Secondary late-onset Lennox-Gastaut syndrome: a critical view

From a group of 66 patients with the Lennox-Gastaut syndrome, 12 whose manifestations had started after the 6th year of life were selected for study. These patients were observed clinically and electroencephalographically for an average period of 2.5 years. We concluded that the late-onset syndrome...

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Main Authors: Amilton Antunes Barreira, Michel Pierre Lison
Format: Article
Language:English
Published: Academia Brasileira de Neurologia (ABNEURO) 1984-06-01
Series:Arquivos de Neuro-Psiquiatria
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X1984000200001&lng=en&tlng=en
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spelling doaj-858b78025ee844d3bb7c8cdcb254852a2020-11-24T23:46:39ZengAcademia Brasileira de Neurologia (ABNEURO)Arquivos de Neuro-Psiquiatria1678-42271984-06-014229510410.1590/S0004-282X1984000200001S0004-282X1984000200001Secondary late-onset Lennox-Gastaut syndrome: a critical viewAmilton Antunes Barreira0Michel Pierre Lison1Universidade de São PauloUniversidade de São PauloFrom a group of 66 patients with the Lennox-Gastaut syndrome, 12 whose manifestations had started after the 6th year of life were selected for study. These patients were observed clinically and electroencephalographically for an average period of 2.5 years. We concluded that the late-onset syndrome can: occur after a long interval between diffuse encephalopathy and the first clinical manifestations, with or without previous alterations in psychomotor development; be associated from the onset with serious mental retardation; exhibit simple, complex and mixed seizures similar to those observed in the early form. These patients can also: suffer complex and mixed epileptic seizures previously unreported; paroxismal interictal EEG abnormalities that overlap those of the early form; and spike-slow wave complexes in the EEG that can be actived by hyperpnea. Our results demonstrate that the incidence of LGS after 6 years of age does not necessarily imply a lower frequency of organic antecedents, or beter neu-ropsychomotor development up to the onset of the syndrome or the presence of a higher rate of nonspecific seizures (generalized or partial seizures, and mainly those with elaborate symptomatolgy). The critical and encephalographic expression of the syndrome, which is secondary and starts after the 6th year of age, may depend at least in part on the age when diffuse encephalopathy started.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X1984000200001&lng=en&tlng=en
collection DOAJ
language English
format Article
sources DOAJ
author Amilton Antunes Barreira
Michel Pierre Lison
spellingShingle Amilton Antunes Barreira
Michel Pierre Lison
Secondary late-onset Lennox-Gastaut syndrome: a critical view
Arquivos de Neuro-Psiquiatria
author_facet Amilton Antunes Barreira
Michel Pierre Lison
author_sort Amilton Antunes Barreira
title Secondary late-onset Lennox-Gastaut syndrome: a critical view
title_short Secondary late-onset Lennox-Gastaut syndrome: a critical view
title_full Secondary late-onset Lennox-Gastaut syndrome: a critical view
title_fullStr Secondary late-onset Lennox-Gastaut syndrome: a critical view
title_full_unstemmed Secondary late-onset Lennox-Gastaut syndrome: a critical view
title_sort secondary late-onset lennox-gastaut syndrome: a critical view
publisher Academia Brasileira de Neurologia (ABNEURO)
series Arquivos de Neuro-Psiquiatria
issn 1678-4227
publishDate 1984-06-01
description From a group of 66 patients with the Lennox-Gastaut syndrome, 12 whose manifestations had started after the 6th year of life were selected for study. These patients were observed clinically and electroencephalographically for an average period of 2.5 years. We concluded that the late-onset syndrome can: occur after a long interval between diffuse encephalopathy and the first clinical manifestations, with or without previous alterations in psychomotor development; be associated from the onset with serious mental retardation; exhibit simple, complex and mixed seizures similar to those observed in the early form. These patients can also: suffer complex and mixed epileptic seizures previously unreported; paroxismal interictal EEG abnormalities that overlap those of the early form; and spike-slow wave complexes in the EEG that can be actived by hyperpnea. Our results demonstrate that the incidence of LGS after 6 years of age does not necessarily imply a lower frequency of organic antecedents, or beter neu-ropsychomotor development up to the onset of the syndrome or the presence of a higher rate of nonspecific seizures (generalized or partial seizures, and mainly those with elaborate symptomatolgy). The critical and encephalographic expression of the syndrome, which is secondary and starts after the 6th year of age, may depend at least in part on the age when diffuse encephalopathy started.
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X1984000200001&lng=en&tlng=en
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