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  • 1
    ISSN: 1432-2129
    Keywords: Schlüsselwörter Trigeminusneuralgie ; CSF ; Neurotransmitter ; Substanz P ; Somatostatin ; Key words Trigeminal neuralgia ; Neurotransmitters ; CSF ; Substance P ; Somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract The etiology of trigeminal neuralgia is unknown, but both peripheral and central causes have been suggested. To investigate the role of central neurochemical mechanisms we measured epinephrine, norepinephrine and their breakdown product, vanilly mandelic acid (VMA), in the cerebrospinal fluid (CSF) of 16 patients (53.3 ± 8.3 years) suffering from trigeminal neuralgia. As markers for the dopaminergic system, we determined CSF levels of dopamine and its metabolite homovanillic acid (HVA). As a marker for the serotonergic system, we measured CSF levels of serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA). In addition, levels of the neuropeptides substance P and somatostatin were determined. The concentration of norepinephrine (P 〈 0.01), VMA (P 〈 0.05) and HVA (P 〈 0.05) were significantly decreased in patients with trigeminal neuralgia and correlated with the duration of the disease and depression scores. 5-HIAA was also significantly decreased (P 〈 0.05) compared to control patients. Whereas substance P was significantly elevated (P 〈 0.05), somatostatin was significantly decreased (P 〈 0.05). Various correlations between the classical neurotransmitters and the neuropeptides could be established. We hypothesize than the sum of complex neurochemical changes plays a role in the etiology of trigeminal neuralgia, which can be separated in local and more central proceedings. The increase in substance P, a major nociceptive neuromodulator, supports the concept of a local neurogenic inflammation, possibly located in the trigeminovascular system. Depending on the duration of the disease and depression, the loss of serotonergic, dopaminergic and noradrenergic innervation seems to reflect more central changes, possibly due to alterations in their antinociceptive descending pathways.
    Notes: Zusammenfassung Bei der Trigeminusneuralgie werden periphere und zentrale Entstehungsmechanismen diskutiert. Daher wurden bei 16 Patienten (53,3 ± 8,3 Jahre) mit einer idiopathischen Trigeminusneuralgie in der Zerebrospinalflüssigkeit (CSF) die Neuropeptide Substanz P und Somatostatin, die Neurotransmitter Noradrenalin und Adrenalin sowie die Metaboliten Homovanillinmandelsäure (HVA), Vanillinmandelsäure (VMA) und 5-Hydroxyindoleessigsäure (5-HIAA) bestimmt. Während die Substanz P in der CSF signifikant (p 〈 0,01) erhöht gefunden wurde, war das Somatostatin gegenüber den Kontrollpersonen signifikant erniedrigt (p 〈 0,05). Noradrenalin (p 〈 0,01), 5-HIAA (p 〈 0,01), HVA (p 〈 0,05) und VMA (p 〈 0,05) waren signifikant erniedrigt. Während die Erhöhung der Substanz P einen Hinweis auf eine lokal beschränkte neurogene Entzündung im trigemino-vaskulären System geben könnte, spricht die Reduktion monoaminerger Transmitter für eine zentral gestörte Schmerzmodulation. Diese scheint mit zunehmender Krankheitsdauer und begleitender Depression stärker zu werden. Die zahlreichen Korrelationen der Neuromediatoren untereinander, insbesondere auch zwischen den Neuropeptiden und den klassischen Neurotransmittern, sprechen für komplexe neurochemische Interaktionen im Rahmen der Schmerzentstehung.
    Type of Medium: Electronic Resource
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