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This article provides a comprehensive review of the interactions between antiepileptics and second-generation antipsychotics. The authors cover pharmacokinetic AED-SGAP DI studies, the newest drug pharmacokinetics in addition to the limited pharmacodynamic DI studies.
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Sudden unexplained/unexpected death (SUDEP) in epilepsy is a major cause of death accounting for 7-17% of the mortality among epileptic patients. Prolongation of QT-interval has been issued as a major mechanism in SUDEP since it is associated with fatal cardiac arrhythmias. This condition may be further precipitated by anti-epileptic treatment. Despite thorough literature research, we did not find any reports suggesting that primidone is responsible for QT-prolongation. On the contrary, all the retrieved reports addressed that the drug shortened QT-interval and corrected signs and symptoms of the underlying disease.
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Anticonvulsant hypersensitivity syndrome is an acute, life-threatening, idiosyncratic drug reaction seen with the aromatic antiepileptic drugs, phenytoin, carbamazepine, phenobarbital, and primidone, with frequent cross sensitivity. It usually occurs 2-8 weeks after initiation of therapy and the hallmark clinical features are fever, rash, and lymphadenopathy. Hematologic abnormalities such as eosinophilia, atypical lymphocytes, and internal organ involvement also occur with varying severity. A case of hypersensitivity syndrome due to carbamazepine with cross sensitivity to phenytoin is reported. It is emphasized that this serious drug reaction with diverse clinical presentations should be recognized and treated promptly.
The present study has been directed to investigate Ursodeoxycholic Acid (UDCA) effect in children, to reduce the high Liver transaminases induced by Anticonvulsant drugs (drug induced hepatitis). This idea has been driven from Cytoprotective and antioxidant properties of UDCA to be used in drug induced inflammation in Liver. Twenty two epileptic patients aged between 4 mo - 3 yr whom were under anticonvulsant therapy with drugs such as valperoic acid, primidone, levetiracetam, Phenobarbital or any combination of them and had shown Liver transaminases rise , after rule out of Viral-Autoimmune, Metabolic and Anatomic causes, have been prescribed UDCA in dose of 10-15 mg/kg/day, at least for 6 months. Any patient who have shown confusing factors such as genetic disorders with liver involvement or spontaneous decline in enzymes or had not treatment compliance has been excluded from the study. Transaminases range changes as well as Probable side effects of the drug have been monitored. The results indicated that UDCA is effective and well tolerable in the children with drug induced hyper transaminasemia. No side effect has been seen and recorded in this study. Based on this study and its results, we recommend UDCA as a safe and effective choice in drug induced hepatotoxicities.
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Controlled trials, case studies, and review articles identified via MEDLINE using the search terms epilepsy, seizures, elderly, phenobarbital, primidone, phenytoin, carbamazepine, valproic acid, felbamate, gabapentin, lamotrigine, topiramate, tiagabine, levetiracetam, oxcarbazepine, and zonisamide. Recently published standard textbooks on epilepsy were also consulted.
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A few neonates born to mothers receiving anticonvulsant drugs during pregnancy have shown defects in vitamin K dependent clotting factors with or without clinical bleeding. Experimentally, phenytoin (diphenyl hydantoin, DPH) has induced clotting defects in cats and inhibited production of clotting factors in rat liver slices. Phenobarbital has produced similar but milder defects. Anticonvulsants have been observed to produce clotting defects in 9 children, 2 weeks to 8 years in age. Elevated levels of phenytoin or other anticonvulsants, or a combination of anticonvulsants were measured in the children. Six patients were on drug combination including two or more of the following: phenytoin, phenobarbital, primidone, carbamazepine, diazepam, ethosuximide. Clotting defects included: elevated prothrombin time, elevated partial thromboplastin time, diminished factors V, VII or X. All children had neurologic symptoms of anticonvulsant toxicity, but the only hematologic problems were oozing from venipuncture sites and increased bruising in 3. All patients were on normal diets and had normal liver function tests. By lowering the level of anticonvulsants, clotting factors returned toward normal. Elevated levels of anticonvulsants can potentially produce clotting defects in neonates and young children.
