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Zanaflex (Tizanidine)

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Generic Zanaflex is a muscle relaxant which is used to help relax certain muscles in your body. It relieves the spasms and increases muscle tone caused by medical problems such as multiple sclerosis or spinal injury. This medication is sometimes prescribed for other uses.

Other names for this medication:

Similar Products:
Lioresal, Soma, Flexeril, Valium


Also known as:  Tizanidine.


Generic Zanaflex is an agonist at (alpha) 2-adrenergic receptor sites and presumably reduces spasticity by increasing presynaptic inhibition of motor neurons. In animal models, Generic Zanaflex has no direct effect on skeletal muscle fibers or the neuromuscular junction, and no major effect on monosynaptic spinal reflexes. The effects of Generic Zanaflex are greatest on polysynaptic pathways. The overall effect of these actions is thought to reduce facilitation of spinal motor neurons.

The imidazoline chemical structure of Generic Zanaflex is related to that of the anti-hypertensive drug clonidine and other (alpha) 2 -adrenergic agonists. Pharmacological studies in animals show similarities between the two compounds, but Generic Zanaflex was found to have one-tenth to one-fiftieth (1/50) of the potency of clonidine in lowering blood pressure.

Zanaflex is also known as Tizanidine, Sirdalud.

Generic name of Generic Zanaflex is Tizanidine-Oral.

Brand name of Generic Zanaflex is Zanaflex.


You should take it by mouth.

It usually is taken two or three times a day.

If you want to achieve most effective results do not stop taking Generic Zanaflex suddenly.


If you overdose Generic Zanaflex and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zanaflex are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Zanaflex if you are allergic to Generic Zanaflex components.

Do not take Generic Zanaflex if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Generic Zanaflex if you have liver disease, have kidney disease, have low blood pressure.

Be careful with Generic Zanaflex if you are taking medication to treat high blood pressure or birth control pills.

Avoid alcohol.

Do not stop take it suddenly.

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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.

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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.

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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.

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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.

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zanaflex 6mg tablets 2015-01-24

Though in the last few decades only a few new drugs have come available for the treatment of spasticity, new insights may revise the role and individual value of several pharmacological treatments. Diazepam, baclofen and tizanidine are the most prescribed drugs for the treatment of spasticity. Intrathecal buy zanaflex baclofen and local infiltration of botulin toxin are added values in selective patients. Gabapentin is a novelty, and the working mechanism of cannabis has been elucidated. Dantrolene sodium appears to owe its selectivity from the recently discovered ryanodine receptor, with a peripheral effect in muscles. In this review the pathophysiology and epidemiology of spasticity, pharmacology, clinical efficacy and unwanted effects of the different drugs for spasticity are updated.

zanaflex dosing 2015-09-07

Baclofen affects in experiments the reactivity of the vestibuloocular reflex by influencing the time constant of buy zanaflex the vestibular nystagmus. The authors compare in three healthy volunteers the reactivity of the vestibular apparatus after administration of Baclofen and a new muscle-relaxant drug tizanidine. The authors evaluate basic parameters of the vestibular and optokinetic nystagmus (gain and time constant), discuss the problem of GABAergic (Baclofen) and monoaminergic (tizanide) receptors kin the area of the vestibular apparatus. As regards the effect on the reactivity of the vestibular system, tizanidine does not affect immediately the response of the vestibuloocular reflex but interferes with processes ensured by the central neuronal integrator.

zanaflex tablets dosage 2015-08-24

Pharmacologic and electrophysiologic studies over the past 20 years have shown tizanidine to be a potent, central-acting myotonolytic agent that principally affects spinal polysynaptic reflexes. This action arises from agonistic activity of the compound at noradrenergic alpha 2 receptors, resulting in both direct impairment of excitatory amino acid release from spinal interneurons and a concomitant inhibition of facilitatory coeruleospinal pathways. Similar alpha 2-receptor-mediated inhibition of interneuronal activity appears to underlie the additional antinociceptive and anticonvulsant activity of tizanidine reported in several species and test paradigms. Despite its structural and biochemical similarity to clonidine, the cardiovscular properties of tizanidine are Lopressor Dosage Iv mild and transitory in relation to its activity as a muscle relaxant. These findings, together with a possible greater separation between myotonolytic and general CNS depressant activity than with other agents, make tizanidine a valuable addition in the pharmacologic treatment of spasticity.

zanaflex 20 mg 2015-05-21

An 85-year-old man with a chief complaint of profound weakness was admitted to the hospital with a blood pressure reading of 60/32 mm Hg and a heart rate of 37 beats/min. His medical history included type 2 diabetes mellitus, congestive heart failure, gastroesophageal reflux disease, chronic obstructive pulmonary disease, osteoarthritis, restless leg syndrome, benign prostatic hyperplasia, generalized anxiety disorder with depression, and severe chronic back pain for which he was receiving treatment at a pain clinic. Two days before hospital admission, he had been seen at the pain clinic and started on ti-zanidine. Additional medications included acetaminophen, chlorpromazine, citalopram, finasteride, lidocaine patch, lisinopril, metformin, pramipexole, omeprazole, simvastatin, theophylline, diclofenac topical gel, hydrocodone-acetaminophen, and ondansetron. After taking three doses of the newly prescribed tizanidine, he developed severe hypotension and bradycardia. Notable laboratory test values included a serum creatinine concentration of 1.90 mg/dL, a blood urea nitrogen concentration of 21 mg/dL, a serum potassium concentration of 5.5 meq/L, and a serum Omnicef Suspension Cost sodium concentration of 128 meq/L. Upon admission, tizanidine, lisinopril, theophylline, omeprazole, and simvastatin were withheld, and i.v. fluids were administered. The patient's vital signs began to gradually improve. Within 24 hours, the patient's blood pressure and heart rate had improved, as had the previously abnormal laboratory test values. Tizanidine was discontinued, and all of his other preadmission medications were restarted at discharge.

