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Topamax (Topiramate)

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Generic Topamax is a medication of high quality, which is taken in treatment of seizures in people with Lennox-Gastaut syndrome and epilepsy. It can also be used to prevent migraine and infantile spasms. Generic Topamax is acting by reducing brain agitation.

Other names for this medication:

Similar Products:
Neurontin, Depakote, Lamictal, Tegretol


Also known as:  Topiramate.


Generic Topamax target is the treatment of seizures in people with Lennox-Gastaut syndrome and epilepsy. It can also be used to prevent migraine and infantile spasms.

Generic Topamax is acting by reducing brain agitation. It is anticonvulsant.

Topamax is also known as Topiramate, Topaz.

Generic name of Generic Topamax is Topiramate.

Brand name of Generic Topamax is Topamax.


Take it orally at the same time every day, with or without food.

Generic Topamax can be taken twice a day (in the morning and in the evening).

Avoid low-carbohydrate and high-fat diet.

Elderly people should be very careful with Generic Topamax.

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


If you overdose Generic Topamax and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Topamax overdosage: feeling drowsy, problems with a speech, blurred vision, double vision, fatigue, lack of coordination, lack of consciousness, lightheadedness, pain of stomach, dyspepsia, vomiting, extreme hunger, agitation, depression, dyspnoea, confusion, decreased appetite, weakness of muscle, pain of bone, convulsion, coma.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Topamax 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 Topamax if you are allergic to Generic Topamax components.

Do not take Generic Topamax if you are pregnant, planning to become pregnant, or are breast-feeding.

Be careful if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful if you are taking ipratropium (such as Atrovent); motion sickness, irritable bowel disease, mental illness, urinary problems, Parkinson's disease, ulcers medicines; oral contraceptives; methazolamide; seizures medicines (carbamazepine (such as Tegretol), phenytoin (such as Phenytek, Dilantin); metformin (such as Glucophage); iron; salicylate pain relievers (such as choline salicylate (such as Arthropan), aspirin, choline magnesium trisalicylate (such as Trisalate), diflunisal (such as Dolobid), magnesium salicylate (such as Doan's); dichlorphenamide (such as Daranide); digoxin (such as Digitek, Lanoxin); zonisamide (such as Zonegran); tranquilizers; acetazolamide (such as Diamox); valproic acid (such as Depakote, Depakene); cholestyramine (such as Questran); sedatives; antidepressants; isoniazid (such as Nydrazid, INH); antihistamines, salsalate (such as Salgesic, Argesic, Disalcid), sleeping pills.

Be careful if you have lung, kidney or liver disease, diabetes, glaucoma, chronic obstructive pulmonary disease, nearsightedness, diarrhea, metabolic acidosis, kidney stones.

Avoid low-carbohydrate and high-fat diet.

Avoid being dehydrated.

Elderly people should be very careful with Generic Topamax.

Be careful with Generic Topamax if you are going to have a surgery (dental or other).

If you experience drowsiness and dizziness while taking Generic Topamax you should avoid any activities such as driving or operating machinery.

To prevent pregnancy, use an extra form of birth control because hormonal birth control pills may not work as well while you are using Generic Topamax.

Avoid alcohol while taking Generic Topamax.

It can be dangerous to stop Generic Topamax taking suddenly.

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We here report on 3 patients with essential tremor, otherwise unresponsive to pharmacological treatment, who greatly benefited from low doses of topiramate (50 mg/d). No side effects were observed and improvement was sustained during a mean of 7 months (range 3-12 months) follow up. Our results suggest that topiramate titration should be performed gradually, so as not to neglect cases responsive to low doses.

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Injury to the ilioinguinal nerve commonly follows during lower abdominal and pelvic surgery, especially with inguinal hernia repair, appendectomy, and hysterectomy. Other potential causes include low abdominal blunt trauma, iliac crest bone graft, psoas abscess, Pott's disease, and prolonged wearing of abdominally constrictive clothing. The actual incidence of ilioinguinal neuralgia is uncertain, as reported percentage ranges between 12% and 62%. Prompt and accurate diagnosis is critical, and appropriate treatments range from conservative pharmacologic management with nonopioid (eg, gabapentin, topiramate) as well as opioid agents, to surgical neurectomy of the proximal portion of the ilioinguinal nerve. Pharmacological treatment is frequently unsuccessful (particularly if delayed) and while surgery is successful in approximately 73% of cases, it can result in problematic paresthesias, and pain may continue to persist in some patients. Thus, minimally invasive techniques, such as peripheral nerve stimulation, may be viable in those patients who are refractory to pharmacological management, as an option to surgery, and who have not gained satisfactory pain relief through surgical intervention. We present three cases of successful pain control of ilioinguinal neuralgia with peripheral nerve stimulation. These cases demonstrate the potential benefits of neurostimulation including durable effective pain relief and decreased use of medication. Putative mechanisms of effect(s) and caveats for continued research to inform prudent employment of this technique are presented.

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Fifteen out of the 30 patients who were administered Sincronil reported an improvement in the clinical condition, with a decrease in the frequency of attacks at the 3rd month of treatment higher than 50% with respect to the run-in period, 9 reported their clinical condition as being substantially unchanged and 6 reported that they had suspended the treatment within the first 4 weeks of therapy due to side effects. Among the 24 patients who continued treatment up to the 3rd month, the frequency of attacks during the 3rd month of treatment was significantly decreased from 7 ± 3.6 to 3.7 ± 3.7 (P<0.0001), migraine severity was reduced from 2.5 ± 0.5 to 1.7 ± 0.7 (P<0.0005) and the MIDAS score was reduced from 14.3 ± 4.9 to 8.6 ± 5.5 (P<0.0001). Sixteen out of the 30 patients who were administered Topamax reported an improvement in the clinical condition with a reduction in the attack frequency at the 3rd month of treatment higher than 50% with respect to the run-in period, 10 reported a substantially unchanged clinical condition and 4 stopped the treatment within the first weeks due to side effects. Among the 26 patients who continued treatment up to the 3rd month, headache frequency during the 3rd month of treatment was significantly reduced, from 7.3 ± 2.6 to 3.5 ± 2.7 (P<0.0001), migraine severity decreased from 2.4 ± 0.6 to 1.6 ± 0.8 (P<0.0005) and the MIDAS score from 14.1 ± 4.2 to 6.8 ± 4.8 (P<0.0001).

