Pain Neurobiology Flashcards
Why things hurt video
Key idea of noceception
nociception of different kinds, all they’re job is to detect something, and send o to the CNS and to the brain and the brain will take that information and make perception of pain, you brain takes things like contex
Classic/Cartesian model of pain
Amount of tissue pathology/damage is directly related to amount of pain you are experiencing in the cartesian model. If there is pain, there must be some sort of pathological damage
Biopsychosocial model of pain
A model of pain that considers how psychological, social, and biological factors affect pain.
The approach to pain, the symptoms you experience have more to do with other things that are not just tissue damage
Biopsychosocial
Biological factors -
Biological factors - changes in the structure (anatomy) or function (physiology) of the body
Biopsychosocial
Psychological factors -
Psychological factors - an individual’s thoughts, emotions and behaviour about pain
Bio psychosocial: Social factors
Social factors - cultural, religious, and occupational beliefs about pain
Models of Pain
Classical/ Cartesian & Biopsychosocial
Classification of Pain
Time: Acute vs.
Chronic (~ >3 months)
Neurobiology: Nociceptive vs Neuropathic vs Nociplastic
Classification of Pain
Time: Acute vs. Chronic (~ >3 months)
Acute pain is Associated with tissue damage, some event that happens now you are experiencing pain, amount of tissue damage might not be the same as the amount of pain, if you are still experiencing pain after three month it transitions into chronic pain
Classification of Pain: Nerobiology- Nociceptive
Pain you get when you activate the peripheral nociceptors.
Pick up things that can potentially damage your tissue. Pin prick is potentially tissue damage or hot. Whereas stroking the Q-tip is not tissue damage and is detective by other things.
Classification of Pain: Nerobiology- Neuropathic
activation of peripheral or centralnociceptive pathways directly (e.g. trauma,pressure)
You may still be activating those nociceptive pathways, but they have to get back to spinal cord though nerve pathways.
If you whack your elbow, that zinger lasts a long time and is not activating nociceptors, but activating axons/pathways that conduct that nociceptive signal back to spinal cord
Classification of Pain: Nerobiology- Nociplastic
neuroplasticity of nociceptive
signaling networks (aka Central sensitization)
Adaptation of neurons. Learning mechanism in nociceptive system leading to changes in pain perception.
What part of the brain is activated during Thermal and Mechanical Pain?
*Both Nociceptive Pain
In the same parts of brain. Both acute nociceptive pain. High degree of overlap b/t acute pain and nociceptive pain networks which include both sensory and affective regions
What part of the brain is activated when Nociplastic Pain is experienced?
All different areas.
Bunch of different parts of brain activated.
These are all active in other types of things such as fear and danger.
No overlap with any noceptive pain active cites
Pain threshold
- the lowest level at which a stimulus is recognized as painful by the person experiencing it
Pain tolerance
- the greatest level of pain a person is prepared to endure
Allodynia
- a normally nonpainful stimulus is perceived as painful
Hyperalgesia
- increased perceived intensity of a “normally” painful stimulus
Hypoalgesia
- decreased response to a normally painful stimulus
Nociplastic Pain: Fear & Danger
➔ Similar brain areas active during: fear, anger, anxiety, frustration, etc.
