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PubMed2004

[The therapy of wearing-off].

Wearing-off, predictable end of dose deterioration, is one of the major problems of long-term levodopa treatment for Parkinson's disease. The mechanisms of wearing-off are (1) loss of striatal dopamine storage, (2) change in the peripheral pharmacokinetics of levodopa and (3) modification of dopamine receptors. The main therapeutic strategy for wearing-off is continuous stimulation of dopamine system. For this purpose, we increase frequency of levodopa doses and use long half-life dopamine agonist(continuous stimulation of dopamine receptors), COMT inhibitor and MAOB inhibitor (prolongation of the half-life of levodopa and dopamine), and zonisamide (long-term increase of dopamine synthesis).

Age Factors↗
PubMedDate not supplied

[West syndrome--new therapeutic approach].

West syndrome (WS) is an age dependent epileptic syndrome caused by various brain disorders. WS has been frequently classified in two groups, cryptogenic and symptomatic. As symptomatic WS consists of patients with numerous types of brain lesions, the prognosis and evolutional changes may be different among the types of brain lesions. WS is resistant to treatment to most conventional antiepileptic drugs, and only valproic acid, benzodiazepines, adrenocorticotropic hormone (ACTH), corticosteroids and vigabatrin have been found efficacious. Benzodiazepine, notably nitrazepam, and less clonazepam had been effective in bringing spasms under control but emerging tolerance and significant side effects (hypotonia and drowsiness) precluded its wider use. ACTH has been the treatment of choice for infantile spasms ever since Sorel and Dusaucy-Bouloye described its effectiveness in 1958. Despite the empirical approach steroids were capable of controlling the spasms and normalizing EEG in about 60% of cases. Corticotropin (ACTH) was used in doses from 5 to 180 I.U. daily, prednizolone 2-10 mg/kg daily, hydrocortisone 5-10 mg/kg daily and dexamethason 0.3-0.5 mg/kg. However, poor consensus was defined regarding the best steroid molecule to use, the dosage, and the duration of treatment. Also frequent and sometimes serious side effects have occurred during ACTH therapy, notably serious infections and hypertension that promoted continuous search for alternative and safer drugs tolerated outpatient treatment, good tolerance and minor side effects. Recently a specific visual field loss has been reported in treated adults that raised concern about safety of vigabatrin. New reports in children claim that vigabatrin treatment of children and adolescents has a lower risk for visual field defect than in adults, because of reported reversibility. Vigabatrin paediatric advisory group recommend the trial of vigabatrin for 12-14 days as first treatment for WS and in the case of good clinical response continuation of therapy for six months. Other new antiepileptic drugs (lamotrigine, topiramate, felbamate and zonisamide) have shown significant efficacy in the treatment of resistant WS to previous medication. The current task is to determine risk/benefit ratios of these two drugs (vigabatine, ACTH) and to delineate the group of patients with WS where their use would be optimal.

Humans↗
PubMed2004

[Treatment guidelines for adult epilepsy].

We reviewed the treatment strategies and choices of drugs for adult patients with epilepsy. As evidence from controlled studies for the older drugs is scarcely available from the literature, we added a clinical study performed in our hospital and an expert consensus study. Published randomized clinical studies revealed carbamazepine (CBZ) to be the treatment of choice, but provided little evidence for the differences in efficacy between phenytoin (PHT), valproate (VPA), phenobarbital (PB) and zonisamide (ZNS). The clinical study in our patients with intractable localization-related epilepsy indicated the superior efficacy of CBZ and PHT over VPA or ZNS. Sixty-nine experts converged on the opinion that monotherapy should be started with VPA for seizures of both idiopathic and symptomatic generalized epilepsy, and with CBZ for seizures of localization-related epilepsy. When the trials with 2-3 monotherapy failed, surgery should be considered for localization-related epilepsy. We proposed practical guidelines for treatment of patients with adult epilepsy, including rehabilitation and care for improvement of quality of life.

Adult↗
PubMed2005

[Clinical efficacy of shortened ACTH therapy --an individualized method for minimization of adverse effects--Part 1. The short-term outcome].

