Talk:Topiramate

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Noted

Noted on this page that the use for bipolar is listed as controversial. there doesn't seem to be any references for that. i'd like to add some if there are no objections, but as i'm new, i wanted to check with whoever's doing this page first? i have experience with the drug and also want to make sure it's npov before posting. thanks for any help & guidance. Wyldchylde78 03:27, 6 December 2006 (UTC)wyldchylde[reply]

Use in alcohol dependence

Can someone more knowledgeable than myself add something about the recent findings that Topiramate maybe indicated in alcohol dependence? Zero sharp 23:41, 9 October 2007 (UTC)[reply]


I know one the outstanding documentary from HBO:Addiction series, it is discussed as being currently a drug they are researching and obtaining positive results for alcololism.Mcateedenise (talk) 14:36, 14 February 2008 (UTC)[reply]

I'm an addict and I will be taking it soon. We shall see how it works. Allanana79 (talk) 06:08, 27 December 2015 (UTC)[reply]

Side effects

New placebo controlled trials have found a 0.43% increase in risk of suicidal behaviour or ideation. Suicide risk was greater for patients taking medication for treatment of epilepsy. Refer warning from FDA


Is this right? "anorexia (loss of appetite) (13.3%) *[5.6%]" Why is it there an asterisk and it showing a lower placebo rate? Or am I reading it wrong? jrun (talk) 09:16, 30 May 2009 (UTC)[reply]


The parashtesias associated with this drug can be quite anoying. Numbness in the fingers, toes, and around the mouth and seem to be dosage related, see PI for rates. ? due to the carbonic anhydrase effect? Potassium has been advocated for improving this however I've found using extended release Riboflavin, or even a extended release B-Complex which is easier to find (B-50) or B-100) works just as well in patients and no extra labs to follow.72.37.171.156 (talk) 18:13, 12 December 2012 (UTC)Addiction Doc[reply]


According to recent lawsuit ads, there seems to be a connection between taking Topiramate during pregnancy and autism or other learning disabilities in the offspring.68.67.254.133 (talk) 22:42, 12 August 2022 (UTC)[reply]
Needs a reliable medical source. See WP:MEDRS MartinezMD (talk) 23:27, 12 August 2022 (UTC)[reply]

Taste perception

Is it really possible that no journals have recorded the taste perception changes? Meats taste like metal, carbonated beverages taste like hydrogen peroxide, greasy foods taste like fat (which they are but people don't normally notice), or the odd psychotropic effects like a shift in perception of detail (noticing things that you don't while ignoring things you normally notice, giving the distinct impression of being in a "sliders universe")? I know Doctors who are well aware of these effects, so I would think one of them would have written them down. 71.198.11.186 (talk) 09:46, 23 September 2012 (UTC)[reply]

Topiramate Use in Familial Tremors

I was placed on Topiramate for familial tremors one month ago. I experienced diarrhea pretty much constantly after 2 weeks, unusual moodiness, depression & mood swings. I found my normal sleeping aid stopped working. I have had trouble falling asleep and continuously wake up with 'troubling thoughts' all night long which keep me from being able to go back to sleep. This is all so unusual for me that I checked the side effects of this drug and found each one of my adverse symptoms. The onset of these reactions are coincidental to starting this med. I have called my doctor to begin coming off of this med as I prefer my familial tremors to this. — Preceding unsigned comment added by 24.125.235.99 (talk) 14:20, 5 September 2013 (UTC)[reply]

Cancer neuropathic pain and opioid-dependence withdrawal

I don't know how to add ref tag links that result in a number, so I'm posting two articles I found tonight, along with their abstracts. They're both behind a paywall, but I have institutional access. My undergrad degree was in biopsychology, so this had some interest with me for further research in prep for a masters program in biology,

