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Simulations have provided quantitative insight, showing that XR formulation is generally more forgiving in nonadherence. They also suggest that in a typical patient, a missed dose should be made up by doubling the next dose. The approach illustrates how a model constructed on clinical trial data can be used to simulate real-world dosing scenarios and guide therapeutics.
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Two pools of citrated whole blood were created by spiking high and low concentrations of gentamicin, vancomycin, phenytoin, lamotrigine and carbamazepine. After recalcification with 15 mmol/L calcium chloride, spiked whole blood was added into four different Becton Dickinson blood collection tubes: RST, serum separator tube, red top tube and polyethylene plain tube. Serum aliquots were collected at baseline (0 h), 2 h, 24 h, day 3 and day 7. Drug concentrations were measured in batch by HPLC and the Architect c8000.
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Cognitive impairments are a major clinical feature of the common neurogenetic disease neurofibromatosis type 1 (NF1). Previous studies have demonstrated that increased neuronal inhibition underlies the learning deficits in NF1, however, the molecular mechanism underlying this cell-type specificity has remained unknown. Here, we identify an interneuron-specific attenuation of hyperpolarization-activated cyclic nucleotide-gated (HCN) current as the cause for increased inhibition in Nf1 mutants. Mechanistically, we demonstrate that HCN1 is a novel NF1-interacting protein for which loss of NF1 results in a concomitant increase of interneuron excitability. Furthermore, the HCN channel agonist lamotrigine rescued the electrophysiological and cognitive deficits in two independent Nf1 mouse models, thereby establishing the importance of HCN channel dysfunction in NF1. Together, our results provide detailed mechanistic insights into the pathophysiology of NF1-associated cognitive defects, and identify a novel target for clinical drug development.
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Although the etiology of NH and EF remains uncertain, both syndromes seem to share a peripheral source. Their association in a number of patients is probably reflecting a pathophysiological connection. Lamotrigine might be a good therapeutic option for those patients presenting with both disorders.
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The objective of this paper is to provide a synopsis of benefits and potential harmful effects of exposure to antiepileptic drugs (AEDs) via breastmilk, and present recommendations for breastfeeding in women with epilepsy.
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The values of the pharmacokinetic parameters of lamotrigine were: clearance over bioavailability (CL/F) 2.60+/-0.40 l/h, renal clearance (CLR) 0.10+/-0.03 l/h, terminal half-life (t1/2) 23.8+/-2.1 h, mean peak serum concentration (Cmax) 0.29+/-0.02 microg/l, time to reach Cmax (tmax) 1.6+/-0.28 h, and total area under the serum concentration-time curve (AUC0-infinity) 703.99+/-82.31 microg/ ml/min (mean +/- SEM). The amount of lamotrigine excreted as glucuronide was 8.90+/-0.77 mg. Rifampicin significantly increased CL/F (5.13+/-1.05 l/h) and the amount of lamotrigine excreted as glucuronide (12.12+/-0.94 mg), whereas both t1/2 (14.1+/-1.7 h) and AUC(0-infinity) (396.24+/-60.18 microg/ml/min) were decreased (P<0.05). Cimetidine failed to affect pharmacokinetics of lamotrigine. Lamotrigine did not change EEG power.
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From the current evidence, lamotrigine cannot be recommended as a mood stabilizer except when conventional therapies have failed.
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Epilepsy is a condition for which regular drug treatment is normally prescribed. We have examined the primary care prescribing rates for anti-epileptic drugs (AEDs) in a region of northern England with a population of 6.8 million. Over the 4-year period 1992-1995 the number of AED prescription items issued rose by 15%. A third of this rise is accounted for by increased prescribing of the new anticonvulsants, vigabatrin, lamotrigine and gabapentin, which are primarily indicated for adjunct use. Prescribing of phenytoin and barbiturates fell over the same period, but this reduction was more than compensated for by increased prescribing of carbamazepine and sodium valproate. There were notable differences in both the overall volume and the choice of AEDs used in different health authority areas and these are probably attributable to the influence of the local secondary-care sector on the therapeutic regimens adopted by general practitioners in the area.
