origin Share +1 Pin Stumble Reddit Shares 0 Topamax (Topiramate) is an anticonvulsant agent discovered in 1979 by Bruce Maryanoff and Joseph Gardocki while working for McNeil Pharmaceutical (a subsidiary of Johnson & Johnson). When compared to other anticonvulsant agents, Topamax is regarded as unique in that it is pharmacologically classified as a sulfamate-substituted monosaccharide derivative, indicating that its chemical structure is similar to that of fructose. After its synthesis, preliminary evaluation lead researchers to speculate that Topamax may prevent seizures. As a result of safety and efficacy in human clinical trials, Topamax received FDA approval in 1996 for the treatment of partial seizures in adults; thereafter it was also approved for usage among pediatrics. Knowing that the mechanisms of anticonvulsants may be useful for the prevention of migraines resulted in some physicians prescribing Topamax (from 1996 to 2004) as an off-label migraine prophylactic. In 2004, Topamax had met clinical trial endpoints and received official FDA approval for the prophylaxis of migraine. Although Topamax is still frequently utilized as a seizure preventative, and is sometimes administered for psychiatric conditions (e.g. bipolar disorder) it remains most commonly prescribed as a migraine prophylactic. Unlike other migraine prophylactics, Topamax is regarded as well-tolerated with few unwanted adverse effects. Moreover, Topamax has robust, Level A evidence to support its clinical usage as a first-line agent the prevention of migraine. How Topamax (Topiramate) May Prevent Migraines (Mechanism of Action) According to the website of the manufacturer, Topamax is hypothesized to function by keeping excitable nerve cells in the brain calm. It does this via modulation of charged particle inflow and outflow. In other words, when a person takes Topamax and the topiramate chemical crosses the blood-brain-barrier (BBB), it essentially relaxes or downregulates overexcitability of neurons, thereby preventing the series of neurologic events that triggers a migraine attack. More specifically, Topamax functions as an inhibitor of voltage-gated sodium channels (VGSC), high-voltage calcium channels, and kainate receptors. It also appears to enhance activity of GABA, the predominant inhibitory neurotransmitter in the brain. It remains unclear as to whether one mechanism contributes more substantially to its efficacy as a migraine prophylactic compared to others, or if all hypothesized mechanisms act synergistically to prevent migraines. Voltage-gated sodium channels (VGSC) inhibition : Many inhibitors of voltage-gated sodium channels are effective in prophylaxis of migraines. Whether this particular mechanism plays a significant role in the migraine prophylactic effect associated with Topamax is unclear. It is well-understood that dysfunction of voltage-gated sodium channels can facilitate neuronal excitability (as is often implicated in the pathogenesis of migraines). Analyses of the human genome have revealed specific mutations in the SCN1A gene can directly cause migraines. The SCN1A gene encodes for the alpha-subunit of voltage-gated sodium channel NaV1.1, and when dysfunctional from a genetic mutation, neurons are more prone to hyperexcitability. Those prone to neuronal hyperexcitability are more likely to experience migraines due to the fact that the increase in homeostatic excitement results in a lower threshold for triggering cortical spreading depression; brief contraction of intracranial blood vessels followed by expansion. For many individuals, especially those with migraines resulting from an SCN1A mutation, the voltage-gated sodium channel inhibition provided by Topamax may be a critical mechanism by which migraines are prevented. Furthermore, blockage of voltage-gated sodium channels can decrease neuroinflammation, ultimately reducing proinflammatory biomarkers and neuropeptides responsible for pain-signaling (e.g. substance P). In other words, voltage-gated sodium channel inhibition may reduce likelihood of migraines caused by inflammation and decrease the perceived pain associated with migraines. While not all voltage-gated sodium channel inhibitors are effective migraine prophylactics (e.g. carbamazepine, phenytoin, etc.), others are (e.g. lidocaine). Based on the literature, we could speculate that those deriving antimigraine benefit from Topamax are responding to its inhibition of voltage-gated sodium channels. That said, other complementary mechanisms may be necessary for clinically effective prophylaxis of migraines. Source: http://www.ncbi.nlm.nih.gov/pubmed/10768295 Source: