What is she best known for?
The fields of study she is best known for:
- Gene
- Mutation
- Internal medicine
Eva Andermann mostly deals with Epilepsy, Genetics, Pathology, Pediatrics and Mutation.
Her Epilepsy research includes elements of Internal medicine, Hippocampus, Central nervous system disease and Electroencephalography.
As part of her studies on Genetics, Eva Andermann often connects relevant subjects like Ataxia.
Her Pathology study incorporates themes from Cortical dysplasia, Perisylvian polymicrogyria, Polymicrogyria and Pachygyria.
Her Pediatrics study combines topics in areas such as Generalized epilepsy with febrile seizures plus, Psychiatry, Myoclonus, Myoclonic epilepsy and Epilepsy syndromes.
The study incorporates disciplines such as Lissencephaly and Bioinformatics in addition to Mutation.
Her most cited work include:
- Intrinsic epileptogenicity of human dysplastic cortex as suggested by corticography and surgical results (614 citations)
- Autosomal dominant nocturnal frontal lobe epilepsy. A distinctive clinical disorder. (417 citations)
- Focal neuronal migration disorders and intractable partial epilepsy: a study of 30 patients. (409 citations)
What are the main themes of her work throughout her whole career to date?
Epilepsy, Genetics, Pediatrics, Pathology and Progressive myoclonus epilepsy are her primary areas of study.
Her Epilepsy study combines topics from a wide range of disciplines, such as Central nervous system disease, Surgery and Electroencephalography.
Her Genetics study which covers Ataxia that intersects with Internal medicine and Endocrinology.
Her research in Pediatrics intersects with topics in Proband, Psychiatry, Age of onset, Alternating hemiplegia of childhood and Neurological disorder.
Her studies in Pathology integrate themes in fields like Cortical dysplasia, Polymicrogyria and Mutation.
Her research integrates issues of Kufs disease and Neuronal ceroid lipofuscinosis in her study of Progressive myoclonus epilepsy.
She most often published in these fields:
- Epilepsy (48.45%)
- Genetics (32.61%)
- Pediatrics (23.60%)
What were the highlights of her more recent work (between 2012-2021)?
- Epilepsy (48.45%)
- Progressive myoclonus epilepsy (18.32%)
- Genetics (32.61%)
In recent papers she was focusing on the following fields of study:
Eva Andermann spends much of her time researching Epilepsy, Progressive myoclonus epilepsy, Genetics, Pediatrics and Pathology.
Her studies deal with areas such as Proband and Bioinformatics as well as Epilepsy.
Her study in Proband is interdisciplinary in nature, drawing from both Temporal lobe, Electroencephalography and Aura.
Her Progressive myoclonus epilepsy research is multidisciplinary, incorporating perspectives in Neuronal ceroid lipofuscinosis, Ataxia and Compound heterozygosity.
Her Pediatrics research incorporates themes from Alternating hemiplegia of childhood, Genetic counseling and Dravet syndrome.
Eva Andermann combines subjects such as Leptomeninges and Polymicrogyria with her study of Pathology.
Between 2012 and 2021, her most popular works were:
- Somatic Mutations in Cerebral Cortical Malformations (242 citations)
- Mutations in DEPDC5 cause familial focal epilepsy with variable foci (215 citations)
- A recurrent de novo mutation in KCNC1 causes progressive myoclonus epilepsy (161 citations)
In her most recent research, the most cited papers focused on:
- Gene
- Mutation
- Internal medicine
Her primary scientific interests are in Epilepsy, Genetics, Exome, Progressive myoclonus epilepsy and Exome sequencing.
Her research on Epilepsy often connects related areas such as Bioinformatics.
The concepts of her Genetics study are interwoven with issues in Generalized epilepsy and Dravet syndrome.
Her Exome research includes themes of Sanger sequencing, Epilepsy syndromes, Genetic variation and Comorbidity.
Her study looks at the relationship between Progressive myoclonus epilepsy and topics such as Ataxia, which overlap with Cognitive decline and Corpus callosum.
Her study on Exome sequencing also encompasses disciplines like
- Neuronal ceroid lipofuscinosis which connect with Parkinsonism and Compound heterozygosity,
- Missense mutation which intersects with area such as Point mutation and PRNP.
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