A total of 9 RCTs involving 1 016 participants were included. Lamotrigine yielded a significantly lower complete control rate of seizure than ethosuximide, but the complete control rate of seizure showed no significant differences between lamotrigine and carbamazepine/sodium valproate. Patients treated with lamotrigine had a significantly lower incidence rate of adverse events than those treated with carbamazepine, but the incidence rate of adverse events showed no significant differences between patients treated with lamotrigine and sodium valproate/carbamazepine. The drop-out rate showed no significant differences between the three treatment groups.
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To provide a qualitative, systematic update and review of the pharmacology, pharmacokinetics, efficacy in mood disorders, adverse effects, and costs of lamotrigine.
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Some studies suggest a higher risk of hypertension in people with epilepsy. Captopril, a potent and selective angiotensin-converting enzyme (ACE) inhibitor, is a well known antihypertensive drug. Besides the peripheral renin-angiotensin system (RAS), ACE inhibitors are also suggested to affect the brain RAS which might participate in the regulation of seizure susceptibility. The purpose of the current study was to evaluate the effect of captopril on the protective action of numerous antiepileptic drugs (carbamazepine [CBZ], phenytoin [PHT], valproate [VPA], phenobarbital [PB], oxcarbazepine [OXC], lamotrigine [LTG] and topiramate [TPM]) against maximal electroshock-induced seizures in mice. This study was accompanied by an evaluation of adverse effects of combined treatment with captopril and antiepileptic drugs in the passive avoidance task and chimney test. Captopril (25 and 50 mg/kg i.p.) did not influence the threshold for electroconvulsions. Among the tested antiepileptics, captopril (25 and 50 mg/kg i.p.) potentiated the antiseizure action of CBZ, decreasing its ED(50) value from 12.1 to 8.9 and 8.7 mg/kg, respectively. Moreover, captopril (50 mg/kg i.p.) enhanced the anticonvulsant activity of LTG. ED(50) value for LTG was lowered from 5.1 to 3.5 mg/kg. The observed interactions between captopril and CBZ or LTG were pharmacodynamic in nature as captopril did not alter plasma and total brain concentrations of these antiepileptics. The combinations of captopril with antiepileptic drugs did not lead to retention deficits in the passive avoidance task or motor impairment in the chimney test. Based on the current preclinical data, it is suggested that captopril may positively interact with CBZ and LTG in epileptic patients. The combinations of captopril with the remaining antiepileptics (PHT, VPA, PB, OXC and TPM) seem neutral.
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Seizure onset occurs in adolescence. All have myoclonias, about 90 % have generalized tonic-clonic seizures, and one third have absences. Myoclonic jerks are frequently the debut symptom, while tonic-clonic seizures appear later on. Patients are particularly susceptible to seizures shortly after waking. It is important to ask specifically about myoclonias as most patients do not report jerks spontaneously. The electroencephalograms of 44-81 % of the patients show discharges of 4-6 Hz polyspike waves. Focal EEG abnormalities may be seen in about 30 %. When patients are treated with valproate and seizure-precipitating factors are avoided, especially sleep deprivation, about 80 % become seizure-free. Lamotrigine and levetiracetam are alternative therapies for women of childbearing age. Attempts to taper off the medication after several years of seizure freedom entail a high risk of seizure relapse.
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Aripiprazole therapy may reduce symptoms in bipolar older adults, and it appears to be reasonably tolerated. However, larger, controlled trials are needed to confirm these preliminary findings.
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We conducted systematic PubMed and SCOPUS reviews (last search =10/01/2015) of randomized controlled trials comparing lamotrigine to placebo or other agents with antidepressant activity in unipolar or bipolar depression. We performed a random-effects meta-analysis of depression ratings, response, remission, and adverse effects calculating standardized mean difference (SMD) and risk ratio (RR) ±95% confidence intervals (CIs).