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The effects of pregabalin for treating essential tremor are uncertain because the quality of the evidence is very low. One small study did not highlight any effect of this treatment; however, the high risk of bias and the lack of other studies on this topic limit further conclusion.
Drug interactions in epileptic children with carbamazepine (CBZ) polytherapy were investigated by analysis of total and free CBZ and its metabolites simultaneously. Heteroinduction effects of CBZ metabolism by other antiepileptic drugs (AEDs), including phenytoin (PHT), phenobarbital (PB), or primidone (PRM), were clearly demonstrated. Serum CBZ level/dose ratios in patients taking CBZ plus other AEDs were decreased while CBZ-10,11-epoxide (CBZ-E) and trans-10,11-dihydroxy-10,11-dihydro-CBZ (CBZ-H) concentrations were significantly increased compared to patients with CBZ alone. Concentration ratios of CBZ-H/CBZ and CBZ-E/CBZ were also significantly higher in patients taking CBZ plus other AEDs. Interactions between CBZ and valproic acid (VPA) involved both protein binding displacement and metabolic inhibition. Patients taking CBZ plus VPA showed significantly increased free fractions of CBZ and CBZ-E and substantially increased serum CBZ-E concentrations and CBZ-E level/dose ratios, while CBZ-H/CBZ-E concentration ratios were decreased compared with patients on CBZ alone. Since this approach investigates the in vivo relationship between substrates and products of the enzymes involved in CBZ biotransformation (the ratios between CBZ and its metabolites), detailed information about the activities of the enzymes may be obtained. This approach appears to be a practical way to improve the monitoring of CBZ metabolism influenced by various physiological or pathological conditions and achieve a better understanding of the drug interactions under different drug regimens (coadministered inhibitor or inducer). This principle may also be adopted for other drugs with similar metabolic characteristics.
Tremor is one of the most frequent neurological signs. The correct clinical classification is mainly clinical. The most frequent primarily neurological tremor is essential tremor (prevalence 2 to 5%). It presents in most cases as a more or less symmetrical postural and kinetic tremor. In about 60% of cases an autosomal-dominant inheritance is found. Tremor may manifest not only in the hands but also in the head and voice. In about 60 to 70% of the patients alcohol may improve the tremor. Parkinsonian tremor is normally a tremor at rest and it starts asymmetrically. The legs and the face are frequently involved. Cerebellar tremor is intentional. Orthostatic tremor, which has a high frequency, mainly manifests in the legs and gives rise to postural instability. Dystonic tremor is an action tremor of the affected region of the body. Drug therapy, which is purely symptomatic, mostly depends on clinical manifestation. Postural and action tremors respond to non selective betablockers (propranolol), primidone, some antiepileptics (gabapentin, toparimate) and benzodiazepines. Classical rest tremors are improved by dopaminergic substances (levodopa, dopamine agonists) or anticholinergics. Dystonic tremor may successfully be treated by injections of botulinum toxin. Orthostatic tremor responds to gabapentin or benzodiazepines in some of the patients. In severely handicapped patients with refractory tremors the implantation of thalamic stimulation electrodes may be considered. This treatment may be very successful, however, its inherent risks have to be taken into account.
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The action of heterocyclic amides series (ethosuximide, phenytoin, primidone) on lipid peroxidation and membrane bound monoamine oxidases A and B under stress condition has been studied. The intraperitoneal injection of the drugs resulted in enhancement of SOD, decrease of brain malondialdehyde content and mitochondrial activity of monoamine oxidases A and B.
