Recognition of interictal and ictal discharges on EEG. Focal vs generalized epilepsy.

INTRODUCTION: The differentiation between focal and generalized epilepsies based on clinical and electroencephalographic features is difficult and sometimes confusing. OBJECTIVE: To review the EEG findings in patients with focal epilepsy. METHODS: An extensive literature review was done. We used the following Pubmed and Medline descriptors alone and in different combinations for database searching: focal, partial, epilepsy, electroencephalographic findings, and EEG. Additional filters included review, original articles, and language limited to Spanish and English. Using the above criteria, a total of 69 articles showed the interictal and ictal EEG findings in focal epilepsy. DEVELOPMENT: Focal epileptiform discharges and persistence of focal abnormalities, characterize the interictal EEG findings in focal epilepsies. To distinguish SBS from primary generalized spike waves are required to note: (a) a lead-in time of at least 2 s, (b) the morphology of the focal triggering spikes clearly differ from that of the bisynchronous epileptiform paroxysms, and (c) the morphology of triggering spikes resemble that of other focal spikes from the same region. Focal and Generalized Epilepsy can coexist. Delayed Lateralization on EEG with inconclusive onset and bizarre semiology confusing semiology should not be confused with generalized onset seizures with focal evolution. CONCLUSIONS: A close attention to localization and morphology of epileptiform discharges, the correct interpretation of secondary bilateral synchrony, and provocative maneuvers help to correctly identify the EEG findings leading to diagnose focal epilepsies. The presence of generalized epileptiform activity does not rule out the existence of a focal epilepsy.

Reelin, tau phosphorylation and psychiatric complications in patients with hippocampal sclerosis and structural abnormalities in temporal lobe epilepsy.

INTRODUCTION: Temporal lobe epilepsy (TLE) is the most common adult epileptic syndrome. About 30-70% of those cases have neuropsychiatric complications. More than 10% of patients have TLE because of focal cortical dysplasia (FCD) type IIIa. OBJECTIVES: The objective of this study was to review the evidence of reelin (RELN) deficiency and tau phosphorylation role in the histopathological, neuropsychiatric, and hyperexcitability features in TLE because of dysplasia type IIIa. METHODS: The current literature was reviewed using Cochrane, EMBASE, PROSPERO, MEDLINE, and PubMed from 1995 to July 2018. Articles of interest were reviewed by one investigator (RAM). RESULTS: Reelin deficit is related to an abnormal migration of neurons in dentate gyrus, and its deficit causes dentate gyrus abnormalities, which in turn has been associated with memory deficits in patients with TLE. A decreased in the expression of RELN ribonucleic acid (RNA) was found in patients with TLE and dysplasia type IIIa compared with patients with TLE and isolated hippocampal sclerosis (HS). Reelin might affect the distribution and dynamic instability of microtubules within neurons in the cerebral cortex and their phosphorylation. Amyloid pathology, tauopathy, or phosphorylated tau (p-tau) overexpression has been reported in epileptic human brain and in animal models of epilepsy. CONCLUSION: Reelin deficit may determine an abnormal cortical lamination and dentate gyrus dispersion and might be associated with an abnormal tau phosphorylation. These processes can be associated with an abnormal hyperexcitability, neuropsychiatric complications, and a myriad of typical histopathological features seen in patients with TLE because of dysplasia type IIIa.