Febrile seizures and temporal lobe epileptogenesis

• Published in: Epilepsy research Vol. 89; no. 1; pp. 27 - 33
• Main Authors: Scantlebury, Morris H, Heida, James G
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Kidlington Elsevier B.V 01.03.2010; Elsevier
• Subjects: Anticonvulsants. Antiepileptics. Antiparkinson agents; Atypical febrile seizures; Biological and medical sciences; Epilepsy, Temporal Lobe - physiopathology; Focal cortical dysplasia; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Hippocampus - physiopathology; Humans; Immature rat; Inflammatory cytokines; Medical sciences; Mesial temporal lobe epilepsy; Mesial temporal sclerosis; Nervous system (semeiology, syndromes); Neurology; Neurons - physiology; Neuropharmacology; Pharmacology. Drug treatments; Seizures, Febrile - physiopathology; Temporal Lobe - physiopathology; N-methyl d-aspartate; AMPA; Focal cortical dysplasia; MTLE; hyperpolarization-activated cyclic-nucleotide gated channels; GEFS; HS; TLE; FS; MTS; TNF; LPS; P; mesial temporal sclerosis; SRS; Atypical febrile seizures; NMDA; postnatal day; malformations of cortical development; interleukin; PFS; generalizes epilepsy and febrile seizures; temporal lobe epilepsy; IL; Inflammatory cytokines; methlyazoxymethanolacetate; spontaneous recurrent seizures; prolonged febrile seizures; α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate; mesial temporal lobe epilepsy; MCD; RA; HCN; hyperthermia-induced seizures; tumor necrosis factor; Immature rat; γ-aminobutyric acid; GABA; MAM; lipopolysaccharide; receptor antagonist; febrile seizures; Mesial temporal lobe epilepsy; Mesial temporal sclerosis; Dysplasia; Nervous system diseases; Rat; Rodentia; Complex partial epilepsy; Febrile convulsion; Cerebral disorder; Vertebrata; Mammalia; Animal; Central nervous system disease; Temporal lobe epilepsy; Neurological disorder
• ISSN: 0920-1211; 1872-6844
• DOI: 10.1016/j.eplepsyres.2009.11.002

Summary Febrile seizures (FS) are a common neurological disorder that affects children. Simple FS are thought to be benign but experimental and clinical evidence support that the risk of developing epilepsy after FS increases if the FS are prolonged and the brain is abnormal. In addition, prolonged FS (PFS) have many deleterious long-term effects characterized mainly in the hippocampus but may involve the whole brain and that prompt abortive treatment of PFS may prevent some of the adverse effects. This review focuses on some of the key factors involved in the generation of FS, factors leading to PFS and potential mechanisms and functional correlates leading to temporal lobe epilepsy (TLE).