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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 243 (1996), S. 121-125 
    ISSN: 1432-1459
    Keywords: Vertebral artery dissection ; Cervical nerve root compression ; Nuchal pain ; Colour-coded Duplex sonography ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Vertebral artery dissection may cause upper limb peripheral motor deficit. We report three young patients presenting with nuchal pain followed by a nearly painless proximal paresis of the arm several days later. The cause, as detected by colour-coded Duplex sonography and MRI, was an extracranial dissection of the vertebral artery. The proximity of the intervertebral segment to the vertebral artery and the nerve roots indicated that compression by an intramural haematoma was the likely cause of the disorder. Subsequent examinations during anticoagulation treatment showed almost complete disappearance of the intramural haematoma and of the neurological deficits within a few weeks. We believe that the occurrence of an upper limb peripheral motor deficit should be added to the spectrum of potentially misleading signs of vertebral artery dissection.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 125 (1999), S. 265-270 
    ISSN: 1432-1106
    Keywords: Key words Tendon reflexes ; Biceps femoris ; Gait ; Ia afferents ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  During gait it is generally accepted that there is a reduction in amplitude of H-reflexes as compared to standing. For short-latency stretch reflexes, however, it is less clear whether a similar reduction in reflex gain is present during locomotion. Stretches of constant amplitude are hard to produce under these circumstances and for this reason some previous studies on the biceps femoris (BF) have used ”reduced gait” in which the stimulated leg is stepping on the spot while the contralateral leg is walking on a treadmill. With this method it was possible to show that BF tendon jerk reflexes are larger at end swing and therefore are likely to contribute to the EMG burst normally occurring in that part of the step cycle when the BF is rapidly stretched. In the present study two questions were addressed: first, whether the reflex is different in size during gait compared to standing and, second, whether it is modulated in size during the gait cycle not only during reduced but also during normal gait. It was found that during both types of gait there was a general reflex depression with regard to the respective control values obtained during standing at similar EMG activity levels. In previous studies on soleus and quadriceps, discrepancies between EMG activity and reflex amplitude have been ascribed to changes in presynaptic inhibition of Ia terminals mediating the afferent volley of the reflex. Based on the data presented, this may also be true for the BF. In both normal and reduced gait the reflex was similarly modulated in size, showing a maximum at the end of swing. This similarity implies that reduced gait may be useful as an acceptable alternative for normal gait in studies on phase-dependent reflex modulation during locomotion.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 227 (1979), S. 279-300 
    ISSN: 1433-8491
    Keywords: Hans Berger ; Early EEG recordings, 1924–1931 ; Cortical and subcortical recordings ; Epilepsy ; Petit mal ; Hans Berger ; Frühe EEG-Registrierungen, 1924–1931 ; Direkte Hirnableitung ; Epilepsie ; Absencen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Zum 50. Jahr seiner ersten EEG-Publikation werden Bergers frühe EEG-Ableitungen von 1924–1931 aus dem Freiburger Berger-Archiv besprochen und illustriert. Drei Arten der frühen Untersuchungen Bergers werden im einzelnen besprochen: 1. Saitengalvanometerableitungen von 1924–1926 vorwiegend bei Patienten mit Knochenlücken, die bei diesen Patienten mit Hirnerkrankungen verlangsamte Grundrhythmen von 6–8/s zeigten. 2. Die direkte Ableitung von Rinde und Mark eines trepanierten Patienten 1930, die den Ursprung des EEG in der Hirnrinde klar nachwies. 3. Typische unpublizierte EEG-Befunde bei Epilepsien 1930–1931 im Anfallsintervall und bei Absencen werden abgebildet. In Bergers ersten 6 Mitteilungen, die alle wesentlichen EEG-Befunde bei Hirnerkrankungen und die EEG-Veränderungen bei Aufmerksamkeit, Schlaf und Narkose beschreiben, fehlen diese in Abb. 4–7 illustrierten EEG-Kurven von Krampfpotentialen. Berger hat seine Epilepsie-Befunde zunächst zurückgehalten, weil er Bewegungsartefakte befürchtete und seine Kontrollen ähnliche Formen bei Lid- und Stirnbewegungen zeigten (Abb. 4a, b). Erst 1933, nachdem andere Untersuchungen über experimentelle Epilepsie bei Tieren das Vorkommen abnorm großer Krampfentladungen der Hirnrinde nachwiesen, wagte Berger in der 7. Mitteilung EEG-Ausschnitte eines Petit-mal-Anfalls und fokaler Anfälle bei Paralyse zu publizieren. In einer Synopsis des EEG 1938 illustrierte Berger den Beginn einer Absence mit großen 3/s-Wellen, die den von Gibbs und Lennox 1934 als „spike and wave“ bezeichneten Formen entsprachen. Berger deutete 1933 die abnormen steilen und unregelmäßigen Hirnpotentialformen als „Afallsbereitschaft des Großhirns“ und die Perioden großer 3/s-Wellen als corticale Begleiterscheinungen der Absencen.
    Notes: Summary For the fiftieth anniversary of Berger's first EEG publication, some of his early recordings obtained between 1924 and 1931 are discussed and illustrated. Examples of his protocols from the Freiburg Berger Archives are reproduced. Three types of Berger's early investigations are described: (1) Stringgalvanometer recordings obtained between 1924 and 1926, mainly from trephined patients with cerebral diseases, which usually showed brain waves slowed to 6–8 per second; (2) Direct recordings from the cortex and white matter proving the cortical origin of the EEG in 1930; (3) Typical unpublished EEG recordings of epileptics and of petit-mal attacks obtained in 1930 and 1931. Berger's first six papers published between 1929 and 1933 described nearly all the main EEG findings of cerebral diseases and the EEG alterations of normals during attention, sleep, and narcosis, but they did not report on convulsive potentials in the EEGs of epileptics. Berger had, however, obtained excellent records of epileptic EEG features, here depicted in Figs. 4 through 7. These remained unpublished until 1933 and 1938, because Berger suspected that they contained artifacts caused by blinks and facial movements which he had recorded in his controls (Fig. 4). Only in 1933, after other authors had described large amplitudes of convulsive potentials in the cortex of animals, did Berger publish parts of the EEGs of a petit-mal attack and of focal attacks in progressive paresis. In 1938, Berger presented the EEG of the beginning of a petit-mal attack with large 3/s spikes and waves recorded in 1931 which were similar to those described by Gibbs and coworkers in 1935. In 1933 and 1938, Berger interpreted the abnormal brain potentials of epileptics as signs of a preconvulsive state of the forebrain and suggested that the periods of 3/s waves were cortical correlates of an epileptic absence.
    Type of Medium: Electronic Resource
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