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We evaluated, prospectively, the carbon dioxide serum levels of 18 patients seen at the epilepsy clinic of our university hospital, before and 3 months after introducing topiramate.

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Obesity is a disease that has historically eluded effective medical therapy. Prior to 2012, phentermine and orlistat were the only medications available to treat obesity in the USA, with phentermine approved only for short-term use. However, as of 2015, the repertoire of pharmacological agents available to treat obesity has greatly expanded to include four new drugs: lorcaserin, phentermine/topiramate extended release (ER), naltrexone ER/wellbutrin ER and liraglutide. Each has a unique mechanism of action and all are intended for long-term use. These newer medications share a common strategy to promote weight loss in that they are designed to manipulate the control of hunger and satiety in the central nervous system. Interestingly, the majority of these new agents are combinations of older medications that have been used for conditions other than obesity. The amount of weight loss seen with these agents beyond placebo varies but generally falls in the range of 3-10% of starting weight and requires continual use of the drug in order for weight loss to be sustained. In addition, each drug has a unique side effect profile that should be carefully considered when selecting the best agent for a given individual. This article provides a review of these recently approved medications focusing on efficacy, side effect profiles and appropriate application to the individual patient.

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Neuroscientific developments have promulgated interest in developing efficacious medications for the treatment of substance dependence. Previous pharmacological strategies that involve the use of relatively specific medications to alter corticomesolimbic dopaminergic neuronal activity--the critical pathway for expression of the reinforcing effects of abused drugs--have yielded modest efficacy in the treatment of alcohol dependence, and no medication has been established as a treatment for cocaine dependence. Since corticomesolimbic dopaminergic neurons interact with other neurotransmitters that modulate the effects of dopamine in the nucleus accumbens, would it not be possible to control these dopaminergic effects more reliably with a medication that acts contemporaneously on more than one neuromodulator of dopaminergic function? Further, since the long-term use of either alcohol or cocaine results in neuronal adaptations as a result of sensitisation, would the chances of effective therapy not be bolstered by administering a medication that was also able to mitigate these chronic effects? Thus, a new conceptual approach is needed. My proposal is that a medication--in this case topiramate--that principally potentiates inhibitory GABA(A) receptor-mediated input and antagonises excitatory glutamatergic afferents to the corticomesolimbic dopaminergic system should have therapeutic potential in treating either alcohol or cocaine dependence or perhaps both. This is because the principal neurochemical effects of topiramate would not only serve to decrease the acute reinforcing effects of alcohol or cocaine, but might also facilitate cessation of their use following a period of long-term use by decreasing neuronal sensitisation. This overview highlights the scientific concepts and clinical evidence for the development of topiramate in the treatment of alcohol dependence and introduces preliminary evidence to indicate that it might also have utility in treating cocaine dependence. Finally, to place the material on topiramate in context, information has been included on the utility and development of other medications that modulate GABA- or glutamate-mediated neuronal systems for the treatment of alcohol or cocaine dependence.

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Novel antiepileptic drugs (AEDs) are thought to act on voltage-sensitive ion channels, on inhibitory neurotransmission or on excitatory neurotransmission. Two successful examples of rational AED design that potentiate GABA-mediated inhibition are vigabatrin (VGB) by irreversible inhibition of GABA-transaminase, and tiagabine (TGB) by blocking GABA uptake. Lamotrigine (LTG) prolongs inactivation of voltage-dependent sodium channels. The anticonvulsant action of remacemide (RCM) is probably largely due to blockade of NMDA receptors and prolonged inactivation of sodium channels induced by its desglycinated metabolite. Felbamate (FBM) apparently blocks NMDA receptors, potentiates GABA-mediated responses, blocks L-type calcium channels, and possibly also prolongs sodium channel inactivation. Similarly, topiramate (TPM) has multiple probable sites of action, including sodium channels, GABA receptors, and glutamate (AMPA) receptors. Gabapentin (GBP) apparently has a completely novel type of action, probably involving potentiation of GABA-mediated inhibition and possibly also inactivation of sodium channels. The therapeutic advantages of the novel AEDs are as yet only partially explained by our present understanding of their mechanisms of action.

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Since 1990 eight new antiepileptic drugs (AEDs) have been developed. Among these new drugs, Topiramate (TPM) is one of the latest AEDs available for treating drug resistant partial epilepsy both in adults and in children. The mechanisms underlying TPM antiepileptic activity are still incompletely understood. However, TPM, a sulfamate-substituted derivative of the naturally occurring monosaccharide D-fructose, has a different structure from other known AEDs. The antiepileptic activity of TPM in animal models of partial and generalized tonic-clonic seizures has been shown to be more effective as compared to other AEDs. Proposed mechanisms of action include reduction of epileptiform discharges through a voltage-dependent block of Na(+) channels, enhancement of the activity of gamma-aminobutyrate at some subtypes of gamma-aminobutyrate receptors, and antagonism of non- N-methyl-D-aspartate (NMDA) glutamate receptors. The pharmacokinetic profile of TPM, which is characterized by its rapid and almost complete absorption after oral administration, linear pharmacokinetics, minimal protein binding and predominantly renal excretion, makes the drug a good option for the treatment. TPM was found to be effective and well tolerated in many studies conducted in adults and pediatric patients suffering from epilepsy. This review, summarising the main studies in this field, provides an overview of the current knowledge about the relevant pharmacological and clinical information on the efficacy and tolerability of TPM.

