Neuropathologic Study of Resected Cerebral Tissue from Patients with Infantile Spasms

Vinters, Harry V.; Rosa, M. J. De; Farrell, Michael

doi:10.1111/j.1528-1157.1993.tb00460.x

Cited by 52 publications

(25 citation statements)

References 42 publications

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“…They do not show Nissl substance but have variable immunoreactivity to GFAP. It had previously been described [3][4][5], and we found in our study, that some of these cells are positive for GFAP, indicating that at least some might have commitment to be astrocytes. However, most of these cells are negative to this glial marker, and we found some balloon cells weakly stained for MAP-2, which is a neuronal marker.…”

Section: Discussionsupporting

confidence: 58%

“…This is especially true if we take into account that there is an association of CD with some slow-growing tumors [4,5]. The high number of patients submitted to surgery is due to the frequent medical intractability of CD.…”

Section: Introductionmentioning

confidence: 99%

“…CD is a term used for a combination of disturbed neuronal migration and abnormal neuronoglial differentiation [10]. There is a range of morphological abnormalities related to disturbed neocortical development called CD [4,5,8]. These lesions can be identified by imaging analyses such as MRI, but normal MRI studies may also show dysplastic areas [11].…”

Section: Introductionmentioning

confidence: 99%

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Focal Cortical Dysplasia in Children

et al. 1999

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Cortical dysplasia (CD) is now recognized as one of the major causes of pediatric focal neocortical epilepsy, and surgical procedures have been considered early in life. However, the mechanisms involved in seizure generation and intractability in these patients are still unknown. We analyzed with immunocytochemistry for various antibodies the brain tissue from 4 children (10 months to 6 years old) with focal epilepsy due to focal CD in order to study the inhibitory and excitatory circuits in dysplastic areas. Our group had similar histopathological and clinical characteristics. In all patients we found areas of cortical disorganization with dysplastic neurons and balloon cells. We studied distributions of glial cells with glial fibrillary acidic protein (GFAP) and neurons with microtubule-associated protein 2 (MAP-2). Gliosis was present in all cases, and GFAP stained also some balloon cells. Dysplastic neurons were darkly stained by MAP-2, and we also found balloon cells weakly stained with MAP-2 in the same areas where GFAP was positive, suggesting coexpression of neuronal and glial markers in some of these cells. There was an increased expression of glutamate receptors, especially GluR2/3, but also N-methyl-D-aspartate receptors in dysplastic cortex. The inhibitory circuit does not seem to be decreased, rather we notice an increased amount of glutamate-decarboxylase-positive terminals around some of the big neurons. We discuss the possible role of these findings as mechanisms of epilepsy.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Focal Cortical Dysplasia in Children

et al. 1999

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“…Because adhesion and extracellular matrix molecules can specify both the time of arrival and the cytoarchitectonic region of innervation (Allendoerfer and Shatz, 1994), cytoskeletal abnormalities could also contribute to anomalous connections. Furthermore, neurons may enlarge if they have undergone abnormal early stage migration or differentiation (Barth, 1987;McConnell, 1989;Vinters et al, 1993).…”

Section: Neuronal Hypertrophymentioning

confidence: 99%

“…Not only are resected tissues obtained from a highly select group, but specimens can also vary in size. Surgically resected tissue is placed in fixative rapidly after removal, whereas autopsy material generally suffers histologically from postmortem delay (Vinters et al, 1993). This difference in handling could potentially affect tissue volume.…”

Section: Tissue Variabilitymentioning

confidence: 99%

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

et al. 2001

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The underlying cause of neocortical involvement in temporal lobe epilepsy (TLE) remains a fundamental and unanswered question. Magnetic resonance imaging has shown a significant loss in temporal lobe volume, and it has been proposed that neocortical circuits are disturbed functionally because neurons are lost. The present study used design-based stereology to estimate the volume and cell number of Brodmann's area 38, a region commonly resected in anterior temporal lobectomy. Studies were conducted on the neocortex of patients with or without hippocampal sclerosis (HS). Results provide the surprising finding that TLE patients have significant atrophy of neocortical gray matter but no loss of neurons. Neurons are also significantly larger, dendritic trees appear sparser, and spine density is noticeably reduced in TLE specimens compared with controls. The increase in neuronal density we found in TLE patients is therefore attributable to large neurons occupying a much smaller volume than in normal brain. Neurons in the underlying white matter are also increased in size but, in contrast to other reports, are not significantly elevated in number or density. Neuronal hypertrophy affects HS and non-HS brains similarly. The reduction in neuropil and its associated elements therefore appears to be a primary feature of TLE, which is not secondary to cell loss. In both gray and white matter, neuronal hypertrophy means more perikaryal surface area is exposed for synaptic contacts and emerges as a hallmark of this disease. Key words: temporal lobe epilepsy; stereology; Brodmann's area 38; ectopia; cortical atrophy; neuronal hypertrophy; hippocampal sclerosisHippocampal sclerosis (HS) is the most frequently encountered pathologic abnormality in intractable epilepsy. There is however increasing evidence of more widespread temporal lobe pathology in HS patients (Nakasato et al., 1992;Sisodiya et al., 1995) and prevalent temporal lobe hypometabolism in patients with temporal lobe epilepsy (TLE) (Rausch et al., 1994). Moreover, magnetic resonance imaging (MRI) studies show a reduction in temporal lobe volume both ipsilateral and contralateral to the seizure focus (Lee et al., 1995Marsh et al., 1997). Volume reduction is also independent of the presence of HS (Sisodiya et al., 1997), which indicates that it underlies a broader spectrum than mesial temporal disease alone.Pathologic studies of TLE neocortex are dominated by those focused on readily detectable lesions and gross developmental abnormalities (Choi and Matthias, 1987;Haines et al., 1991;Raymond et al., 1995). There are far fewer investigations of subtle morphological abnormalities in the neocortex than in the hippocampus (Mathern et al., 1995), even though such studies might be expected to answer basic questions about epileptogenic activity originating outside the hippocampus and gross volume reductions in the temporal lobe.A common view of cortical pathology in TLE is that of neuronal loss. This notion is based on reports of reduced numbers of inhibitory neurons (DeFelip...

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