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Ammon's Horn Sclerosis (ammon + horn_sclerosis)
Selected AbstractsBalloon cells and dysmorphic neurons in the hippocampus associated with epileptic amnesic syndrome: A case reportEPILEPSIA, Issue 5 2008Se Hoon Kim Summary Recently, we encountered a 39-year-old woman with typical epileptic amnesic syndrome. The patient underwent right anterior temporal lobectomy, which removed the right hippocampus. The patient's resected hippocampus showed typical histological features of Ammon's horn sclerosis (AHS) with dysmorphic neurons. In addition, the prominent balloon cells, admixed with dysmorphic neurons, were noted in the hippocampus. To our knowledge, this is the first reported case showing AHS with balloon cells. The presence of balloon cells reinforces the hypothesis that AHS itself might be a maldevelopment disorder. [source] Astrocytes in the hippocampus of patients with temporal lobe epilepsy display changes in potassium conductancesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000Stefan Hinterkeuser Abstract Functional properties of astrocytes were investigated with the patch-clamp technique in acute hippocampal brain slices obtained from surgical specimens of patients suffering from pharmaco-resistant temporal lobe epilepsy (TLE). In patients with significant neuronal cell loss, i.e. Ammon's horn sclerosis, the glial current patterns resembled properties characteristic of immature astrocytes in the murine or rat hippocampus. Depolarizing voltage steps activated delayed rectifier and transient K+ currents as well as tetrodotoxin-sensitive Na+ currents in all astrocytes analysed in the sclerotic human tissue. Hyperpolarizing voltages elicited inward rectifier currents that inactivated at membrane potentials negative to -130 mV. Comparative recordings were performed in astrocytes from patients with lesion-associated TLE that lacked significant histopathological hippocampal alterations. These cells displayed stronger inward rectification. To obtain a quantitative measure, current densities were calculated and the ratio of inward to outward K+ conductances was determined. Both values were significantly smaller in astrocytes from the sclerotic group compared with lesion-associated TLE. During normal development of rodent brain, astroglial inward rectification gradually increases. It thus appears reasonable to suggest that astrocytes in human sclerotic tissue return to an immature current pattern. Reduced astroglial inward rectification in conjunction with seizure-induced shrinkage of the extracellular space may lead to impaired spatial K+ buffering. This will result in stronger and prolonged depolarization of glial cells and neurons in response to activity-dependent K+ release, and may thus contribute to seizure generation in this particular condition of human TLE. [source] Chromogranins as markers of altered hippocampal circuitry in temporal lobe epilepsyANNALS OF NEUROLOGY, Issue 2 2001Susanne Pirker MD Chromogranins are polypeptides which are widely expressed in the central nervous system. They are stored in dense core vesicles of nerve terminals, from where they are released upon stimulation. Using immunocytochemistry, we investigated the distribution of chromogranin A, chromogranin B, secretoneurin, and, for comparison, dynorphin in hippocampal specimens removed at routine surgery from patients with drug-resistant mesial temporal lobe epilepsy and in autopsy tissues from nonneurologically deceased subjects. In post mortem controls (n = 21), immunoreactivity for all four peptides (most prominently for chromogranin B and dynorphin) was observed in the terminal field of mossy fibers. For chromogranins, staining was observed also in sectors CA1 to CA3 and in the subiculum. Chromogranin B immunoreactivity was found in the inner molecular layer of the dentate gyrus, the area of terminating associational-commissural fibers. Secretoneurin and dynorphin immunoreactivity labeled the outer molecular layer and the stratum lacunosum moleculare of sectors CA1 to CA3, where projections from the entorhinal cortex terminate. In specimens with Ammon's horn sclerosis (n = 25), staining for all three chromogranins and for dynorphin was reduced in the hilus of the dentate gyrus. Instead, intense staining was observed in the inner molecular layer, presumably delineating terminals of sprouted mossy fibers. Specimens obtained from temporal lobe epilepsy patients without Ammon's horn sclerosis (n = 4) lacked this pronounced rearrangement of mossy fibers. In the stratum lacunosum moleculare of sector CA1, secretoneurin and dynorphin immunoreactivity was reduced in sclerotic, but not in nonsclerotic, specimens, paralleling the partial loss of fibers arising from the entorhinal cortex. Instead, presumably sprouted secretoneurin-immunoreactive fibers were found in the outer dentate molecular layer in sclerotic specimens. These changes in staining patterns for chromogranins and dynorphin mark profound plastic and functional rearrangement of hippocampal circuitry in temporal lobe epilepsy. [source] What I learnt from studying epilepsy: Epileptology and myselfPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 2 2004HARUO AKIMOTO Abstract, My life work with epilepsy has allowed me to learn a great deal. As an old soldier, I would like to give an account of some important milestones in my lifetime learning. The first factor that linked me to epilepsy was listening to a lecture delivered by Dr Yushi Uchimura on ,The pathogenesis of Ammon's horn sclerosis' at a conference of the Japanese Society of Neurology (now Japanese Society of Psychiatry and Neurology) in 1928 when I was a 4th year medical student at Tokyo University. The following year, I started to study under Dr Uchimura at the Department of Psychiatry, Hokkaido University School of Medicine. Another factor that linked me to clinical care and research of epilepsy as a psychiatrist was my encounter with the two volumes of ,Selected Writing of John Hughlings Jackson' edited by J. Taylor. Jackson's greatest asset and contribution to modern epileptology include (i) the discovery of ,Jacksonian epilepsy', (ii) ,conceptual revolution of epilepsy' by recognizing transient mental disorders as seizures, (iii) modern definition of epilepsy by defining epileptic seizures as discharges in the gray matter, and (iv) discovery of ,new epilepsy' (now temporal lobe epilepsy). In 1940, I reported clinical courses indistinguishable from schizophrenia in epilepsy cases. Through my studies, I disputed the then prevailing interpretation of this condition as epilepsy complicating schizophrenia, and proved that these cases were in fact epileptic mental disorders caused by epilepsy. Many patients with epilepsy require medical care as well as rehabilitation and welfare support. We need to further promote the facilities for rehabilitation and employment in the community for persons with epilepsy, such as co-operatives and welfare worksites. The issues that epileptology and epilepsy face in the 21st century is to realize the goals of liberating epilepsy from social stigma and protecting all the citizen's rights for persons with epilepsy. [source] | ||||||||||