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  • 1
    Electronic Resource
    Electronic Resource
    Subakute Enzephalopathie mit epileptischen Anfällen bei einem Patienten mit chronischem Alkoholismus (SESA-Syndrom) (1998)
    Springer
    Der Nervenarzt 69 (1998), S. 162-165 
    Details
    ISSN: 1433-0407
    Keywords: Schlüsselwörter SESA-Syndrom ; Chronischer Alkoholismus ; Epileptische Anfälle ; Key words SESA syndrome ; Chronic alcoholism ; Seizures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Subacute encephalopathy with seizures in alcoholics (SESA syndrome) is a rare disease entity following chronic alcohol ingestion. It is quite distinct from alcohol withdrawal syndromes, such as delirium, withdrawal seizures or CNS complications of alcohol, such as Wernicke-Korsakow syndrome, central pontine myelinolysis or Marchiafava-Bignami disease, and was proposed in 1981 by Niedermeyer and coworkers. This syndrome consists of multiple neurological deficits, such as hemiparesis or hemianopia, and of recurrent focal and generalized seizures associated with prominent EEG features (peri-odic lateralized discharges, PLEDs). A 72-year-old Caucasian male with chronic alcoholism and an otherwise unremarkable past medical history was admitted to our hospital be-cause of several secondary generalized simple partial seizures. Laboratory investigations revealed elevated levels of gamma-glutamyl-transpeptidase and of mean corpuscular volume. Other laboratory investigations and the CSF examinations on three occasions revealed normal values. Cranial computed and magnetic resonance tomography showed cerebral microangiopathy and generalized atrophy. Despite triple anticonvulsive therapy and an intravenous treatment with acyclovir and thiamine, the epileptic seizures persisted. Several EEGs revealed left parieto-occipital perodic lateralized epileptiform discharges (PLEDs). The patient died of an intercurrent pulmonary infection about 3 months after the onset of symptoms. The described clinical picture resembles the symptoms of SESA syndrome.
    Notes: Zusammenfassung Subakute Enzephalopathie mit epileptischen Anfällen bei Patienten mit chronischem Al-koholismus (SESA-Syndrom) ist neben häufigeren Erkrankungen wie Delirium tremens, Alkoholentzugskrampf, Wernicke-Korsakow-Syndrom, zentraler pontiner Myelinolyse und Marchiafava-Bignami-Syndrom eine seltene Alkoholfolgekrankheit. Multiple neurologische Defizite (Hemiparese, Hemianopsie oder Aphasie), rezidivierende fokale und generalisierte epileptische Anfälle und periodische seitenbetonte steile Potentiale im EEG sind bei diesem Syndrom beschrieben worden. Ein 72jähriger Patient mit chroni-schem Alkoholabusus wurde nach mehreren sekundär generalisierten fokalen Anfällen der rechten Körperseite unter der Verdachtsdiagnose einer Enzephalitis aufgenommen. Die neurologische Untersuchung ergab eine globale Aphasie. Bei den Laboruntersuchungen zeigten sich erhöhte Werte für Gamma-GT und MCV. Sonstige Laboruntersuchungen und Liquoranalysen ergaben Normalbefunde. Im CCT und im zerebralen MRT zeigte sich eine Mikroangiopathie und eine Hirnatrophie. Trotz einer intravenösen Behandlung mit Acyclovir und Vitamin B1 und einer 3fachen antikonvulsiven Therapie wurden weiterhin epileptische Anfälle und eine Verschlechterung des Allgemeinzustandes beobachtet. Mehrere EEG-Untersuchungen ergaben periodische steile links parietookzipital betonte Wellen. Drei Monate nach Beginn der Symptomatik verstarb der Patient an einer Lungenentzündung. Das beschriebene klinische Bild entspricht den Kriterien des SESA-Syndroms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001150050254
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  • 2
    Electronic Resource
    Electronic Resource
    Rapid appearance of β-amyloid precursor protein immunoreactivity in glial cells follwing excitotoxic brain injury (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 23-28 
    Details
    ISSN: 1432-0533
    Keywords: Amyloid precursor protein ; β-amyloid ; Quinolinic acid ; Astrocytes ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical and experimental data have indicated an up-regulation of amyloid precursor protein (APP) after various types of CNS injury. In the present study the cellular source of lesion-induced APP has been investigated an a neurotoxic CNS model. Quinolinic acid injection into the striatum results in neuronal degeneration, while glial cells survive. APP immunoreactivity was detected in glial cells starting at postoperative day 3 and persisted until day 21, the last time point studied. Double immunocytochemistry identified the majority of APP-immunoreactive cells as glial fibrillary acidic protein-immunoreactive astrocytes. There was no evidence of amyloid fibril deposition during this time. It is concluded that following excitotoxic neuronal degneration APP is mainly produced by reactive astrocytes in the lesioned area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294255
