Substanz P, Somatostatin und monoaminerge Transmitter in der Zerebrospinalflüssigkeit von Patienten mit chronischer idiopathischer Trigeminusneuralgie

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.

c-Abl-p38α signaling pathway mediates dopamine neuron loss in trigeminal neuralgia

“…The central mechanism of TN is related to the damage of dopamine neurons in the substantia striatum, and the decrease of dopamine production leads to the decrease of its anti-injury sensitivity. 9,10 Watanabe et al. 24 believe that the maintenance of neuropathic pain is related to the decrease of dopaminergic neurons.…”

“…Strittmatter et al. 9 and Dieb et al. 10 both believe that the central mechanism of TN is related to the damage of dopaminergic neurons in striatum.…”

“…7,8 Studies have shown that oxidative stress can cause the loss of dopaminergic neurons in striatum. Strittmatter et al 9 and Dieb et al 10 both believe that the central mechanism of TN is related to the damage of dopaminergic neurons in striatum. Dopamine can regulate pain at different levels of the body and play a key role in the downward inhibition of pain.…”

Do Low Levels of Beta-Endorphin in the Cerebrospinal Fluid Indicate Defective Top-Down Inhibition in Patients with Chronic Neuropathic Pain? A Cross-Sectional, Comparative Study

“…Given the fact that neuropathic pain processes probably primarily affect a limited portion of the spinal cord, one could argue that a putative localized excess of SP overspilling into the CSF might be too small to be detectable, and hence not as a single substance sufficient to differ between groups. However, Strittmatter and coworkers found that, compared with patients with nonpainful neurological (mostly neuromuscular) disease, mean CSF‐SP was elevated by 33% ( P < 0.05) in patients with trigeminal neuralgia [34], showing that high CSF‐SP can be demonstrated by lumbar puncture far from the locus of putative overproduction of SP (provided this is not a type I error). When trying to assess different studies of CSF‐SP in human neuropathic pain, it is important to remember that neuropathic pain is not a single entity.…”