Typical absences are brief (seconds) generalised seizures of sudden onset and termination. They have 2 essential components: clinically, the impairment of consciousness (absence) and, generalised 3 to 4Hz spike/polyspike and slow wave discharges on electroencephalogram (EEG). They differ fundamentally from other seizures and are pharmacologically unique. Their clinical and EEG manifestations are syndrome-related. Impairment of consciousness may be severe, moderate, mild or inconspicuous. This is often associated with motor manifestations, automatisms and autonomic disturbances. Clonic, tonic and atonic components alone or in combination are motor symptoms; myoclonia, mainly of facial muscles, is the most common. The ictal EEG discharge may be consistently brief (2 to 5 seconds) or long (15 to 30 seconds), continuous or fragmented, with single or multiple spikes associated with the slow wave. The intradischarge frequency may be constant or may vary (2.5 to 5Hz). Typical absences are easily precipitated by hyperventilation in about 90% of untreated patients. They are usually spontaneous, but can be triggered by photic, pattern, video games stimuli, and mental or emotional factors. Typical absences usually start in childhood or adolescence. They occur in around 10 to 15% of adults with epilepsies, often combined with other generalised seizures. They may remit with age or be lifelong. Syndromic diagnosis is important for treatment strategies and prognosis. Absences may be severe and the only seizure type, as in childhood absence epilepsy. They may predominate in other syndromes or be mild and nonpredominant in syndromes such as juvenile myoclonic epilepsy where myoclonic jerks and generalised tonic clonic seizures are the main concern. Typical absence status epilepticus occurs in about 30% of patients and is more common in certain syndromes, e.g. idiopathic generalised epilepsy with perioral myoclonia or phantom absences. Typical absence seizures are often easy to diagnose and treat. Valproic acid, ethosuximide and lamotrigine, alone or in combination, are first-line therapy. Valproic acid controls absences in 75% of patients and also GTCS (70%) and myoclonic jerks (75%); however, it may be undesirable for some women. Similarly, lamotrigine may control absences and GTCS in possibly 50 to 60% of patients, but may worsen myoclonic jerks; skin rashes are common. Ethosuximide controls 70% of absences, but it is unsuitable as monotherapy if other generalised seizures coexist. A combination of any of these 3 drugs may be needed for resistant cases. Low dosages of lamotrigine added to valproic acid may have a dramatic beneficial effect. Clonazepam, particularly in absences with myoclonic components, and acetazolamide may be useful adjunctive drugs.

Treatment of typical absence seizures and related epileptic syndromes.

Ischaemic stroke is the leading cause of severe long-term disability yet lacks drug therapies that promote the repair phase of recovery. This repair phase of stroke occurs days to months after stroke onset and involves brain remapping and plasticity within the peri-infarct zone. Elucidating mechanisms that promote this plasticity is critical for the development of new therapeutics with a broad treatment window. Inhibiting tonic (extrasynaptic) GABA signalling during the repair phase was reported to enhance functional recovery in mice suggesting that GABA plays an important function in modulating brain repair. While tonic GABA appears to suppress brain repair after stroke, less is known about the role of phasic (synaptic) GABA during the repair phase. We observed an increase in postsynaptic phasic GABA signalling in mice within the peri-infarct cortex specific to layer 5; we found increased numbers of α1 receptor subunit-containing GABAergic synapses detected using array tomography, and an associated increased efficacy of spontaneous and miniature inhibitory postsynaptic currents in pyramidal neurons. Furthermore, we demonstrate that enhancing phasic GABA signalling using zolpidem, a Food and Drug Administration (FDA)-approved GABA-positive allosteric modulator, during the repair phase improved behavioural recovery. These data identify potentiation of phasic GABA signalling as a novel therapeutic strategy, indicate zolpidem's potential to improve recovery, and underscore the necessity to distinguish the role of tonic and phasic GABA signalling in stroke recovery.

/pdf/enhanced-phasic-gaba-inhibition-during-the-repair-phase-of-48cmpiggl3.pdf

Enhanced phasic GABA inhibition during the repair phase of stroke: a novel therapeutic target.