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Recent advances in lifestyle intervention programs, pharmacotherapy, and bariatric surgery have enabled the development of medical models for the treatment of obesity. Regarding pharmacotherapy, in 2012 the U.S. Food and Drug Administration approved two new effective and safe weight-loss medications, phentermine/topiramate extended release and lorcaserin, which has greatly augmented options for medically assisted weight loss.

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Full outcome data are available on 203 pregnancies. Of these, 178 resulted in live birth; 16 had an MCM (9.0%; 95% CI 5.6% to 14.1%). Three MCMs were observed in 70 monotherapy exposures (4.8%; 95% CI 1.7% to 13.3%) and 13 in cases exposed to topiramate as part of a polytherapy regimen (11.2%; 95% CI 6.7% to 18.2%). Four of the MCMs were oral clefts (2.2%; 95% CI 0.9% to 5.6%). Four cases of hypospadias were reported (5.1%; 95% CI 0.2% to 10.1%) among 78 known live male births of which two were classified as major malformations.

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In this systematic review, we present information relating to the effectiveness and safety of the following interventions: baclofen (oral); botulinum toxin (intramuscular); capsaicin (intranasal); chlorpromazine; civamide (intranasal); clonidine (transdermal); corticosteroids; ergotamine and dihydroergotamine (oral or intranasal); gabapentin (oral); greater occipital nerve injections (betamethasone plus xylocaine); high-dose and high-flow-rate oxygen; hyperbaric oxygen; leuprolide; lidocaine (intranasal); lithium (oral); melatonin; methysergide (oral); octreotide (subcutaneous); pizotifen (oral); sodium valproate (oral); sumatriptan (oral, subcutaneous, and intranasal); topiramate (oral); tricyclic antidepressants (TCAs); verapamil; and zolmitriptan (oral and intranasal).

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Potential neuroprotective effects of the antiepileptic drug (AED) topiramate (TPM) were evaluated using primary neuronal-astroglial cultures or astroglial-enriched cultures from newborn rats exposed to excitotoxic concentrations of glutamate (Glu) or kainate. Neurons expressed functional Glu receptors of the NMDA and AMPA/kainate types as evaluated by immunocytochemistry and Ca(2+) imaging. When Glu (10 mM) was added to 9-10-day cultures incubated with the fluorescent dye calcein/AM for 5h, there was a marked cell loss in both culture types, but was more pronounced in the neuronal-astroglial cultures. When TPM (5-10 microM) was included in the medium together with Glu, the amount of surviving cells was significantly higher in the neuronal-astroglial cultures, but not in the astroglial-enriched cultures. Immuno-labeling of the cultures revealed an enhanced survival of MAP positive neuronal cells when TPM was included in the Glu containing medium. As TPM has a proven negative modulatory effect on kainate activated receptors, neuronal-astroglial cultures were further exposed to excitotoxic concentrations of kainate (100 microM) and analyzed immunohistochemically. Significantly more MAP positive neurons survived in the TPM containing medium and showed a morphology similar to untreated cells. Valproate and phenytoin were used as reference AEDs. In conclusion, our results demonstrate a protective effect of TPM upon neuronal cells in primary culture, exposed to excitotoxic levels of Glu or kainate.

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Seizure outcome did not differ when patients receiving valproic acid monotherapy (n = 36) were compared with those receiving lamotrigine monotherapy (n = 14), and when patients receiving valproic acid polytherapy (n = 22) were compared with those receiving lamotrigine polytherapy (n = 21) or topiramate polytherapy (n = 15) (P>.05 for all). The combined data of myoclonic seizure control by all 3 AEDs were poorer when compared with the combined data of generalized tonic-clonic seizure control by all 3 AEDs (P =.03), but not when compared with the combined data of absence seizure control by all 3 AEDs (P =.43). Valproic acid, lamotrigine, and topiramate, when compared with phenytoin or carbamazepine, demonstrated significantly better control of myoclonic seizures (P<.01 for all), but not of generalized tonic-clonic seizures (P>.11 for all).

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Hypokalemic periodic paralysis (hypoPP), the most common form of periodic paralysis, is a disorder characterized by attacks of transient muscle weakness associated with a drop in serum potassium level.The mainstay of treatment is potassium supplementation and drugs that inhibit the enzyme carbonic anhydrase. In this report we describe 11-year-old twins with hypoPP who were treated with topiramate, an anti-epileptic drug known to have carbonic anhydrase inhibitory properties. The patients experienced a decrease in the severity of their attacks upon initiation of treatment. Topiramate may warrant further investigation as a treatment option in hypoPP.

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Despite introduction of new antiepileptic drugs the established drugs phenytoin, carbamazepine and valproate still provide the treatment of choice in most forms of epilepsy, being efficacious in approximately two-thirds of all newly referred patients. In 20-60% of patients resistant to treatment with the older drugs, a 50% reduction of seizure frequency can be achieved by adding ethosuximide, clobazam, vigabatrine, oxcarbazepine, lamotrigine, felbamate, tiagabine or topiramate to the classic treatment. The majority of the new drugs are free of the problematic enzyme induction of the older compounds, making monotherapy as well as combination therapy much easier. To what extent the new antiepileptic drugs are going to be used for the treatment of patients with epilepsy will depend on the analysis of cost and benefits. This will be based on efficacy, side effects, interactions and teratogenicity of these new compounds.