To minimize adverse effects and to get good efficacy of ACTH therapy against West syndrome, we tried a new 2-steps therapeutic protocol consisting of the shortened ACTH therapy and the additional ACTH therapy. In a prospective multi-institutional study, 20 patients with newly diagnosed West syndrome who had failed to respond to high-dose vitamin B6 and zonisamide were treated by this shortened ACTH therapy. Synthetic corticotropin (ACTH-Z 0.025 mg/kg/dose, max 0.25 mg) was administrated intramuscularly seven times on every other day for 14 days. At 1 month after discontinuing corticotropin, spasms and hypsarrhythmia disappeared in 10/20 (50%) and 13/17 (59%) patients respectively. Subsequently, 9 out of the 10 patients with persistent spasms received additional therapy for 1 or 2 weeks with daily intramuscular ACTH-Z, which was tapered off over a few weeks. Including the additional ACTH therapy, the disappearance of spasms and hypsarrhythmia were found in 13 patients (65%) and 13 patients (76%). Adverse effects during the shortened ACTH therapy were fewer than additional ACTH therapy but not statistically significant. Severe adverse effects were not observed in both ACTH therapy. In the 2-steps therapeutic protocol according to the response to ACTH, favorable results were obtained in seizure control, EEG findings and the degree of adverse effects.

Adrenocorticotropic Hormone↗
PubMed2005

New antiepileptic drugs--an overview.

The last ten years of the 20th century is called in neuroscience "decade of the brain". This period has brought many new antiepileptic drugs (AEDs) to the practising physician. New AEDs include: vigabatrin, lamotrigine, topiramate, tiagabine, gabapentin, oxcarbazepine, levetiracetam and zonisamide (not registered in Poland). The development of these drugs was under the current epilepsy theory (balance-disturbances between inhibitory and excitatory neurotransmitters in the brain). Mechanism of action of the new AEDs is due to increase of the GABA-system activity and/or reaction with ion-channels events in neurons. The aim of the study was an overview of the current literature on the new AEDs in the treatment of seizures and epileptic syndromes. Data from literature show that the new AEDs are better tolerated, have fewer drug interactions and seem to affect cognitive functions to a lesser degree compared to the conventional drugs. Most of them are recommended to an add-on therapy of partial seizures with/without second generalization, although there are more evidences on efficacy of new AEDs in monotherapy. The new AEDs seemed to be similar to the conventional drugs in efficacy, but superior in tolerability. New AEDs with more selective activity and lower toxicity have been significant improved the quality of life in the epileptic patients. Numerous chemical compounds with potential antiepileptic activity are in experimental and clinical development.

Anticonvulsants↗
PubMed2005

[Subacute encephalitis with anti-glutamate receptor antibodies presented with epilepsia partialis continua].

A previously healthy 32-year-old man visited our clinic with a 5-week history of involuntary movement. Examination demonstrated continuous myoclonic jerks in the left elbow. Two days later, he developed generalized convulsion. Electroencephalography demonstrated small spikes over the right central region. Thus, we made a diagnosis of epilepsia partialis continua (EPC) with a secondary generalization. On admission, serum electrolytes, glucose and ceruloplasmin levels, and amino acid analysis were unremarkable. HIV serology was negative. Anticardiolipin, anti-MPO ANCA, and anti-Hu antibodies were negative. The cerebrospinal fluid (CSF) showed 151/microl lymphocytes and 23/microl polymorphs, 70 mg/dl of glucose, and 61 mg/dl of protein. Autoantibodies against the glutamate receptor subunits epsilon-2 and delta-2 were detected in the serum and CSF. Cranial MRI was unremarkable. Treatment with acyclovir and high-dose methylprednisolone failed to halt the jerks. Two weeks after admission, he developed status epilepticus, which necessitated general anesthesia. Intravenous immunoglobulin infusion gave no beneficial effects. Two months after the onset of the status epilepticus, his convulsions were controlled with zonisamide, clobazam, and carbamazepine. While he had no motor dysfunctions, he had loss of spontaneity and memory impairment. This report suggests that EPC might be the initial symptom of subacute encephalitis with a possible autoimmune mechanism.

Adult↗
PubMed2005

Drug-induced weight gain.

Drug-induced weight gain is a serious side effect of many commonly used drugs leading to noncompliance with therapy and to exacerbation of comorbid conditions related to obesity. Improved glycemic control achieved by insulin, insulin secretagogues or thiazolidinedione therapy is generally accompanied by weight gain. It is a problematic side effect of therapy due to the known deleterious effect of weight gain on glucose control, increased blood pressure and worsening lipid profile. Weight gain may be lessened or prevented by adherence to diet and exercise or combination therapy with metformin. Weight gain is also common in psychotropic therapy. The atypical antipsychotic drugs (clozapine, olanzepine, risperidone and quetiapine) are known to cause marked weight gain. Antidepressants such as amitriptyline, mirtazapine and some serotonin reuptake inhibitors (SSRIs) also may promote appreciable weight gain that cannot be explained solely by improvement in depressive symptoms. The same phenomenon is observed with mood stabilizers such as lithium, valproic acid and carbamazepine. Antiepileptic drugs (AEDs) that promote weight gain include valproate, carbamazepine and gabapentin. Lamotrigine is an AED that is weight-neutral, while topiramate and zonisamide may induce weight loss.

