pain and central sensitisation Flashcards
what does pain mean
danger signal to protect ourselves
Describe features of distinct pain phenotypes
Here are some common pain phenotypes with their key features:
- Nociceptive Pain
Cause: Typically results from tissue damage of non neural tissue (e.g., cuts, burns, bone fractures) or inflammation.
Characteristics: Often described as sharp, aching, or throbbing. It’s usually localized to the area of damage.
Examples: Pain from a surgical incision, arthritis pain, or the pain from a broken bone. - Neuropathic Pain
Cause: Results from damage to the nervous system itself, either peripheral or central. This can be due to diseases (like diabetes), infections, injury, or as a side effect of treatments (e.g., chemotherapy).
Characteristics: Often described as shooting, burning, or tingling. Patients may also experience sensitivity to touch or temperature changes.
Examples: road traffic accident tearing spinal cord, phantom limb pain. - Inflammatory Pain
Cause: Caused by activation of the nociceptive pain pathway via the release of inflammatory mediators produced at a site of tissue inflammation.
Characteristics: The pain is often persistent and associated with redness, swelling, and warmth in the affected area.
Examples: Inflammatory arthritis, appendicitis, inflammatory bowel disease. - Functional/ nociplastic Pain
Cause: Pain without obvious organic cause or clear evidence of tissue damage or inflammation. It’s thought to result from dysregulation of the nervous system.
Characteristics: The pain can be widespread or localized and is often chronic. It may be associated with fatigue, sleep disturbances, and mood changes.
Examples: Fibromyalgia, headaches
what happens during a painful stimulus?
When tissue is damaged or exposed to a harmful stimulus (like extreme heat or pressure), nociceptors (pain receptors) in that area are activated. These specialised sensory neurons are designed to detect signals of potential harm.
Upon activation, the nociceptors transmit signals up the spinal cord via the dorsal root ganglion, which contains the cell bodies of these sensory neurons.
Within the spinal cord, the pain signal is relayed to ascending nerve pathways that carry the signal up to the brain, specifically to areas like the thalamus, somatosensory cortex, and other regions involved in processing the sensation of pain, emotional response, and cognitive evaluation of the pain.
allowing the brain to actively process and modulate the perception of pain through descending pathways. The brain can send signals back down the spinal cord to either enhance or diminish the pain signal.
via activation of descending inhibitory pathways (default mode network). These pathways can release neurotransmitters like endorphins (natural painkillers), serotonin, and norepinephrine, which interact with receptors in the spinal cord to reduce the intensity of pain signals being sent up to the brain, dampening the sensation of pain.
what is the biopsychosocsial model of pain
Bio (Biological): This part looks at the physical or biological reasons for pain. It includes things like an injury to your body, a disease, or changes inside your body that might cause pain.
Psycho (Psychological): This part focuses on how your feelings, thoughts, and mental state can affect your experience of pain. For example, stress, anxiety, and depression can make pain feel worse. On the other hand, being distracted or feeling happy can sometimes make pain feel less intense.
Social: This part considers how your relationships, culture, and the support you get from friends and family can influence your pain. For example, if you have people around you who help and support you, you might feel better and cope with pain more effectively. Or, cultural beliefs about pain can shape how you express and deal with it.
what is osteoarthritis, prevalence of it, what are the environmental risks, genetic risk factors, which neuropsychiatric illness is it associated with, causes of OA related pain, whats the role of inflammation in OA-related pain, what type of sesnitisation is OA
it’s a degenerative joint disease whereby the cartilage, a cushiony material that covers and protects the ends of the bones at joints, wears down over time. when it wears down, it can cause the bones to rub against each other and lead to pain, inflammation, swelling and difficulty moving at the joints
OA affects 10 million people in the United Kingdom who are 45 years or older.
obesity (being overweight puts pressure on joints, making the bones more likely to rub against each other)
previous injury - breakdown of cartilage (ligament injuries, joint fractures, dislocations, repetitive stress injuries like lifting weights)
affects females more, family history
people with a history of depression and anxiety are more likely to have symptoms of OA- lower threshold to pain.
OA related pain:
-psychological factors (mental conditions-low threshold to pain))
-sociocultural factors (support system)
-joint pathology (Injury, disease)
role of inflammation in OA-related pain:
Release of inflammatory cytokines helps mediate and reduce or elevate pain signals such as IL-10 (anti-inflammatory) and IL-4 (downregulates proinflammatory cytokines).
However, pro-inflammatory cytokine mediators such as TNF-alpha and IL-1beta play a crutial role in recruiting more immune cells to site of damage/injury increasing inflammation, contributing to the sensitization of nociceptors.
type of sensitization:
peripheral occurs when the nociceptive neurons (pain receptors) in tissues surrounding the affected joints become more sensitive to stimuli. This can result from inflammation, joint damage, or the degradation of cartilage seen in OA. The damaged tissues release chemicals that increase the sensitivity of nerve endings, leading to an exaggerated pain response to stimuli that might normally be mild or non-painful.
what’s the difference between central and peripheral pain sensitization?
peripheral sensitization:
where does it occur- occurs at the very start of pain pathways, at site of injury/damage/inflammation, in the peripheral nervous system (the nerves outside the brain and spinal cord)
what it does-
after injury or inflammation, the area of damage becomes more sensitive, as the nerve endings of these nociceptors lower their threshold to pain signals, such that even a mild stimulation (gentle touch) can be perceived as painful
example-
If you have a sunburn, your skin becomes so sensitive that even a warm shower can feel scalding, extremely hot, or extremely painful
central sensitization:
where does it occur-
occurs in the central nervous system, including the brain and spinal cord
what it does-
after prolonged or intense pain signals, the way in which the brain processes pain signals changes, such that it becomes more sensitive to any pain signal, even in regions of the body where there is no apparent threat or damage. Thus, it may even interpret a non-painful stimulus as painful
example-
in conditions like fibromyalgia, they may experience widespread pain across the body, even in regions where there is no evidence of threat or damage, due to the increased sensitivity of the spinal cord and brain.