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Anticonvulsants represent one of the main substance classes used for the preventive treatment of migraine. Efficacy has been demonstrated in randomized placebo-controlled trials for topiramate and valproic acid including divalproex sodium. In the case of topiramate, efficacy has recently been proven for chronic migraine and even medication overuse headache, questioning the established concept of medication withdrawal. However, preventive treatment with anticonvulsants is frequently hampered by side effects that occasionally require treatment discontinuation. In addition, these data indicate that some anticonvulsant drugs are effective in migraine, while a number are clearly not useful. Effective anticonvulsants, such as topiramate and valproate, target nociceptive trigeminovascular and trigeminothalamic dural pathways or mechanisms involved in cortical spreading depression. Dissecting out how the anticonvulsants that do not work differ mechanistically from those that do will almost certainly provide avenues through which one can develop new treatments to bring to patients with migraine.

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TPM promptly elevates brain GABA and presumably offers partial protection against further seizures within hours of the first oral dose. Patients may expect to experience the effects of increased homocarnosine and pyrrolidinone within 24 h.

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Diverse brain insults, including traumatic brain injury, stroke, infections, tumors, neurodegenerative diseases, and prolonged acute symptomatic seizures, such as complex febrile seizures or status epilepticus (SE), can induce "epileptogenesis," a process by which normal brain tissue is transformed into tissue capable of generating spontaneous recurrent seizures. Furthermore, epileptogenesis operates in cryptogenic causes of epilepsy. In view of the accumulating information about cellular and molecular mechanisms of epileptogenesis, it should be possible to intervene in this process before the onset of seizures and thereby either prevent the development of epilepsy in patients at risk or increase the potential for better long-term outcome, which constitutes a major clinical need. For identifying pharmacological interventions that prevent, interrupt or reverse the epileptogenic process in people at risk, two groups of animal models, kindling and SE-induced recurrent seizures, have been recommended as potentially useful tools. Furthermore, genetic rodent models of epileptogenesis are increasingly used in assessing antiepileptogenic treatments. Two approaches have been used in these different model categories: screening of clinically established antiepileptic drugs (AEDs) for antiepileptogenic or disease-modifying potential, and targeting the key causal mechanisms that underlie epileptogenesis. The first approach indicated that among various AEDs, topiramate, levetiracetam, carisbamate, and valproate may be the most promising. On the basis of these experimental findings, two ongoing clinical trials will address the antiepileptogenic potential of topiramate and levetiracetam in patients with traumatic brain injury, hopefully translating laboratory discoveries into successful therapies. The second approach has highlighted neurodegeneration, inflammation and up-regulation of immune responses, and neuronal hyperexcitability as potential targets for antiepileptogenesis or disease modification. This article reviews these areas of progress and discusses the challenges associated with discovery of antiepileptogenic therapies.

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Obesity is one of the major problems of health policy in different countries. Pharmacological attempts have been made to help affected people without a definitive solution. Some agents--either with peripheral or central effect--are available in the market. On July 2012, the FDA approved two novel preparations for obese patients: (1) topiramate-phentermine--the first one an anticonvulsant and the second one a sympathomimetic amine--and (2) lorcaserin, a 5-HT2CR agonist. Both preparations emerged as new options for weight management.

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To evaluate anticraving action and tolerability of topiramate in cocaine user treatment.

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The choice of the adequate antiepileptic treatment is based on the clinical experience more than rationality. During some decades, the combination of two antiepileptic drugs was considered the initial treatment but monotherapy showed more advantages (effectiveness, fewer adverse events, fewer teratogenic effects and better compliance). New antiepileptic drugs have increased our interest and knowledge of the epilepsies. They have changed some of our therapeutical schemes. Sodium valproate continues to be considered the choice treatment for all the idiopathic, cryptogenic and symptomatic generalized epilepsies. Lamotrigine and topiramate are two valid alternatives in these epileptic syndromes. In West's syndrome vigabatrin is considered the initial treatment. Carbamacepine, vigabatrine and tiagabine are not indicated in the treatment of generalized idiopathic epilepsies especially in patients with absence seizures. In focal epilepsies, both cryptogenic and symptomatic all the antiepileptic drugs have shown efficacy and the choice treatment is based on the adverse events and the teratogenic power. Prospective studies in patients with the same type of seizures and epileptic syndromes will allow us to determine the more adequate antiepileptic treatment.

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Sleep-related eating disorder (SRED) is a condition characterized by recurrent episodes of eating at the transition from night-time sleep to arousal. SRED patients describe eating in an out-of-control manner with preference for high-caloric foods and sometimes with inedible or toxic items. Level of consciousness during SRED episodes ranges from partial consciousness to dense unawareness typical of somnambulistic episodes. SRED is sometimes associated with psychotropic medication, in particular sedative hypnotics, and other sleep disorders, including parasomnias, narcolepsy, and restless legs syndrome. Night eating syndrome (NES) is another important condition in the disordered night-time eating spectrum showing hyperphagia episodes at full arousal from nocturnal sleep without accompanying amnesia. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset. The two conditions often overlap and possibly share a common pathophysiology. Studies have suggested that central nervous system serotonin modulation may lead to an effective treatment of NES, while the anti-seizure medication topiramate may be an effective SRED treatment.

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The purpose of this study was to investigate changes in utilisation of antiepileptic drugs (AEDs) in epilepsy and non-epilepsy disorders in Norway and furthermore to study the retention rates of the most commonly used AEDs in these indications in long-term use.