http://www.ncbi.nlm.nih.gov/pubmed/10768299 Source: http://www.ncbi.nlm.nih.gov/pubmed/16054936 Source: http://www.ncbi.nlm.nih.gov/pubmed/26718459 Glutamate receptor inhibition : An important mechanism by which Topamax may prevent migraines is via inhibition of glutamate receptors. Glutamate is the chief excitatory neurotransmitter in the CNS and binds to ionotropic receptors such as NMDA, AMPA, and kainate receptors. Numerous studies have linked glutamatergic abnormalities in the pathogenesis of migraines. Research has shown that Topamax selectively inhibits kainate receptors containing the GluR5 subunit. Kainate receptors with the GluR5 subunit are responsible for mediating excitatory synaptic currents, and as is understood, excess excitement resulting from glutamate stimulation could trigger cortical spreading depression and inevitably, migraine attacks. In 2011, researchers Andreou and Goadsby published a study assessing the effect of Topamax on trigeminovascular activity in the trigeminocervical complex (TCC) and ventroposteromedial thalamic nucleus (VPM). They also used a technique called microiontophoresis to assess the effect of Topamax on ionotropic glutamate receptors. Results indicated that Topamax inhibited trigeminovascular activity in the TCC and VPM, as well as substantially blunted kainate receptor firing. It is thought that kainate receptor antagonism induced by Topamax altered the trigeminovascular activity within the trigeminothalamic pathway, possibly decreasing the release of neurochemicals and neuropeptides such as: substance P, CGRP, and gastrin-releasing peptide. In addition to preventing migraine attacks by antagonizing kainate receptors, this mechanism may also reduce migraine-related pain due to the fact that kainate receptors can be found in the central pain neuraxis. Therefore, users of Topamax may not only experience fewer migraines from its modulation of kainate receptors, but also less migraine-related pain. Source: http://www.ncbi.nlm.nih.gov/pubmed/17691981 Source: http://www.ncbi.nlm.nih.gov/pubmed/12904467 Source: http://www.ncbi.nlm.nih.gov/pubmed/21893557 Source: http://www.ncbi.nlm.nih.gov/pubmed/23095167 Voltage-gated calcium current reduction (L-type) : Another way by which Topamax may prevent migraines is via reducing activity of L-type voltage-gated calcium channels. It is understood that L-type calcium channels play a role in modulating excitability of dendrites. An overactive L-type calcium channel current may facilitate overexcitability, which could induce neurological events preceding cortical spreading depression and migraines. Evidence suggests that Topamax attenuates activity of L-type (long-lasting) voltage-gated calcium channels. This reduces dendritic excitability and possibly increases the stimulatory threshold required to provoke a migraine. It is known that mutations in CACNA1A, a gene that encodes for the alpha-1 subunit of CaV2.1 (P/Q-type) channels causes familial hemiplegic migraine type 1 (FHM1). This finding suggests that voltage-gated calcium currents may play a role in the pathogenesis of migraines (for certain individuals). Although Topamax does not appear to modulate the P/Q-type voltage-gated calcium channels, its modulation of the L-type channels may be enough to reverse some calcium channel abnormalities exhibited among migraine patients. Other drugs such as Verapamil, an L-type calcium channel blocker, are useful in migraine prophylaxis; possibly from the L-type channel blocking. That said, other drugs that inhibit L-type calcium channels also tend to act on P/Q-type calcium channels. P/Q-type channels are more implicated in the pathogenesis of migraines compared to L-type, and since Topamax doesn t appear to block P/Q-type calcium channels, it may be wrong to assume that a reduction of L-type calcium channel activity facilitates an antimigraine effect. Nonetheless, L-type calcium channel modulation provided by Topamax cannot be fully ruled out as a possible prophylactic mechanism. Source: http://www.ncbi.nlm.nih.gov/pubmed/10768302 Source: http://www.ncbi.nlm.nih.gov/pubmed/23165010 GABA modulation : Studies evaluating the pharmacodynamics of Topamax reveal that it increases the frequency of GABA-mediated chloride channel opening. GABA is the chief inhibitory neurotransmitter of the CNS and abnormalities in GABAergic turnover have been implicated in migraines and migraine-related pain. Researchers believe that GABAergic modulation induced by Topamax may be most important for the treatment of common migraine (or migraine without aura). Topamax s ability to augment GABAergic activity may ensure proper stimulation