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Tizanidine used in back pain accompanied by muscle spasm results in quick pain relief (initial relief on the 2nd day of treatment, complete relief after 4 days, vs. initial relief on the 3rd day of treatment, complete after 7 days in the control group). The daily dosage and cumulative dose needed to achieve analgesic effect is low (lowest recommended dose by the producer). Tizanidine is well tolerated: adverse effects were rare (<6%, vs. 13% in the control group) and transient. The clinical effect of tizanidine was prompt in acute pain and more delayed in chronic disease.
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It was possible to reduce the infiltration pain of local anesthetic during epidural catheterization by oral administration of 3 mg of tizanidine as premedication. Blood pressure and rate-pressure product in the operating room were also attenuated by receiving tizanidine. Therefore, we recommend premedication with tizanidine for patients undergoing epidural catheterization.
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Many commonly used migraine medications may be compatible with breast-feeding based on expert recommendations. Ibuprofen, diclofenac, and eletriptan are among acute medications with low levels in breast milk, but studies of triptans are limited. Toxicity is a concern with aspirin due to an association with Reye's syndrome; sedation or apnea is a concern with opioids. Finally, preventive medications not recommended include zonisamide, atenolol, and tizanidine.
Health systems have developed interventions to reduce harm associated with drug-drug interactions. Pharmacy benefit managers are in an important position to identify the coprescribing of medications known to interact, since they process data on a large portion of prescription claims in the United States. Electronic health records and electronic prescribing also include alerts through their systems' clinical decision support. However, limited data are available that assess prescribers' perceptions of processes that screen for potential drug-drug interactions (PDDIs).
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The effects of intravenous clonidine and tizanidine on nociceptive neurons in the nucleus ventralis posterolateralis (VPL) of the thalamus, a key station in the lateral system of ascending pain pathways, were evaluated in urethane-chloralose anesthetized cats. Intravenous clonidine and tizanidine produced a dose-dependent (5 and 10 micrograms/kg, and 25 and 50 micrograms/kg, respectively) suppression of responses of nociceptive specific (NS) and wide dynamic range (WDR) neurons in the VPL to high threshold splanchnic input. In contrast, the responses of both NS and WDR units to electrical stimulation of spinothalamic tract fibers in the ventrolateral funiculus (VLF) were little affected. We conclude that a site of suppressive action of the alpha 2-adrenoceptor agonists, as observed in nociceptive VPL neurons, is at the level of the spinal dorsal horn rather than in the VPL itself.
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This open-label, phase I study comprised two protocols: protocol 1, tizanidine HCl solution (32.73 mg/mL) intranasally at single doses of 2 and 4 mg versus 4 mg tizanidine oral tablets (randomized, three periods crossover, 12 healthy subjects); and protocol 2, tizanidine HCl solution (16.36 mg/mL) intranasally at a single dose of 1 mg vs. 4 mg tizanidine oral tablets (randomized, two periods crossover, 12 healthy subjects, one dropout). Tizanidine plasma concentrations were determined by liquid chromatography/mass spectrometry.
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Sensitivity (pD2 value, negative logarithm of the molar concentration producing the half maximum response) and affinity (pKA value, negative logarithm of dissociation constant) of norepinephrine were determined in 6 arteries from rabbits. A positive correlation was found in the pD2 and pKA values of norepinephrine. The slope was not significantly different from 1. The pD2 and pKP (a negative logarithm of dissociation constant of a partial agonist) values of tizanidine, an alpha 1-partial agonist, were also determined. There were positive correlations between the pD2 and pKP values of tizanidine and also between the two pD2 values of norepinephrine and tizanidine. The slopes were not significantly different from 1. These results suggest that the regional differences in pD2 values of norepinephrine and tizanidine in the arteries are partly due to the affinity and suggest that both drugs interact with one recognition site in the alpha 1-adrenoceptors. The dissociation constants, KD values, and the maximum binding sites, Bmax, for [125I]-HEAT were also estimated by Scatchard analysis of the specific binding of [125I]-HEAT to the membrane fractions from rabbit arteries. The KD values for [125I]-HEAT were also identical. However, Bmax varied considerably among rabbit arteries. There was a positive correlation between the logarithm of Bmax and the pD2 values for norepinephrine. The present results suggest that the regional difference in the pD2 values for norepinephrine in rabbit arteries is due to variations in the affinities to the alpha 1-adrenoceptors as well as the receptor densities.
The effect of tizanidine given as a premedication on perioperative hemodynamics (mean blood pressure, heart rate), sedation, hypnosis and midazolam requirements for induction were assessed in 68 patients scheduled for elective surgery under general anesthesia. Patients were assigned to three groups. Group 1 was premedicated 90 min prior to induction with tizanidine 4 mg po (n = 28); group 2 was premedicated with tizanidine 2 mg po (n = 12); group 3 received no premedication (n = 28). In group 1, increase of mean blood pressure on anesthesia induction was attenuated significantly and sedative and hypnotic effects were stronger significantly compared with other groups. We also found that the amounts of midazolam necessary for loss of consciousness were significantly less in patients who had received tizanidine 4 mg. In conclusion, tizanidine is a useful drug as preanesthetic medication for general anesthesia.