PAIN Flashcards
Describe pain, name 5 features of pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
- subjective
- always unpleasant
- psychological state
- emotional experience
- a senssation
What is acute pain?
Pain that lasts less than 12 weeks
What is chronic pain?
Continous pain that lasts more than 12 weeks
or persistent pain that lasts longer than the expected healing period
What is nocieceptive pain?
This is pain that arises from actual or threatened damage to non-neural tissue and is dude to the activation of nociceptors (in conjunction with normally functioning somatosensory system)
What is neuropathetic pain?
Pain that is initiated or caused by a primary lesion or dysfunction of the nervous system
eg. trigeminal neuralgia - pain due to spinal cord damage/stroke
Name the 3 types of sensory fibres in the PNS
- Alpha-delta-fibres
- Alpha-beta
- C-fibres
What are A-delta-fibres (Aδ-fibres)
Aδ-fibres = short, sharp pain
- smaller in diameter and
- thinly myelinated
- possess higher activation thresholds.
- They respond to both thermal and mechanical stimuli.
What are Aβ-fibres ? Alpha-beta
Aβ-fibres
- Large diameter and highly myelinated, = quick!
- low activation thresholds
- respond to light touch and are responsible for conveying tactile information.
What are C-fibres
- Smallest primary efferent
- Unmyelinated
=slowest conduction
=highest activation thresholds
therefore detect selectively nociceptive or ‘painful’ stimuli
Which fibres are ‘pain fibres’?
A-gamma and C-fibres are pain fibres or nocieptors
-they respond to thermal and mechanical stimuli
Where are nociceptors located?
- External - skin, cornea, mucosa
- Internal - viscera, joints, muscles, connective tissue
(cell bodies of neurons are in either dorsal root ganglion (body) or trigeminal ganglion (face, head, neck))
How does nociceptor transduction work?
- Peripheral terminals are nociceptors contain numerous types of transducers/receptors
- These can be selectively activated by noxious mechanical, thermal and chemical stimuli
- If the stimulus is strong enough to stimulate the transducer a GENERATOR POTENTIAL occurs
- If the generator potential causes sufficient depolarisation of the membrane (reaches the threshold) an action potential is generated. This travels up the axon to its central terminal in the dorsal horn.
- results in the release of synaptic NEUROTRANSMITTERS
=Substance P or glutamate
What are the 3 phases of pain?
- ACUTE PAIN, short-lived response in CNS
- Prolonged noxious stimulation leads to an inflammatory response and continued discharge which modifies the behaviour of dorsal horn neurons and leads to changes in excitability of dorsal horn neurons
- Peripheral nerve damage
may lead to spontaneous discharge, which modifies behaviour of dorsal horn neurons - allows non-nociceptive peripheral nerves access to ascending pain system (eg A-delta fibres that are response to light touch)
What is peripheral sensitization?
- phosphorylation of key enzymes that regulate transducer receptor function
- this leads to an amplified response of pain :(
How does GLUTAMATE work?
Glutamate is a pain neurotransmitter - it acts on a number of receptors 1. AMPA receptors 2. NMDA receptors 3. mGLuR receptors GLU is released in response to acute and persistant noxic stimuli
What is primary hyperalgesia or peripheral sensitisation?
- The peripheral terminals of small diameter neurons are excited by a wide range of endogenous chemical mediators, especially in conditions of tissue inflammation.
- These inflammatory chemicals can be released by local tissues, immune cells or by the neurons themselves.
- These chemicals can cause SENSITSATION of the nociceptor, such that afferent activity can result in an AMPLIFIED response.
- This is achieved by intracellular changes such as phosphorylation of key enzymes which can regulate transducer / receptor function
- This modulation leads to modification (altered gene regulation, altered connectivity, cell death)
Explain how neural plasticity can occur
- Activation. external stimuli causes generator potentials and action potentions
- modulation, repetitive and high frequency activation of C fibres results in amplification and prolongation of the response (windup)
activation of receptors promotes downstream changes such as phosphorylation on enzymes , these more long term changes are called LONG-TERM POTENTIALS, this leads to central sensitization - This manifests as increased response to painful stimuli
modification = cell death, altered connectivity and altered gene expression
How can the brain and spinal cord affect pain perception
Brain and spinal cord can modulate and create pain perception
Describe general pain pathway
- Primary afferent fibres (A-delta, A-gamma, C-fibres)
- Dorsal root ganglia to dorsal horn
- Descending pathways are activated
- projects to thalamus
- projects to primary/secondary somatosensory 3, 1, 2
- also projects to insular, anterior cingulate, prefrontal cortex
What is the insular cortex’s role in pain perception
Insular cortex is deep in the lateral fissue
- This is where the degree of pain is judged
- Contributes to subjective aspect of pain perception
- Perception, motor control, self awareness, interpersonal experience
- plays a role in addition
What is the cingulate cortex’s role in pain perception?
-The cingulate cortex maintains connections with other pain processing area
What is the peri-aqueductal-grey’s role in pain perception?
Peri aqueductal grey - is the gray mater around the cerebral aqueduct
- it has input from cortical and sub-cortical areas
- nor adrengic and serotonergic neurons
- it projects onto neurons in the dorsal horn to modulate noxious transmission
What are optoids?
Opioids are substances that act on opioid receptors to produce morphine-like effects.
- relieve pain
- Opioids include opiates eg morphine
- usually moderate to severe pain
