Ignite Creation Date:
2025-12-24 @ 1:28 PM
Ignite Modification Date:
2025-12-29 @ 2:57 PM
Study NCT ID:
NCT01172795
Status:
UNKNOWN
Last Update Posted:
2010-07-30
First Post:
2010-07-29
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Diffuse Noxious Inhibitory Controls (DNIC): Nociceptive Modulation and Interaction With Neurocognitive Performance in Chronic Pain
Sponsor:
Vrije Universiteit Brussel
Organization:
Study Overview
Official Title:
None
Status:
UNKNOWN
Status Verified Date:
2010-07
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Diffuse noxious inhibitory control In order to quantify central sensitization in chronic pain patients, the Diffuse Noxious Inhibitory Control (DNIC) model has been used frequently. DNIC relies on painful conditioning stimulation of one part of the body to inhibit pain in another part, to remove the "noise" and to focus on relevant stimuli.
Earlier studies provided evidence for malfunctioning of DNIC in Fibromyalgia (FM) patients. However, the cause of this impairment is not yet elucidated, and further study is required to unravel the pathophysiology of DNIC in FM.
Hypothalamus-Pituitary-Adrenal (HPA) axis Besides neural mechanisms, also hormonal abnormalities could cause altered pain processing. Cortisol is released in answer to pain to suppress the pain. Given the evidence for hypofunction of the hypothalamic-pituitary-adrenal axis and the lower cortisol release in response to stressors in a proportion of FM patients and in chronic whiplash associated disorders (WAD) patients, the relation between pain and cortisol in these patients may be an interesting topic to consider.
Neurocognitive performance Besides chronic pain, people with chronic WAD and FM suffer from severe concentration difficulties and decreased neurocognitive capabilities (reduced reaction time, short term memory deficits etc. The decreased neurocognitive performance is known to be related to pain severity in various chronic pain populations. It is hypothesized that malfunctioning of descending inhibitory pathways and subsequent chronic pain experience precludes optimal neurocognitive performance.
Objectives The present investigation addresses the (patho)physiological mechanisms of DNIC in chronic pain populations.
1. Firstly, patients with FM, chronic WAD and healthy controls are compared regarding functioning of DNIC, cortisol levels and response and neurocognitive performance (case-control).
2. Secondly, the possible interaction between the functioning of DNIC, cortisol and neurocognitive performance is studied in patients with FM, WAD and healthy control subjects (cross-sectional).
3. Thirdly, to examine whether a fatiguing neurocognitive stressor changes DNIC and cortisol levels in patients with FM, chronic WAD or healthy sedentary control subjects.
Earlier studies provided evidence for malfunctioning of DNIC in Fibromyalgia (FM) patients. However, the cause of this impairment is not yet elucidated, and further study is required to unravel the pathophysiology of DNIC in FM.
Hypothalamus-Pituitary-Adrenal (HPA) axis Besides neural mechanisms, also hormonal abnormalities could cause altered pain processing. Cortisol is released in answer to pain to suppress the pain. Given the evidence for hypofunction of the hypothalamic-pituitary-adrenal axis and the lower cortisol release in response to stressors in a proportion of FM patients and in chronic whiplash associated disorders (WAD) patients, the relation between pain and cortisol in these patients may be an interesting topic to consider.
Neurocognitive performance Besides chronic pain, people with chronic WAD and FM suffer from severe concentration difficulties and decreased neurocognitive capabilities (reduced reaction time, short term memory deficits etc. The decreased neurocognitive performance is known to be related to pain severity in various chronic pain populations. It is hypothesized that malfunctioning of descending inhibitory pathways and subsequent chronic pain experience precludes optimal neurocognitive performance.
Objectives The present investigation addresses the (patho)physiological mechanisms of DNIC in chronic pain populations.
1. Firstly, patients with FM, chronic WAD and healthy controls are compared regarding functioning of DNIC, cortisol levels and response and neurocognitive performance (case-control).
2. Secondly, the possible interaction between the functioning of DNIC, cortisol and neurocognitive performance is studied in patients with FM, WAD and healthy control subjects (cross-sectional).
3. Thirdly, to examine whether a fatiguing neurocognitive stressor changes DNIC and cortisol levels in patients with FM, chronic WAD or healthy sedentary control subjects.
Detailed Description:
None
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?: