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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 103 (1996), S. 917-924 
    ISSN: 1435-1463
    Keywords: Silent period ; transcallosal stimulation ; magnetic stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was performed in order to determine the influence of ipsilateral transcranial magnetic stimulations (TMS) on the silent period evoked by contralateral cortical stimulations. Ipsilateral TMS preceded the contralateral magnetic or electrical cortex stimulation by 0–50ms. In all subjects, the duration of the silent period was decreased in interstimulus intervals of 20–30ms when using magnetic ipsi- and contralateral stimuli. No change in the silent period was seen with ipsilateral magnetic and contralateral electrical stimulations. Decreases of motor evoked potential amplitudes were an inconsistant phenomenon. The results indicate that ipsilateral TMS in activate inhibitory cortical interneurons, probably via transcallosal pathways. Different time courses and different degrees of inhibition indicate that motor excitation and inhibition may be mediated by different neuronal circuits.
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 104 (1997), S. 1207-1214 
    ISSN: 1435-1463
    Keywords: Transcranial magnetic stimulation ; riluzole ; glutamate ; intracortical inhibition ; intracortical facilitation ; silent period
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the glutamate antagonist riluzole on excitatory and inhibitory phenomena in the human motor system was studied by transcranial magnetic stimulation (TMS) and peripheral electrical nerve stimulation. The motor threshold, the intracortical inhibition and intracortical facilitation as assessed by paired TMS, the cortical and peripheral silent periods, F wave amplitudes and F wave latencies were measured. Riluzole suppressed the intracortical facilitation whereas other parameters remained unchanged, indicating that the neurotransmitter glutamate is mainly involved in facilitatory mechanisms in the motor system.
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 221 (1979), S. 133-136 
    ISSN: 1432-1459
    Keywords: Meralgia paresthetica ; Familial occurrence ; Autosomal dominant trait
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Familiär auftretende Meralgia parästhetica ist ungewöhnlich: in der Literatur sind bisher nur wenige Beobachtungen mitgeteilt worden. Ein eindeutiger Erbgang ließ sich nicht ablesen. Es wird hier über eine Familie berichtet, in der sich eine Meralgia parästhetica mit dominantem Erbgang feststellen ließ.
    Notes: Summary Familial occurrence of Meralgia paresthetica is uncommon. Only few familial case studies have been reported up to now. The author presents a family with Meralgia in four generations, suggesting a distinctly autosomal dominant trait.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 66 (1988), S. 227-227 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 5
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Frontalhirnsyndrom ; Schädel-Hirn-Trauma ; Zerebrovaskuläre Erkrankungen ; Key words Frontal lobe syndrome ; Severe head injury ; Cerebrovasular diseases ; Prefrontal cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The term „frontal lobe syndrome” comprises a variety of different clinical syndromes produced by focal lesions involving the prefrontal cortex. However, similar syndromes can be observed after lesions involving subcortical structures connected with the prefrontal cortex in neuronal networks. With respect to the different clinical pictures and underlying brain lesions, prefrontal lobe dysfunction may be divided into a disorganized type, caused by lesion of the dorsolateral prefrontal lobe and its connections, a disinhibited type that can be observed following lesions of the orbitofrontal cortex, and an apathetic type following lesions affecting the functional balance between the cingulum and the supplementary motor area. As intracerebral lesions are rarely limited to the brain regions described, in the majority of patients various degrees of behavioural dysfunction can be observed. The case reports of four patients illustrating the three major prefrontal syndroms following severe head injury (n=2) or cerebrovascular disease (n=2) are presented and diagnostic implications as well as possible treatment strategies are discussed.
    Notes: Zusammenfassung Der klinisch gebräuchliche Terminus des „Frontalhirnsyndroms” beschreibt eine heterogene Symptomatik, welche nicht nur nach Schädigung des präfrontalen Kortex, sondern auch bei Läsionen von tieferliegenden, mit dem präfrontalen Kortex in Verbindung stehenden Strukturen beobachtet werden kann. Nach den im Vordergrund stehenden klinischen Merkmalen und unter Berücksichtigung der dabei geschädigten anatomischen Strukturen können Schädigungen des präfrontalen Kortex in 3 Untergruppen unterteilt werden: 1. das desorganisierte Syndrom, welchem eine Schädigung der dorsolateralen Konvexität und ihrer Verbindungen zugrunde liegt; 2. das enthemmte Syndrom, welches durch Läsionen des orbitofrontalen Kortex und seiner Verbindungen verursacht wird und 3. das apathische Syndrom infolge mittelliniennaher Läsionen mit Schädigung der Verbindungen zwischen Gyrus cinguli und supplementär-motorischem Areal. Da intrazerebrale Läsionen nur selten auf die beschriebenen Regionen beschränkt sind finden sich häufig Mischbilder mit bisweilen bizzarren psychopathologischen Auffälligkeiten. Anhand von 4 Fallbeispielen von Patienten mit Schädel-Hirn-Trauma (n=2) oder zerebrovaskulärer Erkrankung (n=2) werden die klinische Problematik veranschaulicht und diagnostische sowie therapeutische Maßnahmen besprochen.