Anticonvulsants↗
PubMed2004

Treatment of refractory primary generalized epilepsy.

Although complete seizure control is achievable in 54% to 82% of patients with primary (idiopathic) generalized epilepsy syndromes, there remains a substantial group with inadequate control. Valproate has been considered the drug of choice but is not always effective and might produce unacceptable adverse effects. Several newer drugs have emerged as potential alternatives to valproate, including lamotrigine, levetiracetam, topiramate, and zonisamide. Sedation and tolerance limit the utility of benzodiazepines. For severely refractory patients, drug combinations, vagal nerve stimulation, or felbamate might be considered. Only a few controlled clinical trials have been conducted for these syndromes; more are needed.

Adolescent↗
PubMedDate not supplied

[Carbamazepine-induced systemic lupus erythematosus--a case report].

Epileptic seizures may be an early symptom of systemic lupus erythematosus, while at the same time some of the epileptic drugs, namely carbamazepine (CBZ), phenytoin (PHT), valproic acid (VPA), ethosuximide (ETM), primidone (PRM), lamotrigine (LTG), zonisamide (ZNS) can cause lupus. A separate clinical problem is the fact that few cases of systemic lupus have as yet been identified by giving antiepileptic drug. We present the case of a 30-year-old woman with frequent simple partial seizures and few secondarily generalized seizures since the age of 18. She was treated with VPA for three years. Then, because of side effects the drug had to be withdrawn and was replaced by CBZ. After eight months duration of the treatment with CBZ, the dose was increased because a secondarily generalized seizure occurred again. After another two months, painful swelling of all joints and leucopenia were observed. During additional studies, LE cells and high titer of ANA antibodies were found. Systemic lupus erythematosus was diagnosed and prednisone therapy was introduced. In spite of the withdrawal of CBZ, the increased titer of ANA antibodies persisted for several years and skin and muscle biopsy performed five years from the onset of clinical symptoms disclosed inflammatory infiltration and presence of IgG and IgM deposits in skin and vessel walls. Control serological examinations, skin and muscle biopsy carried out after eight years of observation and lack of clinical manifestations permitted to exclude a connective tissue disease in our patient.

Adult↗
PubMedDate not supplied

[The interactions of antiepileptic drugs in oncology practice].

AIMS: Antiepileptic drugs, which often have to be used in patients with cancer, can have important effects on the results offered by antineoplastic agents. Here, we review the influence of antiepileptic drugs on antineoplastic agents and the influence of antineoplastic agents on antiepileptic drugs; measures to prevent such interactions are also suggested. DEVELOPMENT: Antiepileptic drugs that induce cytochrome P450, such as carbamazepine, phenytoin and phenobarbital, can reduce the levels and effects of antineoplastics that metabolise by means of this enzyme, for example, taxanes, Vinca alkaloids, methotrexate, teniposide and camptothecin. Furthermore, enzyme-inducing antiepileptic drugs diminish the levels and effects of many other drugs that can be administered to oncology patients, such as other antiepileptic drugs used in polytherapy, narcotic analgesics, antidepressants, antipsychotics or antibiotics. In contrast, valproate can increase the toxicity of etoposide or nitrosoureas. Moreover, antineoplastic agents like cisplatin or corticoids can lower the effectiveness of phenytoin and methotrexate has a similar effect on valproate. In contrast, 5-fluorouracil can increase the toxicity of phenytoin. Pharmacodynamic interactions are also possible. CONCLUSIONS: Information about the clinical consequences of the interactions between antiepileptics and antineoplastic agents is often based on cases or series of cases, but a growing body of evidence from pharmacokinetic studies shows that enzyme-inducing antiepileptics exert an important influence on the effectiveness of the antineoplastic agents. It is therefore recommendable to avoid them and replace them with non-enzyme-inducing antiepileptics, such as gabapentin, lamotrigine, levetiracetam, pregabalin, topiramate or zonisamide. When enzyme-inducing antiepileptics have to be used, it is likely that higher doses of antineoplastic agents or other inducible drugs will have to be utilised.

