Library

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
    Springer
    Der Nervenarzt 71 (2000), S. 927-928 
    ISSN: 1433-0407
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    ISSN: 1432-0533
    Keywords: Key words     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 in 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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    ISSN: 1432-0533
    Keywords: Key words Spinal cord injury ; Stroke ; B7 molecules ; Macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lesion-induced microglial/macrophage responses were investigated in post-mortem human spinal cord tissue of 20 patients who had died at a range of survival times after spinal trauma or brain infarction. Caudal to the spinal cord injury or brain infarction, a strong increase in the number of activated microglial cells was observed within the denervated intermediate grey matter and ventral horn of patients who died shortly after the insult (4–14 days). These cells were positive for the leucocyte common antigen (LCA) and for the major histocompatibility complex class II antigen (MHC II), with only a small proportion staining for the CD68 antigen. After longer survival times (1–4 months), MHC II-immunoreactivity (MHC II-IR) was clearly reduced in the grey matter but abundant in the white matter, specifically within the degenerating corticospinal tract, co-localising with CD68. In this fibre tract, elevated MHC II-IR and CD68-IR were still detectable 1 year after trauma or stroke. It is likely that the subsequent expression of CD68 on MHC II-positive microglia reflects the conversion to a macrophage phenotype, when cells are phagocytosing degenerating presynaptic terminals in grey matter target regions at early survival times and removing axonal and myelin debris in descending tracts at later survival times. No T or B cell invasion or involvement of co-stimulatory B7 molecules (CD80 and CD86) was observed. It is possible that the up-regulation of MHC II on microglia that lack the expression of B7 molecules may be responsible for the prevention of a T cell response, thus protecting the spinal cord from secondary tissue damage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 55 (1984), S. 317-324 
    ISSN: 1432-1106
    Keywords: Sinusoidal analysis ; Stretch reflex ; Long latency ; Tremor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reflex stiffness of the flexing human index finger was studied using sinusoidal movements at 3–16 Hz. The Nyquist stiffness diagram indicates the presence of a ‘presonance’ at around 4 Hz, its ‘C’ shape after correction for the mechanical properties of the relaxed finger is consistent with the involvement of a stretch reflex in its generation. This contention was supported by the presence of negative friction around 4 Hz and the disappearance of the modulation of the stiffness curve after afferent ischaemic block. Correction for the mechanical properties of active muscle, measured after afferent block, permitted the isolation of the reflex compo nent of stiffness. The circular form of the Nyquisdiagram indicates a relatively flat frequency response for the reflex over the range tested, and its radius gives a measure of reflex gain. The low value of the frequency at which the frictional force is minimal, suggests the involvement of a reflex of longer than spinal latency. This is discussed in relation to mechanisms of tremor genesis and the interaction of spinal and long latency reflexes in distal hand muscles.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 326 (1971), S. 231-239 
    ISSN: 1432-2013
    Keywords: Extensor γ-Motoneurones ; Low-Threshold Muscular Afferents ; Extensor-Gamma-Motoneurone ; Niedrigschwellige Muskelafferenzen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In der intercolliculär dezerebrierten Katze wurden Gamma-Efferenzen aus dem N. gastroc. funktionell isoliert und abgeleitet. In der Regel hemmt die elektrische Tetanisierung niedrigschwelliger Afferenzen aus dem ipsilateralen N. peron. prof. die Gamma-Motoneurone, während die gleiche Reizung des kontralateralen N. gastroc. die Gamma-Motoneurone erregt.
    Notes: Summary Functionally isolated γ-efferents to the triceps surae have been recorded in the intercollicular decerebrate cat. As a rule, repetitive stimulation of low-threshold afferents from the ipsilateral pretibial flexors decreases the activity of the γ-efferents, whereas the same stimulation of the contralateral gastrocnemius nerve activates the γ-motoneurones.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...