Chronic Tension Type Headache, An Analog for Fibromyalgia and Depression Disorder?
|Ping Qu1, Jin-Xia Yu2, Lan Xia1 and Gui-Hai Chen3*|
|1Department of Neurology, the Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China|
|2Official Hospital of The people's Government, Anhui Province, Hefei 230001, China|
|3Department of Neurology, The Affiliated Chaohu Hospital of Anhui Medical University, Chaohu 238000, China|
|Corresponding Author :||Gui-Hai Chen
Department of Neurology
The Affiliated Chaohu Hospital
of Anhui Medical University
Chaohu 238000, China
E-mail: [email protected]
|Received: September 08, 2015 Accepted: October 13, 2015 Published: October 17, 2015|
|Citation: Qu P, Yu JX, Xia L, Chen GH (2015) Chronic Tension Type Headache, An Analog for Fibromyalgia and Depression Disorder? Biochem Pharmacol (Los Angel) 4:190. doi:10.4173/2167-0501.1000190|
|Copyright: © 2015 Qu P, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
Background: Chronic tension type headache (CTTH) is the most prevalent headache and is associated with a high socio-economic impact. The exact pathogenesis of CTTH remains unclear. It has been shown CTTH has many similar clinic features with fibromyalgia (FM) and major depression disorder (MDD). Several studies have found some changes of hypothalamic-pituitary-adrenal (HPA) and hypothalamus-pituitary-thyroid (HPT) axes, sex hormones and pro-inflammatory cytokines in FM and MDD. We speculated CTTH has the same changes. Striving to provide new insights into the pathophysiology of CTTH, we designed this trial to address the common and specific aspects of these three disorders in their clinic features and pathophysiological mechanisms, especially from neuroendocrine system and inflammatory pathways. Method: The patients with CTTH, FM and MDD were recruited, and the healthy subjects were selected as controls. The sleep quality, depressive mood and cognitive function of all subjects were evaluated. The serum levels of corticotrophin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol, thyrotrophin releasing hormone (TRH), thyroid stimulating hormone (TSH), total triiodothyronine (TT3), total thyroxine (TT4) , gonadotrophin releasing hormone (GnRH), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected to find the changes of neuroendocrine system and inflammatory pathways which are believed to be linked with these disorders. Results: Compared with the controls, the HAMD-17 and PSQI scores were significantly higher (Ps<0.001) and the MoCA-C score was significantly lower (P=0.029) in the CTTH, FM and MDD patients. The patients with the CTTH, FM and MDD showed different degrees of damage in spatial and object memories compared to the controls (Ps<0.05). The changes of the HPA and HPT axes, GnRH and pro-inflammatory cytokines in the CTTH, FM and MDD patients were similar. In addition, the serum levels of CRH, cortisol, GnRH, TRH, IL-1β and TNF-α were significantly higher (P<0.001) while TT3, TT4 were significantly lower (P<0.001) in the CTTH, FM and MDD groups relative to the controls. The FM patients showed lower value in the pituitary level of HPA and HPT axis. Conclusion: The patients with CTTH had similar patterns of memory damage and changes of the HPA and HPT axes, GnRH and pro-inflammatory cytokines with the FM and MDD patients.