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Lamictal (Lamotrigine)

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Generic Lamictal is a single antiepileptic drug(AED) of the phenyltriazine class. Generic Lamictal is a medication indicated for adjunctive therapy for infancy with the following types of seizure: partial seizures, primary generalized tonic-clonic seizures, generalized seizures of Lennox-Gastaut syndrome; monotherapy for adult patients with partial seizures who are also receiving their treatment with carbamazepine, phenytoin, phenobarbital,primidone and valproate.

Other names for this medication:
Apo-lamotrigine, Arvind, Convulsan, Crisomet, Dafex, Daksol, Danoptin, Dezepil, Doclamotri, Dyna-lamotrigine, Elmendos, Epilepax, Epimil, Epiral, Epitec, Epitrigine, Epizol, Espa-trigin, Flamus, Fringanor, Gerolamic, Labileno, Lafigin, Lagotran, Lamal, Lambipol, Lamdra, Lamepil, Lameptil, Lametec, Lameton, Lamez, Lamia, Lamicstart, Lamictin, Lamidus, Lamilept, Lamirax, Lamitor, Lamitrin, Lamo tad, Lamo-q, Lamodex, Lamogin, Lamogine, Lamolep, Lamorin, Lamoro, Lamotax, Lamotaxyl, Lamotiran, Lamotor, Lamotren, Lamotri hexal, Lamotrig-isis, Lamotrigin, Lamotrigina, Lamotriginum, Lamotrihexal, Lamotrin-mepha, Lamotrix, Lamox, Laribax, Larig, Latrigil, Latrigin, Latrigine, Logem, Lomarin, Medotrigin, Meganox, Mogine, Neurium, Plexxo, Pms-lamotrigine, Protalgine, Ratio-lamotrigine, Sandoz lamotrigine, Seaze, Symla, Tradox, Trigila, Triginet, Triglyx, Trogine

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Also known as:  Lamotrigine.


Generic Lamictal is a medication indicated for adjunctive therapy for infancy with the following types of seizure such as partial seizures, primary generalized tonic-clonic seizures, generalized seizures of Lennox-Gastaut syndrome; monotherapy for adult patients with partial seizures who are also receiving their treatment with carbamazepine, phenytoin, phenobarbital,primidone and valproate; bipolar disorder treatment for adults. Generic Lamictal helps to control mood episodes (depression, mania, hypomania and mixed episodes).

Generic Lamictal remains an effect of sodium channels. Generic Lamictal keeps off sodium channels thereby stabilizing nervous membranes and hereupon modulate presynaptic transmitter release of excitatory amino acids.

Lamictal is also known as Lamotrigine, Lametec.

Generic name of Generic Lamictal is Lamotrigine.

Brand name of Generic Lamictal is Lamictal.


Take it orally.

Generic Lamictal can be used by children and adults.

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


If you overdose Generic Lamictal and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Lamictal overdosage: ataxia, nystagmus, increased seizures, decreased level of consciousness, coma, intraventricular conduction delay.


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

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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 Lamictal if you are allergic to Generic Lamictal components.

Be careful with Generic Lamictal if you are pregnant, planning to become pregnant, or are breast-feeding.

Be careful with Generic Lamictal in case of different types of contraception usage, hepatic impairment, renal impairment.

It can be dangerous to stop Generic Lamictal taking suddenly.

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They may be especially useful in the treatment of certain resistant epilepsy syndromes such as Lennox-Gastaut and West syndromes for which conventional drugs often fail.

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Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels have a key role in the control of heart rate and neuronal excitability. Ivabradine is the first compound acting on HCN channels to be clinically approved for the treatment of angina pectoris. HCN channels may offer excellent opportunities for the development of novel anticonvulsant, anaesthetic and analgesic drugs. In support of this idea, some well-established drugs that act on the central nervous system - including lamotrigine, gabapentin and propofol - have been found to modulate HCN channel function. This Review gives an up-to-date summary of compounds acting on HCN channels, and discusses strategies to further explore the potential of these channels for therapeutic intervention.

