Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Perilesional neurochemical changes in focal epilepsies (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 376-384 
    Details
    ISSN: 1432-0533
    Keywords: Key words Epilepsy ; Immunohistochemistry ; Neurotransmitter ; Pathology ; Tumor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Circumscribed cortical lesions are frequently encountered in patients with chronic focal epilepsies. However, the pathogenesis of seizures is poorly understood. To determine whether the perilesional cortex shows evidence for abnormal excitatory or inhibitory neurochemical activity, we immunohistochemically examined the distribution of the α1 subunit of the GABAA receptor (GABAR), the N-methyl-d-aspartate receptor subunit 1 (NR1), and glutamate decarboxylase (GAD) in 30 surgical specimens of neocortical epilepsy-associated lesions. These comprised 7 low-grade gliomas, 2 gangliogliomas, 2 dysembryoplastic neuroepithelial tumors, 4 glioneuronal malformations, 5 vascular malformations, and 10 glial or gliomesodermal scars. All specimens originated from patients with chronic pharmacoresistant epilepsy. In 73% of the cases there was a distinct difference in immunoreactivity for GABAR, GAD or NR1 between the perilesional zone and the normal cortex. With each of the markers there was reduced perilesional immunoreactivity in 30% of the specimens. Increased staining for GAD was seen in 17%, for GABAR in 7%, and for NR1 in 13% of the cases. The age at surgery, onset of seizures, epilepsy duration, and maximal seizure frequency did not differ significantly between patients with normal and those with altered perilesional immunoreactivity patterns. Although the perilesional changes for GAD, GABAR or NR1 were heterogeneous, they suggest a disturbed balance between excitatory and inhibitory synaptic transmission which may contribute to the pathogenesis of focal seizures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050439
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Tuberous sclerosis-like lesions in epileptogenic human neocortex lack allelic loss at the TSC1 and TSC2 regions (1996)
    Springer
    Acta neuropathologica 93 (1996), S. 93-96 
    Details
    ISSN: 1432-0533
    Keywords: Key words Chromosome 9 ; Chromosome 16 ; Epilepsy ; Hamartoma ; Pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Glioneuronal malformations with a striking histological resemblance to cortical tubers of tuberous sclerosis, but no extracerebral stigmata of this phacomatosis, are frequently encountered in patients with chronic pharmacoresistant epilepsies. It is controversial as to whether these lesion represent a forme fruste of tuberous sclerosis or a distinct entity. The recently reported loss of heterozygosity (LOH) at the regions of the TSC1 or TSC2 locus in hamartomas obtained from different organs of patients with established tuberous sclerosis, including cortical tubers, stimulated us to examine epilepsy-associated tuberous sclerosis-like glioneuronal malformations with respect to LOH at the TSC1 and TSC2 loci of chromosomes 9q34 and 16p13.3, respectively. The analysis was carried out on DNA derived from paraffin-embedded brain tissues of 11 patients. For 5 patients, peripheral blood leukocytes were also available for DNA extraction. We performed microsatellite analysis with five markers on chromosome 9 and four markers on chromosome 16. In addition, polymerase chain reaction-restriction fragment length polymorphism (RFLP) analysis was performed using a polymorphic EcoRV restriction site in exon 40 of the TSC2 gene. No LOH was identified in any of the cases. These findings do not support a relationship between the epilepsy-associated glioneuronal lesions and tuberous sclerosis. However, tuberous sclerosis is genetically heterogeneous and microsatellite and RFLP analysis cannot exclude small deletions or point mutations. Thus, given the histopathological similarity of glioneuronal malformations in epilepsy patients to cortical tubers, further molecular genetic studies will be needed as our understanding of the molecular basis of tuberous sclerosis increases to completely clarify the relationship of these lesions to tuberous sclerosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050587
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Neuronal loss and gliosis of the amygdaloid nucleus in temporal lobe epilepsy (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 606-610 
    Details
    ISSN: 1432-0533
    Keywords: Key words Ammon’s horn sclerosis ; Amygdala ; Hippocampus ; Pathology ; Seizures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although clinical and electrophysiological evidence indicates that the amygdaloid body plays an important role in the pathogenesis of temporal lobe epilepsy, there are very few detailed data on histopathological changes in this nucleus in epilepsy patients. In the present study we have examined the lateral nucleus of the amygdaloid body in 70 surgical specimens from patients with temporal lobe epilepsy and in 10 control specimens with respect to neuronal density and gliosis. The results were compared to the neuronal loss in the hippocampal formation. Our goal was to examine the pathological alterations of the amygdaloid body and their correlation with other morphological changes in temporal lobe epilepsy. In epilepsy patients with Ammon’s horn sclerosis or focal lesions of the temporal lobe, the neuronal density of the lateral amygdaloid nucleus was significantly decreased as compared to normal controls (P 〈 0.001). Overall, the mean volumetric density in epilepsy patients was reduced to 59% of that in normal individuals. There was no correlation between the neuronal density in the lateral amygdaloid nucleus and that in the different segments of the hippocampal formation or to the age at onset or the duration of epilepsy. The neuronal loss of the amygdaloid nucleus correlated well with the presence of fibrillary gliosis. Our findings demonstrate that the amygdaloid body is severely altered in most patients with temporal lobe epilepsy and that these changes are independent of those in the hippocampus. The presence of neuronal loss and gliosis in the amygdaloid nucleus of patients with focal lesions but no Ammon’s horn sclerosis is compatible with an involvement of the amygdala in secondary epileptogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050658
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...