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Elevation of CSF Tumor Necrosis Factor α Levels in New Daily Persistent Headache and Treatment Refractory Chronic Migraine
Author(s) -
Rozen Todd,
Swidan Sahar Z.
Publication year - 2007
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.2006.00722.x
Subject(s) - medicine , pathogenesis , tumor necrosis factor alpha , proinflammatory cytokine , inflammation , headaches , cytokine , migraine , tumor necrosis factor α , immunology , gastroenterology , surgery
Objective.—To determine if patients with new daily persistent headache (NDPH) have elevated levels of tumor necrosis factor α (TNF α) in the CSF. Background.—NDPH is considered one of the most treatment resistant of all headache syndromes. This reflects a lack of understanding of its pathogenesis. As a certain percentage of NDPH patients have their headaches start after an infection, the possibility of a persistent state of systemic or CNS inflammation comes into question. TNF α is a proinflammatory cytokine involved in brain immune and inflammatory activities, as well as in pain initiation. The goal of this study was to look at TNF α levels in the CSF of NDPH patients, to determine if CNS inflammation may play some role in the pathogenesis of this condition. Methods.—CSF TNF α levels were studied in 38 patients: 20 with NDPH and a control population of 16 patients with chronic migraine (CM), and 2 with post‐traumatic headache (PT). Results.—CSF TNF α levels were elevated in 19 of 20 NDPH patients, 16 of 16 CM patients, and both PT patients. Serum TNF α levels were normal in most of the study subjects. Conclusion.—An elevation of CSF TNF α levels was found in almost all NDPH patients and suggest a role for TNF α in the pathogenesis of this condition. Surprisingly, all CM and PT patients tested had elevated CSF TNF α levels. In most patients with elevated CSF levels, serum TNF α levels were normal. All of these syndromes may be manifestations of CNS inflammation. As most of the positive‐tested patients showed minimal to no improvement during aggressive inpatient treatment, persistent elevation of CSF TNF α levels may be one of the causes of treatment refractory CDH.