of GABAA and GABAB receptor sites. Stimulation of GABAA and GABAB sites decreases excitability of nociceptive neurons, thereby blunting the perception of migraine-related pain. Essentially, this may raise a user s threshold for enduring the throbbing or sharp pain that occurs during a migraine attack. What s more, those with migraines often exhibit abnormally low levels of GABA prior to an attack, however, during an attack, GABA concentrations tend to spike. This suggests that those with migraines exhibit [possibly predictable] abnormal GABAergic metabolism with peaks (during attacks) and valleys (between attacks). Agents such as Valproate (inhibitors of GABA transaminase) appear to effectively treat migraines by increasing baseline concentrations of GABA. Although Topamax doesn t inhibit GABA transaminase (the enzyme that metabolizes GABA), it appears to enhance GABAergic activity possibly generating a similar neural effect to that of Valproate. We also know that polymorphisms of GABA receptor genes (particularly those encoding GABAA receptors) tend to increase migraine susceptibility. For these reason, we can hypothesize that GABAergic enhancement elicited by Topamax may be an important antimigraine mechanism, at least in a subset of patients. Source: http://www.ncbi.nlm.nih.gov/pubmed/24040174 Source: http://www.ncbi.nlm.nih.gov/pubmed/19300616 Source: http://www.ncbi.nlm.nih.gov/pubmed/9332882 It should also be noted that Topamax enhances the conductance of potassium, as well as functions as an enzymatic inhibitor of carbonic anhydrase. While it is unclear as to whether potassium conductance inhibition helps prevent migraines, it is unlikely that carbonic anhydrase inhibition contributes to antimigraine properties. In fact, inhibition of carbonic anhydrase has been documented as causing vasodilation (the opposite of what migraine sufferers need during an attack). Finally, a lesser discussed mechanism by which Topamax may prevent migraines is through action on mitochondrial permeability transition pores. Benefits of Topamax for Migraines (Possibilities) There are many potential benefits to be attained from taking Topamax for the prevention of migraines. Not only will it likely reduce the number of migraine attacks you experience per month, but it may prevent seizures (among those with comorbid epilepsy), preserve brain function, and facilitate weight loss. Topamax may also be perceived as advantageous compared to other interventions based on its ability to reduce non-migraine headaches. Adjunctive option : Those who are only deriving partial benefit from an existing migraine prophylactic may be able to add Topamax to their regimen for additional symptomatic relief. In some cases, Topamax may act synergistically with another prophylactic to prevent migraine attacks better than either as a standalone. Furthermore, Topamax can often be taken along with triptans (abortive therapies) without any interactions. For cases of refractory migraines, Topamax may serve as a much-needed adjuvant prophylactic. All ages : It is extensively documented that Topamax can prevent the occurrence of migraine attacks in adults. What s more, it appears as though Topamax may be safe and well-tolerated among pediatrics (children and adolescents). Some studies have discovered that Topamax prevents migraines among pediatrics (at a low dose less than 2 mg/kg/day). Although not formally FDA approved to treat pediatric migraines, it appears effective and may be a much-needed (safe / effective) intervention for younger migraine patients. Clinical efficacy : Topamax is considered clinically effective with Level A evidence (among much of the medical community), as well as the FDA for the prophylaxis of migraines among adult patients. It was FDA approved for adult migraine prevention in 2004 and was considered a safe anticonvulsant medication in 1996. Many professionals prescribe Topamax to adult migraine patients as a first-line therapy. Comorbidities : A subset of patients may be able to essentially treat multiple conditions simultaneously with Topamax. It is FDA approved for the treatment of partial seizures, potentially making it an optimal intervention for patients with both migraines and seizures; it seems to prevent them both. Additionally, though not approved as a standalone agent for weight loss, it may help treat obesity among overweight migraine patients. Headaches : Not only does Topamax prevent migraines, but it also is capable of preventing non-migraine headaches. Some studies measuring number of migraines per month, as well as number of non-migraine headaches per month discovered that Topamax