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We previously demonstrated that converting patients from the enzyme-inducers phenytoin or carbamazepine to the non-inducers levetiracetam or lamotrigine reduces serum lipids and C-reactive protein (CRP). We sought to determine if the same changes would occur when patients were switched to topiramate, which has shown some evidence of enzyme induction at high doses. We also examined the effects of drug switch on low-density lipoprotein (LDL) particle concentration.

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Medications administered long term, such as those used for migraine prophylaxis, are often associated with weight change as a side effect. Such effects may compromise general health status, exacerbate coexisting medical conditions, and affect medication adherence. Weight gain should be of particular concern in patients with migraine, as there is evidence that overweight and obese patients with migraine are at risk for an increased frequency and severity of migraine attacks.

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Cognitive behavioral therapy, lisdexamfetamine, SGAs, and topiramate reduced binge eating and related psychopathology, and lisdexamfetamine and topiramate reduced weight in adults with binge-eating disorder.

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These studies further investigate the ability of topiramate (TPM) to enhance gamma-aminobutyric acid (GABA)-mediated inhibition through a benzodiazepine-insensitive pathway.

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Topiramate (TPM) is a broad-spectrum antiepileptic drug with various mechanisms of action including an inhibitory effect on some isozymes of carbonic anhydrase (CA). Binding to CA-I and CA-II, which are highly concentrated in erythrocytes, may affect drug pharmacokinetics. Consequently, the objectives of this study were: (a) to comparatively assess TPM pharmacokinetics in healthy subjects, based on plasma and whole blood data, by simultaneously measuring TPM concentrations in plasma and whole blood following different therapeutic doses; (b) to rigorously establish the affinity of TPM for CA-I and CA-II in order to gain insight into how binding to these isozymes in erythrocytes influences TPM pharmacokinetics. TPM (100, 200 and 400 mg, single dose) was given in a randomized three-way crossover design to 27 healthy subjects and the drug concentrations in plasma and whole blood were simultaneously measured for 168 h after dosing. The pharmacokinetics of TPM in plasma was linear, but TPM clearance from whole blood increased with increasing dose. At low therapeutic concentrations, the blood-to-plasma ratio for TPM decreased from 8 to 2 as its concentration increased, indicating a substantial and saturable binding of TPM to erythrocytes. The kinetics (dissociation binding constant -Kd and maximum binding rate -Bmax) of the binding of TPM to erythrocytes was determined from the measured concentrations of TPM in whole blood and plasma. This analysis indicated the existence of two binding sites with Kd values of 0.54 and 140 microM, and Bmax values of 22 and 124 micromol/L of erythrocyte volume, respectively. These Bmax values are similar to literature values for the molar concentration of human CA-II (14-25 micromol/L) and CA-I (115-125 micromol/L). TPM inhibition constant (Ki) values for the inhibition of purified human CA obtained using assays based on CO2 hydration or 4-nitrophenylacetate hydrolysis were 0.62 and 0.49 microM for CA-II, and 91 and 93 microM for CA-I. The results of these studies indicate that virtually all of the binding of TPM to erythrocytes is attributable to CA-I and CA-II. Because CA-I and CA-II are highly concentrated in erythrocytes, a large portion of TPM in whole blood is bound and serves as a depot. This contributes to the lower oral clearance (CL/F), apparent volume of distribution (Vss/F) and longer half-life (t(1/2)) that TPM has in blood compared to the CL/F, Vss/F and t(1/2), estimated from plasma data. The difference between TPM blood and plasma pharmacokinetics was more profound at low doses (< or = 100 mg/day).

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Epidermal nevus syndrome is a kind of neurocutaneous syndrome that is associated with epidermal nevus and a variety of congenital CNS disorders. Clinical presentations include seizures, paresis, mental retardation, and developmental delay. We report three cases with MR imaging and magnetoencephalography findings; one patient underwent ictal and interictal single photon emission CT. Both structural and functional imaging studies indicated that the frontal lobes had lesser involvement or were intact. One patient underwent hemispherectomy because of the medically intractable seizure. He remained seizure free with topiramate monotherapy.

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Adjunctive sibutramine and topiramate may have comparable weight loss effects in overweight or obese bipolar patients with psychotropic-associated weight gain, but are each associated with similarly high discontinuation rates. In addition, they may have different attrition profiles. Compared to sibutramine, discontinuation of topiramate may be more likely to occur early in treatment and may be more dependent upon manic and depressive symptoms.

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topamax medicine 2016-12-13

Twenty papers describing 17 unique trials met the inclusion criteria. Analysis of data from nine trials (1737 participants) showed that topiramate reduced headache frequency by about 1.2 attacks per 28 days as compared to placebo (MD -1.20; 95% confidence interval (CI) -1.59 to -0.80). Data from nine trials (1190 participants) show that topiramate approximately doubled the proportion of responders relative to placebo (RR 2.02; 95% CI 1.57 to 2.60; NNT 4; 95% CI 3 to 6). Separate analysis of different topiramate doses produced similar MDs versus placebo at 50 mg (-0.95; 95% CI -1.95 to 0.04; three studies; 520 participants), 100 mg (-1.15; 95% CI -1.58 to -0.71; six studies; 1620 participants), and 200 mg (-0.94; 95% CI -1.53 to -0.36; five studies; 804 participants). All three doses significantly increased the proportion of responders relative to placebo; ORs were as follows: for 50 mg, 2.35 (95% CI 1.60 to 3.44; three studies; 519 participants); for 100 mg, 3.49 (95% CI 2.23 to 5.45; five studies; 852 participants); and for 200 mg, 2.49 (95% CI 1.61 to 3.87; six studies; 1025 participants). All three doses also significantly improved three or more domains of quality of life as compared to placebo. Meta-analysis of the three studies that included more than one dose of topiramate suggests that 200 mg is no more effective than 100 mg. With regard to mean headache frequency and/or responder rate, seven trials using active comparators found (a) no significant difference between topiramate and amitriptyline (one study, 330 participants); (b) no significant difference between topiramate and flunarizine (one study, 83 participants); (c) no significant difference between topiramate and propranolol (two studies, 342 participants); (d) no significant difference between topiramate and relaxation (one study, 61 participants); but (e) a slight significant advantage of topiramate over valproate (two studies, 120 participants). Relaxation improved migraine-specific quality of life significantly more than topiramate. In trials of topiramate against placebo, seven adverse events (AEs) were reported by at least three studies. These were usually mild and of a non-serious nature. Except for taste disturbance and weight loss, there were no significant differences in the frequency of AEs in general, or of the seven specific AEs, between placebo and topiramate 50 mg. AEs in general and all of the specific AEs except nausea were significantly more common on topiramate 100 mg than on placebo, with NNHs varying from 3 to 25, buy topamax and the RDs versus placebo were even higher for topiramate 200 mg, with NNHs varying from 2 to 17.