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We describe a sensitive, precise high-pressure liquid chromatographic method in which 5-(p-methylphenyl)-5-phenylhydantoin is used as the internal standard for simultaneous determination of diphenylhydantoin, phenobarbital, and primidone in whole blood and plasma. These anticonvulsant drugs are well separated from each other and from normal blood constituents in less than 10 min. The lower limit of detection for each drug is 100 ng for primidone, 200 ng for dilantin, and 300 ng for phenobarbital. The eluted drugs were detected by their absorption at 254 nm, and evaluated from their peak heights as compared to internal standard. The method was successfully adapted for pediatric samples (100 to 500 mul of whole blood or plasma). Fifty specimens were analyzed for phenobarbital and diphenylhydantoin and 25 specimens for primidone by a standard gas-chromatographic method and by our liquid-chromatographic method; the resulting correlation coefficient was greater than 0.98.
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Despite the recent entry into the market-place of a range of new pharmacological treatments for epilepsy, most patients still receive the standard antiepileptic drugs. This review considers the clinical place and practical use of these agents. Detailed consideration is given to carbamazepine, phenytoin, sodium valproate, phenobarbital and ethosuximide, with lesser emphasis on primidone, clobazam and clonazepam. Individualization of therapy, polypharmacy, refractory epilepsy, therapeutic drug monitoring, pregnancy, withdrawing treatment, epilepsy prophylaxis and referral to an epilepsy centre are also discussed. The paper concludes with a statement of 12 basic rules in prescribing established antiepileptic drugs.
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Psychometric, adaptive ability, motor proficiency, and sensory discrimination measures were administered to adult seizure patients within 36 hours of blood serum determinations of diphenylhydantoin, phenobarbital, and primidone. Thirty-five subjects in whom at least one of the three drug levels fell within stated mug per milliliter toxicity ranges were compared with 28 subjects of comparable age and IQ who were identified by the same procedure to be nontoxic. The toxic group consistently obtained poorer mean test scores, and significant intergroup differences were found on several measures of attention and concentration and on tests of motor coordination and static tremor.
To date, serendipitous observations have provided most of our understanding of tremor cellular physiology. Based on similarities to currently effective drugs or rational approximations and inferences, several currently available agents should be considered for tremor trials.
Epilepsy is the most common neurological disorder affecting approximately 50 million people worldwide. In India, overall prevalence of epilepsy is reported to be 5.59/1000 population. Antiepileptic drugs (AEDs) constitute the main-stay of treatment with a large number of AEDs available in the market. High incidence of adverse effects is a major limitation with AEDs. One of the major concerns is significant metabolic effects on the bone. However, little attention has been paid to this issue because most of the bone effects remain subclinical for a long time and may take years to manifest clinically. The main effects include hypocalcemia, hypophosphatemia, reduced serum levels of Vitamin D, increase in parathormone (PTH) levels, and alterations in bone turnover markers. The CYP450 enzyme-inducing AEDs such as phenytoin, phenobarbital, carbamazepine, and primidone are the most common AEDs associated with bone disorders while the data regarding the effect of valproate and newer AEDs such as lamotrigine, gabapentin, vigabatrin, levetiracetam, and topiramate on bone metabolism and bone density are scanty and controversial. Deficiency of Vitamin D is commonly described as a cause for the bone loss in epileptic patients while others being decreased absorption of calcium, increased PTH levels, and inhibition of calcitonin secretion, etc. However, there are no formal practical guidelines for the management of bone disease among those taking AEDs. Evidence-based strategies regarding monitoring, prevention, and treatment of bone diseases in patients on AED therapy are needed.