Anticonvulsants↗
PubMedDate not supplied

Post traumatic epilepsy: a review of scientific evidence.

Post traumatic epilepsy is the development of recurrent seizures following head trauma and has a high clinical relevance. Several risk factors including some genetic factors increase the susceptibility of post traumatic epilepsy. The precise mechanisms of epileptogenesis in post-traumatic epilepsy are still poorly understood. Many structural, physiologic and biochemical changes in the brain may account for epileptogenesis. The reactive oxygen species (ROS), especially *OH and excitotoxicity are primarily involved. Antioxidants, like tocopherol, antiepileptic drug zonisamide, condensed tannins, melatonin, adenosine, trans-resveratrol, and some other agents have been proposed to prevent epileptogenic focus formation. The review also discusses various aspects of post traumatic epilepsy, mechanisms of epileptogenesis, and clinical implications.

Animals↗
PubMed2005

[Current pharmacotherapy of epilepsy in adults].

The availability of new antiepileptic drugs (AEDs) has expanded the spectrum of medical treatment options in epilepsy. However, the development of ten new compounds (vigabatrin, felbamate, gabapentin, lamotrigine, topiramate, tiagabine, oxcarbazepine, levetiracetam, zonisamide, and pregabalin) has not changed the basic principles of epilepsy treatment. The choice of an AED depends upon seizure type or seizure syndrome, efficacy, safety, tolerability, patient age and gender, concomitant medication, and comorbid conditions. In general, most of the newer AEDs are not necessarily more effective but usually better tolerated than the traditional agents mainly because of their favorable pharmacokinetic profiles and fewer drug interactions. Because treatment options have been widened with the introduction of these new compounds, drug therapy can now be tailored to the requirements of the individual patient. Nevertheless, significant safety and efficacy issues continue to exist and there is a strong need for the development of even better agents. This clinical review focuses on current aspects of drug therapy in epilepsy.

Adult↗
PubMed2006

Targets for antiepileptic drugs in the synapse.

Antiepileptic drugs (AEDs) have many proposed mechanisms of action and are still not fully understood. AEDs are widely used today to treat epilepsy, migraine, neuropathic pain, and bipolar disorder, and other disorders are also being investigated. The focus in this review is the main targets for AEDs in the GABAergic and glutamatergic synapses and possible future sites of action for AEDs to clarify their wide spectrum of activity. The study is a review of recently published investigations of the mechanisms of action of AEDs. The main targets for AEDs in the synapses include enhancement of GABAergic inhibitory neurotransmission, decrease in glutamatergic excitatory neurotransmission directly or via inhibition of voltage-dependent sodium and calcium channels, and interference with intracellular signaling pathways. Vigabatrin, tiagabine, and valproate possess their main actions in the GABAergic synapse. Levetiracetam, topiramate, lamotrigine, carbamazepine, oxcarbazepine, gabapentin, pregabalin, felbamate, and zonisamide decrease glutamatergic excitability. In addition, valproate, carbamazepine, and oxcarbazepine modulate intracellular signaling pathways. Several AEDs of a new generation based on the existing drugs are in development. Future targets to decrease excitability may include GABA and glutamate ionotropic and metabotropic receptors and astrocytes. Knowledge of the sites of action of AEDs in the synapse is important to improve our understanding of their broad spectrum of clinical efficacy and to develop future effective drugs for the treatment of both epilepsy and other neurological and psychiatric disorders.

Animals↗
PubMed1993

[A case of carbamazepine-induced lupus with myositis].

This is the report with muscle disorder associated carbamazepine (CBZ)-induced lupus. A 39-year-old female had been treated with CBZ 400 mg per day for 2 years because of complex partial seizure. In November, 1992 laboratory studies showed elevation of serum CK, IgG and titers of antinuclear antibody. Physical examination on admission revealed muscle weakness of neck flexors and iliopsoas but no rash or arthralgia. The electromyography showed myogenic change in the right biceps. CBZ was discontinued and replaced by zonisamide. Prednisolone 40 mg daily was started and the patient steadily improved. In the literature, there have been a few cases with muscle symptoms in CBZ-induced lupus, but muscle involvement with highly elevated CK associated with CBZ-induced lupus has not been reported.

Adult↗
PubMed1996

[A case of adult Reye's syndrome with favorable outcome despite status epilepticus].

