Inflammatory theory of diseases: What has it got to do with late-onset LGS?

Lennox-Gastaut syndrome (LGS) is the most common epileptic encephalopathy in children presenting between 3 and 5 years of age. It is a complex age-related epilepsy syndrome with multiple possible etiologies such as hypoxic ischemic injuries, genetic syndromes, cerebral cortical malformations, and tumors. The etiology may remain elusive in approximately 25% of the cases.1 Similar to many other childhood epilepsy syndromes, the age at onset can be variable but can be delayed into adulthood. LGS is characterized by multiple seizure types, abnormal EEG characteristics, and cognitive decline. Nonconvulsive status epilepticus, previous diagnosis of West syndrome, earlier age at onset, and a symptomatic etiology are the known independent risk factors for progressive neuropsychological decline. Multiple seizures types, such as tonic-atonic drop attacks, tonic seizures, focal impaired awareness seizures, atypical absences, myoclonic seizures, focal to bilateral tonic-clonic seizures, or generalized seizures, can be encountered. Diffuse generalized slowing, generalized paroxysmal fast activity of 10–20 Hz mainly during non-REM sleep, and slow spike and slow wave (<2.5 Hz) are some of the electroencephalographic hallmarks of this syndrome. Both pediatric and adult epileptologists are well familiar with the diagnostic challenges and delays and medical intractability of LGS. Brain MRI can help clinicians to exclude focal or diffuse structural abnormalities. Genetic/chromosomal DN...
Source: Neurology Clinical Practice - Category: Neurology Authors: Tags: All Neuropsychology/Behavior, All Epilepsy/Seizures, Antiepileptic drugs, EEG Editorial Source Type: research