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mesial_temporal_lobe_epilepsy

Mesial temporal lobe epilepsy

The seizures involve sensory changes, for example smelling an unusual odour that is not there, and disturbance of memory.

Mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) is the most common type of focal epilepsy.

Etiology

Pathophysiology

In order to understand the pathophysiology of temporal lobe epilepsy (TLE), and thus to develop new pharmacological treatments, in vivo animal models that present features similar to those seen in TLE patients have been developed during the last four decades. Some of these models are based on the systemic administration of chemoconvulsants to induce an initial precipitating injury (status epilepticus) that is followed by the appearance of recurrent seizures originating from limbic structures.

Kainic acid and pilocarpine models, have been widely employed in basic epilepsy research. Their behavioral, electroencephalographic and neuropathologic features and response of these models to antiepileptic drugs and the impact they might have in developing new treatments are explained in the work of Lévesque et al. 1).


The transition to the ictal stage is accompanied by increasing global synchronization and a more ordered spectral content of the signals, indicated by lower spectral entropy. The interictal connectivity imbalance (lower ipsilateral connectivity) is sustained during the seizure, irrespective of any appreciable imbalance in the spectral entropy of the mesial recordings 2).

Diagnosis

A pilot study demonstrates that seizures in mesial temporal and temporal-plus epilepsies (i.e., temporoperisylvian) can be detected reliably in the anterior thalamic nucleus (ATN). Further studies are needed to validate these findings 3).

Fractional anisotropy asymmetry (FAA) values can be potentially used to identify the seizures of origin of TLE and to help understand the relationship between fiber tracts with the side of seizure origin of TLE 4).

The area of predominant perifocal 18F positron emission tomography hypometabolism and reduced [11C]flumazenil (11C-FMZ) -binding on PET scans is currently considered to contain the epileptogenic zone and corresponds anatomically to the area localizing epileptogenicity in patients with temporal lobe epilepsy (TLE).

Complicactions

Drug resistant epilepsy is a major clinical challenge affecting about 30% of temporal lobe epilepsy (TLE) patients.

The reasons for failure of surgical treatment for mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS) remain unclear.

Treatment

Surgery

see Temporal lobe epilepsy surgery.

Surgical resection is the gold standard treatment for drug-resistant focal epilepsy, including mesial temporal lobe epilepsy (MTLE) and other focal cortical lesions with correlated electrophysiological features.

Surgical approaches for medically refractory mesial temporal lobe epilepsy (MTLE) that previously have been reported include anterior temporal lobectomy (ATL), transcortical selective amygdalohippocampectomy, transsylvian amygdalohippocampectomy, and subtemporal amygdalohippocampectomy.

Each approach has its advantages and potential pitfalls.

Anterior temporal lobectomy

Outcome

After surgery for intractable mesiotemporal lobe epilepsy (mTLE) seizures recur in 30-40%. One predictor for seizure recurrence is the distribution of seizure onset and interictal epileptiform discharges (IED).

Preoperative bilateral ictal foci are a negative predictor for seizure outcome. Contrarily, IED exceeding the affected temporal lobe in the ipsilateral hemisphere or even bilateral IED had favorable seizure outcome if seizure onset is strictly limited to the affected temporal lobe. Reoperation for seizure persistence constitutes a promising therapeutic option 5).


The extent of pre-surgical perifocal PET abnormalities, the extent of their resection, and the extent of non-resected abnormalities were not useful predictors of individual freedom from seizures in patients with TLE 6).

Case series

1)
Lévesque M, Avoli M, Bernard C. Animal Models of temporal Lobe Epilepsy Following Systemic Chemoconvulsant Administration. J Neurosci Methods. 2015 Mar 10. pii: S0165-0270(15)00091-6. doi: 10.1016/j.jneumeth.2015.03.009. [Epub ahead of print] PubMed PMID: 25769270.
2)
Vega-Zelaya L, Pastor J, de Sola RG, Ortega GJ. Disrupted Ipsilateral Network Connectivity in Temporal Lobe Epilepsy. PLoS One. 2015 Oct 21;10(10):e0140859. doi: 10.1371/journal.pone.0140859. eCollection 2015. PubMed PMID: 26489091.
3)
Pizarro D, Ilyas A, Toth E, Romeo A, Riley KO, Esteller R, Vlachos I, Pati S. Automated detection of mesial temporal and temporoperisylvian seizures in the anterior thalamic nucleus. Epilepsy Res. 2018 Jul 23;146:17-20. doi: 10.1016/j.eplepsyres.2018.07.014. [Epub ahead of print] PubMed PMID: 30055392.
4)
Li H, Xue Z, Dulay MF Jr, Verma A, Karmonik C, Grossman RG, Wong ST. Fractional anisotropy asymmetry and the side of seizure origin for partial onset-temporal lobe epilepsy. Comput Med Imaging Graph. 2014 Jul 2. pii: S0895-6111(14)00102-5. doi: 10.1016/j.compmedimag.2014.06.009. [Epub ahead of print] PubMed PMID: 25037096.
5)
Schmeiser B, Zentner J, Steinhoff BJ, Brandt A, Schulze-Bonhage A, Kogias E, Hammen T. The role of presurgical EEG parameters and of reoperation for seizure outcome in temporal lobe epilepsy. Seizure. 2017 Sep 6;51:174-179. doi: 10.1016/j.seizure.2017.08.015. [Epub ahead of print] PubMed PMID: 28888215.
6)
Stanišić M, Coello C, Ivanović J, Egge A, Danfors T, Hald J, Heminghyt E, Mikkelsen MM, Krossnes BK, Pripp AH, Larsson PG. Seizure outcomes in relation to the extent of resection of the perifocal fluorodeoxyglucose and flumazenil PET abnormalities in anteromedial temporal lobectomy. Acta Neurochir (Wien). 2015 Sep 8. [Epub ahead of print] PubMed PMID: 26350516.
mesial_temporal_lobe_epilepsy.txt · Last modified: 2018/08/01 13:01 by administrador