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  • 1
    Electronic Resource
    Electronic Resource
    Schilddrüsenfunktion bei Lithiumbehandlung (1998)
    Springer
    Der Nervenarzt 69 (1998), S. 189-195 
    Details
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Lithium ; Affektive Störungen ; Schilddrüse ; Schilddrüsenhormone ; Schilddrüsenstoffwechsel ; Key words Lithium ; Affective disorders ; Thyroid ; Thyroid hormones ; Thyroid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Lithium is widely used in the acute and prophylactic treatment of affective disorders. Lithium affects thyroid hormone metabolism via different mechanisms. In patients this leads to a compensatory increase in pituitary thyroid stimulating hormone (TSH) which usually maintains the euthyroid status. This is probably the reason for the relatively high prevalence of goitre in lithium-treated patients; however, the enlargement of the gland is only moderate in most cases. Due to its immunostimulating effects lithium may support the appearance of thyroid autoantibodies and the developement of thyroiditis, which may be the reason for a higher prevalence of hypothyroidism in patients receiving lithium. However, also cases of hyperthyroidism in such patients have been reported repeatedly. Therapeutic recommendations for the treatment of disturbances of thyroid function during lithium treatment are given.
    Notes: Zusammenfassung Lithium ist ein in der Akut- und Langzeitbehandlung von affektiven Psychosen weitverbreitetes Medikament. Über verschiedene Mechanismen übt es einen thyreostatischen Einfluß auf den Schilddrüsenstoffwechsel aus. Dies führt zu einem kompensatorischen Anstieg des Hypophysenhormons Thyreotropin (TSH), wodurch in der Regel eine euthyreote Stoffwechsellage aufrecht erhalten werden kann. Das nach neueren Untersuchungen recht häufige Auftreten einer Struma bei Lithiumpatienten wird hierdurch erklärt. Die Vergrößerung der Schilddrüse ist zumeist jedoch nur mäßig ausgeprägt. Aufgrund seiner immunstimulatorischen Eigenschaften kann Lithium das Auftreten von Schilddrüsenautoantikörpern und die Manifestation einer Thyreoiditis begünstigen. Das bei Lithiumpatienten etwas gehäufte Vorkommen von Hypothyreosen ist überwiegend hierdurch bedingt. Immer wieder werden auch Einzelfälle von Hyperthyreosen während einer Lithiummedikation mitgeteilt. Empfehlungen für das therapeutische Vorgehen bei den verschiedenen Störungen des Schilddrüsenstoffwechsels im Laufe einer Lithiumbehandlung werden im Text gegeben.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001150050259
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  • 2
    Electronic Resource
    Electronic Resource
    Nerve cell loss in the thalamic centromedian-parafascicular complex in patients with Huntington's disease (1996)
    Springer
    Acta neuropathologica 91 (1996), S. 161-168 
    Details
    ISSN: 1432-0533
    Keywords: Key words Huntington's disease ; Human brain ; Thalamus ; Nuclei centromedianus-parafascicularis ; Neurone number
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The centromedian-parafascicular complex represents a nodal point in the neuronal loop comprising striatum – globulus pallidus – thalamus – striatum. Striatal neurone degeneration is a hallmark in Huntington's disease and we were interested in estimating total neurone and glial number in this thalamic nuclear complex. Serial 500-μm-thick gallocyanin-stained frontal sections of the left hemisphere from six cases of Huntington's disease patients (three females, three males) and six age- and sex-matched controls were investigated applying Cavalieri's principle and the optical disector. Mean neurone number in the controls was 646,952 ± 129,668 cells versus 291,763 ± 60,122 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.001). Total glial cell number (astrocytes, oligodendrocytes, microglia, and unclassifiable glial profiles) was higher in controls with 9,544,191 ± 3,028,944 versus 6,961,989 ± 2,241,543 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.021). Considerable increase of fibrous astroglia within the centromedian-parafascicular complex could be observed after Gallyas' impregnation. Most probably this cell type enhanced the numerical ratio between glial number and neurone number (glial index: Huntington's disease patients = 24.4 ± 8.1; controls = 15.0 ± 5.2; Mann-Whitney U-test, P 〈 0.013). The neurone number in the centromedian-parafascicular complex correlated negatively, although statistically not significantly, with the striatal neurone number. This lack of correlation between an 80% neuronal loss in the striatum and a 55% neurone loss in the centromedian-parafascicular complex points to viable neuronal circuits connecting the centromedian-parafascicular complex with cortical and subcortical regions that are less affected in Huntington's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050408
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  • 3
    Electronic Resource
    Electronic Resource
    Hochdosierte Thyroxinbehandlung bei therapie- und prophylaxe- resistenten Patienten mit affektiven Psychosen (1998)
    Springer
    Der Nervenarzt 69 (1998), S. 1019-1022 
    Details
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Thyroxin ; Schilddrüsenhormone ; Therapieresistente Depression ; Prophylaxeresistenz ; Major Depression ; Bipolare Störungen ; Key words Thyroxine ; Thyroid hormones ; Therapy- resistant depression ; Prophylaxis-resistance ; Major depression ; Bipolar disorde
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The following review summarizes current knowledge on the treatment of therapy-resistant patients with affective disorders with supraphysiological doses of thyroxine (T4). Several groups have reported independently of each other that administration of 200–500 µg T4/day has excellent effects in 50–65% of patients a) with bipolar disorder, with or without „rapid cycling” course, who were previously resistant to all prophylactic drugs and b) in the treatment of therapy-resistant depression. T4 is effective only in combination with an antidepressant or a prophylactic drug. Side effects are minimal, even when T4 is administered over several years. These results now justify to recommend high dose T4-augmentation as „last-resort” treatment also beyond research purposes, i. e. in psychiatric wards and in private practice. Recommendations for clinical applications are given and hypotheses on possible mechanisms underlying the efficacy of T4 treatment are discussed.