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The inflammation process with MS is promoted by several inflammatory cytokines produced by the immune cells themselves and local resident cells like activated microglia. Consecutive damaging pathways involve the transmigration of activated B lymphocytes and plasma cells, which synthesize antibodies against the myelin sheath, boost the immune attack, and result in ultimate loss of myelin. Likewise, activated macrophages and microglia are present outside the lesions in the normal-appearing CNS tissue contributing to tissue damage. In parallel to inflammatory demyelination, axonal pathology occurs in the early phase which correlates with the number of infiltrating immune cells, and critically contributes to disease severity. The spectrum of neuronal white matter and cortical damage ranges from direct cell death to subtle neurodegenerative changes such as loss of dendritic ramification and the extent of neuronal damage is regarded as a critical factor for persisting neurological deficits. Under normal conditions, CNS microglia safeguards organ integrity by constantly scanning the tissue and responding rapidly to danger signals. The main task of microglial cells is to encapsulate dangerous foci and remove apoptotic cells and debris to protect the surrounding CNS tissue; this assists with tissue regeneration in toxin-induced demyelination. In the absence of lymphocytic inflammation and in the context of non-autoimmune, pathogen-associated triggered inflammation, microglial cells protect the neuronal compartment. These mechanisms seem to be inverted in MS and other chronic neurodegenerative disorders because activated microglia and peripherally derived macrophages are shifted towards a strongly pro-inflammatory phenotype and produce the proinflammatory cytokines TNF-α and interleukin (IL)1-β, as well as potentially neurotoxic substances including nitric oxide, oxygen radicals and proteolytic enzymes. Microglial silencing reduces clinical severity, demonstrating their active involvement in damage processes and in the immune attack against the CNS. In light of this, it is questionable whether microglia and monocyte-derived macrophages, the very last downstream effector cells in the immune reaction, actually have the capacity to influence their fate. It is more likely that the adaptive immune system orchestrates the attack against CNS cells and drives microglia and macrophages to attack oligodendrocytes and neurons.
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There is growing concern about the over-diagnosis of bipolar disorder, and increasing evidence that bipolar depression may present differently to unipolar depression. Antipsychotics are the initial agents of choice for the acute treatment of mania. For preventive treatment, lithium and atypical antipsychotics have the strongest evidence base. Lithium has been shown to be more effective than valproate. The main effect of lithium and most of the atypical antipsychotics is on prevention of manic relapse; only olanzapine and quetiapine also protect against depression. Lamotrigine is an agent with evidence for prevention of depressive relapse, but have minimal activity against mania. The role of antidepressants remains contentious, while there is strong support for quetiapine. Finally, there is growing evidence from randomised controlled trials of the benefit of psychological therapies in conjunction with medications.
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Total SWD duration, SWD number, and mean SWD duration were significantly decreased in rats that received 35-day LTG treatment compared with rats that received vehicle treatment. Rats with spontaneous SWDs versus rats with no SWDs showed significant levels of anxiety and depression in the OF, EPM, and SC tests. Rats with SWDs also showed longer immobility in the FS test. However, the LTG-treated group compared with the vehicle group presented with significantly lower manifestations of anxiety and depression in the OF, EPM, SC, and sucrose preference tests and shorter immobility in the FS test.
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We found two novel SNPs associated with LTG-induced MPE: rs12668095 near CRAMP1L/TMEM204/IFT140/HN1L (P=4.89×10(-7)) and rs79007183 near TNS3 (P=3.15×10(-10)), both of which were replicated in an independent cohort.
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The patients with epilepsy (n=109) on treatment with conventional and newer AEDs (levetiracetam, lamotrigine and clobazam) for > 6 months were enrolled. Of these, 70 were on monotherapy: levetiracetam (n=12), VPA (n=16), carbamazepine (n=20) and phenytoin (n=22) and the remaining on polytherapy. Their body composition [body fat mass, lean dry mass (LDM), total body water (TBW), intracellular water (ICW), extracellular water (ECW) and basal metabolic rate (BMR) was estimated and biochemical parameters were assessed.
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Borderline personality disorder (BPD) has long defined definitive treatment. Such failure is reflected in repeated suicidal crises, often associated with dysphoric symptoms of a chronic fluctuating nature, whose labile intermittent character does suggest a subthreshold bipolar depressive mixed state. For all these reasons, we hypothesized that the anticonvulsant lamotrigine, touted to be a mood stabilizer with antidepressant properties, might be uniquely beneficial for these patients.