L17 - Pain Flashcards
(17 cards)
What is pain
A localised or generalised unpleasant bodily sensation (or complex of sensations) that causes mild to severe physical discomfort and/or emotional distress. typically results from bodily disorder (such as injury or disease)
- acute: arises suddenly, usually has a specific cause, resolves quickly
- intermittent: pain that comes and goes
- chronic: lon term (mots to more), persists long after original stimulus has subsided
- typically begins with activation of nociceptors
- product of CNA processing a variety of neural signals
- perception is highly context-dependent
- usually regarded by clinicians as a symptom of an underlying condition
why is pain important?
- alerts us to injuries, diseases ad infections
- helps prevent additional, and more severe tissue damage
- promotes behaviours that minimise the severity and/or duration of the triggering event
- the value of pain is evident when we see what happens to those who cannot sense pain
describe loss of pain sensation
Congenital Insensitivity to Pain with Anhidrosis (CIPA)
- sensory and autonomic neuropathy
- caused by mutation of a nerve growth factor receptor: developmental failure of a subset of sensory and autonomic nerves
- inability to sense pain and temperature, don’t sweat
- repeated injuries and self mutilation eg. bone fractious, biting tongue and lips
- at risk of fever-inducing seizures, infections - appendicitis, periodontitis etc.
describe the origins of pain signals (what receptors, and two fibre types)
Nocicepetors:
- widespread, joints, skin, muscles , viscera
- absent from the brain
- usually free nerve endings of primary sensory neurons
- 3 main classes: mechanical (activated by intense mechanical deformation/pressure), thermal (activated by extremes of temperature, high >45, low <5), chemcial (activated by H+, histamine, cytokines etc), can be polymodal (activated by combinations of mechanical, thermal, chemical)
Pain fibres are thinly myelinated or unmyelinated axons.
C fibres:
- smallest diameter, unmyelinated axons
- slow conduction velocity
- single ongoing pain, dull throbbing (polymodal receptors)
A-delta fibres:
- small diameter, thinly myelinated axons
- faster conduction velocity
- signal acute onset of pain, sharp pain (thermo and mechanoreceptors)
Nociceptors typically feature members of the TRP (transient receptor potential) family of receptors
what is the pathway for pain transmission (diagram on slides)
- painful stimulus activated nerve endings
- signal conducted along afferent axon
- cell body in dorsal root or cervical nerve ganglion
- synapse in CNS released glutamate or substance P (both excitatory)
ascending somatosensory pathway is what carries sensation of pain
what are allodynia and hyperalgesia
Increased perception of pain
Allodynia:
- pain from an innocuous stimuli eg. feather-light touch causes pain
Hyperalgesia:
- persistent ot enhances sensation pain sensation
- often due to inflammation and release of chemicals (prostaglandins, cytokines etc)
what are the mechanisms of hyperalgesia (at the site of peripheral injury and at CNS)
Sensation at site of peripheral injury:
Damaged cells release chemicals:
- causes inflammation
- increases nociceptor activation
- can lead to changes in blood vessel permeability and swelling
- APs can propagate along axon branches innervating neighbouring skin regions
Sensation in CNS:
- strength of synapses can change in CNS
- chronic activation of nociceptors can lead to chronic enhancement of central pain-processing circuits
describer pain modulation for aanalgesia
- selective suppression of pain without effects on conciousness
- pain signalling can be ‘gated’ by stimulation of non-pain sensory fibres from same area (rubbing injured area, teething babies chewing objects)
- this theory ‘gate control model’ led to development of therapies such as: TENS (trans epidermal nerve stimulation) and implantable spinal cord stimulators - pain signalling can be modulated by descending pathways from brain
- pharmacological intervention is very complex, but generally targeted at either preventing stimulation of pain fibres, or enhancement of central pathways that interfere with pain transmission
describe the gate control model (how it works)
“Gating” of pain signal transmission in the spinal cord by non-painful stimulation of nearby nerves
- C-fibres activate projection neurons in spinal cord
- signals sent via anterolateral tract to thalamus
- stimulating non-pain sensory fibres from same region (eg. rubbing the area of the wound) activated inhibitory interneurons in dorsal horn
- reduction in output of projection neurons
describe endogenous opiates in pain modulation
- opiates (eg. opium, morphine, heroine) are powerful analgesics because many brain (and spinal cord) pathways involved in transmission of pain information have opiate receptors
- endogenous opiates bind with opiate receptors in the CNS (endorphins, enkephalins, dynorphins)
- opiate receptors found in spinal cord and brain regions inhibit pain signalling
how are prostaglandins involved in pain modulation
- prostaglandine binding to their receptors lead to ion channels opening
- makes nerve terminal more exitable
- can also increase growth of nerve endings (which can result in more activation and more pain)
- many pain medications inhibit cyclooxygenase enzymes to reduce prostaglandin synthesis (aspirin, ibuprofen, paracetamol, etc. [NSAIDs]
- this has pain-suppression effect both at site of injury and in sensory neurons in DRG and CNS
describe how pain perception and processing works
A variety of brain regions are associated with pain perception and processing.
Not just felt from the somatosensory cortex, lots of brain regions involved, quite complicated.
describer pain localisation and referred pain
- somatotopic mapping of sensory input (including pain) from the body onto somatosensory cortex means we can normally localise the origin of somatic sensations accurately
- convergence of visceral and somatic efferent neurons onto ascending pathways leads to penomenon of referred pain as th brain cannot distinguish whether the stimulus arose in skin or viscera
- in case of visceral stimulation, brain ‘refers’ pain to most common site of stimulation (skin)
- eg. pain in left upper chest may be sign of heart attack
describe trigeminal referred pain and how this relates to ‘tooth pain’
Not all ‘tooth pain’ is actually caused by damage in oral cavity
Because of convergence of afferents from the cervical and trigeminal nerves in the trigeminal nucleus it is quite common for patient stop report pain originating from the beck/base of skill as pain felt in the temporomandibular area
Important to confirm the source of pain before performing remedial dental procedures
describe tooth nerves and pain
- periodontal afferents provide info on tooth load, vibration etc.
- dental pulp is richly innervated
- pulpal nerve fibres excited by noxious stimuli including thermal, osmotic (eg. sweet), mechanical and chemical
- sensations arising from pulp go to central pain pathways, so sensation is predominantly pain
- blood vessels in pulp have sympathetic innervation
describer the two different types of pulpal nerves
Myelinated, (relatively) fast conduction A-delta fibres
- periphery of pulp, inner dentine, dentinal tubules
- cell bodes in trigeminal ganglion
- respond to heat, cold, desiccation and mechanical stimulation of exposed dentine
- movement of dentinal fluid generates action potentials via mechanosensityive channels
- nerve endings with temperature sensitive ion channels also common
- rapid onset sharp pain
Unmyelinated slow conducting C-fibres:
- body of pulp
- polymodal - heat, cold and inflammatory mediator
- depper, duller, aching pain. poorly localised
describe tooth pain
- many nerve endings are likely to be low threshold mechanoreceptors, thermoreceptors, as well as classical nociceptors
- stimuli typically need to be applied to exposed dentinal tubules
- stimulated pulp nerves release inflammatory mediator which reduce thresholds for nerve activation resulting in hyperalgesia and allodynia
- plural inflammation can result in increased expression of voltage gated Na+ channels, reducing threshold for activation of pain fibres, and also trigger sprouting of nociceptive endings
- central branches of tooth trigeminal neurons project to sub nucleus caudal of trigeminal nucleus
- tooth pulp driven neurons located in thalamus and insula
