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cyclobenzaprine
- skeletal muscle relaxant
- MoA: decreases activity of locus coeruleus, so decreases activity of descending facilitative influence on motor neuron excitability
- decreases muscle tone (less flexion and extension)
- aka "disfacilitation"
- structurally similar to TCA
- SE: antimuscarinic: sedation, confusion, dry mouth, dizziness, urinary retention
- OoA: 1 hr
- t1/2: 18 hrs
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methocarbamol
- muscle relaxant
- MoA: unclear...may suppress excitatory interneurons in spinal cord -> decrease amp of polysynaptic reflexes.
- less excitatory drive to motor neurons -> muscle relaxation
- said to decrease muscle tension without reducing basal muscle tone to maintain posture.
- SE: sedation (v. significant), dizziness, blurred vision, dyspepsia, metallic taste
- OoA: 30 mins
- t1/2: 1-2 hours
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baclofen
- GABA-mimetic, spasmolytic
- agonist at GABAb receptors. does not requre presence of GABA for action.
- reduces muscle spasticity, equally effective but less sedating than BZD
- OoA: rapid after oral admin
- t1/2: 3-4hrs
- can be given intrathecally for refractory spasticity
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benzodiazepines (e.g. diazepam) for lower back pain
- act on GABAa receptors but require GABA to exert action (not bind to same part as GABA)
- enhances effect of GABA, increases frequency of chloride channel opening
- OoA: almost immediate. oral 15-30mins.
- t1/2: 5-50 hours (depends on metabolism and properties of diff agents)
- SE: sedation, confusion, slurred speech, hypotension, brady, apnea
- DEPENDENCE, withdrawal if stop. Important to taper dose.
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triptans
- selective agonist for 5-HT1d and 5-HT1b receptors
- e.g. suma, riza, nara, zoli, almo, ele
- MoA: 1) bind to presyn 5-HT1d and inhibit release of neuropeptides, 2) direct VC/px of VD of meningeal bv, 3) block afferent input to 2o neurons in trigeminal nucleus caudalis.
- PK: most effective when given in early stages of migraine (within 2 hours of onset). hepatic metab via MAO-A enzymes
- dosage routes: PO, SL, intranasal, IV, IM
- OoA: 15 mins with SC/IV
- suma F 15%, newer agents F 50-70%, but not 100% so IV is most preferred.
- SE: well tol'd...ass'd with stroke and CVD?
- risk of serotonin syndrome if: MAOI in past 2 weeks, Ergot in last 24 hrs.
- SSRIs and SNRIs not absolute CI...but must tell pt how to monitor for serotonin syndrome.
- CI: ischemic vascular disease
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ergotamine
- ergot alkaloid, purified
- agonist, partial agonist, antagonist: 5-HT & alpha-adreno
- agonist, partial agonist: dopamine receptors
- MoA: VC of meningeal blood vessels. stronger affinity, up to 24 hours before dissociates from receptors.
- dosage routes: IM, IV, SC, intranasal
- SE: may worsen N/V, cause rebound headache, dependence, prolonged vasospasm
- Administer with antiemetic.
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dihydroergotamine
- ergot alkaloid, semi-synthetic
- agonist, partial agonist, antagonist: 5-HT & alpha-adreno
- agonist, partial agonist: dopamine receptors
- MoA: VC of meningeal blood vessels. Higher affinity to alpha-adrenoreceptors, but lower receptor affinity vs. ergotamine for all other receptrs...mmore rapid hepatic elimination.
- dosage routes: IM, IV, SC, intranasal
- OoA: 15-30 mins
- CI: hypertension, ischemic cardiovascular disease, current use of MAOI or strong CYP3A4 inhibs (azoles, macrolides)
- SE: may worsen N/V, not cause rebound h/a or dependence.
- Administer with antiemetic.
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metoclopramide (chlorpromazine, prochlorperazine)
- antiemetic, used as monotherapy or adjunctive therapy in tx migraines
- block dopamine and alpha-adrenoreceptors
- - chemoreceptor trigger zone: decrease N/V
- - trigeminovascular system: vasoconstriction...helpful for migraines?
- metoclopramide enhances ACh action...accelerates gastric motility, increases lower esophageal sphincter tone.
- SE: extra-pyramidal (akathisia, tardive dyskinesia, dystonia) if long term, and drowsiness
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