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  • 3
    Electronic Resource
    Electronic Resource
    Structural changes of anterior horn neurons and their synaptic input caudal to a low thoracic spinal cord hemisection in the adult rat: a light and electron microscopic study (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 552-564 
    Details
    ISSN: 1432-0533
    Keywords: Glia ; Motoneuron ; Ribosome ; Spinal cord injury ; Synapse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Structural changes in lumbosacral ventral horn neurons and their synaptic input were studied at 3, 10, 21, 42, and 90 days following low thoracic cord hemisection in adult rats by light microscopic examination of synaptophysin immunoreactivity (SYN-IR) and by electron microscopy. There was an ipsilateral transient decrease in SYN-IR at the somal and proximal dendritic surfaces of anterior horn neurons which extended caudally from the site of injury over a postoperative (p.o.) period of 42 days. Concomitantly, at 21 days p.o., perineuronal SYN-IR started to recover in upper lumbar segments. By 90 days p.o., a normal staining pattern of SYN was noted in upper and mid lumbar segments, but the perineuronal SYN-IR was still slightly below normal levels in low lumbar and sacral segments. Electron microscopy revealed ultrastructural changes coincident with the alterations in SYN-IR. At 3 days p.o., phagocytosis of degenerating axon terminals by activated microglial cells was observed at the somal and proximal dendritic surfaces of ventral horn neurons. These changes were most prominent up to two segments caudal to the lesion. At 10 days p.o., advanced stages of bouton phagocytosis were still detectable in all lumbosacral motor nuclei. Additionally, abnormal axon terminals, with a few dispersed synaptic vesicles and accumulations of large mitochondria, appeared at the scalloped somal surfaces of anterior horn neurons. At 21 days p.o., several large lumbosacral motoneurons had developed chromatolysis-like ultrastructural alterations and motoneuronal cell bodies had become partially covered by astrocytic lamellae. At 42 days p.o., there was a transient appearance of polyribosomes in some M-type boutons. In addition, at 42 and 90 days p.o., a few degenerating motoneurons were detected in all lumbosacral segments, but most displayed normal neuronal cell bodies contacted by numerous intact synapses as well as by astrocytic processes. In contrast to these striking alterations of synaptic input at somal and proximal dendritic surfaces of motoneurons, relatively few degenerating boutons were detected in the neuropil of motor nuclei at all the p.o. times studied. We suggest that the preferential disturbance of the predominantly inhibitory axosomatic synapses on ventral horn neurons may be involved in the mechanisms which influence the well-established increase in motoneuronal excitability after spinal cord injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318567
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  • 4
    Electronic Resource
    Electronic Resource
    Distribution of B-50(GAP-43) mRNA and protein in the normal adult human spinal cord (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 378-386 
    Details
    ISSN: 1432-0533
    Keywords: Key words B-50(GAP-43) ; Spinal cord ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract B-50(GAP-43) is a phosphoprotein mainly found in the nervous system which plays a major role in neurite growth during development and regeneration as well as in synaptic remodelling. In the mature intact central nervous system, intense B-50 immunoreactivity (B-50-IR) can still be detected in regions which maintain residual capacity for structural re-organization. B-50 expression has been studied extensively in laboratory animals; however, its distribution and regulation in the human spinal cord is largely unknown. As a first step to analyze lesion-induced structural alterations, we investigated the distribution of B-50 protein and mRNA in the normal adult human spinal cord and dorsal root ganglia. Intense B-50-IR was localized to the superficial laminae of the dorsal horn at all segmental levels, the intermediolateral nucleus at thoracic levels and Onuf’s nucleus at sacral levels. Scattered neurons, particularly in the ventral horn of lumbar and sacral segmental levels (and occasionally also in Clarke’s nucleus) displayed intense B-50-IR in close apposition to the perikaryal and proximal dendritic surfaces. Nonradioactive in situ hybridization indicated that B-50 mRNA could also be detected in neurons of the ventral horn and also in the intermediolateral nucleus. The distribution of B-50 mRNA and protein in the normal human spinal cord shows a marked similarity to that reported in experimental animals, including the selective labelling of Onuf’s nucleus. However, the strong B-50-IR on the surface of some large anterior horn motor neurons has not been observed in other mammals. This finding might reflect a particular state of readiness for synaptic plasticity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050814