A case of adult Reye's syndrome is described. A previously healthy 17-year-old man developed convulsions 2 days after resolution of an upper respiratory infection with parainfluenza virus type 3. During the preceding infection, he took aspirin. On admission, he was drowsy. There was no focal signs. Cranial CT scan was unremarkable. A lumbar puncture revealed an opening pressure of 180 mm H2O; the cerebrospinal fluid was acellular with normal protein level. Serum chemistry showed elevated transaminase activities and normal bilirubin level. Blood ammonia level was high; urea and citrulline levels were abnormally low. These abnormalities disappeared later, suggesting transient cysfunction of mitochondrial urea-cycle enzymes. Free and acyl carnitine levels were unremarkable. Both metabolic acidosis and ketonuria were absent. Thus, a variety of aminoacidurias and organic acidemias are unlikely. All these findings meet diagnostic criteria for Rye's syndrome proposed by the CDC of the USA. Status epilepticus was treated with intravenous infusion of thiamylal sodium. He was treated with hypertonic glucose solution and osmotic diuretic. Three months after the onset of the illness, his convulsions were controlled only with zonisamide, clonazepam, and carbamazepine. He had motor dysfunctions. This case is unique in that a patient with adult Reye's syndrome and status epilepticus favorably recovered.

Adolescent↗
PubMed1996

New antiepileptic drugs.

No fewer than eight new antiepileptic drugs (AEDs) with diverse mechanisms of action have been introduced into clinical practice in the 1990s. Short monographs on lamotrigine, vigabatrin, gabapentin, oxcarbazepine, felbamate, topiramate and vigabatrin have been prepared for this review. Details are provided of mechanisms of action, clinical pharmacokinetics and adverse drug interactions. Each section concentrates on the efficacy, tolerability and practical use of these drugs. The areas where they have potential for superiority over the established AEDs have been highlighted. Specific indications and dosage schedules have been provided. As many of these AEDs have, as yet, limited licences, an attempt has been made to identify ongoing studies and important omissions. Where possible, the eventual place of the new agent in the pharmacological management of epilepsy has been assessed. A more limited summary has been included of zonisamide which, although licensed in Japan, is still regarded as an investigational drug elsewhere. Short discussions of three of the most promising investigational compounds, namely remacemide, losigamone and levetiracetam, complete the picture.

Acetates↗
PubMed1997

[A novel epilepsy animal model (NER)].

A mutant showing convulsive seizures spontaneously in a CJ: Wistar colony was named the Noda epileptic rat (NER). The NER exhibits tonic-clonic convulsion without any external stimuli once every 30 h. However, we succeeded in inducing similar convulsive seizures by applying priming sound stimuli (95 dB, 8 kHz, 30 sec) from 3 weeks of age in all 24 NER examined. When the effects of clinically available antiepileptics were tested on the seizures of such primed NER, the most potent agents were carbamazepine, diazepam, valproate, phenobarbital and trimethadione, while phenytoin and zonisamide showed lower potency. Furthermore, ethosuximide was not effective in inhibiting the seizures. In hippocampal slices of NER with convulsive seizures, repetitive firing accompanied by long-lasting depolarization was observed when a single stimulation was delivered to the mossy fibers in the CA3 pyramidal cell. This depolarization shift was completely blocked with a Ca2+ antagonist (nicardipine 10 nM). The long-lasting hyperpolarization that followed the repetitive firing was also observed with mossy fiber stimulation in the hippocampal CA3 pyramidal cells of the NER. These findings suggest that Ca2+ channel abnormality of the hippocampal CA3 pyramidal cells may be involved in the convulsive seizures.

Animals↗
PubMed1997

[Partial seizures following aseptic meningoencephalitis: an unusual case].

We reported a case of partial seizures following aseptic meningoencephalitis. A 2-year-10-month-old boy was admitted to our hospital because of generalized seizures with fever. He had no history of previous seizures and had been well until 8 days before admission. He had been given a 4th DPT (diphtheria, tetanus toxoid and pertussis) vaccine 9 days before admission, and had developed fever and exanthema on the trunk the following day. Both fever and exanthema recurred repeatedly thereafter. After admission, he suffered from generalized seizures without fever and many kinds of partial seizures with psychiatric symptom. Despite administration of several antiepileptic drugs, these seizures persisted for one and half months, occurring 5 to 18 times a day. Thirty-six days after admission, MRI showed multiple dark areas on T1-weighted images and bright areas on T2-weighted images in the bilateral frontal area. We considered these to be due to cerebral vasculitis associated with aseptic meningitis. The patient's seizures were finally controlled by zonisamide administration. At the same time, fever went down. He has since shown normal development without seizures for 18 months.

Child, Preschool↗