or spread of toxin to unwanted areas may be problematic

CNS stimulant; sympathomimetic

Uses: ADHD and Narcolepsy

ADHD because: 

Mechanism: Increase release of catecholamines, especially dopamine; reverse transporter/inhibits vesicular storage; Inhibites DAT and VMAT

Behavior and cardio effects: through the mesolimbic system, euphoria, alertness, reduced fatigue, increased energy, decreased appetit Psychosis at high dose (repetition of meaningess activity);increases HR and BP

Side effects: Low - increased BP, euphoria, alertness, loss of appetite; Moderate - stimulate respiration, tremor, increases motor activity, restlesness and agitation; High - continual purposeless repetitive tasks, severe anorexia and weight loss, paranoia, delusions, hallucinations, suddent outbursts of aggression and violence, behavioral fixations, psychosis

Other: Meth - can be smoked, psychosis, meth mouth

CNS stimulant

Uses: ADHD (less CNS stim), narcolepsy

Mechanism: Decreases hyperactivity, improves attention; long acting preparations minimize rebound

SNRI

Uses: ADHD

Mechanism: Inhibits reuptake of NE

Side effects: may increase BP w/ other drugs, little addictions potential; nausea, anorexia, dizziness

No MAOI combo

CNS stimulant

Mechanism: Blocks adenosine receptors, inhibits PDE, increasing cAMP

Effects: increased mental alertness, faster and clearer though, wakefulnesss, restlessness

Side effects: constrict cerebral blood vessels (headache use), bronchodilation, increased gastric acid, diuresis, withdrawal