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We have investigated the dose- and time-dependency of myocyte apoptosis and necrosis induced by the beta2-adrenergic receptor agonist, clenbuterol, with the aim of determining whether myocyte apoptosis and necrosis are two separate processes or a continuum of events. Male Wistar rats were administered subcutaneous injections of clenbuterol, and immunohistochemistry was used to detect myocyte-specific apoptosis and necrosis. Myocyte apoptosis peaked 4 h after, and necrosis 12 h after, clenbuterol administration. In the soleus, peak apoptosis (5.8 +/- 2.0%; P < 0.05) was induced by 10 mug and peak necrosis (7.4 +/- 1.7%; P < 0.05) by 5 mg x kg(-1) clenbuterol. Twelve hours after clenbuterol administration, 73% of damaged myocytes labeled as necrotic, 27% as apoptotic and necrotic, and 0% as purely apoptotic. Administrations of clenbuterol (10 microg x kg(-1)) at 48-h intervals induced cumulative myocyte death over 8 days. These data show that the phenotype of myocyte death is dependent on the magnitude of the insult and the time at which it is investigated. Only very low doses induced apoptosis alone; in most cases apoptotic myocytes lysed and became necrotic and the magnitude of necrosis was greater than that of apoptosis. Thus, it is important to investigate both apoptotic and necrotic myocyte death, contrary to the current trend of only investigating apoptotic cell death.
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In 47 children followed for 1 year after the first "simple" febrile convulsion, dipropylacetate (Depakine, 20 mg/kg) was as effective in preventing new febrile convulsions (a single recurrence in 4% of 47 children) as was phenobarbital (5 mg/kg) or primidone (25 mg/kg) (a single recurrence in 4% of 47 children), and there were no side effects. Of 47 untreated children followed for 1 year, 55% had 1 to 4 new febrile convulsions. All medications were given in divided doses morning and evening.
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Decreased basal and calcium-stimulated calcitonin serum levels have been found in children with congenital hypothyroidism and in those receiving anticonvulsant drugs. The purpose of our investigation was to confirm these results using a new technique for calcitonin measurement and to study the effect on bone turnover. Calcitonin serum levels were measured with two different antibodies before and after a low-dose Ca infusion in patients receiving phenytoin, primidone, carbamazepine, or valproate and in patients with congenital hypothyroidism receiving L-thyroxine. In comparison with control values, basal and Ca-stimulated extractable calcitonin, representing the monomeric and biologically active form of the hormone, were moderately decreased in patients with epilepsy receiving phenytoin and primidone, and severely decreased in patients with hypothyroidism. Ca and bone metabolism were normal, except for an elevated renal threshold for phosphate (indicating phosphate conservation) in patients receiving phenytoin and primidone, and increased fasting urinary excretion of Ca and hydroxyproline (indicating increased bone resorption) in patients with hypothyroidism. The secretory capacity of the C cells for monomeric calcitonin is decreased in children receiving treatment with some, but not all, anticonvulsant drugs, and lacking in patients with hypothyroidism. Patients with calcitonin deficiency may be prone to osteopenia if the tendency to increased osteoclastic activity is aggravated by secondary hyperparathyroidism in patients with epilepsy receiving phenytoin and primidone or by inappropriate thyroid replacement therapy in patients with hypothyroidism.
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Prolonged QT or QU intervals can be caused by a variety of conditions which include drugs, electrolyte imbalance, and acquired and congenital diseases. This finding is associated with life-threatening ventricular arrhythmias that, at times, have unusual morphologies characteristically named "torsade de pointes." Treatment, when iatrogenic, is obvious--when due to acute acquired diseases, therapy is supportive until the acute phase passes. In congenital prolonged QT syndromes, primidone (Mysoline) recently has been found to be successful in long-term management.