➔ Unresolved trauma
Pain is a learned response
- Tissue damage sends nociceptive signals to SC and brain
- If brain senses danger it creates more neural activity to solve the problem
- The pain processing pathways get larger and steal resources from other brain areas
What occurs when resources in the brain are being used for one thing (pain processing)
That means that resources are not available for another thing such as cognitive processes like memory recall and what not
Pain prevalence: MS, SCI, PD
MS: overall 63%
27% dysesthetic extremity pain: described as a continuous ‘‘burning’’ pain that is typically bilateral, affecting the legs and feet, usually worse at night and can be exacerbated by physical activity. (Less likely to respond to exercise prescription, classical model, will make individual believe that they are damaging tissues)
SCI: 26-96%
PD: 40-85%
Nociceptive broad system
Musculoskeletal (bone, joint, muscle trauma, inflammation)
Visceral (renal, bowel, sphincter)
Compressive mononeuropahies
Something pushing on a nerve, purple tunnel syndrome, often comes with numb press tingling, inflammation at the wrist, pushing at the median nerve and it starts to disintegrate and starts to send signals that is precised as discomforting
Phantom pain
Leads to limb loss, after a massive injury, doctor cut off a limb, after that, the individual will experience phantom pain
Peripheral nerve fibers
nociceptors: A-delta (little bit of myelin) & C (no myelin)
All sensitive to chemical, mechanical and thermo stimuli
What do A-delta and C nociceptors do
GO up slightly different pathways but they relay nociceptive signals into SC
A-Delta localize the pain signals. C fibers help your perception of pain
What are the central pathways of pain
- spinal cord & ascending pathways
- supraspinal centres (Thalamus, sensorysomatocortex)
Descending inhibition -
5-HT (serotonin) and NE
Region of brain stem that has descending fibers that put serotonin or NE is region of SC where pain signals are being processed to modulate the signals coming up to the brain.
Your brain can decide at spinal cord level if pain can ascend to brain
Characteristics of acute pain
- Pain is a symptom
- Defined time of onset
- Pathology identifiable
- Response to tissue injury
- Relieved by treatment at pain
- Responsive to meds
- Works well in classic model
Characteristics of chronic pain
- Pain’s a disease
- Ill-defined time of onset
- Pathology unidentifiable
- Absent or adapted ANS activity
- Does not respond to treatment at pain
- Less responsive to meds
- Associated with depression, weight loss, low sex
- Does not work well in classical model
Paleospinothalamic tract
Anterior spinal thalamic system, activates the limbic system, which is associated with emotion, hypersensitive to neuropastic pain
slow impulses; chronic pain
Neospinothalamic tract
Same as lateral spinal thalamic track
fast impulses; acute pain
Paleospinothalamic pathway
indirect spinothalamic pathway
1. first order neuron synapses in dorsal horn
2. second order neuron synapses in reticular formation + medial thalamus
3. third order neuron synapses in cingulate, frontal, limbic cortices
Basic pathway for brain to recognize pain
Info comes into SC and has to synapse with a second region neuron and that synapses with another neuron that ascends info to the brain
Neospinothalamic pathway
direct spinothalamic pathway
1. First order neuron synapses in dorsal horn
2. second order neuron synapses in thalamus (VPL)
3. third order neuron synapses in the primary somatosensory cortex
What is vicerosomatic convergence
Referred pain due to WDR convergence
Nociceptive specific cells
superficial Lamina 1 and 2 in dorsal horn receive contacts from both A-delta and C-fibers only respond to noxious stimuli
What are noxious stimuli?
Thermal, chemical, mechanical stimuli capable of causing tissue damage
What are wide dynamic range neurons (WDR)
Project via neospinothalamic tract to the thalamus and on to the ‘pain matrix’ areas
What do WDR respond to
stimuli ranging from nonpainful touch - to noxious mechanical (pinch, pierce), heat and chemicals.
What does the paleospinothalamic tract include?
(C-fibre)
Limbic System
Hypothalamus
Basal ganglia
- If these are active, patient have an emotional response, localaization is diffuse (struggle to make where the pain is coming from).
What does the neospinothalamic tract include
(A-delta)
Primary somato sensory cortex: Localization of pain of the body, it tells you the where, very important cause this art of the pain need top be activated if a patient want to identify where they are having the pain
Neuroplasticity and Chronic pain
The spinal and brain pathways that process acute nociceptive pain, are ‘overtrained’. Neuroplasticity has become maladaptive and is causing the chronic pain.
If it gets to the point where it is self reinforcing and won’t shut itself down
Nociplastic pain
- There is not any tissue damage. Nociceptors are not saying there is tissue damage. But chronic activation of them have trained them to say there is damage
Neuroplasticity has become maladaptive and is causing the chronic pain.
Overtrained
It can go wrong when it overtrains, it’s hyper sensitive and becomes maladaptive and leads to chronic pain
What is the route to cure chronic pain
Maybe neuroplasticity is also the route to cure.
