Evidence of Enhanced Kindliig and Hippocampal Neuronal Injury in Immature Rats with Neuronal Migration Disorders

Germano, Isabelle M.; Sperber, Ellen F.; Ahuja, Shalini; Moshé, Solomon L.

doi:10.1111/j.1528-1157.1998.tb01322.x

Cited by 67 publications

(40 citation statements)

References 24 publications

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“…19,20 Experimentally, hyperthermia-induced seizures themselves did not lead to spontaneous seizures in an immature rat model, 17,21 which was interpreted as evidence for febrile seizures constituting only one step in a multistage process. 17 The observation that experimentally induced migrational disorders increased the susceptibility to hyperthermia-induced seizures 22 and kindling 23 further substantiated this view. However, in the clinical setting most cases of MTLE show only the preoperative MR signs of hippocampal sclerosis.…”

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confidence: 65%

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Kasper¹,

Stefan²,

Paulus

2003

Annals of Neurology

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The interrelationship of mesial temporal lobe epilepsy (MTLE), hippocampal sclerosis, and febrile convulsions still remains an enigma. Additional microscopical cortical dysplasia or microdysgenesis has been suggested as pre-existent susceptibility factor rendering the affected brain vulnerable to the development of MTLE after initial precipitating injuries such as febrile convulsions. Twenty-four MTLE cases with histopathologically definite hippocampal sclerosis were examined for clearly defined features of microdysgenesis and further signs of neocortical dysplasia. Although unequivocal signs of dysplasia were absent, 29.2% of cases showed cortical neuronal clustering, 25.0% showed perivascular clustering, and 20.8% showed increased white matter neurons. The features of microdysgenesis studied here were not linked with each other and were not related to initial precipitating injuries, positive family history, or any other clinical parameter. Their suggested fundamental role as dysplastic factor within development of hippocampal sclerosis and MTLE is not confirmed.

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confidence: 65%

Microdysgenesis in mesial temporal lobe epilepsy: A clinicopathological study

Kasper¹,

Stefan²,

Paulus

2003

Annals of Neurology

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“…This suggests that a preexisting underlying structural or functional abnormality likely facilitated the development of epilepsy. Similarly, in animal models, Germano et al (43) demonstrated that rats with neuronal migration brain lesions had a lower afterdischarge threshold, and their hippocampi would kindle more quickly than those of the control rats.…”

Section: Discussionmentioning

confidence: 93%

Proton Magnetic Resonance Spectroscopic Imaging Studies in Patients with Newly Diagnosed Partial Epilepsy

Dubeau

Andermann

et al. 2000

Epilepsia

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Summary:Purpose: To assess whether the N-acetyl aspartate (NAA) to creatine ratio (NAA/Cr) is abnormally low at the onset of epilepsy and whether successful treatment of seizures with antiepileptic drugs is sufficient for normalization of NAA/Cr.Patients and Methods: Proton magnetic resonance spectroscopic imaging ('H-MRSI) was used to measure NAA/Cr in temporal lobes of eight patients with newly diagnosed epilepsy before or soon after starting medication. Six patients had follow-up ' H-MRSI examinations 7 months later. Clinical pattern of the seizures and the EEG findings suggested partial seizures in all and TLE in five patients. None of the patients had lesional epilepsy according to magnetic resonance imaging.Results: Initial 'H-MRSI of the temporal lobes showed significantly low NAA/Cr values in five of eight patients. Five of six patients who had follow-up 'H-MRSI were seizure-free after using medication; the remaining patient did not take medication and continued to experience occasional auras. Wilcoxon rank sign comparison of NAA/Cr on initial 'H-MRSI examination and follow-up 'H-MRSIs showed no significant difference (Z = 135, p = 0.893, 2-tailed) for five seizure-free patients.Conclusions: Neuronal dysfunction is present at an early stage of the epileptic process. NAA/Cr recovery in seizure-free patients controlled with antiepileptic drugs is less evident, compared with successful surgical treatment. Thus, absence of seizures is not necessarily coupled with NAAlCr improvement and observed variable response warrants further investigation. Key Words: MRS-Epilepsy-Newly diagnosed epilepsyNeuronal recovery. In brain proton magnetic resonance spectroscopy ('H-MRS), the most intense signal is visible at 2.02 ppm and corresponds to N-acetyl groups, mainly N-acetyl aspartate (NAA) (1). NAA is synthesized in brain mitochondria from acetyl-coenzyme A and aspartate by the enzyme L-aspartate N-acetyltransferase (2-4), and is confined to neurons and neuronal processes of the mature brain (5,6). The NAA signal in the mature brain derives only from the neuronal pool, areas of decreased NAA signal intensity are interpreted as neuronal loss and dysfunction. The assumption of neuronal loss is supported by both experimental (7-12) and clinical observations (13,14). The assumption of neuronal dysfunction is supported by in vivo (15-17) and in vitro (12,18,19) (17) performed proton magnetic resonance spectroscopic imaging ( 'H-MRSI) in 16 patients with symptomatic carotid artery stenosis before and after endarterectomy. They found that metabolic changes seen preoperatively (LNAA, Tiactate) normalized 4 days after endarterectomy. Matthews et al. (18) showed that neurons under stress conditions in vitro express less NAA, and this reverses with optimization of the culture media, reflecting the survival of a population of viable neurons. Bates et al. (19) showed that inhibition of mitochondrial oxygen consumption and ATP synthesis also inhibited NAA production, suggesting that impaired neuronal mitochondria function, if ...

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“…8 In addition, studies on animal models of dysplasia have shown that cortical and heterotopic subcortical structures display excessive excitability, which is manifested as a reduction in seizure threshold both in vivo and in vitro, but not with the occurrence of spontaneous seizures. [9][10][11] None of these models resemble the most clinically epileptogenic forms in humans; however, neuronal heterotopia is the most commonly reported histopathologic abnormality in resected tissue.…”

Section: Developmental Neocortical Lesionsmentioning

confidence: 95%