W. Allen Hauser
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
W. Allen Hauser has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
Torbjorn Tomson
Karolinska Institutet, Stockholm, Sweden
2 shared publications- Arturo Carpio
University of Cuenca
1 shared publication Dale C. Hesdorffer
Department of Epidemiology and Department of Neurology, Columbia University, New York, New York, U.S.A.
1 shared publication- Dale C. Hesdorffer
Gertrude H. Sergievsky Center and Department of Epidemiology, Columbia University, New York, NY 10032, USA
1 shared publication Dale Hesdorffer
G.H. Sergievsky Center, New York, NY
1 shared publicationElias Olafsson
G.H. Sergievsky Center, New York, NY
1 shared publication
Latest Publications
- Top Cited Papers
Recommendation for a definition of acute symptomatic seizure
Summary: 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.
Top Cited PapersRecommendation for a definition of acute symptomatic seizure
Summary: 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.
- 1 July 2007
- Published by Elsevier in Epilepsy Research
- Vol. 75 (2-3) , 220-223
Co-occurrence of major depression or suicide attempt with migraine with aura and risk for unprovoked seizure
- 1 July 2007
- Published by Elsevier in Epilepsy Research
- Vol. 75 (2-3) , 220-223
Co-occurrence of major depression or suicide attempt with migraine with aura and risk for unprovoked seizure
- 22 December 2005
- Published by Wiley in Annals of Neurology
- Vol. 59 (1) , 210-213
Migraine with aura is a risk factor for unprovoked seizures in children
Objective: Migraine is associated with epilepsy, but the time order and nature of the relationship are unclear. We conducted a population based case control study to clarify the time order to determine whether migraine is a risk factor for epilepsy.Methods: Migraine symptoms were evaluated in a population‐based case–control study of all incident epilepsy in Icelandic children and in matched controls (next two same sex births in the country).Results: Migraine was associated with a fourfold increased risk for developing epilepsy, an association explained by migraine with aura (odds ratio, 8.1; 95% confidence interval, 2.7–24.3). Migraine without aura did not increase risk for epilepsy.Interpretation: Children with migraine with aura have a substantial increased risk to develop subsequent epilepsy. This finding is consistent with the hypothesis that migraine with aura and migraine without aura may be different disorders. Ann Neurol 2006;59:210–213
- 22 December 2005
- Published by Wiley in Annals of Neurology
- Vol. 59 (1) , 210-213
Migraine with aura is a risk factor for unprovoked seizures in children
Objective: Migraine is associated with epilepsy, but the time order and nature of the relationship are unclear. We conducted a population based case control study to clarify the time order to determine whether migraine is a risk factor for epilepsy.Methods: Migraine symptoms were evaluated in a population‐based case–control study of all incident epilepsy in Icelandic children and in matched controls (next two same sex births in the country).Results: Migraine was associated with a fourfold increased risk for developing epilepsy, an association explained by migraine with aura (odds ratio, 8.1; 95% confidence interval, 2.7–24.3). Migraine without aura did not increase risk for epilepsy.Interpretation: Children with migraine with aura have a substantial increased risk to develop subsequent epilepsy. This finding is consistent with the hypothesis that migraine with aura and migraine without aura may be different disorders. Ann Neurol 2006;59:210–213