Sodium Valproate: Monotherapy and Polytherapy

Covanis, Athanasios; Gupta, AK; Jeavons, P. M.

doi:10.1111/j.1528-1157.1982.tb05085.x

Cited by 259 publications

(149 citation statements)

References 42 publications

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“…Sodium valproate (VPA), the sodium salt of 1982), which is now recognised as a first line valproic acid, is a broad spectrum anticonvulsant agent for the management of partial and generaldrug (Richens & Ahmed, 1975; al., ized seizures (Callaghan et al, 1985;Turnbull et 1979;Covanis et al, 1982;Callaghan et al, al., 1985). Its branched chain fatty acid structure Correspondence: Dr M. J.…”

Section: Introductionmentioning

confidence: 99%

Effect of sodium valproate on carbamazepine disposition and psychomotor profile in man.

Macphee

Mitchell

Wiseman

et al. 1988

Brit J Clinical Pharma

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1 The effect of sodium valproate (VPA; 500 mg thrice daily for 7 days) and matched placebo on the disposition and psychomotor profile of a single dose of carbamazepine (CBZ; 10 mg kg-1) was studied in eight healthy male subjects using a randomised balanced crossover design.2 VPA alone had no effect on antipyrine clearance, urinary 6p-hydroxycortisol excretion and a battery of psychomotor function tests after 3 days' treatment despite achieving a mean steady-state concentration (90 ± 6 mg 1-1) well within the target range (50-100 mg I-1) for the drug.3 VPA pre-treatment did not alter total CBZ area under the concentration-time curve (AUC 0-59 h) but did prolong CBZ elimination half life by 12% (P < 0.01). AUC 0-59 h for free plasma CBZ was 13% higher (P < 0.02) and half-life of unbound CBZ 16% longer (P < 0.02) during VPA treatment. CBZ-10, 11 epoxide (CBZ-E) levels (52%) and CBZ-E/ CBZ ratios (45%) were both elevated by concurrent VPA (P < 0.05) and free CBZ fraction was increased by 7% (P < 0.02). 4 The sole effect of VPA on the psychomotor profile of CBZ was prolongation of card sorting time (P < 0.05), although CBZ-related side effects were reported as more severe when VPA was also taken (P < 0.01). 5 These data suggest that VPA displaces CBZ from plasma protein binding sites and inhibits the metabolism of both the parent drug and its epoxide. The effect of VPA on the psychomotor profile of a large single dose of CBZ was minimal. 6 Further studies in epileptic patients receiving both these anticonvulsant drugs are warranted to appraise the extent and clinical relevance of their interaction.

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Section: Introductionmentioning

confidence: 99%

Effect of sodium valproate on carbamazepine disposition and psychomotor profile in man.

Macphee

Mitchell

Wiseman

et al. 1988

Brit J Clinical Pharma

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“…However, the controlled evidence for efficacy is mostly for juvenile myoclonic epilepsy [43,44]. Less impressive results are seen in other childhood myoclonic epilepsy syndromes [45]. Why is valproic acid seemingly more effective for cortical-subcortical myoclonus than levetiracetam, while the relative efficacy is reversed for cortical myoclonus?…”

Section: Cortical-subcortical Myoclonus Treatmentmentioning

confidence: 99%

Treatment of Myoclonus

Caviness

2014

Neurotherapeutics

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Myoclonus creates significant disability for patients. This symptom or sign can have many different etiologies, presentations, and pathophysiological mechanisms. A thorough evaluation for the myoclonus etiology is critical for developing a treatment strategy. The best etiological classification scheme is a modified version from that proposed by Marsden et al. in 1982. Clinical neurophysiology, as assessed by electromyography and electroencephalography, can be used to classify the pathophysiology of the myoclonus using a neurophysiology classification scheme. If the etiology of the myoclonus cannot be reversed or treated, then symptomatic treatment of the myoclonus itself may be warranted. Unfortunately, there are few controlled studies for myoclonus treatments. The treatment strategy for the myoclonus is best derived from the neurophysiology classification scheme categories: 1) cortical, 2) cortical-subcortical, 3) subcorticalnonsegmental, 4) segmental, and 5) peripheral. A cortical physiology classification is most common. Levetiracetam is suggested as first-line treatment for cortical myoclonus, but valproic acid and clonazepam are commonly used. Corticalsubcortical myoclonus is the physiology demonstrated by myoclonic seizures, such as in primary epileptic myoclonus (e.g., juvenile myoclonic epilepsy). Valproic acid has demonstrated efficacy in such epileptic syndromes with other medications providing an adjunctive role. Clonazepam is used for subcortical-nonsegmental myoclonus, but other treatments, depending on the syndrome, have been used for this physiological type of myoclonus. Segmental myoclonus is difficult to treat, but clonazepam and botulinum toxin are used. Botulinum toxin is used for focal examples of peripheral myoclonus. Myoclonus treatment is commonly not effective and/or limited by side effects.

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“…En relación al ácido valproico, estudios no controlados describen que se obtiene un control de más del 50% de las crisis en: 55% de pacientes con drop attacks; 25-30% de pacientes con crisis de ausencia atípica y Mioclónicas; y menor tasa de respuesta para las crisis tónicas y tónico-clónicas (25,26). Sus principales efectos adversos son la hepatotoxicidad y la trombocitopenia que puede empeorar con la politerapia.…”

Section: Resultados De Ensayosunclassified

Síndrome de Lennox Gastaut. Aproximación diagnóstica y avances terapéuticos: Fármacos antiepilépticos, Canabidiol y otras alternativas.

Herrera

Burneo²

2018

Rev Neuropsiquiatr

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El Síndrome de Lennox Gastaut es una encefalopatía epiléptica catastrófica de inicio en la infancia con características electro-clínicas definidas de la siguiente manera: 1) presencia de múltiples tipos de crisis epilépticas especialmente tónicas; 2) deterioro cognitivo asociado a cambios conductuales; 3) presencia de complejos punta-onda lenta generalizados en el electroencefalograma (EEG) y paroxismos generalizados de actividad rítmica rápida durante el sueño. Su etiología puede ser estructural o genética (antes denominadas sintomáticas y criptogénicas, respectivamente). El diagnóstico inicial puede ser difícil ya que con frecuencia no se identifican todos los criterios al comienzo del cuadro y el diferencial considera otros síndromes epilépticos de inicio en la infancia, tales como las epilepsias mioclónicas. El tratamiento es muy complejo, se carece de guías definidas de práctica clínica, por lo cual la experiencia de expertos es relevante. Se sugiere inicio de medicación con valproato. Lamotrigina, felbamato, topiramato, rufinamida y clobazam son los fármacos de elección de segunda línea aprobados por la Administración Federal de Alimentos y Drogas de los Estados Unidos. (FDA). El manejo quirúrgico incluye cirugía resectiva y callosotomía total o parcial. Otras alternativas son estimulación del Nervio Vago, dieta cetogénica, estimulación cerebral profunda y el uso médico de cannabis.

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Sodium Valproate: Monotherapy and Polytherapy

Cited by 259 publications

References 42 publications

Effect of sodium valproate on carbamazepine disposition and psychomotor profile in man.

Effect of sodium valproate on carbamazepine disposition and psychomotor profile in man.

Treatment of Myoclonus

Síndrome de Lennox Gastaut. Aproximación diagnóstica y avances terapéuticos: Fármacos antiepilépticos, Canabidiol y otras alternativas.

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