zanaflex cost 2015-05-04

Addition of therapeutic CFJ injections to a multimodal treatment program is a useful therapeutic modality for patients, especially young patients, suffering from long-standing MPS with Lopid Reviews referral pain of CFJ syndrome.

zanaflex drug 2016-04-30

Intrathecal administration of baclofen via programmable pump is a highly effective treatment method in severe spasticity resistant to oral medications. The authors describe a case of severe spasticity with tetraplegia Lanoxin Dosage Iv and painful (> 10 a day) muscle spasms in the upper and lower limbs and paraspinal muscles, in a patient with clinically definite diagnosis of multiple sclerosis (MS). The 34-year-old female patient with a 15-year history of MS, suffering from lower limb spasticity with pes equinovarus since 1995, was treated with very good results with botulinum toxin injections of calf muscles (14 sessions of Dysport 1500iu till 2002). In the early 2002 she developed tetraplegia with severe, generalized and intractable spasticity. After 4 months of ineffective polytherapy (with high doses of oral baclofen, tizanidine, gabapentine, clonidine, diazepam) and the patient's enormous sufferings (she could neither sit up nor voluntarily change her position in bed), a programmable baclofen pump (Medtronic) was implanted. As soon as a few days after the surgery she could stand, sit and move voluntarily, her painful spasms disappeared, and her bladder catheter was removed. At a 6-month follow-up the effect was stable--she was able to walk a long distance outdoors with the aid of a crutch. The daily dose of the drug is 500 micrograms. No side effects of complications were noted.

zanaflex online 2016-11-20

The role of descending noradrenergic fibers in the spinal motor systems was investigated using spinal reflexes in acutely spinalized rats. In rats pretreated with the MAO inhibitor clorgyline-HCl (1 mg/kg, i.v.), L-3,4-dihydroxyphenylalanine ( Nizoral Medicine L-dopa) (5 mg/kg, i.v.), a precursor of dopamine and noradrenaline, markedly potentiated the mono- (MSR) and polysynaptic reflexes (PSR). Selective blockade of alpha 1-adrenoceptors by pretreatment with prazosin-HCl abolished these facilitatory effects on the MSR and the PSR and revealed the inhibitory effect of L-dopa on the PSR. The depression of PSR was antagonized by the alpha 2-antagonist piperoxan. Clonidine-HCl (0.05 mg/kg, i.v.), a so-called alpha 2-agonist, and tizanidine-HCl (0.1 mg/kg, i.v.) decreased the MSR and the PSR in rats pretreated with prazosin. These inhibitions were antagonized by piperoxan. These results suggest that alpha 1- and alpha 2-adrenoceptors mediate facilitation and attenuation of motor transmission in the rat spinal cord, respectively.

zanaflex reviews 2017-10-26

Projections of group II afferents from intrinsic foot muscles to lower limb motoneurones were investigated in humans after electrical stimuli were applied to the tibial nerve (TN) at ankle level, using modulation of the quadriceps H reflex, on-going EMG of the quadriceps and peroneus brevis, and PSTHs of single quadriceps, biceps, semitendinosus, tibialis anterior, and peroneus brevis motor units. TN stimulation evoked late and high-threshold excitation in all leg and thigh muscles investigated. The mean latency of the late excitation was 13.5+/-0.4 ms longer than that of the heteronymous monosynaptic Ia excitation, and the more caudal the motor nucleus the longer the central delay of the late effect, suggesting mediation through interneurones located rostral to motoneurones. The electrical threshold and conduction velocity of the largest diameter fibres evoking the late excitation were estimated to be approximately 2 and 0.67 times, respectively, those of the fastest Ia afferents, i.e. consistent with a mediation by group II afferents. Stimulation of the skin areas innervated by TN did not evoke late excitations. Further Celebrex Pill support for mediation through group II afferents was provided by the findings that: 1. the latency of the TN-induced late and high-threshold excitation in Per brev units was more delayed by cooling the nerve than that of the excitation evoked by group I afferents, and 2. tizanidine intake (known to depress selectively transmission of group II effects) suppressed the TN-induced late and high-threshold excitation whereas the group I facilitation was not modified.

zanaflex scheduled drug 2016-12-12

We conducted an observational study within our pharmacoepidemiological database derived from electronic medical records of a tertiary care hospital. Among all users of MQAB associated with TdP, we determined the prevalence of additional QT-prolonging drugs and risk factors and identified contraindicated co-administrations of simvastatin, atorvastatin, or tizanidine. Electrocardiographic (ECG) monitoring and associated adverse events were validated in Urispas 200 Tablets medical records.