topamax alcohol 2015-12-27

According to the revised 2nd Edition of the International Classification of Headache Disorders, primary headaches can be categorized as chronic or episodic; chronic migraine is defined as headaches in the absence of medication overuse, occurring on ≥15 days per month for ≥3 months, of which headaches on ≥8 days must fulfill the criteria for migraine without aura. Prevalence and incidence data for chronic migraine are still uncertain, owing to the heterogeneous definitions used to identify the condition in population-based studies over the past two decades. Chronic migraine is severely disabling and difficult to manage, as affected patients experience substantially more-frequent headaches, comorbid pain and affective disorders, and fewer buy topamax pain-free intervals, than do those with episodic migraine. Data on the treatment of chronic migraine are scarce because most migraine-prevention trials excluded patients who had headaches for ≥15 days per month. Despite this lack of reliable data, a wealth of expert opinion and a few evidence-based treatment options are available for managing chronic migraine. Trial data are available for topiramate and botulinum toxin type A, and expert opinion suggests that conventional preventive therapy for episodic migraine may also be useful. This Review discusses the evolution of our understanding of chronic migraine, including its epidemiology, pathophysiology, clinical characteristics and treatment options.

topamax 25mg reviews 2017-12-31

Of 60 patients randomized to treatment (mean buy topamax age, 36.8 +/- 10.3 years; 90% female), 36 completed the study at the end of the 9 months of active treatment (onabotulinumtoxinA, 19/30 [63.3%]; topiramate, 17/30 [56.7%]). In the topiramate group, 7/29 (24.1%) discontinued study because of treatment-related AEs vs 2/26 (7.7%) in the onabotulinumtoxinA group. Between 68% and 83% of patients for both onabotulinumtoxinA and topiramate groups reported at least a slight (25%) improvement in migraine; response to treatment was assessed using Physician Global Assessment at months 1, 3, 6, and 9. Most patients in both groups reported moderate to marked improvements at all time points. No significant between-group differences were observed, except for marked improvement at month 9 (onabotulinumtoxinA, 27.3% vs topiramate, 60.9%, P = .0234, chi-square). In both groups, HA/migraine days decreased and MIDAS and HIT-6 scores improved. Patient-reported quality of life measures assessed using MIQ after treatment with onabotulinumtoxinA paralleled those seen after treatment with topiramate in most respects. At month 9, 40.9% and 42.9% of patients in the onabotulinumtoxinA and topiramate groups, respectively, reported > or =50% reduction in HA/migraine days. Forty-one treatment-related AEs were reported in 18 onabotulinumtoxinA-treated patients vs 87 in 25 topiramate-treated patients, and 2.7% of patients in the onabotulinumtoxinA group and 24.1% of patients in the topiramate group reported AEs that required permanent discontinuation of study treatment.

topamax high dose 2017-10-24

The treatment of epilepsy in pregnancy is particularly challenging in that the fetal and maternal risks associated with maternal seizures need to be balanced against the potential teratogenic effects of antiepileptic drugs (AEDs). Pregnancy is known to affect the pharmacokinetics of older-generation AEDs. Understanding such alterations is important in the effort to optimise drug therapy since they may affect seizure control as well as fetal drug exposure. Therapeutic drug monitoring has therefore been recommended to control for changes in the disposition of the older-generation AEDs during pregnancy. Much less is known about gestation-induced alterations in the pharmacokinetics of the newer AEDs that have been introduced in the last 15 years. Lamotrigine is by far the most extensively studied of the newer AEDs. Pronounced alterations have been reported in the apparent clearance of lamotrigine, with an increase of >300% from baseline in late pregnancy in some patients on monotherapy, most likely due to enhanced metabolism. The available data suggest that the corresponding decline in plasma concentrations can be associated with loss of seizure control. More limited data indicate that a similar decline in plasma concentrations of the active monohydroxy derivative of oxcarbazepine buy topamax may occur in late pregnancy. Preliminary experience also suggests that a significant fall in plasma concentrations of levetiracetam may occur during pregnancy. No systematic information is available on the pharmacokinetics during pregnancy of other newer AEDs (e.g. gabapentin, pregabalin, tiagabine, topiramate or zonisamide). Given the importance of maintaining optimal treatment of epilepsy during pregnancy, therapeutic drug monitoring appears to be justified for lamotrigine and oxcarbazepine in particular. Systematic studies of the effects of pregnancy on the pharmacokinetics of the other newer-generation AEDs are urgently needed.