A controlled clinical trial of the anti-epileptic efficacy and toxic side effects of diphenylsilanediol was conducted on 24 client-owned epileptic dogs. Data obtained from an abbreviated procedural treatment program indicated that diphenylsilanediol compared favorably with primidone as an anti-epileptic compound, but had limiting toxic side effects to the liver, pancreas, and possibly to other tissues. There was a mean reduction of 60.7% in seizure frequency in 15 epileptic dogs treated with diphenylsilanediol when compared with their pretreatment frequency. There was a mean reduction of 55.6% in seizure frequency in 9 spileptic control dogs treated with primidone. Samples of blood obtained from the dogs in the program on the 4th, 8th, 12th, 24th, and 36th weeks of treatment were examined for complete blood cell count, blood urea nitrogen, liver function, and pancreatic function. Toxic side effects were not seen among the primidone-treated control dogs, with the exception of occasional dose-related drowsiness. Among the diphenylsilanediol-treated dogs, 3 developed liver disease, 2 developed definite pancreatic changes, and 2 showed evidence of bone marrow suppression. Four dogs died during treatment with diphenylsilanediol, whereas no deaths occurred during the same interval of primidone therapy.
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A case of a patient with astrocytoma who showed somnolence and asterixis one month after tumour resection is presented. Although primidone had been prescribed preoperatively for five years and the same dose was maintained after the operation, the serum concentration of the primidone metabolite phenobarbital was elevated and she demonstrated hyperammonemic encephalopathy, which disappeared on withdrawal of the drug. A description of this seldom reported phenomenon during primidone therapy is given, with reference to valproate cases.
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The effects of concomitant antiepileptic drugs on the serum carbamazepine concentration (C1) were analyzed quantitatively. Primidone (PRM), phenobarbital (PB), phenytoin (PHT), valproic acid (VPA), zonisamide (ZNS), clonazepam (CZP), and ethosuximide (ETS) were coadministered with carbamazepine (CBZ). Routine therapeutic drug monitoring data, obtained from epileptic patients who were treated with the repetitive oral administration of CBZ fine granules/tablets, were used for the analysis. A total of 119 patients were administered CBZ alone, and 91, 39, 19, and 6 patients were coadministered one, two, three, and more than four different antiepileptic drugs, respectively. Using the data obtained from the patients administered CBZ alone, Ct could be expressed approximately as a function of the daily dose per extracellular water volume (D/VECW) as Ct = A(D/VECW)B (A, B: parameter). By comparing the regression line on log Ct vs. log(D/VECW) for CBZ alone with that for CBZ plus another concomitant drug, Ct was thus found to be affected at each definite ratio by PB and PHT, but not by VPA and ZNS. We postulated a model showing that Ct is affected by each concomitant antiepileptic drug i at each definite ratio. We defined the parameter Ri(i = 1, 2, ..., 7) representing the effect of each concomitant antiepileptic drug on Ct. A linear polynomial expression, in which both members of this model are converted into common logarithms, was used for a multiple regression analysis. The analysis clarified that PB and PHT lowered Ct to 0.770 and 0.710 the value of CBZ alone, respectively. On the other hand, VPA and ZNS did not affect Ct. The number of patients coadministered PRM, CZP, and/or ETS was not sufficient to detect the effect on Ct based on a test of significance. In the case of the addition or discontinuation of concomitant antiepileptic drugs in the same patient, the estimated Ct values were calculated using the value of each Ri and compared with the measured Ct values. Both values were in good agreement, and thus our results appear valid.
Despite a worldwide decline in barbiturate use, cases of acute poisoning with severe toxicity are still noted, particularly in developing countries. Severe poisonings often require prolonged admission to an intensive care unit, so enhanced elimination might be useful to hasten recovery. Information regarding the efficacy of these techniques for individual barbiturates is not available in standard textbooks.
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Adequate prepregnancy planning is essential for women who have epilepsy. Women receiving folate-lowering drugs may be at increased risk of adverse pregnancy outcomes. Therefore, epileptic women contemplating pregnancy should be treated with the minimum number of folate-lowering drugs possible and receive folic acid supplementation.
