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).
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).
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.
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.
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.