The medial temporal lobe epilepsy is a bilateral disease – novel aspects

Abstract

SummaryIntroduction.Medial temporal lobe epilepsy (MTLE) is the most frequent form of epilepsy in adulthood. It is classified as local/regional epilepsy. However, there is increasing evidence of the involvement of both temporal lobes and this provides abundant arguments to question this view, and consider MTLE as one of the typical bilateral system epilepsies.Aim.To provide a contemporary review of medial temporal lobe epilepsy, discussing the bilateral aspects, with reference to epilepsy surgery.Methods.A literature review and a resume of the author’s own experiences with MTLE patients.Results.Recent electrophysiological and neuroimaging data provide convincing data supporting that MTLE is a bilateral disease. The uni-and bilateral features form a continuum and the participation rate of the two temporal lobes determine course and surgical perspective of the individual patient.Conclusions.The contradictory data of invasive presurgical evaluations of MTLE patients suggest that there need to identify further indicatory markers of bilaterality and thus change the presurgical evaluation from the non-invasive towards the invasive ways. The mechanisms of the interrelationship between the two temporal lobes in MTLE warrants further research.

Long term sequelae of amygdala enlargement in temporal lobe epilepsy

“…In our study, AE persisted in 25 (73 %), resolved in 6 (18 %), evolved into bilateral HS in 1, bilateral mesial temporal atrophy in 1 and ipsilateral mesial temporal atrophy in 1.Coan et al [9] proposed that AE may be the result of hypertrophy secondary to hypoxic insult and could progress to atrophy and HS later as was seen with Patient 1. Our findings showing progression to bilateral HS reiterate bilaterality of mTLE [23] and that these changes could represent a continuum to HS [24]. The same patient had history of status epilepticus.…”

Biomarkers of Drug Resistance in Temporal Lobe Epilepsy in Adults

“…Experimental and clinical data demonstrate that neuroinflammation and neurodegeneration involved in epileptogenesis make a significant contribution to the development of drug resistance and the chronicity of TLE [ 16 , 17 ]. The mechanism of development of neuroinflammation and neurodegeneration in TLE has been studied in experimental models as well as in clinical samples of biological fluids and tissues of patients [ 17 , 18 , 19 ]. In TLE cases with hippocampal sclerosis (HS), there is a progressive loss of neurons and gliosis in the hippocampus and amygdala, which may be caused by uncontrolled processes of neuroinflammation and neurodegeneration accompanied by disruptions in the blood–brain barrier and damage to brain cells [ 20 ].…”