Seizure outcome and hippocampal atrophy in familial mesial temporal  lobe epilepsy

Kobayashi, Eliane; Lopes-Cendes, Íscia; Guerreiro, Carlos A. M.; Sousa, Solange Carvalho de; Guerreiro, Marilisa M.; Cendes, Fernando

doi:10.1212/wnl.56.2.166

Cited by 132 publications

(149 citation statements)

References 24 publications

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“…Experimental studies in rats show that hyperthermia stimulates epileptiform activity in hippocampus and that hyperthermia also stimulates seizures in rats, on which neuronal migration defect has been generated. Similar to the results obtained from animal experiments, evidence proving the presence of pre-seizure neuro-developmental hippocampal pathology in some cases with FS and it is asserted that FS occurs as this hippocampal pathology leads to febrile sensitivity [29]. We have applied the hyperthermia model developed by the authors for rats in our study as well [17].…”

Section: Discussionsupporting

confidence: 75%

Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced Seizures

Bican¹

2012

J Clinic Experiment Pathol

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Epidemiological and recent prospective analyses of long Febrile Seizures (FS) support the idea that such seizures can provoke Temporal Lobe Epilepsy (TLE) in some children. Because of the high prevalence of these seizures, if epilepsy was to arise as their direct consequence, this would constitute a significant clinical problem. Animal studies have revealed that exposure of hippocampal neurons to FS early in life, particularly prolonged or frequently repetitive FS, or together with brain malformation, may lead to sustained dysfunction of these cells including long-term memory impairment or epileptogenesis, in spite of the absence of neuronal damage. We established a hyperthermia model of febrile convulsions in young adult rats, and studied the effects of propofol treatment general anesthetic acting via GABA-A receptor on epileptiform activity and the morphological features of medial temporal lobe.We found statistically significant neuronal losses in the CA1, CA3 and dentate gyrus regions of hyperthermiaapplied rats as compared to the control rats. We also observed that propofol administration suppressed epileptic discharges in EEG and prevented clinical seizures behaviors. It took a median of 11 (range, 6-40) minutes for propofol to stop seizures. We conclude that prevention of epilepsy-related damage can be achieved via epileptogenesis-based clinical approaches, and that propofol is an effective agent in the hyperthermia-induced status epilepticus model.

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Section: Discussionsupporting

confidence: 75%

Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced Seizures

Bican¹

2012

J Clinic Experiment Pathol

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“…It is believed that the studies performed using coronal plane MRI have overestimated the actual size of the amygdala. Post-mortem studies have reported that the amygdala volume ranges from 1.1 to 1.6 cm 3 after correction for fixation-related shrinkage, but different (25)(26)(27) volumetric MRI analyses have reported values ranging from 1 to near 4 cm 3 (15,(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28). The accuracy of the volumetric MRI study of the amygdala is influenced by some factors.…”

Section: Discussionmentioning

confidence: 99%

The importance of accurate anatomic assessment for the volumetric analysis of the amygdala

Bonilha

Kobayashi

Cendes

et al. 2005

Braz J Med Biol Res

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There is a wide range of values reported in volumetric studies of the amygdala. The use of single plane thick magnetic resonance imaging (MRI) may prevent the correct visualization of anatomic landmarks and yield imprecise results. To assess whether there is a difference between volumetric analysis of the amygdala performed with single plane MRI 3-mm slices and with multiplanar analysis of MRI 1-mm slices, we studied healthy subjects and patients with temporal lobe epilepsy. We performed manual delineation of the amygdala on T1-weighted inversion recovery, 3-mm coronal slices and manual delineation of the amygdala on three-dimensional volumetric T1-weighted images with 1-mm slice thickness. The data were compared using a dependent t-test. There was a significant difference between the volumes obtained by the coronal planebased measurements and the volumes obtained by three-dimensional analysis (P < 0.001). An incorrect estimate of the amygdala volume may preclude a correct analysis of the biological effects of alterations in amygdala volume. Three-dimensional analysis is preferred because it is based on more extensive anatomical assessment and the results are similar to those obtained in post-mortem studies.