topamax drug abuse 2015-05-09

This preliminary report suggests that the point prevalence of the metabolic syndrome in patients with schizoaffective disorder appears to be higher than that reported in the general population of the USA. Targeted weight reduction and life buy topamax style change strategies (increased exercise, smoking cessation, stress reduction) may provide useful interventions to decrease the morbidity and mortality that accompanies the presence of the metabolic syndrome in patients with psychiatric illnesses.

dosage topamax 2015-04-08

Five dogs with naturally occurring epilepsy were used for this study. Three were getting at buy topamax least one antiseizure drug as maintenance therapy including phenobarbital (PB). Four (ID 1-4) were used for the 10 mg/kg IV TPM + PO TPM study, and three (ID 3-5) were used for the 20 mg/kg IV TPM study. IV TPM was infused over 5 min at both doses. The animals were observed for vomiting, diarrhea, ataxia, and lethargy. Blood samples were collected at scheduled pre- and post-dose times. Plasma concentrations were measured using a validated high-performance liquid chromatography-mass spectrometry method. Non-compartmental and population compartmental modeling were performed (Phoenix WinNonLin and NLME) using plasma concentrations from all dogs in the study. iEEG was acquired in one dog. The difference between averaged iEEG energy levels at 15 min pre- and post-dose was assessed using a Kruskal-Wallis test.

topamax generic cost 2015-03-12

We found a definite electro-clinical response in 2/11 patients, already evident after 12-96 h after TPM introduction, and a possible response in 2/11 patients ( buy topamax concomitantly with other AEDs); 7/11 did not respond. Partial-complex SE appeared to better respond than generalized-convulsive SE. One patient developed a severe nephrolithiasis.

topamax pill 2016-12-07

These findings highlight the need to assess neuropsychiatric adverse events comprehensively using sensitive and validated methods early in the clinical development of candidate antiobesity drugs with a buy topamax central mechanism of action.

topamax pills 2015-11-28

This paper highlights the development of pharmacological and nonpharmacological treatments for pathological buy topamax gambling and is based on a review of the literature published in the past 12 months.

topamax alcohol addiction 2016-05-23

Many studies showed that Topiramate (TPM) may be a useful drug in a wide spectrum of childhood epilepsies. We report a 3-month-old female with stormy onset of secondarily generalized partial seizures. She showed a high seizure frequency and a progressive worsening electroencephalogram (EEG), despite standard antiepileptic drugs administration. TPM succeeded in controlling seizures, even after the other drugs were discontinued. This case suggests that TPM may represent a buy topamax good choice for the treatment of partial seizures refractory to conventional drugs in infants.

topamax max dose 2017-04-18

The treatment of obesity is often met with a myriad of challenges in the primary care setting. Nevertheless, a modest 5% weight loss is considered clinically significant and may be associated with health benefits. Phentermine/topiramate (Qsymia), available in the United buy topamax States since September 2012, achieves clinically meaningful weight loss along with improvements in weight-related comorbidities. This combination drug therapy could be an additional tool for primary care providers in their quest for effective management of obesity. Special precautions and close monitoring are indicated when prescribing phentermine/topiramate for women of childbearing potential. Monitoring of heart rate and psychiatric and cognitive side effects is important.

topamax 50mg tab 2016-11-27

Two reviewers independently selected trials for inclusion and extracted the relevant data. The following outcomes were assessed: (a) 50 per cent buy topamax or greater reduction in seizure frequency; (b) treatment withdrawal (any reason); (c) side effects. Primary analyses were intention-to-treat. Summary relative risks (RR) with 95% confidence intervals (95% CI) are presented. Dose response was evaluated in regression models.

topamax positive reviews 2015-07-04

Network analysis is an emerging tool for the study of complex systems. Antiepileptic drug (AED) polytherapy in children with medically intractable epilepsy may be considered a complex system, given the heterogeneity of drug combinations that are frequently modified according to clinical indications. The current article presents a buy topamax concise review of network theory and its application to the characterization of AED use in children with refractory epilepsy. Current and previous AEDs prescribed to 27 children with refractory, localization-related epilepsy were recorded, and network theory was applied to identify patterns of drug administration. Of the fifteen unique AEDs prescribed, levetiracetam possessed the highest betweenness centrality within the network. Furthermore, first generation AEDs were often discontinued, while lacosamide and topiramate were most likely to be initiated. We also identified three subnetworks of AEDs that were commonly coadministered. We conclude that network analysis is an effective method to characterize the complexity of AED administration patterns in children with epilepsy with many promising future applications.

topamax 100mg tablets 2016-07-25

Migraine and depression coincide in some 20-30% of patients. Although antidepressants (namely tricyclics) are not considered as first-line prophylactic compounds in patients with migraine alone, several clinical trials support a remarkable benefit in the treatment of migraine and related headache disorders. However, treatment with one antidepressant alone often does not suffice to treat both disorders effectively. Therefore, combinations of classical antidepressants with both newer antidepressants and established prophylactic drugs (e.g. beta-adrenergic receptor antagonists [beta-blockers], topiramate and sodium valproate) are required. In addition, acute attack medication (such as triptans, ergotamines or buy topamax analgesics) is regularly combined with the preventive medication, thus requiring elaborate knowledge about the complex network of potential interactions and contraindications. Fear of potentially serious interactions can frequently lead to insufficient treatment of both underlying disorders, with an enormous impact on the patient's life. Pathophysiologically, multiple neurotransmitters have been attributed an important role in the aetiology of migraine (mainly serotonin and calcitonin gene-related peptide) and depression (among others, serotonin, dopamine and noradrenaline [norepinephrine]). Most drugs used to treat both disorders influence at least one of these transmitter systems, such as classical tricyclics. This review discusses the efficacy of antidepressants in migraine prevention. In addition, recommended combinations in patients with concomitant depression and migraine are presented with regard to their proposed pharmacological mechanism of action and their potential interactions.

