TY - JOUR
T1 - The role of biomarkers in drug-resistant trigeminal neuralgia: a prospective study in patients submitted to surgical treatment
AU - Rapisarda, Alessandro
AU - Baroni, Silvia
AU - Gentili, Vanessa
AU - Moretti, Giacomo
AU - Burattini, Benedetta
AU - Sarlo, Francesca
AU - Olivi, Alessandro
AU - Urbani, Andrea
AU - Montano, Nicola
PY - 2022
Y1 - 2022
N2 - Background: Molecular mechanisms underlying trigeminal neuralgia (TN) have been poorly understood. Recently, different biomarkers have been studied in several chronic neuropathic diseases or in neuronal damage, but their role in TN has not yet been investigated. Here, we firstly analyzed the serum levels of the neuron-specific enolase (NSE) (as an index of neuronal tissue damage) in TN patients submitted to surgical treatment. Different cytokines and interleukins related to inflammation were also studied. Methods: Blood samples from 40 patients were prospectively collected preoperatively and after the surgical procedure, namely microvascular decompression (MVD) and percutaneous balloon compression (PBC). Serum levels of uric acid, NSE, ferritin, CRP, IL-2R, and IL-6 were studied. The acute pain relief (APR) and the pre- and postoperative BNI were used to evaluate the clinical outcome. Results: Overall, we obtained an APR in 87.5% of patients and a significant reduction of BNI after surgery (p < 0.0001). We observed a significant reduction of postoperative NSE values in the group of patients undergoing MVD (p = 0.0055) and a significant increase of postoperative NSE values in patients undergoing PBC (p < 0.05). Furthermore, in the group of patients undergoing MVD, we found a significant postoperative increase of CRP (p < 0.0001), ferritin (p = 0.001), and IL-6 (p = 0.01) values. The only patient who did not respond to MVD had NSE levels unchanged. Conclusion: Our results suggest the hypothesis that TN would be related to the neural damage instead of the systemic inflammatory status and indicate NSE as a possible biomarker of response in patients submitted to MVD.
AB - Background: Molecular mechanisms underlying trigeminal neuralgia (TN) have been poorly understood. Recently, different biomarkers have been studied in several chronic neuropathic diseases or in neuronal damage, but their role in TN has not yet been investigated. Here, we firstly analyzed the serum levels of the neuron-specific enolase (NSE) (as an index of neuronal tissue damage) in TN patients submitted to surgical treatment. Different cytokines and interleukins related to inflammation were also studied. Methods: Blood samples from 40 patients were prospectively collected preoperatively and after the surgical procedure, namely microvascular decompression (MVD) and percutaneous balloon compression (PBC). Serum levels of uric acid, NSE, ferritin, CRP, IL-2R, and IL-6 were studied. The acute pain relief (APR) and the pre- and postoperative BNI were used to evaluate the clinical outcome. Results: Overall, we obtained an APR in 87.5% of patients and a significant reduction of BNI after surgery (p < 0.0001). We observed a significant reduction of postoperative NSE values in the group of patients undergoing MVD (p = 0.0055) and a significant increase of postoperative NSE values in patients undergoing PBC (p < 0.05). Furthermore, in the group of patients undergoing MVD, we found a significant postoperative increase of CRP (p < 0.0001), ferritin (p = 0.001), and IL-6 (p = 0.01) values. The only patient who did not respond to MVD had NSE levels unchanged. Conclusion: Our results suggest the hypothesis that TN would be related to the neural damage instead of the systemic inflammatory status and indicate NSE as a possible biomarker of response in patients submitted to MVD.
KW - Biomarkers
KW - Inflammation
KW - NSE
KW - Neuron-specific enolase
KW - Trigeminal neuralgia
KW - Biomarkers
KW - Inflammation
KW - NSE
KW - Neuron-specific enolase
KW - Trigeminal neuralgia
UR - http://hdl.handle.net/10807/199767
U2 - 10.1007/s10072-022-05971-7
DO - 10.1007/s10072-022-05971-7
M3 - Article
SN - 1590-1874
SP - N/A-N/A
JO - Neurological Sciences
JF - Neurological Sciences
ER -