Nationwide analyses of drug use can provide a prevalence estimate of the underlying disease and can help in understanding the characteristics of treatment. This study aimed for such analyses regarding the utilization of antiepileptic drugs (AED) for epilepsy in Germany. In 2009, all 4,115,705 AED prescriptions of all German patients with statutory health insurance (70,011,508 persons) were retrospectively analyzed. The IMS(®) LRx database served as data source, which accesses nationwide pharmacy data centers processing all German prescription data. To establish the age and sex-specific percentage of patients taking AED because of epilepsy, we used a second database, Disease Analyzer(®), which covered a representative sample of the German population (7.2 million patients) and contained ICD10 codes alongside with prescription data. The period prevalence of patients taking AED because of epilepsy was 9.1/1,000 (children/adolescents: 5.2/1,000; elderly: 12.5/1,000). Of the patients, 83.1 % took at least one of four AED: valproate (29.8 %), carbamazepine (26.4 %), lamotrigine (21.4 %), and levetiracetam (16.9 %). Oxcarbazepine and sultiame were popular with pediatricians. Elderly patients frequently received phenytoin and primidone. More than half of the patients were treated by family physicians; 68 % took AED in monotherapy and 7.9 % received >2 AED (children/adolescents: 12.5 %). The costs for AED prescribed for epilepsy amounted to €285.1 Mio (median AED costs/patient: €158/a). The German 2009 prevalence of epileptic patients taking AED was 9.1/1,000. Family physicians cared for the majority of patients. Prevalence and prescribing patterns changed with age. Costs of AED against epilepsy added up to 1 % of total medication costs in Germany.
Using a newly developed microdialysis probe which allows continuous monitoring of drugs in blood, we have studied the pharmacokinetics of various antiepileptic drugs (carbamazepine, and its primary metabolite carbamazepine-epoxide, phenytoin primidone and phenobarbitone) in 5 patients (2 male, 3 female, aged 40-50 years) with intractable epilepsy. It was observed that microdialysate pharmacokinetic profiles were comparable to those obtained by direct blood sampling. Furthermore, patients found the microdialysis probe highly acceptable and desirable and indeed preferable to that of blood sampling.
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Two patients with intractable epilepsy who had been treated with various combinations of anticonvulsant drugs developed phenytoin encephalopathy. In both patients choreo-athetoid involuntary movements were prominent. Blood phenytoin concentrations were above 30 mug/ml. When phenytoin was given in smaller doses and its level in the blood fell the involuntary movements and other clinical manifestations disappeared.
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A high performance liquid chromatographic (HPLC) method is described for the quantitative determination of primidone in tablets. A ground tablet sample is diluted directly in the mobile phase, at a concentration of about 1 mg/mL of primidone, mixed and deaerated, and filtered. The resulting solution is then quantitated by HPLC. The average spike recoveries for the 50 mg and 250 mg tablets were 101.2% and 99.0%, respectively. The average recovery for an authentic mixture formulated at the 250 mg level was 100.1% with a relative standard deviation of 0.45%.
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Permanent freedom from fits can be achieved in a large proportion of children with a history of epilepsy through precise individual adjustment and careful maintenance of the therapeutic regimen. A review of the cases treated at the Pediatric Clinic, out-Patient-Department for Epileptics, University of Vienna, reveals that at present about 70% of the patients have a good prognosis (the figures vary from 50 to 85%, depending on the seizure type). An important question which has received only scant attention in the literature arises in the case of patients who have remained free from epileptic fits over a period of many years, namely whether longterm antiepileptic therapy can be terminated and, if so, then when and how. Only very few studies deal specifically with this problem and even these do not provide entirely satisfactory answers to all the posed questions, not only with regard to the optimum time and mode of drug reduction, but also with regard to the principles underlying the choice of apparently suitable candidates for attempted termination of therapy. An attempt is made in this retrospective study comprising 375 patients who have been followed up over a period of at least 5 years, to throw some light on these problems. Indeed, results of statistical significance were obtained by the use of a new mathematical technique, which enables the formulation of new guiding principles in the resolution of all three above-mentioned questions. In consequence, it now appears within the power of the pediatrician to markedly reduce the risk of relapse, which in the case of childhood epilepsies, is about 20%, at present. In general, several basic principles must be adhered to. Total freedom from convulsions over an uninterrupted period of at least 3 years' duration is an absolute prerequisite for consideration of cessation of therapy. Reduction in antiepileptic drug dosage should be carried out as a stepwise procedure over a period of about 2 years. Regular clinical and EEG follow-up examinations should be performed over this period of drug reduction and for 5 years subsequently, in order to recognise and counteract promptly any early signs of possible relapse. The prerequisite convulsionfree period is raised to 4 to 5 years or even longer and the time over which therapy is tailed off increased accordingly in the presence of any of the following criteria: 1. "Endogenous" tendency to relapse, 2. persistence of paroxysmal EEG abnormalities or deterioration of the EEG during the attempt to reduce the dosage of antiepileptic drugs, 3. inveterate epilepsy. The cessation of fits and the termination of medication do not yet signify that all the after-effects of epilepsy are overcome. Social integration must also be achieved before this goal is reached. The psychopathological symptomatology of the patient plays an important role in determining the outcome, whereby the level of intelligence of the patient is the decisive factor...
