Portrait of My Father: Frida Kahlo’s Intimate Relation to Epilepsy

European Neurology ◽

10.1159/000516321 ◽

2021 ◽

pp. 1-5

Author(s):

Enrique J. Carrazana

Keyword(s):

Absence Epilepsy ◽

Posttraumatic Epilepsy ◽

Frida Kahlo ◽

Intimate Relation ◽

Juvenile Absence Epilepsy

The painting <i>Portrait of My Father</i> (1951) by the Mexican painter, Frida Kahlo, is discussed by the author within the context of epilepsy and biographical events in the lives of both Frida and her father, the German Mexican photographer Guillermo Kahlo. The biographical accounts of the photographer’s seizures are suggestive of juvenile absence epilepsy but cannot discount the possibility of posttraumatic epilepsy of mesial frontal origin.

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Juvenile Absence Epilepsy Exacerbated by Valproic Acid

Pediatric Neurology ◽

10.1016/j.pediatrneurol.2006.08.011 ◽

2007 ◽

Vol 36 (2) ◽

pp. 121-124 ◽

Cited By ~ 9

Author(s):

Robbie D. Buechler ◽

Jeffrey R. Buchhalter

Keyword(s):

Valproic Acid ◽

Absence Epilepsy ◽

Juvenile Absence Epilepsy

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Juvenile Absence Epilepsy

10.1007/springerreference_188260 ◽

2012 ◽

Keyword(s):

Absence Epilepsy ◽

Juvenile Absence Epilepsy

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Genetic generalized epilepsy

10.1093/med/9780199688395.003.0027 ◽

2016 ◽

Author(s):

Friederike Moeller ◽

Ronit M. Pressler ◽

J. Helen Cross

Keyword(s):

Clinical Presentation ◽

Age Of Onset ◽

Juvenile Myoclonic Epilepsy ◽

Absence Epilepsy ◽

Childhood Absence Epilepsy ◽

Juvenile Absence Epilepsy ◽

Generalized Epilepsy ◽

Treatment Prognosis ◽

Electroencephalogram Eeg ◽

Eeg Features

This chapter provides an overview of generalized epilepsies (GGE), which comprises a group of epilepsy syndromes of presumed genetic origin. They are classified into several syndromes according to their age, depending on clinical manifestation and associated electroencephalogram (EEG) features. The chapter introduces the concept of GGE before addressing different GGE syndromes, describing their clinical presentation, EEG features, treatment, prognosis, and underlying genetics. The following GGE syndromes are discussed in order of their age of onset—myoclonic astatic epilepsy, childhood absence epilepsy, epilepsy with myoclonic absences, eyelid myoclonia with absences, juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic seizures on awakening. This is followed by an overview on pathophysiological mechanisms underlying GGE.

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Clinical and genetic aspects of juvenile absence epilepsy

Journal of Neurology ◽

10.1007/bf00919710 ◽

1994 ◽

Vol 241 (8) ◽

pp. 487-491 ◽

Cited By ~ 21

Author(s):

Tahir Obeid

Keyword(s):

Absence Epilepsy ◽

Juvenile Absence Epilepsy

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Seizure Exacerbation by Antiepileptic Drugs

Epilepsy Currents ◽

10.1111/j.1535-7511.2005.00061.x ◽

2005 ◽

Vol 5 (5) ◽

pp. 192-193 ◽

Cited By ~ 2

Author(s):

Jacqueline A. French

Keyword(s):

Antiepileptic Drugs ◽

De Novo ◽

Focal Epilepsy ◽

Juvenile Myoclonic Epilepsy ◽

Absence Epilepsy ◽

Absence Seizures ◽

Incorrect Diagnosis ◽

Juvenile Absence Epilepsy ◽

Generalized Epilepsy

Worsening of Seizures by Oxcarbazepine in Juvenile Idiopathic Generalized Epilepsies Gelisse P, Genton P, Kuate C, Pesenti A, Baldy-Moulinier M, Crespel A Epilepsia 2004;45:1282–1286 Purpose Several studies have shown that carbamazepine (CBZ) may aggravate idiopathic generalized epilepsy (IGE). Oxcarbazepine (OXC) is a new drug chemically related to CBZ. We report six cases of juvenile IGE with a clear aggravation by OXC. Methods We retrospectively studied all patients with IGE first referred to our epilepsy department between January 2001 and June 2003 and treated with OXC. Results During this period, six patients were identified. All had an aggravation of their epilepsy in both clinical and EEG activities. OXC had been used because of an incorrect diagnosis of focal epilepsy or generalized tonic–clonic seizures (GTCSs) of undetermined origin (no syndromic classification of the epilepsy). Before OXC, only one patient had experienced a worsening of seizures with an inadequate drug (carbamazepine; CBZ). Four had juvenile myoclonic epilepsy, one had juvenile absence epilepsy, and one had IGE that could not be classified into a precise syndrome. OXC (dosage range, 300–1,200 mg/day) was used in monotherapy in all of them except for one patient. Aggravation consisted of a clear aggravation of myoclonic jerks (five cases) or de novo myoclonic jerks (one case). Three patients had exacerbation of absence seizures. One patient had worsened dramatically and had absence status, and one had de novo absences after OXC treatment. The effects of OXC on GTCSs were less dramatic, with no worsening in frequency in three and a slight increase in three. Conclusions OXC can be added to the list of antiepileptic drugs that can exacerbate myoclonic and absence seizures in IGE.

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