treatment significantly reduced counts of both. Although it is unclear as to whether Topamax is capable of preventing every subtype of headache, it appears effective in the prevention of cluster headaches. Inhibits migraine progression : Some migraine experts believe that individuals with migraines may experience a worsening of attacks over time (e.g. years). They speculate that migraines can become more severe and numerous over extended durations especially if left untreated. In other words, someone with episodic migraine (less frequent) may eventually develop chronic migraine (highly frequent) if they fail to seek treatment. Researchers believe that Topamax could prevent the progression of episodic to chronic migraine if administered at an early stage of the disease. Migraine subtypes : Evidence suggests that Topamax can effectively prevent both classic migraine (with aura) and common migraine (without aura). It can also treat cases of episodic migraine, chronic migraine, as well as transformed migraine. It may be more effective among patients with episodic migraine that chronic migraine, but appears to benefit both subtypes. Neuroprotective agent : An added benefit associated with using Topamax is that you may preserve brain cells. It is known that epileptic seizures are capable of damaging the brain and killing brain cells in multiple regions. More troubling is the fact that anticonvulsants used to prevent seizures (and migraines) can also trigger apoptosis (programmed neuronal death). Thankfully, at clinically recommended concentrations, Topamax can function as a neuroprotective agent , possibly protecting your precious neurons. (Source: https://www.ncbi.nlm.nih.gov/pubmed/15727029). Side effects : Compared to most drugs, Topamax is considered well-tolerated and unlikely to provoke unwanted side effects. Most side effects resulting from treatment are of mild-to-moderate severity. Due to the fact that side effects resulting from Topamax aren t as substantial as those associated with many other anticonvulsants and migraine prophylactics, users may prefer this drug as a treatment. Weight loss : On average, users of Topamax lose around 5 lbs. body weight after several months of treatment. The exact mechanisms responsible for facilitating this weight loss remain unclear, however, weight loss is often welcomed by patients. Many women deliberately seek out Topamax for weight loss because no upfront effort is required to lose the weight. Furthermore, medical professionals may prefer to use a drug that promotes weight loss among obese patients (or those at risk of obesity) as opposed to a drug associated with weight gain. Drawbacks of Topamax for Migraines (Possibilities) Although there are a significant number of potential benefits to be attained by Topamax users, not everyone responds well to this drug. In some cases, a patient may take the clinically recommended dose of Topamax and find that it is completely useless as a migraine prophylactic. Others may dislike its side effects (e.g. cognitive deficits) and the fact that it carries withdrawal symptoms (upon discontinuation). Cognitive deficits : One of the biggest drawbacks associated with using Topamax is that it causes cognitive impairment and brain fog (impaired clarity of thinking) in many users. You may feel spaced out and perhaps a bit dopey while using this drug, hence the reason some patients have nicknamed the drug Dopamax (a portmanteau of dopey and Topamax). The most commonly reported cognitive deficits among migraine patients include: memory loss and inability to concentrate. Assuming these cognitive deficits impair your ability to perform in an occupational or educational setting, you may need to opt for a different treatment. (Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707352/). Daily administration required : To derive sufficient prophylactic benefit from Topamax, it needs to be administered on a daily basis for at least 1-3 months. Users cannot take breaks by skipping a day or two if they expect to continuously prevent migraine attacks daily administration is required. This means that your body will be under the influence of a drug (topiramate) potentially for years or decades; probably not something most people want. Ineffective : Most research suggests that while a majority of patients may derive therapeutic benefit from Topamax, not everyone will. This means that for some individuals the drug will be completely ineffective as a migraine prophylactic. There are many underlying causes of migraine attacks, each of which are subject to interindividual variation. Since Topamax doesn t correct or target