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  • 6
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Adrenomyleoneuropathie ; Adrenoleukodystrophie ; Genmutation ; Peroxisomale Stoffwechselerkrankung ; X-chromosomaler Erbgang ; Key words Adrenoleukodystrophy ; Adrenmyeloneuropathy ; Genetic analysis ; Peroxisomal disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Adrenoleukodystrophy (ALD) is an X-linked peroxisomal disease affecting 1 in 20000 males either as cerebral ALD in childhood or as adrenomyeloneuropathy (AMN) in adulthood. Recently, the ALD gene has been identified by positional cloning. We report three males patients with AMN and a fourth patient with juvenile ALD. Biochemical studies showed elevated plasma concentration of saturated very-long-chain fatty acids. Genomic DNA of the patients was analysed for possible sequence variations in the ALD gene by PCR amplification and single strand conformation polymorphism analysis. Three missense mutations (Ser515Phe, Glu267Lys and Arg401Trp) and a 9-bp deletion were detected predicting, respectively, the replacement and absence of amino acids in the deduced amino acid sequence of the ALD protein. In the patients’ families, detection of the respective mutations allows the identification of carriers of ALD/AMN. Mutational screening in ALD families is of practical importance in improving genetic counseling.
    Notes: Zusammenfassung Die Adrenoleukodystrophie (ALD) ist eine X-chromosomal erbliche peroxisomale Stoffwechselerkrankung, deren häufigste Manifestationsform die kindliche ALD gefolgt von der adulten Adrenomyeloneuropathie (AMN) ist. Es werden 3 Patienten mit einer AMN und ein Patient mit einer juvenilen Verlaufsform einer ALD vorgestellt. Die Konzentrationen der überlangkettiger Fettsäuren im Plasma waren bei diesen Patienten pathologisch erhöht. Das ALDP-Gen wurde bei diesen Patienten mittels PCR amplifiziert und mit Hilfe der Einzelstrang-Konformations-Polymorphismus-(SSCP-)Analyse auf Mutationen hin untersucht. Dabei fanden sich drei Missense-Mutationen (Ser515Phe, Glu267Lys, Arg401Trp) und eine Deletion von 9 Nukleotiden. Diese Mutationsanalyse ermöglicht eindeutige Aussagen bezüglich der Anlageträgerschaft für ALD in den jeweils betroffenen Familien und ist daher für eine adäquate humangenetische Beratung von Bedeutung.
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  • 7
    ISSN: 1432-0533
    Keywords: Key words Schwann cell inclusions ; Demyelination ; Myelinated nerve fibers ; Morphometry ; Peripheral ; neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the cytoplasm of Schwann cells of a sural nerve biopsy from a 21-year-old female patient with chronic neuropathy we noted numerous unique, usually double membrane-bound, osmiophilic, granular or globular inclusions, approximately 30–600 μm in diameter. Some of these membrane-bound vesicular or tubular structures contained less dense or no osmiophilic inclusions. Morphometry revealed a reduction of the myelin area per endoneural area to approximately 13% (normal value: 20– 30%) and of the density of myelinated nerve fibers to 5,412/mm2 (normal value at this age: 6,000–9,000/mm2). Large myelinated nerve fibers were predominantly reduced in number, and no myelinated nerve fibers with diameters larger than 4.5 μm were seen. Numerous, usually small onion bulb formations indicated a predominantly demyelinating type of neuropathy. This is to the best of our knowledge the first case of a chronic demyelinating neuropathy in which this kind of presumably pathognostic deposits in the cytoplasm of Schwann cells was detected.