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  • 5
    Electronic Resource
    Electronic Resource
    Structural changes of anterior horn neurons and their synaptic input caudal to a low thoracic spinal cord hemisection in the adult rat: a light and electron microscopic study (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 552-564 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glia ; Motoneuron ; Ribosome ; Spinal cord injury ; Synapse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Structural changes in lumbosacral ventral horn neurons and their synaptic input were studied at 3, 10, 21, 42, and 90 days following low thoracic cord hemisection in adult rats by light microscopic examination of synaptophysin immunoreactivity (SYN-IR) and by electron microscopy. There was an ipsilateral transient decrease in SYN-IR at the somal and proximal dendritic surfaces of anterior horn neurons which extended caudally from the site of injury over a postoperative (p.o.) period of 42 days. Concomitantly, at 21 days p.o., perineuronal SYN-IR started to recover in upper lumbar segments. By 90 days p.o., a normal staining pattern of SYN was noted in upper and mid lumbar segments, but the perineuronal SYN-IR was still slightly below normal levels in low lumbar and sacral segments. Electron microscopy revealed ultrastructural changes coincident with the alterations in SYN-IR. At 3 days p.o., phagocytosis of degenerating axon terminals by activated microglial cells was observed at the somal and proximal dendritic surfaces of ventral horn neurons. These changes were most prominent up to two segments caudal to the lesion. At 10 days p.o., advanced stages of bouton phagocytosis were still detectable in all lumbosacral motor nuclei. Additionally, abnormal axon terminals, with a few dispersed synaptic vesicles and accumulations of large mitochondria, appeared at the scalloped somal surfaces of anterior horn neurons. At 21 days p.o., several large lumbosacral motoneurons had developed chromatolysis-like ultrastructural alterations and motoneuronal cell bodies had become partially covered by astrocytic lamellae. At 42 days p.o., there was a transient appearance of polyribosomes in some M-type boutons. In addition, at 42 and 90 days p.o., a few degenerating motoneurons were detected in all lumbosacral segments, but most displayed normal neuronal cell bodies contacted by numerous intact synapses as well as by astrocytic processes. In contrast to these striking alterations of synaptic input at somal and proximal dendritic surfaces of motoneurons, relatively few degenerating boutons were detected in the neuropil of motor nuclei at all the p.o. times studied. We suggest that the preferential disturbance of the predominantly inhibitory axosomatic synapses on ventral horn neurons may be involved in the mechanisms which influence the well-established increase in motoneuronal excitability after spinal cord injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00318567
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  • 6
    Electronic Resource
    Electronic Resource
    Facilitation of picture naming by focal transcranial magnetic stimulation of Wernicke’s area (1998)
    Springer
    Experimental brain research 121 (1998), S. 371-378 
    Details
    ISSN: 1432-1106
    Keywords: Key words Transcranial magnetic stimulation ; Semantic processing ; Speech motor systems ; Picture naming
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  On the basis of an evolutionary concept of language it was postulated that activation of the motor systems for arm movements, which are phylogenetically older, should facilitate language processes. In aphasic subjects picture naming can be improved by a concomitant movement of the dominant arm. In the present study it was investigated whether a similar facilitation can be observed in normal subjects by studying the effects of transcranial magnetic stimulation (TMS) on picture naming latencies. Suprathreshold focal TMS was applied to the left motor cortex for proximal arm muscles in right-handed subjects. The effects were compared with TMS of Wernicke’s area. While TMS of the motor cortex and the non-dominant temporal lobe had no facilitatory effects, TMS of Wernicke’s area decreased picture naming latencies significantly when TMS preceded picture presentation by 500 or 1000 ms. The observed effects depended on the intensity of the stimulus used. While clearly present with intensities of 35% and 55% of maximum output the facilitation disappeared with higher stimulation intensities. It is concluded that focal magnetic stimulation is able to facilitate lexical processes due to a general preactivation of language-related neuronal networks when delivered over Wernicke’s area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002210050471
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