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Despite a satisfactory grade of recommendation, general pharmacological treatments are limited by adverse events and lack of evidence of functional benefit. Intrathecal baclofen should be discussed for upper-limb spasticity, but further studies are needed before its use can be recommended. The place of chemical neurolysis with use of alcohol or phenol should be evaluated with surgical neurotomy and botulinum toxin therapy. The use of botulinum toxin is the only treatment supported by scientific results, but many questions remain about the site of injection, how to improve efficacy and influence on neurological recovery.
Effects of tizanidine were studied with special reference to the effect on motor systems. The drug effectively reduced the intercollicular decerebrate rigidity and gamma-activity indirectly recorded from muscle spindle afferent discharges without showing the direct inhibitory effect on muscle spindles in rats. The drug dose-dependently inhibited the phasic responses of alpha-rigidity in anemic decerebrate rats without showing marked inhibition of the tonic response. Tizanidine effectively depressed the crossed extensor reflex in chicks and depressed mono- and polysynaptic reflex potentials in rats; dorsal root reflex was increased transiently. Tizanidine had no effect on the neuromuscular junction in rats and [3H]diazepam binding in rat brain membrane. It is suggested that the depression by tizanidine of gamma-system and spinal reflexes contribute to muscle relaxation and anti-spastic effects and that mechanisms of action are different from those of other centrally acting muscle relaxants such as mephenesin and benzodiazepines.
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Spinal cord injury (SCI) is a traumatic condition that can lead to both functional and neuromuscular impairments. Spasticity in the muscles surrounding the ankle joint caused by hypertonia is often reported as a complication. We investigated whether a pharmacological intervention using Tizanidine, an anti-spastic medication acting as an α2-adrenergic agonist, could lead to improvements in walking endurance. We placed subjects on a 4-week program and measured the change in clinical measures of walking speed, endurance, and mobility. We used growth mixture modeling (GMM) to class subjects into groups based on recovery patterns. Two classes of recovery were found by GMM: high and low functioning. Radom coefficient regression (RCR) was then used to identify significant changes over time. Statistically significant improvements in walking endurance were shown for the high functioning group. However, a small number of subjects in the high functioning group showed improvement greater than the smallest real difference (SRD), which indicates a clinical significance as well. We also investigated the extent to which these recovery patterns can be predicted using baseline measures. Baseline walking endurance was found to be a robust predictor of recovery in walking endurance. Subjects that began the intervention with already higher endurance showed a greater chance of improvement in endurance over time. This information could potentially be used as a fast and reliable assessment tool for clinicians to predict which patient can benefit the most from this intervention prior to prescribing the medication, and thus optimizing cost and resources. Our findings demonstrate that these techniques can be used to characterize and predict the progress of changes to functional impairments due to various types of intervention.
Alpha-2-adrenergic agonists, such as clonidine, produce antinociception in animal pain models after intrathecal administration. However, clinical usage is limited by cardiovascular side effects. To investigate alternative alpha(2)-adrenergic agonists as analgesics, we implanted six dogs with an intrathecal catheter and infusion pump. After baseline saline infusion, animals received clonidine or tizanidine (crossover study) each week at escalating doses of 125-750 microg/h. Analgesia, blood pressure, heart rate, respiratory rate, sedation, and coordination were evaluated. A 28-day safety study was performed with another nine dogs receiving intrathecal tizanidine (3 or 6 mg/d) or saline. Equal doses of clonidine and tizanidine produce the same antinociception in thermal withdrawal tests. Blood pressure was reduced with 125-500 microg/h of clonidine, but not with tizanidine at any dose. Clonidine 250 microg/h reduced heart rate by 45.8%, and five of six animals had bradyarrhythmias (marked bradycardia), whereas tizanidine decreased heart rate by 15.1% without arrhythmias, even at the largest dose. Respiratory rate decreased with 250 microg/h of clonidine and larger doses. Sedation or incoordination occurred only at the largest dose for either drug. The safety study indicated that 3 mg/d of tizanidine in dogs produced no side effects or histopathologic changes. Tizanidine may be a useful alternative in patients experiencing cardiovascular side effects with intrathecal infusion of clonidine.
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The effect of a novel imidazoline derivative (tizanidine) on stimulated gastric acid secretion was studied in the perfused stomach of anesthetized rats. Tizanidine, which did not prevent peripherally-stimulated gastric acid secretion, inhibited 2DG- or TRH-stimulated gastric acid secretion. Yohimbine and phentolamine reduced the inhibition of TRH-stimulated acid secretion by tizanidine. Clonidine was found to have similar effects to tizanidine at a lower dose. These results indicate that tizanidine may inhibit gastric acid secretion via the central alpha-adrenergic system similar to clonidine in anesthetized rats.
The electrochemical behaviour of tizanidine [5-chloro(delta-2-imidazolinyl-2-amino)-4-benzothiadiazole-2,1,3], a centrally-active skeletal muscle relaxant has been investigated in aqueous media at the carbon paste electrode (CPE). Cyclic voltammetry at different pH values, controlled potential coulometry and comparative studies on three structurally related molecules have permitted identification of the oxidation site of tizanidine and suggest possible oxidation products in acidic media. The electrochemical reduction at the CPE occurred in one irreversible step and the reduction product (diamine derivative) was detected and characterized on the positive going scan in cyclic voltammetry. Quantitative measurements of tizanidine within the range 2 x 10(-5) M and 1 x 10(-4) M have been realized at the CPE using the differential pulse technique.
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Dysfunction of nervous system plays the main role in this pain syndrome. The efficacy of the drugs in the early/late recovery period was estimated as follows: nonsteroidal anti-inflammatory drugs - 33%/12%, amitriptyline - 24%/42%, gabapentin - 10%/13%, lidocaine - 95%/100%, tizanidine - 29%/33%. Seventy-six percent of patients were free of pain after treatment using a regimen suggested by the authors.
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Changes in clinical and electrophysiologic measurements in the cold group were statistically significant compared with those of the tizanidine and patient control groups.