what are the three clinical clues to sensitization in OA
Allodynia:
is a condition whereby a non-painful stimuli, such as a gentle pressure or touch, is interpreted as very painful
Hyperalgesia:
refers to exaggerated response to painful stimuli, meaning that a person would experience more intense pain that what is considered normal for a certain injury or condition
radiating pain:
when the sensation of pain spreads from the source of injury to other parts of the body where there is no apparent threat or damage.
how to assess pain
Quantitative sensory testing, such as:
-pressure pain threshold
-temporal summation
-conditioned pain modulation
somatosensory abnormalities:
-allodynia
-hyperalgesia
-brain imaging
How do pressure pain thresholds, temporal summation and conditioned pain modulation work to assess pain?
PPT:
we can do this by applying pressure to an area of the body, measuring in kilopascals what pressure is and asking the person when does that pressure change to pain (they can press a button to indicate that)
TS:
When there’s repeated stimulation of nociceptors, each subsequent stimulation is perceived as more intense or painful than the one before. This is because the second, subsequent stimulation arrives before the effect of the first one dissipates, leading to greater depolarization and increasing the overall signal to the brain.
Thus, temporal summation can make a series of small, individually non-painful stimuli, feel intense and painful.
CPM:
this is a way in which the body can modulate or control pain by using one pain to lessen the other.
In CPM, there are usually two sites of pain, the primary pain is the one you are interested in studying or treating, and the secondary pain is a separate, controlled pain that you introduce to another part of the body, which is known as the conditioned stimulus.
This conditioned stimulus could be like immersing a hand in ice cold water, which is uncomfortable and mildly painful but not harmful. this creates a second source of pain that is different and separate to the primary one that you are interested in. The idea is, that the brain can only handle so much pain at once, so by introducing the conditioned stimulus, the brain ‘distracts’ itself,dealing with this new pain, decreasing the intensity of the first pain.
By observing how the introduction of the second pain affects the perception of the first pain, researchers and doctors can learn about an individual’s pain modulation system. If the first pain lessens significantly, it indicates that the person’s pain modulation system is functioning well. If there’s little change, it might suggest issues with pain processing, which can be important for diagnosing and treating chronic pain conditions
what is maladaptive pain?
when the pain persists beyond the natural healing process and stopped being a useful signal to the body and has instead become a chronic, often debilitating condition. Unlike acute pain, which serves as an important warning system for injury or illness (telling you something is wrong and needs attention), maladaptive pain persists beyond the normal healing process and doesn’t have a clear biological purpose. It can arise from changes in the nervous system where the pain pathways become overly sensitive or continue to fire signals even in the absence of an actual injury or threat.
treatments for OA
-remove fluid from knee that was swollen to reduce pressure on joints
-capsaicin creams
Capsaicin works by binding to TRPV1 receptors found on the surface of pain and heat-sensing neurons; upon activation of this receptor, this leads to calcium influx and thus the release of substance P, which is involved in transmitting pain signals to the brain. With repeated application of capsaicin, the stores of substance P become depleted; this then reduces the ability of nerves to transmit pain signals to the brain, ultimately desensitising these neurons and allowing them to become less sensitive to painful stimuli in regions where capsaicin was applied.
-duloxetine (SNRI- serotonin norepinephrine reuptake inhibitor), aids in blocking transporters that take up these chemical messengers, increasing their abundance in synapses, and improving communication between brain cells and neurons. contributes to increasing a good mood and alleviating pain or anxiety.
Outline features of inflammatory versus neuropathic pain, including causes, mechanisms, characteristics and function.
Inflammatory Pain
Cause:
Inflammatory pain is caused by tissue damage and the subsequent inflammatory response. Conditions like arthritis, infections, injuries, and surgeries can lead to inflammatory pain.
Mechanism:
When tissues are damaged, the body releases proinflammatory cytokines (chemicals) that increase blood flow and attract immune cells to the area, causing inflammation. This process sensitizes nerve endings in the affected area, leading to pain by lowering their pain threshold.
Characteristics:
Often described as a constant throbbing.
The affected area may be red, swollen, warm, or tender to touch.
Usually localized to the injured or inflamed area but can spread to surrounding regions.
May improve with anti-inflammatory medications (e.g., NSAIDs) or steroids which are anti-inflammatory.
Function:
Serves as a protective mechanism, signaling the body to avoid using the injured or inflamed area to allow for healing.
Neuropathic Pain
Cause:
Neuropathic pain arises from damage to the nervous system itself, either peripheral or central. It can be due to conditions like a spinal cord injury or stroke.
Mechanism:
Damage to nerves alters nerve function both at the site of injury and in the surrounding areas. This can lead to abnormal signals being sent to the brain, which are interpreted as pain including non-painful stimuli.
Characteristics:
Often described as burning or stabbing.
May be accompanied by sensations like tingling, numbness, or pins and needles.
The pain is often out of proportion/not aligned to the physical findings or may occur without an obvious injury.
Function:
Unlike inflammatory pain, neuropathic pain does not serve a protective function. It’s considered a malfunction of the nervous system.