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 38 (1996), S. S111 
    ISSN: 1432-1920
    Keywords: Key words Vitamin E deficiency ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe a patient with a progressive neurological disorder consisting of ataxia, loss of proprioception and pyramidal tract dysfunction in his sixth decade. He had severe vitamin E deficiency due to fat malabsorption secondary to chronic inflammatory bowel disease. Sural nerve biopsy revealed a reduced number of myelinated fibres. MRI of the cervical spine showed high-signal lesions on T2-weighted images in the posterior columns, correlating well with the clinical findings.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 38 (1996), S. S111 
    ISSN: 1432-1920
    Keywords: Vitamin E deficiency ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We describe a patient with a progressive neurological disorder consisting of ataxia, loss of proprioception and pyramidal tract dysfunction in his sixth decade. He had severe vitamin E deficiency due to fat malabsorption secondary to chronic inflammatory bowel disease. Sural nerve biopsy revealed a reduced number of myelinated fibres. MRI of the cervical spine showed high-signal lesions on T2-weighted images in the posterior columns, correlating well with the clinical findings.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Der Schmerz 13 (1999), S. 201-204 
    ISSN: 1432-2129
    Keywords: Schlüsselwörter Zönästhesie ; Chronischer Schmerz ; Wahnhafte Störung ; Key words Chronic pain ; Coenesthesia ; Delusional disorder
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Background: Coenesthesias can be defined as disorders of body perception or body hallucinations, projected in different parts of the body. Patients complain of intractable pain or dysesthesia. These symptoms are reported even from organs where we usually have no perception. Coenesthesia must be regarded as a symptom that can be observed in various psychiatric diseases, e.g., schizophrenia. However, in rare cases coenesthesias can be documented in neurological diseases, e.g., intracranial tumors or infections. Therefore, accurate assessment of possible differential diagnoses is important. In late stages, coenesthesias can easily be recognized because of their ”bizarre” character. In early stages, however, patients often complain of intractable, unlocalizable burning pain. They frequently undergo operations because of their great suffering. The drug treatment of first choice is neuroleptics, but the results are unpredictable. Cases and therapie: The case studies of three patients are presented and discussed (patient 1 with coenaesthetic schizophrenia, patient 2 with coenesthesia in the course of a delusional (paranoid) disorder; patient 3 with coenesthesia caused by carcinomatous meningitis).
    Notes: Zusammenfassung Hintergrund: Zönästhesien sind als abnorme Körpermißempfindungen oder leibliche Beeinflussungserlebnisse im Sinn von Leibhalluzinationen definiert, welche in verschiedene Teile des Körpers projiziert werden. Die Patienten klagen häufig über unerträgliche Schmerzen oder Mißempfindungen, welche auch Organe betreffen können, von denen normalerweise keine bewußte Empfindung besteht. Zönästhesien sind als Symptome zu werten, die bei verschiedenen psychiatrischen Erkrankungen, z.B. Erkrankungen aus dem schizophrenen Formenkreis, beobachtet werden. Sie können jedoch auch Symptome neurologischer Erkrankungen sein, z.B. von entzündlichen oder tumorösen Erkrankungen des ZNS, weshalb eine ausführliche Differentialdiagnostik erforderlich ist. Während Zönästhesien in späten Krankheitsstadien aufgrund ihres „bizarren” Charakters leicht zu erkennen sind, kann die Einordnung in Frühstadien, in denen häufig nur schwer lokalisierbare Brennschmerzen oder Mißempfindungen berichtet werden, schwierig sein. Trotz der unspezifischen Beschwerdeschilderung werden aufgrund des hohen Leidensdrucks der Patienten nicht selten wiederholt weitreichende, z.T. invasive und manchmal unnötige diagnostische und therapeutische Maßnahmen veranlaßt. Als Therapie erster Wahl gelten in Abhängigkeit von der Grunderkrankung Neuroleptika, wobei sich die therapeutische Beeinflußbarkeit der Symptome schwierig gestalten kann. Fälle und Therapie: Anhand von 3 Patientenbeispielen [1. Patient mit zönästhetischer Schizophrenie, 2. Patient mit Zönästhesien im Rahmen einer wahnhaften Störung (Paranoia), 3. Patient mit symptomatischen Zönästhesien im Rahmen einer Meningiosis carcinomatosa] werden die klinische Symptomatik der Zönästhesie dargestellt und die Differentialdiagnosen sowie therapeutische Möglichkeiten besprochen.
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