In spite of common guidelines, AED treatment differed significantly among adults with epilepsy in Germany. Besides gender, type of health insurance and place of residence strongly influenced AED administration.
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This paper describes the preparation of primidone-loaded poly-epsilon-caprolactone nanocapsules according to the interfacial deposition technique. The colloidal suspension obtained showed a monomodal size distribution with a mean diameter ranging from 308 to 352 nm. By adjusting the process parameters, the encapsulation efficiency was about 74% with good reproducibility. Primidone release from the nanocapsules was found to be slower as compared to the oily control solution despite an important burst-effect. The release profile was not influenced by the pH of the release medium.
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A new simple extraction method, e.g., for subsequent quantitative determination of some antiepileptic drugs by GLC is described. HCl and an internal standard are added to 100 microliter of plasma or any biological fluid. This mixture is applied directly to an Extrelut column. Lipophilic substances (i.e. the antiepileptic drugs diphenylhydantoin, primidone and phenobarbital) are then extracted into 20 ml of ether and the solvent is evaporated to dryness. Direct GLC analysis of the on-column methylated drugs is performed using a P-N-detector.
We report a 15-year-old female with stimulus-induced drop episodes occurring many times a day that resulted in failure to perform her daily activities. Because her SIDEs were misdiagnosed as atonic seizures, she was treated with several antiepileptic drugs, including valproic acid, levetiracetam, lamotrigine, primidone, carbamazepine, and clobazam.
An enzyme multiplied immunoassay technique is compared with a gas-liquid chromatographic technique for the measurement in blood serum of the anticonvulsants phenytoin, carbamazepine, phenobarbitone, primidone, and ethosuximide. The correlation between results obtained by each method was excellent, and both systematic and random errors were well within acceptable limits.
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A review of 50 adult epileptics who had taken anticonvulsant drugs for 10 or more years showed a decrease in the concentration of serum phosphate and calcium and an increase in the activity of alkaline phosphatase in 22% of the patients. Plasma albumin and gamma-globulin levels were higher than in control subjects. All the patients lived at home and the dietary intake of calcium and vitamin D was often borderline normal or low. Six patients were submitted to bone biopsy and of these, 4 showed histological osteomalacia. Gastrointestinal disease did not appear to be a significant factor. None of the patients had symptoms or signs attributable to osteomalacia which does not seem to be of serious significance. All the patients were taking at least two drugs and it was not possible to assess the relative importance of the various drugs. A prospective study is needed. Measurements of serum calcium, phosphorus, and alkaline phosphatase should be performed at intervals on patients who are receiving anticonvulsant therapy. Treatment with calciferol may be indicated.
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A few reports have shown elevated fasting total plasma homocysteine (tHcy) in patients taking antiepileptic drugs (AEDs). In this study we determined the influence of AEDs on plasma tHcy levels prior to and following methionine loading.