  • Bendaly, Edmond A ; Jordan, Carol A ; Staehler, Sandra S ; Rushing, Daniel ATopiramate in the treatment of neuropathic pain in patients with cancer. Supportive cancer therapy, 2007, Vol.4(4), pp.241-6
http://www.sciencedirect.com/science/article/pii/S1543291213601678
Topiramate in the Treatment of Neuropathic Pain in Patients with Cancer
Edmond A. Bendalya, , , Carol A. Jordanb, Sandra S. Staehlerc, Daniel A. Rushingc
a Division of Hematology-Oncology, New York University Medical Center
b Roudebush Veterans Affairs Medical Center, Indianapolis, IN
c Division of Hematology-Oncology, Indiana Cancer Pavilion, Indiana University School of Medicine, ::Indianapolis
Received 11 April 2007, Revised 6 August 2007, Accepted 14 August 2007, Available online 21 January 2013
DOI: 10.3816/SCT.2007.n.021
Abstract
Introduction
Neuropathic pain has been reported to affect 40%–50% of patients with cancer.
Patients and Methods
Consecutive patients selected from the outpatient/adult patient palliative care clinic of the Roudebush Veterans Affairs Medical Center and the Indiana University Palliative Clinic were reviewed. A verbal pain linear analogue assessment scale was used to assess neuropathic pain. Pain medication history was also reviewed in addition to percent pain relief. The following variables were extracted from the medical record: pain characteristics, location, cause, date of initiation of therapy, maximal tolerated dose, pain scores on the visit of optimal tolerated dose, other concurrent medications, number of months of pain before initiation of topiramate therapy, and total duration of topiramate therapy. Decrease in worst, best, and average pain was recorded, as were the development of any adverse effects.
Results
Of the 13 patients on second- and third-line therapy, 53.8% had ≥ 30% decrease in worst pain; 69.2% had ≥ 30% decrease in average pain, and 53.8% had ≥ 30% decrease in best pain. Eight of 13 patients (61.5%) experienced adverse effects. Five patients discontinued (38.5%) topiramate because of adverse events.
Conclusion
Because our retrospective study showed topiramate to be a beneficial second- and third-line therapy in patients with cancer who did not experience adequate pain control on previous regimens, further prospective studies are needed to establish this medication in the armamentarium of neuropathic cancer pain management.

and:

  • Zullino, Daniele F ; Cottier, Anne-Claude ; Besson, Jacques. Topiramate in opiate withdrawal. Progress in Neuropsychopharmacology & Biological Psychiatry, 2002, Vol.26(6), pp.1221-1223
DOI: 10.1016/S0278-5846(02)00251-8
http://www.ncbi.nlm.nih.gov/pubmed/12452551 | http://www.sciencedirect.com/science/article/pii/S0278584602002518
Abstract
The α2-adrenergic agonist clonidine is the mainly used drug for the opiate withdrawal. Its efficacy and tolerance in treating withdrawal symptoms is, however, suboptimal. The pharmacological profile of topiramate suggests it could be rather valuable for opiate withdrawal, as there is some evidence that topiramate acts, among others, through inhibition of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, which play an important role in the withdrawal-induced activation of the locus coeruleus (LC) by glutamate. Three patients undergoing an inpatient opiate detoxification program were treated with topiramate, which achieved a nearly complete control of withdrawal symptoms.
Keywords
Anticonvulsant; Opioid-related disorders; Narcotics; Substance withdrawal syndrome
Abbreviations
AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; LC, locus coeruleus; NMDA, N-methyl-d-aspartic acid
1. Introduction
The treatment of opioid withdrawal is aimed to safely ameliorate acute symptoms of withdrawal and to facilitate entry into recovery and/or rehabilitation programs. Two principal pharmacologic strategies are in general use: (1) substitution with an agonist or a partial agonist and gradual tapering, (2) abrupt discontinuation of opioids and use of nonopiate medications to reduce withdrawal symptoms (American Psychiatric Association, 1995). The antihypertensive drug clonidine, which acts by stimulating midbrain α2-adrenergic receptors, thereby reducing the noradrenergic hyperactivity of the locus coeruleus (LC) that accounts for many of the symptoms of opioid withdrawal, has become the mainly used drug for the second strategy. The efficacy of clonidine in treating withdrawal symptoms has, though, to be considered as suboptimal, as symptoms like anxiety, restlessness, insomnia, muscular aching and craving may not respond. Furthermore, the side effects of clonidine include insomnia, sedation, and hypotension. Contraindications to the use of clonidine comprise acute or chronic cardiac disorders, renal or metabolic disease and moderate to severe hypotension. Clonidine-assisted detoxification is therefore more difficult to carry out in outpatient settings and can be administered only to a restricted number of patients (American Psychiatric Association, 1995).
Whereas anticonvulsants have repeatedly been proposed as a treatment of alcohol and benzodiazepine withdrawal Bertschy et al., 1997 and Myrick et al., 1998, and some data exist on their utility in reducing cocaine and opiate consumption Chatterjee and Ringold, 1999, Mendelson and Mello, 1996 and Myrick et al., 1998, there is only one study with regard to treatment of opiate withdrawal.
In a randomized double-blind study realized in Lausanne, Bertschy et al. (1997) compared a carbamazepine/mianserin combination with clonidine in 32 patients. The two treatments did not differ in the intensity of the withdrawal, according to the rate of retention in treatment, symptoms and psychic distress.
The use of carbamazepine may, however, be limited in drug dependent patients by some health conditions like liver disease, allergic conditions, alcohol toxic thrombocytopenia or interactions with concomitant medication due to induction of hepatic cytochrome P450 enzymes.
Available data indicate that activation of the noradrenergic cells in the LC plays an important role in the symptoms of opiate withdrawal (Rasmussen, 1995). A glutamatergic projection from the nucleus paragigantocellularis seems to be important in the withdrawal-induced activation of the LC. Whereas N-methyl-d-aspartic acid (NMDA) receptors seem to play a minor role in the withdrawal-induced activation of the LC by glutamate, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors play an important role. NMDA antagonists may, moreover, not be clinically useful for opiate withdrawal due to their PCP-like effects, but AMPA antagonists may be of benefit for alleviating opiate withdrawal symptoms in humans.
Topiramate is a sulphamate-substituted monosaccharide derived from d-fructose and it is unrelated to other antiepileptic agents. There is some evidence that topiramate acts, among others, through inhibition of kainate-activated (AMPA) receptors (Langtry et al., 1997). In vitro, topiramate has, on the other hand, no effect on NMDA mediated excitatory amino acid receptors.
Topiramate may therefore be a promising alternative to clonidine or opiate tapering as a treatment for opiate withdrawal. The authors report on three patients treated successfully with topiramate.

