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1.
Ann Intensive Care ; 13(1): 85, 2023 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-37712992

RESUMO

BACKGROUND: Acute symptomatic epileptic seizures are frequently seen in neurocritical care. To prevent subsequent unprovoked seizures, long-term treatments with antiseizure medications are often initiated although supporting evidence is lacking. This study aimed at prospectively assessing the risk of unprovoked seizure relapse with respect to the use of antiseizure medications. It was hypothesized that after a first acute symptomatic seizure of structural etiology, the cumulative 12-month risk of unprovoked seizure relapse is ≤ 25%. METHODS: Inclusion criteria were age ≥ 18 and acute symptomatic first-ever epileptic seizure; patients with status epilepticus were excluded. Using telephone and mail interviews, participants were followed for 12 months after the acute symptomatic first seizure. Primary endpoint was the occurrence and timing of a first unprovoked seizure relapse. In addition, neuro-intensivists in Germany were interviewed about their antiseizure treatment strategies through an anonymous online survey. RESULTS: Eleven of 122 participants with structural etiology had an unprovoked seizure relapse, resulting in a cumulative 12-month risk of 10.7% (95%CI, 4.7%-16.7%). None of 19 participants with a non-structural etiology had a subsequent unprovoked seizure. Compared to structural etiology alone, combined infectious and structural etiology was independently associated with unprovoked seizure relapse (OR 11.1; 95%CI, 1.8-69.7). Median duration of antiseizure treatment was 3.4 months (IQR 0-9.3). Seven out of 11 participants had their unprovoked seizure relapse while taking antiseizure medication; longer treatment durations were not associated with decreased risk of unprovoked seizure relapse. Following the non-representative online survey, most neuro-intensivists consider 3 months or less of antiseizure medication to be adequate. CONCLUSIONS: Even in case of structural etiology, acute symptomatic seizures bear a low risk of subsequent unprovoked seizures. There is still no evidence favoring long-term treatments with antiseizure medications. Hence, individual constellations with an increased risk of unprovoked seizure relapse should be identified, such as central nervous system infections causing structural brain damage. However, in the absence of high-risk features, antiseizure medications should be discontinued early to avoid overtreatment.

2.
Epilepsy Behav ; 14(2): 429-31, 2009 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-19130901

RESUMO

Treatment of status epilepticus usually requires intravenous anticonvulsant therapy. Lacosamide is a novel anticonvulsant drug that is available as infusion solution. We describe a patient with nonconvulsive status epilepticus who was successfully treated with intravenous lacosamide.


Assuntos
Acetamidas/administração & dosagem , Anticonvulsivantes/administração & dosagem , Estado Epiléptico/tratamento farmacológico , Adulto , Eletroencefalografia , Feminino , Humanos , Injeções Intravenosas/métodos , Lacosamida , Resultado do Tratamento
3.
Seizure ; 23(2): 151-4, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24295895

RESUMO

PURPOSE: Oxcarbazepine (OXC) is an effective anticonvulsant used for treatment of partial and secondarily generalized seizures. However, there is almost no data regarding its effectiveness and tolerability when used for treatment of status epilepticus (SE). METHODS: We retrospectively identified all patients who received OXC for treatment of SE in our hospital between July 2008 and December 2010 in our hospital and analyzed all available data. RESULTS: We identified 13 patients (median age 79 years) who were treated with OXC for refractory SE after failure of first- and second-line therapy in our institution. In the majority of patients, etiology was remote symptomatic (10/13), and semiology was nonconvulsive (10/13). OXC was initiated as third or later agent in almost all patients after median latency of 81 h with a median maximum daily dose of 1800 mg. OXC was the last drug before SE cessation in 8/13 patients. Relevant hyponatriemia <125 mmol/l was seen in 3 patients. CONCLUSION: OXC may be an effective alternative in refractory SE, but patients need to be monitored closely for hyponatriemia. PRACTICE IMPLICATIONS: OXC could be used for refractory SE under close electrolyte monitoring when standard agents fail or are unsuitable.


Assuntos
Anticonvulsivantes/uso terapêutico , Carbamazepina/análogos & derivados , Estado Epiléptico/tratamento farmacológico , Idoso , Idoso de 80 Anos ou mais , Anticonvulsivantes/efeitos adversos , Carbamazepina/efeitos adversos , Carbamazepina/uso terapêutico , Epilepsia/complicações , Feminino , Humanos , Hiponatremia/etiologia , Masculino , Pessoa de Meia-Idade , Oxcarbazepina , Estudos Retrospectivos , Estado Epiléptico/etiologia , Fatores de Tempo , Resultado do Tratamento
4.
J Neurol ; 256(10): 1634-42, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19458986