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“…6 Moreover, several family studies have provided some evidence for a genetic predisposition to HS. 7,8 These findings appear to be inconsistent with evidence from twin studies in which 4 monozygous twin pairs were all discordant for TLE and HS.9,10 The findings from twin studies argue against a strong genetic basis for TLE with HS or HS itself. To further clarify this issue, we studied family members of probands that had TLE with HS to search for evidence of HS or more subtle anatomical abnormalities in relatives.…”

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confidence: 87%

Etiology of hippocampal sclerosis

et al. 2013

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Objective: We sought evidence of a hereditary component for hippocampal sclerosis (HS) by determining whether close relatives of probands with temporal lobe epilepsy (TLE) with HS also had asymptomatic HS or subtle variation in hippocampal morphology.Methods: First-degree relatives from 15 families in which probands had TLE with HS and 32 age-and sex-matched controls were included in the study. Left and right hippocampal volumes and T2 relaxometry were measured using 3-tesla MRI.Results: Thirty-two asymptomatic first-degree relatives and 3 relatives with a history of seizures or epilepsy were studied. None of the first-degree relatives had HS on visual analysis and T2 relaxation times were normal, excluding the presence of HS. Mean hippocampal volume was smaller (6.4%) in asymptomatic relatives (2.94 6 0.27 cm 3 , 95% confidence interval 5 2.87-3.01) than in controls (3.14 6 0.22 cm 3 , 95% confidence interval 5 3.09-3.19, p , 0.005); the effect was greater in relatives of probands with a positive family history of epilepsy. The relatives also had more asymmetric hippocampi (asymmetric index 0.92 6 0.05) than controls (0.96 6 0.03, p 5 0.001).Conclusions: Small asymmetric hippocampi in healthy relatives are likely to represent a familial developmental variant that may predispose to the formation of TLE with HS. The underlying histopathology of these small hippocampi is unknown. This observation may provide an imaging marker for future studies seeking susceptibility genes for HS. Neurology Hippocampal sclerosis (HS) is a common pathologic finding in patients with temporal lobe epilepsy (TLE). The etiology of HS is controversial and likely multifactorial. It is widely considered an acquired phenomenon, secondary to postnatal injury such as prolonged febrile seizures (FS). Prospective studies of large cohorts of children with FS have not shown a convincing association, 1-5 although the recent FEBSTAT study suggests that children with prolonged FS may have acute hippocampal injury and an increased frequency of hippocampal developmental change. 6 Moreover, several family studies have provided some evidence for a genetic predisposition to HS. 7,8 These findings appear to be inconsistent with evidence from twin studies in which 4 monozygous twin pairs were all discordant for TLE and HS.9,10 The findings from twin studies argue against a strong genetic basis for TLE with HS or HS itself. To further clarify this issue, we studied family members of probands that had TLE with HS to search for evidence of HS or more subtle anatomical abnormalities in relatives.METHODS Patients and participants. We recruited the families of probands with TLE and HS in which their first-degree relatives lived in proximity to our medical center. Diagnosis of TLE in probands was made based on clinical and electroencephalographic findings. Clinical features such as déjà vu, stereotyped flashbacks of a past event, rising epigastric/visceral sensation, or stereotyped/unpleasant olfactory or gustatory hallucinations at seizure onset were co...

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Seizure outcome and hippocampal atrophy in familial mesial temporal lobe epilepsy

Cited by 132 publications

References 24 publications

Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced Seizures

Effects of Propofol on Epileptiform Activity and Hippocampal Morphology in Febrile Convulsions and Pilocarpine Induced Seizures

The importance of accurate anatomic assessment for the volumetric analysis of the amygdala

Etiology of hippocampal sclerosis

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