topamax alcohol abuse 2017-09-11

Several classes of medications are used both on- and off-label for the prevention of migraine, including β-blockers (eg, propranolol, timolol), tricyclic antidepressants (eg, amitriptyline), anti-epileptic drugs (eg, topiramate Augmentin S Suspension , valproic acid), and neurotoxins (eg, onabotulinumtoxinA).

topamax alcohol treatment 2016-02-12

Tobacco cessation rates and tobacco dependence Zyloprim Renal Dosing .

topamax 250 mg 2017-03-28

An important step during the development of high-performance liquid chromatography (HPLC) methods for quantitative analysis of drugs is choosing the appropriate detector. High sensitivity, reproducibility, stability, wide linear range, compatibility with gradient elution, non-destructive detection of the analyte and response unaffected by changes in the temperature/flow are some of the ideal characteristics of a universal HPLC detector. Topiramate is an anticonvulsant drug mainly used for the treatment of different types of seizures and prophylactic treatment of migraine. Different analytical approaches to quantify topiramate by HPLC have been described because of the lack of chromophoric moieties on its structure, such as derivatization with fluorescent moieties and UV-absorbing moieties, conductivity detection, evaporative light scattering detection, refractive index detection, chemiluminescent nitrogen detection and MS detection. Some methods for the determination of topiramate by capillary electrophoresis and gas chromatography have also been published. This systematic review provides a description of the main analytical methods presented in the literature to analyze topiramate in the drug substance and in pharmaceutical formulations. Each of these Triphala Recommended Dosage methods is briefly discussed, especially considering the detector used with HPLC. In addition, this article presents a review of the data available regarding topiramate stability, degradation products and impurities.

topamax xr dosage 2016-03-08

Of the 30 patients, 21 had a >10% decrease in HCO3- levels. The mean decrease in HCO3- among the 21 patients was 4.7 mEq/L, and maximum was 10 mEq/L. No clinical symptoms occurred, and HCO3- supplement was not needed, except for one patient who developed tachypnea from worsened acidosis after prolonged status epilepticus during a suspected viral illness Mestinon Medication . Among the 21 patients, TPM was discontinued in seven children because of a lack of efficacy, and in two because of anorexia. After discontinuing TPM, the serum HCO3- returned to the previous level before starting TPM in all nine.

topamax user reviews 2015-05-21

The analysis of residual organic solvents (methanol, ethanol and toluene) in topiramate drug substance was investigated. Topiramate is a potent anticonvulsant drug under clinical evaluation. The drug is recrystallized from ethanol denatured by either methanol or toluene, and each residual solvent is controlled at 0.1% (w/w) level. A capillary gas chromatography (GC) method described in this manuscript utilizes a DB-WAX, 1 micron thick, 30 m x 0.53 mm i.d., column. Since topiramate is a thermally labile compound, the selection of the proper injector temperature is critical to the success of the analysis. The injector temperature was set at 120 degrees C to prevent degradation. The Purchase Generic Viagra initial oven temperature was set at 55 degrees C for 8 min and programmed at a rate of 30 degrees C min-1 to a final temperature of 160 degrees C for 11 min. Helium was used as a carrier gas. The sample solvent selected was dimethylformamide pretreated with molecular sieves to remove trace amounts of alcohols that may interfere with the assay. The method was validated to be specific, linear, precise, sensitive, rugged and showed excellent recovery.

topamax 100 mg 2017-04-23

Literature was obtained through searches in PubMed (Mid 1950s-March 2007), Iowa Drug Information Service/Web (1966-February 2007), International Pharmaceutical Abstracts (1970-February 2007), and the Cochrane Library. The terms migraine, prophylaxis, child, and children were used and cross referenced with all drug names Trental Online Buy . Reference citations from publications identified were also reviewed and included.

topamax overdose 2015-11-23

All patients treated with lamotrigine, levetiracetam or topiramate in the Epilepsy Centre were identified. Each Aggrenox Capsule drug was analyzed from introduction of the drug in the Netherlands up to a final assessment point 2 years later.

topamax brand name 2015-06-14

These preliminary data suggest that adjunctive topiramate may reduce depressive symptom severity in acute bipolar depression. The Plavix 300 Mg antidepressant efficacy of this compound requires confirmation via double-blind placebo controlled investigation.

topamax high dosage 2015-12-20

Patients randomized either to sibutramine or topiramate lost comparable amounts of weight (4.1 +/- 5.7 and 2.8 +/- 3.5 kg, respectively) and displayed similar rates Paxil Drug Test of weight loss (0.85 and 0.82 kg/week, respectively). However, only four (22%) patients receiving sibutramine and six (21%) patients receiving topiramate completed the 24-week trial. In addition, the attrition patterns for the two drugs were different, with patients discontinuing topiramate doing so early in treatment and patients discontinuing sibutramine doing so throughout treatment. Also, higher ratings of manic and depressive symptoms significantly increased risk for early topiramate discontinuation compared to that for sibutramine.

topamax 800 mg 2015-12-10

To compare the efficacy and safety of onabotulinumtoxinA (BOTOX Luvox Drug Class ), Allergan, Inc., Irvine, CA) and topiramate (TOPAMAX), Ortho-McNeil, Titusville, NJ) prophylactic treatment in patients with CM.

topamax 100mg tab 2016-01-29

TPM (0, 10, 30, 90 mg/kg) injected subcutaneously into B6 mice 60 min prior to access to a 12% ethanol solution (v/v) over 8 days produced dose-responsive reduction in consumption during the first 2-h period after injection.