RESUMO

There are established drugs for the treatment of status epilepticus (SE) but their potentially hazardous side-effects are well known. Levetiracetam (LEV) is a novel anticonvulsant available for intravenous (i.v.) application. It could be an alternative when standard drugs fail or should be avoided. We retrospectively identified patients from two German teaching hospitals who were treated with LEV i.v. for SE. Their charts were reviewed regarding sociodemographic data, type, etiology, onset and duration of SE, dose of LEV, concurrent antiepileptic drugs (AED) treatment, tolerability, and outcome. Thirty-two patients (15 female) were found who were treated with i.v. LEV for SE (median age 71 years). Two patients were exclusively treated with LEV. Eight received a low and further 20 patients a high dose of benzodiazepines before LEV. Two patients were treated with LEV to enable discontinuation of narcosis. SE was generalized convulsive in five, nonconvulsive in 20, and simple focal in seven patients. Etiology was acute 13 times and remote symptomatic 16 times; three SE were of unknown etiology. Therapy was initiated within a median time of 3 h and LEV i.v. was applied within a median time of 6 h. Median LEV bolus was 2,000 mg; median total dose on day 1 was 3,500 mg. Benzodiazepines plus i.v. LEV terminated SE in 23 patients without application of additional anticonvulsants, 10 within 30 min. LEV could not terminate SE in seven patients. We documented nausea and emesis in one and elevation of liver enzymes in another patient that were likely to be attributed to LEV. LEV i.v. seems to be safe with relevant efficiency for the treatment of SE in elderly and multimorbid patients when comorbidity and respiratory insufficiency precludes high doses of benzodiazepines or phenytoin.


Assuntos
Anticonvulsivantes/uso terapêutico , Piracetam/análogos & derivados , Estado Epiléptico/tratamento farmacológico , Adulto , Idoso , Idoso de 80 Anos ou mais , Anticonvulsivantes/administração & dosagem , Anticonvulsivantes/efeitos adversos , Feminino , Humanos , Injeções Intravenosas , Levetiracetam , Masculino , Pessoa de Meia-Idade , Piracetam/administração & dosagem , Piracetam/efeitos adversos , Piracetam/uso terapêutico , Estudos Retrospectivos , Estado Epiléptico/epidemiologia , Estado Epiléptico/etiologia , Fatores de Tempo , Resultado do Tratamento , Adulto Jovem
5.
Anesth Analg ; 99(2): 416-22, table of contents, 2004 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-15271716

RESUMO

Ca-activated Cl currents (I(Cl(Ca))) are used frequently as reporters in functional studies of anesthetic effects on G protein-coupled receptors using Xenopus laevis oocytes. However, because anesthetics affect protein kinase C (PKC), they could indirectly affect I(Cl(Ca)) if this current is regulated by phosphorylation. We therefore studied the effect of modulation of either PKC or protein phosphatases PP1alpha and PP2A on I(Cl(Ca)) stimulated either by lysophosphatidate (LPA) signaling or by microinjection of Ca. X. laevis oocytes were studied under voltage clamp. Rat PP1alpha and PP2A were overexpressed in oocytes. PP, inositoltrisphosphate (IP(3)), the PP inhibitor okadaic acid (OA), the PKC inhibitor chelerythrine, or CaCl(2) were directly injected into the oocyte. Responses to agonists (LPA 10(-6) M, IP(3) 10(-4) M, CaCl(2) 0.5 M) were measured at a holding potential of -70 mV in the presence or absence of the PP inhibitors cantharidin or OA. PP1 alpha and PP2A inhibited I(Cl(Ca)) from 7.6 +/- 0.9 microC to 2.5 +/- 0.9 microC and 3.2 +/- 1.4 microC, respectively. PP inhibition enhanced I(Cl(Ca)) in control oocytes and reversed the inhibitory effect in oocytes expressing PP1 alpha or PP2A. PKC inhibition by chelerythrine enhanced both LPA- and CaCl(2)-induced I(Cl(Ca)). Our data indicate that the Xenopus I(Cl(Ca)) is modulated by phosphorylation. This may complicate design and interpretation of studies of G protein-coupled receptors using this model.


Assuntos
Anestésicos/farmacologia , Cálcio/fisiologia , Canais de Cloreto/efeitos dos fármacos , Canais de Cloreto/fisiologia , Fosfoproteínas Fosfatases/fisiologia , Proteína Quinase C/fisiologia , Algoritmos , Animais , Canais de Cálcio/efeitos dos fármacos , Canais de Cálcio/fisiologia , DNA Complementar/genética , Eletrofisiologia , Inibidores Enzimáticos/farmacologia , Feminino , Inositol 1,4,5-Trifosfato/fisiologia , Receptores de Inositol 1,4,5-Trifosfato , Potenciais da Membrana/efeitos dos fármacos , Oócitos/metabolismo , Técnicas de Patch-Clamp , Fosfoproteínas Fosfatases/antagonistas & inibidores , Fosfoproteínas Fosfatases/biossíntese , Plasmídeos/genética , Proteína Quinase C/antagonistas & inibidores , Proteína Quinase C/biossíntese , Receptores Citoplasmáticos e Nucleares/efeitos dos fármacos , Receptores Citoplasmáticos e Nucleares/fisiologia , Xenopus laevis
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