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Lamotrigine (LTG) is an antiepileptic drug (AED) that was approved in Japan in 2008. We evaluated the influence of AEDs that induce hepatic enzymes (including phenytoin (PHT), phenobarbital (PB), carbamazepine (CBZ)), valproic acid (VPA), and various combinations of these drugs, on plasma LTG concentration in adult Japanese epilepsy patients. A total of 621 patients (mean age 34.4±11.8 years) were evaluated retrospectively. We calculated the concentration to dose ratio (CD ratio) for LTG with different AED regimens, and employed multiple regression analysis to determine factors influencing the LTG concentration. There was a linear correlation between the dose and concentration of LTG in patients treated with LTG (group I), LTG+VPA (group II), LTG+inducers (group III), or LTG+VPA+inducers (group IV). The mean CD ratio of patients on LTG monotherapy was 1.43±0.4 (μg/mL)/(mg/kg). When LTG was combined with VPA, the CD ratio increased about 2.2-fold, but there was no significant correlation between the CD ratio and VPA concentration. The mean CD ratios calculated in patients receiving LTG+PHT, LTG+PB, and LTG+CBZ were 0.56, 0.84, and 0.91, respectively. Addition of PHT significantly reduced the CD ratio in a concentration-dependent manner, in comparison with PB and CBZ (p<0.005 and p<0.001, respectively). Stepwise multiple regression analysis showed that the coefficient of determination of groups I, II, III, and IV were 0.94, 0.94, 0.90, and 0.91, respectively. In the clinical setting, these findings can help to estimate LTG concentrations and predict the inducing or inhibiting effects of concomitant AEDs.

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The utilization of most AEDs included in our analysis remained stable over the study period. The greatest increases in utilization of drugs established in Israel were observed for lamotrigine (33%), oxcarbazepine (31%), and primidone (18%). Decreases in use were recorded for carbamazepine (18%) and phenobarbital (15%). Use of older AEDs appeared to be relatively high, compared with the use of newer AEDs.

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CBZ and VPA, but not LTG and OXC, are associated with changes in serum sex-hormone levels in boys and young men with epilepsy. However, the long-term health consequences of these reproductive endocrine changes during pubertal development remain to be established.

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We included 100 patients with epilepsy on stable dosing with lamotrigine as mono or adjunctive therapy. Lamotrigine and lamotrigine N-2-glucuronide concentrations were determined in up to two plasma samples per patient. Patients were genotyped for UGT1A4, UGT2B7, ABCB1 and SLC22A1. Population pharmacokinetic analysis was performed by non-linear mixed effects modelling. Prior knowledge from previous pharmacokinetic studies was incorporated to stabilize the modelling process. A parent-metabolite model was developed to get a more detailed view on the covariate effects on lamotrigine metabolism.

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Quantitative EEG (QEEG) effects of therapeutic doses of carbamazepine (CBZ), oxcarbazepine (OXC), valproate (VA) and lamotrigine (LA) monotherapy were investigated in patients with beginning epilepsy. Baseline waking EEG (EEG1) was recorded in the untreated state, the second EEG (EEG2) was done after 8 weeks of reaching the therapeutic dose. Left occipital data were used for analysis. QEEG target parameters were absolute band-power (delta: AD, theta: AT, alpha: AA, beta: AB), and alpha mean frequency (AMF). Group effects (untreated versus treated condition in the CBZ, VA, OXC, LA groups) were computed for each target parameter. One group with benign rolandic epilepsy remained untreated for clinical reasons and served to estimate the QEEG test-retest differences. In addition, the individual QEEG response to each drug was calculated as (EEG2-EEG1).

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Lyell's disease is a rare, life-threatening, acute dermatologic disease. The mucous membranes are also often involved. Nearly all cases are induced by medications. There is currently no specific treatment and interdisciplinary cooperation is very important. The authors present a case report of a 15 year old boy with the ocular manifestations of Lyell's disease, triggered by lamotrigine. He was admitted to the burn unit with involvement of 85% of his body surface area. Ocular manifestations documented during hospitalization were classified as mild (lid edema, conjunctival injection) and later severe (multiple symblepharons). The patient was treated with antibiotic eyedrops/ointment, corticosteroid eyedrops/ointment, topical lubricants and a glass rod was used to lyse the symblepharons. At 23 months of follow-up our patient had a symblepharon which blocked the superior and inferior punctum in both eyes, without conjunctival fornix foreshortening or corneal abnormalities, minimal ocular discomfort.

