The Relationship Between Chronic OA Pain and Cognition Deficits in OA Patients.
Condition: Knee Osteoarthritis; Neuroinflammatory Response
MeSH terms: Osteoarthritis; Osteoarthritis, Knee
Study type: Observational

Summary: 
      The goal of this observational study is to learn about the association between pain
      characteristics and cognitive functions in chronic knee osteoarthritis. The main questions it
      aims to answer are:

        1. If pain characteristics affect cognitive functions in severe knee OA patients?

        2. If concentration of neuroinflammation mediators were raised in severe knee OA patients
           with comparing with control group participants?

      Participants will receive pain and cognition questionnaire before surgery and their blood and
      CSF will be collected for further analysis of neuroinflammation mediators.
    

Detailed description: 
      In the previous studies, which revealed that because neural systems involved in cognition and
      pain processing are closely linked, they may affect with each other. In addition to sensory
      symptoms, cognitive functioning is thought to be affected in chronic pain patients. Pain uses
      cognitive resources, alters neural plasticity and affects expression and activity of a
      variety of chemical and cellular neuromediators. There are several brain regions such as
      amygdala and hippocampus which are most commonly activated during pain
      processing.Osteoarthritis (OA) of the knee is one of the leading causes of disability among
      noninstitutionalized elderly adults. One population-based study revealed that osteoarthritis
      increases the risk of cognitive deficits diseases such as dementia. However the possible
      mechanism had not be elucidated. Recent study revealed that OA-induced hyperalgesia was
      associated with increased nerve growth factor (NGF)/tropomycin receptor kinase A (TrkA)
      signaling. NGF activation of extracellular signal-regulated kinase (ERK)/ mitogen-activated
      protein kinase (MAPK) may play a role in centralization of OA pain. Otherwise NGF has also
      been shown to produce a dramatic upregulation of brain-derived neurotrophic factor (BDNF) in
      trkA-expressing dorsal root ganglion (DRG) cells, and there is now growing evidence that BDNF
      may serve as a central regulator of excitability and is a neuromodulate or of central pain
      processing. On the other hand, in previous studies they showed that BDNF plays a critical
      role in synaptic plasticity, memory processes and storage of long-term memory. The
      BDNF/tropomycin receptor kinase B (TrkB) system in the hippocampus plays a crucial role not
      only in the memory acquisition, but also in the retention and / or recall of spatial memory.

      Besides ongoing pain in chronic knee OA is characterized by increased brain activity in
      limbic-affective regions thus providing novel evidence for a strong emotional component of
      arthritis pain. There are feedback loops exist between pain, emotion and cognition. How is
      the role of BDNF in such loop? The objective of the study was the evaluation of association
      between pain characteristics and cognitive functions in severe knee OA patients. Besides, we
      will try to explore the possible mechanisms by which chronic OA like pain develops to
      cognitive deficits in animal models. The relationship between BDNF levels in body fluids
      (serum and CSF) and pain characteristics and cognitive function was also evaluated in the
      whole sample.
    

Observational model: Case-Control
Time perspective: Prospective
Sampling method: Non-Probability Sample
Study population: 
        People with chronic knee osteoarthritis pain who will receive total knee replacement
        surgery. They have no other chronic pain except chronic knee pain. Furthermore they did not
        have any cerebral diseases such as stroke or brain tumor.
      
Keywords: Chronic pain; Knee osteoarthritis; Cognitive deficits