Most children with new-onset epilepsy achieve seizure freedom with appropriate antiepileptic drugs (AEDs). However, nearly 20 % will continue to have seizures despite AEDs, as either monotherapy or in combination. Despite the growing market of new molecules over the last 20 years, the proportion of drug-resistant epilepsies has not changed. In this review, we report the evidence of efficacy and safety based on phase III randomized controlled clinical trials (RCTs) of AEDs currently used in the paediatric population. We conducted a literature search using the PubMed database and the Cochrane Database of Systematic Reviews. We also analysed the RCTs of newer AEDs whose efficacy in adolescents and adults might suggest possible use in children. Most of the phase III trials on AEDs in children have major methodological limitations that considerably limit meaningful conclusions about comparative efficacy between old and new molecules. Since the efficacy of new drugs has only been reported versus placebo, the commonly held opinion that new and newer AEDs have a better safety profile than old ones does not appear to be supported by evidence. Despite limited solid evidence, pharmacological management has improved over the years as a consequence of increased awareness of some degree of specificity of treatment in relation to different epilepsy syndromes and attention to adverse events. Future research should be directed taking these factors, as well as the diversity of epilepsy, into consideration.

/pdf/antiepileptic-drug-treatment-in-children-with-epilepsy-2a2lla6c2l.pdf

Antiepileptic Drug Treatment in Children with Epilepsy

Several factors characterize the current medical treatment of epilepsy during childhood. Children do not present the same types of seizures or epilepsies as adults, and certain epilepsy syndromes are seen only during childhood. Accordingly, the choice of antiepileptic drugs (AEDs) may differ in children. In addition, certain medical therapies, such as ACTH or pyridoxine, are used only in children. It is also common practice to prescribe AEDs in children for indications that are "off-label," such as the treatment of partial-onset seizures with carbamazepine before the age of 6 years. The natural history of epilepsy and the risk for seizure recurrence may be different in the pediatric age range, and this may influence the decision to institute chronic prophylactic therapy in children. Similar considerations may apply to the decision to discontinue AED therapy. The pharmacokinetics of several AEDs are age-dependent, and dosages are more variable among patients. The adverse effects of AEDs may be age-dependent, and the pattern of exacerbation of certain seizures by AEDs may be different in children. In addition, several new AEDs are now available, or are about to be released, and the preferential sequence of AEDs of choice in children with epilepsy will need to be reassessed as experience grows and as the results of comparative studies become available.

Antiepileptic drugs in pediatric practice.

Nanoparticle Formulation Improves the Anticonvulsant Effect of Clonazepam on the Pentylenetetrazole-Induced Seizures: Behavior and Electroencephalogram

• In a controlled clinical investigation based on ten patients with simple absences and ten patients with myoclonic atonic seizures, all patients who had insufficient response to conventional antiepileptic treatment received clonazepam (Rivotril [Denmark]; Clonopin, comparable US product) combined with previous antiepileptic drugs The effects of the combined use of clonazepam and the previous antiepileptic drugs were compared with the effects of placebo combined with the same drugs The trial was single-blind crossover with sequential analysis In a daily dose of usually 3 to 6 mg, depending on patient age, the antiepileptic effect of clonazepam was significantly superior to placebo and was estimated as remarkably good Side-effects of somnolence, fatigue, drowsiness, and coordination disturbances occurred in most of the patients, but subsided spontaneously or could be controlled by slow increase or slight reduction of dosage Mental sideeffects such as agitation, confusion, and aggressiveness were more troublesome and caused discontinuation of clonazepam in two patients

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=NEUR&articleId=574463&pdfFileName=archneur_33_5_002.pdf

Clonazepam in the Treatment of Epilepsy: A Controlled Clinical Trial in Simple Absences, Bilateral Massive Epileptic Myoclonus, and Atonic Seizures

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Clonazepam in the Treatment of Epilepsy: A Controlled Clinical Trial in Simple Absences, Bilateral Massive Epileptic Myoclonus, and Atonic Seizures