Epilepsia
-
Takotsubo cardiomyopathy is characterized by chest pain, dyspnea, electrocardiographic changes resembling an acute coronary syndrome, and transient wall-motion abnormalities without identifiable coronary culprit lesion explaining the wall-motion abnormality. Takotsubo cardiomyopathy occurs frequently after emotional or physical stress. Seizures have been reported as triggers of takotsubo cardiomyopathy. ⋯ Compared with 974 patients reported in takotsubo cardiomyopathy -series, patients with seizure-associated takotsubo cardiomyopathy were younger (61.5 vs. 68.5 years, p < 0.0001), more frequently males (17 vs. 9%, p = 0.004), had less frequent chest pain (6 vs.76%, p < 0.005), more frequent cardiogenic shock (25 vs. 8%, p = 0.003), and more frequent recurrency (14 vs. 3%, p = 0.004). Seizure-associated takotsubo cardiomyopathy manifests frequently as sudden hemodynamic deterioration, which could result in death in the absence of adequate help. Probably some cases of sudden unexpected death in epilepsy are attributable to takotsubo cardiomyopathy.
-
There is significant variability and controversy regarding the interpretation, nomenclature, and clinical implications of many EEG patterns seen in encephalopathic patients. The American Clinical Neurophysiology Society has attempted to create well-defined, objective rules for naming these patterns in order to allow scientific investigation into their significance. ⋯ A perfect system for describing complex wave forms with words will never be perfect; scalp EEG itself has substantial limitations, as intracranial recordings in neurocritical care patients have shown. The latest version of the nomenclature is available at http://www.acns.org.
-
Patients with status epilepticus that proves refractory to anesthetic agents represent a daunting challenge for treating clinicians. Animal data support the neuroprotective action of brain hypothermia, and its efficacy in status epilepticus models. ⋯ Conversely, mild hypothermia has a high-evidence level and is increasingly used in postanoxic encephalopathy, both in newborns and adults. Due to the paucity of available clinical data, prospective studies are needed to assess the value of hypothermia in status epilepticus.
-
Current standard treatment of established status epilepticus after failure of benzodiazepines is intravenous phenytoin/fosphenytoin, phenobarbital, or valproate. Since 2006 two new antiseizure drugs have become available as intravenous formulation: levetiracetam (2006) and lacosamide (2008). ⋯ Future randomized controlled trials are needed to inform clinicians better about the best choice of treatment in established status epilepticus. The experimental evidence as well as the current clinical experience with levetiracetam and lacosamide are summarized in this review.
-
Brain slices incubated with glucose have provided most of our knowledge on cellular, synaptic, and network driven mechanisms. It has been recently suggested that γ-aminobutyric acid (GABA) excites neonatal neurons in conventional glucose-perfused slices but not when ketone bodies metabolites, pyruvate, and/or lactate are added, suggesting that the excitatory actions of GABA are due to energy deprivation when glucose is the sole energy source. In this article, we review the vast number of studies that show that slices are not energy deprived in glucose-containing medium, and that addition of other energy substrates at physiologic concentrations does not alter the excitatory actions of GABA on neonatal neurons. ⋯ In keeping with extensive observations in a wide range of animal species and brain structures, GABA depolarizes immature neurons and the reduction of the intracellular concentration of chloride ([Cl(-)](i)) is a basic property of brain maturation that has been preserved throughout evolution. In addition, this developmental sequence has important clinical implications, notably concerning the higher incidence of seizures early in life and their long-lasting deleterious sequels. Immature neurons have difficulties exporting chloride that accumulates during seizures, leading to permanent increase of [Cl(-)](i) that converts the inhibitory actions of GABA to excitatory and hampers the efficacy of GABA-acting antiepileptic drugs.