The phrase "attenuate pain" is correct and usable in written English.
It can be used in medical or psychological contexts when discussing methods or treatments that reduce the intensity of pain.
Example: "The new medication is designed to attenuate pain in patients suffering from chronic conditions."
Alternatives: "reduce pain" or "diminish pain".
This study was designed to test the hypothesis that exogenous administration of recombinant mouse granulocyte-colony-stimulating factor (rmG-CSF) to enhance the recruitment of inflammatory cells to painful inflamed sites could attenuate pain in a chronic neuropathic pain model in mice.
Nerve growth factor (NGF) has a pivotal role in peripheral hyperalgesia and inflammation; anti-NGF antibodies attenuate pain responses in inflammatory pain models, and in people with osteoarthritis (OA) or low back pain.
The agents which are being used to attenuate pain either by acting in the central nervous system (CNS) or by peripheral pain mechanisms except altering the consciousness are called analgesic [1].
Hypothesis 2 represents the view that although opioid-based pain systems are maximally engaged in fibromyalgia, they insufficiently attenuate pain [22].
CB1 receptors attenuate pain by reducing peripheral nerve excitability and through inhibition of sensory transmitter release [ 38].
We demonstrate that intrathecal injection of RvD1 could significantly attenuate pain of CP, in a dose-dependent manner.
However, as finger movements [18] and muscle contractions [19] attenuate pain-related cortical responses, all responses acquired after such movement were discarded from the analysis.
Although there are many caveats to keep in mind when interpreting the literature, there is growing evidence to suggest that interfering with HDAC activity can attenuate pain-related behavior in several preclinical inflammatory pain models [ 82- 84].
We found that intrathecal injection of LV-mediated GDNF RNAi (Lvs-siGDNF) may be a novel strategy to attenuate pain-related behaviors by inhibiting the level of substance P (SP) and blocking the pain-related ERK signaling pathway.
We used a model of lumbar radiculopathy and behavioural and electrophysiological analyses to investigate whether sympathectomy could attenuate pain-related behaviour and alter the electrical properties of the DRG neurons.
Moreover, hypnotic sedation (e.g., midazolam and propofol) does not attenuate pain-related ML-SSEPs (like opioids do), as ML-SSEPs seem to be the neurophysiological expression of the activation of the brain-area network involved both in pain perception [ 11, 32] and other salient sensory input [ 33].