all possible migraine causes, it will be an ineffective intervention for some. Pregnancy : Another drawback associated with Topamax is that it should be avoided during pregnancy. Some small-scale studies suggest that administration of Topamax during pregnancy may elevate risk of birth defects. Examples of some birth defects resulting from Topamax included: cleft palates and genital abnormalities. Side effects : Many people dislike taking Topamax due to its side effect profile. Perhaps most problematic are the cognitive deficits such as memory loss, inability to concentrate, and feeling spaced out. Additionally, other side effects such as paresthesia (numbness and tingling), anorexia, fatigue, and change in taste. Unwanted weight loss : Though weight loss resulting from Topamax is not a guarantee for all users, many notice decreases in body weight after several months of treatment. Weight loss may be a small amount (e.g. 5 lbs.) or more substantial (e.g. 15-20 lbs.). Some individuals that are already at low body weight and small statured may consider the weight loss to be a problematic reaction. Withdrawal : Assuming you were using Topamax for awhile and wish to discontinue treatment, you re likely going to experience some discontinuation effects. Users are often uninformed of potential Topamax withdrawal symptoms that they may experience when stopping treatment. These withdrawal symptoms may be long-lasting (e.g. months) and impair quality of life. Even more problematic is that users may experience rebound migraines of greater frequency and severity during withdrawal than pre-treatment. Topamax (Topiramate) For Migraines (Review of Research) Nearly all of the published research suggests that Topamax is a highly-effective medication for the prophylaxis of migraines. The drug has undergone sufficient testing to satisfy the United States FDA, and was officially approved in 2004 for the prophylaxis of migraines in adults. An issue of American Family Physician published January 2006 indicates that Topamax as a migraine prophylactic is backed by Level A evidence. In other words, there appear to be ample, well-designed trials suggesting that the drug is capable of preventing adult migraines. Though it isn t FDA approved to treat pediatric migraines, it appears effective at low-doses. Moreover, Topamax is considered well-tolerated and may be preferred over other agents due to the fact that it causes weight loss (rather than gain). Source: http://www.aafp.org/afp/2006/0101/p72.html 2013 : Efficacy and safety of topiramate in migraine prophylaxis: an open controlled randomized study comparing Sincronil and Topamax formulations. A study conducted by Cosentino et al. (2013) aimed to analyze the efficacy, tolerability, and safety of topiramate for the prophylaxis of migraine without aura. It should be noted that topiramate is the active ingredient in the brand name drug Topamax, as well as Sincronil (an Italian version of Topamax). For the study, researchers implemented an open-label, parallel-group, randomized, controlled design. A total of 60 patients (between 18 and 65 years of age) were recruited for participation, all of which experienced a migraine frequency between 3 and 15 attacks per month. After trial enrollment and acceptance, dosages of Topamax and Sincronil were titrated upwards over a period of 20 days until patients were taking 25 mg (b.i.d.). Thereafter, the twice-daily dosing of 25 mg was maintained for a 3-month duration. Of the 30 patients receiving Sincronil, 15 patients experienced improvement in clinical symptoms of migraine without aura and exhibited reductions in frequency of migraine attacks greater than 50% compared to the baseline (run-in) phase. A total of 6 patients experienced some benefit from the Sincronil, but discontinued treatment due to adverse reactions. The remaining 9 patients (of the 30) experienced no change in clinical symptoms from the medication. Results indicated that patients able to continue Sincronil for the entire 3 months experienced a decrease in attack frequency from 7 days per month to 3.7 days per month. Additionally, by the third month, migraine severity had plummeted from a score of 2.5 to just 1.7 and the MIDAS (migraine disability assessment) scores dropped from 14.3 to 8.6. Among those receiving Sincronil (or topiramate marketed in Italy), migraines were successfully prevented. Of the 30 patients that received Topamax, a total of 16 patients experienced a reduction in migraine attack frequency by at least 50% (compared to the baseline run-in phase) by the third month of treatment. A total of 4 of the remaining patients ended up