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Beghi E.,Mario Negri Institute for Pharmacological Research | Carpio A.,University of Cuenca | Forsgren L.,Umea University | Hesdorffer D.C.,Columbia University | And 5 more authors.
Epilepsia | Year: 2010

Purpose: To consider the definition of acute symptomatic seizures for epidemiological studies, and to refine the criteria used to distinguish these seizures from unprovoked seizures for specific etiologies. Methods: Systematic review of the literature and of epidemiologic studies. Results: An acute symptomatic seizure is defined as a clinical seizure occurring at the time of a systemic insult or in close temporal association with a documented brain insult. Suggestions are made to define acute symptomatic seizures as those events occurring within 1 week of stroke, traumatic brain injury, anoxic encephalopathy, or intracranial surgery; at first identification of subdural hematoma; at the presence of an active central nervous system (CNS) infection; or during an active phase of multiple sclerosis or other autoimmune diseases. In addition, a diagnosis of acute symptomatic seizure should be made in the presence of severe metabolic derangements (documented within 24 h by specific biochemical or hematologic abnormalities), drug or alcohol intoxication and withdrawal, or exposure to well-defined epileptogenic drugs. Discussion: Acute symptomatic seizures must be distinguished from unprovoked seizures and separately categorized for epidemiologic purposes. These recommendations are based upon the best available data at the time of this report. Systematic studies should be undertaken to better define the associations in question, with special reference to metabolic and toxic insults, for which the time window for the occurrence of an acute symptomatic seizure and the absolute values for toxic and metabolic dysfunction still require a clear identification. © 2009 International League Against Epilepsy.

Azmanov D.N.,University of Western Australia | Zhelyazkova S.,Medical University-Sofia | Dimova P.S.,Medical University-Sofia | Radionova M.,Medical University-Sofia | And 11 more authors.
Epileptic Disorders | Year: 2010

SCN1A mutations account for a large proportion of Dravet syndrome patients, and are reported in other cases of epilepsy, such as some families with genetic epilepsy with febrile seizures plus (GEFS+). While most Dravet syndrome cases are caused by de novo mutations, 5% inherit a mutation from a mildly affected or symptom-free parent. Parental mosaicism has been identified, with documented cases involving truncating mutations or gene rearrangements. We describe a Roma/Gypsy family, where a missense mutation in SCN1A, p.D194N, is transmitted from a mosaic GEFS+ father to a child with Dravet syndrome. Mosaicism may be more common than assumed and should be considered regardless of the nature of the mutation.

Wieling W.,University of Amsterdam | Krediet C.T.P.,University of Amsterdam | Solari D.,Arrhythmologic Center | De Lange F.J.,University of Amsterdam | And 5 more authors.
Journal of Internal Medicine | Year: 2013

The aim of this review is to provide an update of the current knowledge of the physiological mechanisms underlying reflex syncope. Carotid sinus syncope will be used as the classical example of an autonomic reflex with relatively well-established afferent, central and efferent pathways. These pathways, as well as the pathophysiology of carotid sinus hypersensitivity (CSH) and the haemodynamic effects of cardiac standstill and vasodilatation will be discussed. We will demonstrate that continuous recordings of arterial pressure provide a better understanding of the cardiovascular mechanisms mediating arterial hypotension and cerebral hypoperfusion in patients with reflex syncope. Finally we will demonstrate that the current criteria to diagnose CSH are too lenient and that the conventional classification of carotid sinus syncope as cardioinhibitory, mixed and vasodepressor subtypes should be revised because isolated cardioinhibitory CSH (asystole without a fall in arterial pressure) does not occur. Instead, we suggest that all patients with CSH should be thought of as being 'mixed', between cardioinhibition and vasodepression. The proposed stricter set of criteria for CSH should be evaluated in future studies. © 2013 The Association for the Publication of the Journal of Internal Medicine.

Surges R.,University College London | Adjei P.,University College London | Kallis C.,University College London | Kallis C.,London School of Hygiene and Tropical Medicine | And 6 more authors.
Epilepsia | Year: 2010

Purpose: To determine whether abnormal cardiac repolarization and other electrocardiography (ECG) predictors for cardiac mortality occur in epilepsy patients and whether they are associated with an increased risk for sudden unexpected death in epilepsy (SUDEP). Methods: In a matched-pair case-control study, recordings of adult patients with pharmacoresistant focal epilepsies who died from SUDEP and who had previously had presurgical video-EEG (electroencephalography) telemetry were reviewed. Living controls were matched for age, gender, and date of admission for video-EEG telemetry. Periictal heart rate (HR), corrected QT interval (QTc), postictal HR recovery, HR variability, and cardiac rhythm were assessed. QT dispersion was analyzed with 12-lead ECG. Results: A total of 38 patients (19 per group) had 91 recorded seizures. QTc was prolonged above pathologic upper limits in 9 of 89 seizures and 5 of 38 patients. Nine of 34 patients displayed pathologic QT dispersion. Presence of neither pathologic cardiac repolarization nor other ECG features were specifically associated with SUDEP. SUDEP patients were, however, more likely to lack pathologic cerebral magnetic resonance imaging (MRI) findings, less likely to experience antiepileptic drug reduction during telemetry, and had more secondarily generalized tonic-clonic seizures (SGTCS) per year. Discussion: Our study did not reveal a clear-cut ECG predictor for SUDEP. Pathologic cardiac repolarization is not uncommon in adult patients with pharmacoresistant focal epilepsy and could favor occurrence of fatal tachyarrhythmia as one plausible cause for SUDEP. SGTCS are a risk factor for SUDEP, have, as compared to complex-partial seizures, a greater, unfavorable impact on heart activity, and may thereby additionally compromise cardiac function. © 2009 International League Against Epilepsy.

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