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Age as well as estrogen levels may have an impact on the pharmacokinetics of lamotrigine (LTG) and monohydroxycarbazepine (MHD), the active metabolite of oxcarbazepine (OXC). To assess the effects of age and menopause, we evaluated retrospectively a therapeutic drug-monitoring database. Samples from 507 women and 302 men taking LTG and 464 women and 319 men taking OXC were used to develop a population pharmacokinetic model. Data were analyzed using NONMEM software and were compared with a population pharmacokinetic model based on samples of 1705 women and 1771 men taking carbamazepine (CBZ). Age was a significant factor contributing to pharmacokinetic variability in individuals using LTG, OXC, and CBZ with increasing clearance as a function of bioavailability (Cl/F) over age 18, a maximum Cl/F at 33years (CBZ) and 36 years (LTG and OXC), and a gradual decrease of Cl/F towards older age. We found no effect of perimenopausal age range on LTG and MHD clearance.

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Eighty-two patients undergoing LTG monotherapy were reported seizure free as defined above. In 34 the TT could not be calculated because they became seizure free on the first chosen dose. TTs of the remaining 48 patients ranged from 4.0 to 42.0 micromol/l. There were no differences between children and adults, and between generalized and localization-related epilepsies. The therapeutic levels of patients with undefined TT tended to be lower. The level-dose ratio in both groups varied only moderately indicating absence of major exogenous influences.

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On the basis of six years of clinical experience with lamotrigine in the treatment of psychiatric disorders, supplemented by three case reports and a comprehensive literature review of empirical studies, we discuss the possible indications for lamotrigine in psychiatric disorders.

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Lamotrigine, an antiepileptic drug, is cleared from the systemic circulation mainly by glucuronidation. The possibility of changes in the pharmacokinetics of lamotrigine in plasma owing to hepatic dysfunction has been evaluated.

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Fourteen treatment studies that included patients with bipolar disorder with either a syndrome-defined anxiety disorder or nonspecific anxiety were selected.

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Data from cross-sectional and prospective studies revealed that patients with epilepsy and on long-term treatment with antiepileptic drugs (AEDs) are at increased risk for metabolic bone diseases. Bone diseases were reported in about 50% of patients on AEDs. Low bone mineral density, osteopenia/osteoporosis, osteomalacia, rickets, altered concentration of bone turnover markers and fractures were reported with phenobarbital, phenytoin, carbamazepine, valproate, oxcarbazepine and lamotrigine. The mechanisms for AEDs-induced bone diseases are heterogeneous and include hypovitaminosis D, hypocalcemia and direct acceleration of bone loss and/or reduction of bone formation. This article reviews the evidence, predictors and mechanisms of AEDs-induced bone abnormalities and its clinical implications. For patients on AEDs, regular monitoring of bone health is recommended. Prophylactic administration of calcium and vitamin D is recommended for all patients. Treatment doses of calcium and vitamin D and even anti-resorptive drug therapy are reserved for patients at high risk of pathological fracture.

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Two similar formulations (A and B) and one reference (C) were tested in nine epileptic refractory patients. The study was divided into three periods of 42 days, one for each formulation, and medical data about the frequency of seizures, the occurrence of side effects and measurement of plasma concentrations of lamotrigine were collected.

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lamictal max dose 2015-05-11

To describe the pharmaceutical use, health care resource utilisation patterns, and annual direct medical cost of epilepsy as well as determining the impact of Stromectol Online Kaufen various demographic and clinical characteristics on total costs of epilepsy in Oman.

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Evaluation of daily clinical practice in prescribing lamotrigine in refractory epilepsy patients. Atarax Suspension

lamictal pediatric dose calculator 2016-09-13

Utilisation of newer AEDs in UK primary care has Cymbalta Reviews Weight Gain increased between 1993 and 2008 with increasing use of diverse combinations of AEDs. The data quantify exposure to AEDs relevant to planning analytical pharmaco-epidemiological studies, as well as providing information to inform prescribing policies.

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Results suggest that lamotrigine attenuated the Lopressor Iv Dose effects of corticosteroids on the left amygdala. Larger trials are warranted to confirm these findings.

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The incidence of extrapyramidal side effects was considerably higher than expected. We suggest that these medications be Albenza Tab 200mg used with considerable caution in these patients.