discontinuing Topamax within 1 week as a result of adverse effects, whereas the other 10 patients derived insufficient therapeutic benefit in regards to migraine reduction. Evaluation of the 26 patients able to continue Topamax through the third month of the trial indicated that it significantly: decreased headache frequency (from 7.3 days to 3.5 days), diminished migraine severity (from scores of 2.4 to 1.6), and axed MIDAS (migraine disability assessment) scores (from 14.1 to 6.8). Pooling results from each trial suggests that topiramate is clinically effective in over 51% of patients with common migraine, ineffective for approximately 32%, and intolerable in around 17% of patients. Though these were two relatively small-scale trials with just 30 participants in each, we can conclude that topiramate (administered as Topamax and Sincronil) effectively prevents migraines. It also reduces the severity of migraine attacks and attenuates migraine-related disability. Source: http://www.ncbi.nlm.nih.gov/pubmed/24088805 2013 : Prophylaxis of childhood migraine: topiramate versus propranolol. Although select medications are safe and tolerable among children with migraines, their respective efficacies are often considered questionable. In effort to determine the therapeutic values of prophylactics among children, Tonekaboni et al. (2013) conducted a study comparing the efficacy of topiramate (an anticonvulsant) to that of propranolol for migraine. The study was classified as a randomized clinical trial and recruited 78 children that had been diagnosed with migraine (in accordance with International Headache Association criteria). Participants were randomly assigned to receive either: Topamax or Propranolol groups were matched by age and sex. A total of 38 patients received Topamax and were labeled Group A whereas the remaining 40 patients received Propranolol and were labeled Group B. Efficacy was determined based on changes in frequency, severity, and duration of migraine attacks after 1 and 4 months of treatment. Results indicated that frequency, severity, and duration of migraine attacks significantly decreased in both the Topamax and Propranolol groups, but neither treatment was more efficacious than the other. It was concluded that Topamax and Propranolol equally viable migraine prophylactics for children with migraine. Authors suggested that the decision to use one intervention over the other should be made based on the specific patient. Source: http://www.ncbi.nlm.nih.gov/pubmed/24665283 2012 : Effective dose of topiramate in pediatric migraine prophylaxis. A study by Abbaskhanian et al. (2012) was carried out to determine optimal dosing of Topamax among pediatrics for migraine prophylaxis. Researchers discussed the fact that migraine is a common neurological disorder that can occur throughout childhood and adolescence. They mentioned that Topamax (at the time) was a newer anticonvulsant agent that was effective for prophylaxis of migraine in adults. It was emphasized that the FDA had not yet approved Topamax for the prophylaxis of migraines among pediatric populations. Knowing that Topamax was considered safe with few adverse effects in adults, they decided to test it as a prophylactic in pediatrics at a low-dose. A total of 60 pediatrics that had been diagnosed with migraines were recruited for participation. The 60 pediatrics were divided into two treatment groups and randomly assigned to receive Topamax at a dose of either: less than 2 mg/kg/day OR more than 2 mg/kg/day for a period of 2 months. To determine efficacy of each dosage, patients underwent symptomatic evaluation at baseline (0 weeks), 4 weeks, and 8 weeks. Results suggested that pediatrics receiving a dosage under 2 mg/kg/day experienced reductions in: migraine frequency (from 6.2 to 3 episodes per month), headache intensity (from 7.2 to 3.7 on a severity scale), and headache duration (from 5.4 to 2.2 hours). Among those taking dosages over 2 mg/kg/day, reductions were noted in: headache frequency (from 6.9 to 3.24), headache intensity (from 7.11 to 3.14), and headache duration (from 5.2 to 1.8 hours). Side effects noted in the pediatrics included: paresthesia, anorexia, and drowsiness. Based on the results, it is apparent that dosages exceeding 2 mg/kg/day were no more effective than those under 2 mg/kg/day. In conclusion, it appears as though low-dose Topamax (under 2 mg/kg/day) is safe, tolerable, and effective among pediatrics with migraines. Since it is not formally approved by the FDA, it could be considered as an off-label alternative for pediatric patients that do not respond to other recommendations. Source: