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Cerebrospinal fluid biomarkers of inflammation in trigeminal neuralgia patients operated with microvascular decompression

Ericson, Hansa,*; Abu Hamdeh, Samia; Freyhult, Evab; Stiger, Fredrikc; Bäckryd, Emmanueld; Svenningsson, Anderse; Gordh, Torstenc; Kultima, Kimb

doi: 10.1097/j.pain.0000000000001649
Research Paper
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Compression of the trigeminal root entry zone by a blood vessel can cause trigeminal neuralgia (TN). However, a neurovascular conflict does not explain all cases of TN, and TN can exist without a neurovascular contact. A common observation during microvascular decompression surgery to treat TN is arachnoiditis in the region of the trigeminal nerve. Thus, aberrant inflammatory mechanisms may be involved in the pathophysiology of TN but information about the role of inflammation in TN is scarce. We used Proximity Extension Assay technology to analyse the levels of 92 protein biomarkers related to inflammation in lumbar cerebrospinal fluid from patients with TN (n = 27) before and after microvascular decompression compared to individuals without TN. We aimed to analyse the pattern of inflammation-related proteins in order to improve our understanding of the pathophysiology of TN. The main finding was that immunological protein levels in the cerebrospinal fluid from patients with TN decreased after surgery towards levels observed in healthy controls. Two proteins seemed to be of specific interest for TN: TRAIL and TNF-β. Thus, inflammatory activity might be one important mechanism in TN.

Inflammatory protein biomarkers in the CSF of trigeminal neuralgia patients decreased after microvascular decompression surgery.

aDepartment of Neuroscience, Neurosurgery, Uppsala University, Uppsala, Sweden

bDepartment of Medical Sciences, Chemical Chemistry, Uppsala University, Uppsala, Sweden

cDepartment of Surgical Sciences, Anesthesiology and Intensive Care, Uppsala University, Uppsala, Sweden

dDepartment of Medical Health Sciences, Pain and Rehabilitation Centre, Linköping University, Linköping, Sweden

eDepartment of Clinical Sciences, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden

*Corresponding author. Address: Department of Neuroscience, Neurosurgery, Uppsala University Hospital, Uppsala SE-751 85, Sweden. Tel.: +46 (0)18 611 5271; fax: +46 (0)18 611 5586. E-mail address: hans.ericson@akademiska.se (H. Ericson).

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

© 2019 International Association for the Study of Pain
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