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Our group developed a new psychostimulant animal model reflecting some clinical aspects of schizophrenia better than the conventional model does. In this model, long-lasting prepulse inhibition (PPI) deficit at the basement state is induced via repeated administration of methamphetamine (METH, 2.5mg/kg) without challenge injection of this psychostimulant. This study elucidates the effects of Topamax 5 Mg lamotrigine (LTG, 30mg/kg) on the initiation and expression of a steady-state PPI deficit induced by the repeated METH administration. We assessed the effect of coadministration of LTG and METH on the initiation of PPI deficit. The LTG was injected 120min after each METH injection for 5 times on every alternate day and for an additional 5 times every day, amounting to a total of 10 times. After 11-13 days of the withdrawal period, we measured PPI using the SR-LAB system. Using other animals after 20min of LTG injection, we subsequently examined the effect of a single injection of LTG on the expression of PPI deficit caused by the repeated METH administration. The LTG blocked the initiation of PPI deficit induced by the repeated METH administration at 68dB of prepulse intensity, but had no effect on the startle amplitude. The LTG prevented the initiation and expression of neuroplastic PPI deficit detected at the baseline state without any METH challenge injection, which was induced by the repeated administration of this psychostimulant. Results suggest that LTG is useful for blocking progressive deterioration of neurocognitive function and recovering the neurocognitive deficit in schizophrenia.

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Clinical trials of lamotrigine (LTG) began in 1984. By November 1992 about 5,800 patient-years' experience of adverse effects had been compiled. In general, LTG has an acceptable safety profile. Mild central nervous system adverse effects such as ataxia, dizziness, and headache occur significantly more frequently with LTG than with Avodart 10 Mg placebo but seldom demand discontinuation of LTG therapy. Dosage-related allergic skin rash occurs in about 5% of patients. The rash rarely is severe enough to require hospitalization. The adverse-reaction profile of LTG compares favorably with that of traditional antiepileptic drugs.

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We report about a 3-day-old full-term newborn who suffered from series of tonic-clonic and myoclonic seizures. His mother was treated with lamotrigin for epilepsy. It is Zocor Generic Name worthy of note that the drug level of the neonate had already decreas-ed to 37% of the basic level of his mother. At the same time, there was a catabolic metabolic situation and a mild hyponatriaemia. We believe that the neonatal seizures were caused by lamotrigin withdrawal.

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Studies were performed to investigate the UDP-glucuronosyltransferase enzyme(s) responsible for the human liver microsomal N2-glucuronidation of the anticonvulsant drug lamotrigine (LTG) and the mechanistic basis for the LTG-valproic acid (VPA) interaction in vivo. LTG N2-glucuronidation by microsomes from five livers exhibited atypical kinetics, best described by a model comprising the expressions for the Hill (1869 +/- 1286 microM, n = 0.65 +/- 0.16) and Michaelis-Menten (Km 2234 +/- 774 microM) equations. The UGT1A4 inhibitor hecogenin abolished the Michaelis-Menten component, without affecting the Hill component. LTG N2-glucuronidation by recombinant UGT1A4 exhibited Michaelis-Menten kinetics, with a Km of 1558 microM. Although recombinant UGT2B7 exhibited only low activity toward LTG, inhibition by zidovudine and fluconazole and activation by bovine serum albumin (BSA) (2%) strongly suggested that this enzyme was responsible for the Hill component of microsomal LTG N2-glucuronidation. VPA ( Avapro Generic Alternative 10 mM) abolished the Hill component of microsomal LTG N2-glucuronidation, without affecting the Michaelis-Menten component or UGT1A4-catalyzed LTG metabolism. Ki values for inhibition of the Hill component of LTG N2-glucuronidation by VPA were 2465 +/- 370 microM and 387 +/- 12 microM in the absence and presence, respectively, of BSA (2%). Consistent with published data for the effect of fluconazole on zidovudine glucuronidation by human liver microsomal UGT2B7, the Ki value generated in the presence of BSA predicted the magnitude of the LTG-VPA interaction reported in vivo. These data indicate that UGT2B7 and UGT1A4 are responsible for the Hill and Michaelis-Menten components, respectively, of microsomal LTG N2-glucuronidation, and the LTG-VPA interaction in vivo arises from inhibition of UGT2B7.

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The Second Eilat Conference on New Antiepileptic Drugs was held at the King Solomon's Palace Hotel from October 31 to November 3, 1994. Epileptologists and scientists from 20 countries attended the conference, which was held to discuss new trial designs, drug approval, early use of new antiepileptic drugs, and new drugs in development. Over the last six years, several novel antiepileptic drugs have been introduced worldwide, and new information on their safety and efficacy has become available. These include felbamate, gabapentin, lamotrigine, oxcarbazepine, and vigabatrin. Drugs in development include those at an advanced stage, such as topiramate Paracetamol Overdose In Infant and tiagabine, as well as those just entering clinical trials, such as remacemide and levetiracetam. The following is a summary of the presentations for drugs in development and newly marketed drugs. The meeting concluded with a presentation, 'Still Searching for the Magic Bullet'.