http://www.ncbi.nlm.nih.gov/pubmed/23559999 2011 : Zonisamide versus topiramate in migraine prophylaxis: a double-blind randomized clinical trial. A study by Mohammadianinejad et al. (2011) compared the efficacy of the drug Zonegran (Zonisamide) to that of Topamax (Topiramate) for the prevention of migraines. Researchers noted that Topamax is an antiepileptic agent that is FDA approved as a migraine prophylactic, but a subset of patients are unable to tolerate its side effects. Therefore, they sought to determine whether Zonegran would be an effective, well-tolerated alternative for migraine patients unable to tolerate Topamax. For the study, a total of 80 patients diagnosed with migraines were assigned to receive either Zonegran (titrated from 50 mg to 200 mg per day) or Topamax (titrated from 25 mg to 100 mg per day). All patients were evaluated at pre-treatment baseline, after 4 weeks, and after 12 weeks. Evaluations sought to determine whether there were significant changes in: frequency of migraine, headache severity, abortive medication usage, migraine disability scores, and adverse reactions. Results indicated that both Zonegran and Topamax significantly reduced frequency of migraines, severity of migraines, usage of abortive medication, and migraine-related disability among sufferers. Interestingly, on measures of general headache severity, Zonegran was more effective than Topamax. That said, both drugs were considered well-tolerated with few adverse events. This study provides evidence to support the usage of Topamax for the prophylaxis of migraines. There remains more clinical evidence to support the prophylactic efficacy of Topamax than to support the prophylactic efficacy of Zonegran. Nevertheless, it appears as though Zonegran may be equally as effective as Topamax as a prophylactic and serve as a feasible alternative among patients unable to tolerate Topamax. Source: http://www.ncbi.nlm.nih.gov/pubmed/21738025 2011 : Topiramate vs divalproex sodium in the preventive treatment of migraine: a prospective real-world study. Researchers Krymchantowski and Jevoux compared the efficacy of Topamax and Depakote for the prevention of migraine. Prior to the study, researchers were aware of the fact that both agents were capable of preventing migraine attacks. However, it was unclear as to whether one agent (e.g. Topamax) was more effective than the other as a prophylactic. For the study, researchers recruited a total of 120 patients that had been diagnosed with migraine. Of the 120 patients, 69 received Topamax and the remaining 51 received Depakote for a duration of 12 months. Those receiving Topamax started at a dose of 25 mg/day and titrated the dosing upwards every 10 days by an additional 25 mg until they reached 150 mg/day (in 2 divided doses). Participants receiving Depakote began at a dosage of 250 mg/day and titrated their dosing upwards to 500 mg (b.i.d.). It should be mentioned that none of the participants had ever utilized Topamax nor Depakote prior to this study. To determine efficacy of each treatment, researchers collected data from each participant, documenting: headache frequency, tolerability (after 3 months), and adherence to treatment. At pre-treatment baseline, headache frequency of the Topamax and Depakote groups were similar at around 8 headache days per month. After 3 months of treatment, 40/69 (58%) patients receiving Topamax experienced a reduction in headache frequency of at least 50%. By comparison, 26/51 (51%) patients receiving Depakote for 3 months experienced a reduction in headache frequency of at least 50%. Documentation of side effects revealed that Topamax users experienced: weight loss, paresthesia, and cognitive deficits whereas those taking Depakote experienced: weight gain, hair loss, and gastrointestinal disturbances. Despite the fact that this study was open-label and non-randomized, it appears as though Topamax and Depakote are equally effective and well-tolerated for the prophylaxis of migraine. That said, some patients may prefer one over the other based on side effects; typically weight loss is preferred. Source: http://www.ncbi.nlm.nih.gov/pubmed/21457240 2009 : Topiramate treatment of chronic migraine: a randomized, placebo-controlled trial of quality of life and other efficacy measures. A study by Silberstein et al. (2009) sought to assess the therapeutic value of Topamax for the treatment of chronic migraine. Previously conducted research by Silberstein (in 2007) demonstrated that Topamax (at 100 mg/day) is effective in reducing the number of migraine days per mo reduce
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