    Notes: Zusammenfassung Die nachfolgende Übersicht faßt die bisherigen Erfahrungen mit einer hochdosierten Thyroxin(T4)-Behandlung bei therapie- und prophylaxeresistenten Patienten mit affektiven Psychosen zusammen. Mehrere voneinander unabhängige Arbeitsgruppen berichteten in offenen Studie über ausgezeichnete prophylaktische bzw. therapeutische Ergebnisse einer Behandlung mit „supraphysiologischen” Dosen von T4 (200 bis 500 µg pro Tag) bei 50 bis 65% aller bislang prophylaxeresistenten bipolaren Patienten mit oder ohne Rapid-cycling-Verlauf sowie bei bisher therapieresistenten Depressionen. T4 ist nur bei gleichzeitiger Medikation eines Antidepressivums bzw. Phasenprophylaktikums wirksam. Die Nebenwirkungen sind – auch bei Langzeitbehandlung – in fast allen Fällen minimal. Diese Ergebnisse rechtfertigen, die hochdosierte T4-Behandlung als „Mittel der letzten Wahl” bei therapie- und prophylaxeresistenten Patienten mit affektiven Psychosen in Zukunft auch außerhalb der Forschung, d. h. auf den Stationen Psychiatrischer Abteilungen sowie in Nervenarztpraxen durchzuführen. Praktische Empfehlungen zur Durchführung dieser Behandlung werden gegeben und die möglichen Wirkungsmechanismen diskutiert.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001150050378
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  • 4
    Electronic Resource
    Electronic Resource
    Cortical and striatal neurone number in Huntington's disease (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 320-333 
    Details
    ISSN: 1432-0533
    Keywords: Key words Huntington's disease ; Human cerebral cortex ; Striatum ; Neurone number ; Stereology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five age- and sex-matched control cases. Serial 500-μm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36 – 72 years) was 5.97×109±320×106, the average number of small striatal neurones was 82×106±15.8×106. The left striatum (caudatum, putamen, and accumbens) contained a mean of 273×106±53×106 glial cells (oligodendrocytes, astrocytes and unclassifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36 – 75 years) was diminished by about 33  % to 3.99×109±218×106 nerve cells (P≤ 0.012, Mann-Whitney U-test). The mean number of small striatal neurones decreased tremendously to 9.72 × 106± 3.64×106 ( – 88  %). The decrease in total glial cells was less pronounced (193 × 106±26 × 106) but the mean glial index, the numerical ratio of glial cells per neurone, increased from 3.35 to 22.59 in Huntington's disease. Qualitatively, neuronal loss was most pronounced in supragranular layers of primary sensory areas (Brodmann's areae 3,1,2; area 17, area 41). Layer IIIc pyramidal cells were preferentially lost in association areas of the temporal, frontal, and parietal lobes, whereas spared layer IV granule cells formed a conspicuous band between layer III and V in these fields. Methodological issues are discussed in context with previous investigations and similarities and differences of laminar and lobar nerve cell loss in Huntington's disease are compared with nerve cell degeneration in other neuropsychiatric diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310376
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Cortical and striatal neurone number in Huntington's disease (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 320-333 
    Details
    ISSN: 1432-0533
    Keywords: Huntington's disease ; Human cerebral cortex ; Striatum ; Neurone number ; Stereology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five age-and sex-matched control cases. Serial 500-μm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36–72 years) was 5.97×109±320×106, the average number of small striatal neurones was 82×106±15.8×106. The left striatum (caudatum, putamen, and accumbens) contained a mean of 273×106±53×106 glial cells (oligodendrocytes, astrocytes and unclassifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36–75 years) was diminished by about 33% to 3.99×109±218×106 nerve cells (P≦0.012, Mann-Whitney U-test). The mean number of small striatal neurones decreased tremendously to 9.72×106±3.64×106 (−88%). The decrease in total glial cells was less pronounced (193×106±26×106) but the mean glial index, the numerical ratio of glial cells per neurone, increased from 3.35 to 22.59 in Huntington's disease. Qualitatively, neuronal loss was most pronounced in supragranular layers of primary sensory areas (Brodmann's areae 3,1,2; area 17, area 41). Layer IIIc pyramidal cells were preferentially lost in association areas of the temporal, frontal, and parietal lobes, whereas spared layer IV granule cells formed a conspicuous band between layer III and V in these fields. Methodological issues are discussed in context with previous investigations and similarities and differences of laminar and lobar nerve cell loss in Huntington's disease are compared with nerve cell degeneration in other neuropsychiatric diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310376
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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