<snip because it's the article, and I can't justify leaving it in for fair-use>

3. Discussion
The pharmacological profile of topiramate suggests it could be rather valuable for opiate withdrawal, which seems to be confirmed by the three presented cases. Compared to clonidine, topiramate seemed to be associated with less side effects and to be efficacious on more manifestations of the withdrawal syndrome. This should, however, be further examined in studies comparing topiramate with clonidine.
Compared to the methadone-tapering method, topiramate has also some advantages in that it does not produce opioid-like tolerance or physical dependence, it avoids the postmethadone rebound in withdrawal symptoms, and patients completing a course of topiramate-assisted withdrawal can be immediately given an opioid antagonist (e.g., naltrexone) if indicated. A further advantage may be its mood stabilizing properties (Teter et al., 2000).
Preclinical data suggest a dissociation between neurobiological mechanisms of tolerance and dependence (Jackson et al., 2000). The role of glutamatergic mechanisms in synaptic plasticity and long-term behavioral adaptation to drugs has repeatedly been emphasized. Experiments on behavioral sensitization indicate that NMDA-receptors are involved in induction, AMPA-receptors may mediate expression of the established response. Preclinical studies of withdrawal from opioids suggest that whilst AMPA-receptor antagonists may not be able to prevent tolerance or dependence from developing, they may ameliorate both the physical and emotional consequences of withdrawal. Therefore, AMPA-receptor antagonists like topiramate may represent a promising new approach for treating the consequences of drug abuse. — Preceding unsigned comment added by Kassorlae (talk • contribs) 02:50, 19 August 2014 (UTC)[reply]

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ARE MY MEDICATIONS STEROIDS?

IS TOPAMAX A STEROID? — Preceding unsigned comment added by 2600:8800:FF10:0:A1BF:5AA5:5375:BAE3 (talk) 02:35, 15 May 2016 (UTC)[reply]

Side effects

The "Side effects" section seems to violate WP:MEDMOS: "Try to avoid cloning drug formularies such as the BNF and online resources like RxList and Drugs.com. Extract the pertinent information rather than just dumping low-level facts in a big list, which should be avoided per WP:NOTMANUAL and Wikipedia:LAUNDRYLIST. For example, a long list of side effects is largely useless without some idea of which are common or serious." --Nbauman (talk) 03:52, 8 October 2017 (UTC)[reply]

"Topamax®" listed at Redirects for discussion

An editor has identified a potential problem with the redirect Topamax® and has thus listed it for discussion. This discussion will occur at Wikipedia:Redirects for discussion/Log/2022 April 15#Topamax® until a consensus is reached, and readers of this page are welcome to contribute to the discussion. BD2412 T 05:20, 15 April 2022 (UTC)[reply]

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