NS 6: Pain Flashcards
why can non-painful stimuli be perceived as painful after injury?
tissue damage releases substances e.g. bradykinin, PGs and histamine, which lower threshold of nociceptive nerve fibres so sensation of pain is easier to bring about.
what name is used to refer to non painful stimuli being perceived as painful?
allodynia
also pain which occurs in an area other than the 1 stimulated
where do some pain fibres of spinothalamic tract go off to on their way to somatosensory cortex?
to activate reticular formation of pons and medulla
enter periaqueductal grey matter of mid-brain
what do pain fibres from face and front of head enter?
trigeminothalamic system
what do pain fibres from back of head travel in?
cervical nerves
where is pain mainly represented in the cerebral cortex?
the cingulate gyrus= convolution of cortex lying next to corpus callosum
and in sensory and motor association areas
why can direct electrical stimulation of periaqueductal grey matter have an analgesic effect?
this area consists of a collection of cells highly sensitive to opioid neuropeptides e.g. enkephalins, endorphins and dynorphin, and which regulates serotoninergic pathways to the substantia gelatinosa- stimulating inhibitory interneurones that inhibit neurotransmitter release from 1st order afferents so nociceptive pathway inhibited.
what are descending serotoninergic pathways from reticular formation regulated by?
fibres from periaqueductal grey matter of mid-brain
what do descending serotoninergic fibres end on?
cells in substatia gelatinosa (lamina II), causing release of enkephalin- modulates activation of ascending pain pathway
what is thought to ‘gate’ the input into the anterolateral system of ascending sensory fibres?
enkephalin
why is normal cutaneous sensation not painful?
enkephalinergic neurones inhibit pain pathway
how is pain pathway activated following tissue damage?
mediators e.g. PGs, bradykinin and histamine are released which inhibit cells of substantia gelatinosa which contain enkephalinergic neurones which inhibit the pain pathway, so inhibiting these cells causes pain pathway activation.
descending serotoninergic fibres may now reactivate cells of substantia gelatinosa, partially reimposing inhibition to modulate the pain.
define chronic pain
pain that persists beyond the period of removal of provoking stimulus (pain for more than 3 months)
what features of peripheral nerves indicate that they are ‘mixed spinal nerves’?
Each spinal nerve has 2 nerve roots, apart from the 1st which has no sensory root, an anterior and posterior spinal root, come together in spian lcanal so mixed nerve emerges from IV foramen. Anterior= motor function, Posterior= sensory function, so peripheral nerves have sensory, motor and autonomic functions all represented within the same nerves.
Different directions for APs to travel are represented= afferents- AP towards CNS from sense organs, efferents- AP from CNS to PNS.
General or special modalities= cranial nerves
Myelination or lack of, lightly and heavily myelinated
Speed of AP conduction, related to degree of myelination- conduction velocity directly proportional to fibre diameter in myelinated axons, and directly proportional to square root of fibre diameter in unmyelinated.
Fibre thickness- thicker if myelinated, and cross-sectional diameter of axon directly proportional to size of its cell body.
Which sensory modalities will be activated at just threshold potential in nerve conduction studies and why?
proprioceptors, in part. muscle spindle afferents as these are most heavily myelinated nerves in body, and myelination reduces capacitance, so these nerves will require less current to activate them and so will be brought to threshold more easily on stimulation.
Which sensory modality will be activated at maximum intensities of stimulation in nerve conduction studies and why?
C-fibres (unmyelinated axons)= slow pain fibres and warmth
as really high capacitance, so higher current required to reach threshold.
why does paraesthesia occur with nerve fibre compression?
compression acts as a non-physiological stimulus to nerve AP firing, but as these APs have not been coded correctly, the nervous system is unable to make sense of them, and this produces the strange feeling of pins and needles.
what non-imaging technique can be used to determine if sciatic nerve problem is cause of pain in back of leg?
straight-leg raise test- patient lies down on their back and examiner raises their leg with knee straight. If sciatic pain experienced when leg between 30 and 70 degrees, then +ve disc, and herniated IV disc= likely cause of pain.
why may only a mild pain be felt initially in a RTA?
stressful situation- high order regions of CNS e.g. frontal cortex and somatosensory cortex can interact with nociceptive pathway to reduce pain. Fibres from here release opioid-like neuropepetides which act on cells of periaqueductal grey matter, and descending fibres from here activate serotoninergic fibres and noradrenergic fibres in medulla which then activate enkephalinergic neurones in dorsal horn of SC and trigeminal nucleus which moderate nociceptive pathway. Opioid receptors in PAG engaged by ascending nociceptive fibres and hypothalamus, forming a pain modulating feedback loop.
Release of ACTH accompanied by release of endorphin like chemicals.
What 2 regions may pain be referred from the diaphragm and why?
central part of diaphragm innervated by phrenic nerve= C3, C4 and C5, so pain may be referred to C3-C5 dermatomes= shoulder region and costal margins.
peripheral part of diaphragm and skin over costal margins innervated by inferior IC nerves= T5-T11, so pain is referred to the chest wall.
why is cardiac pain referred to left arm?
visceral pain fibres from heart travel in cardiac plexus to superior cervical ganglion. Heart develops at same segmental level as structures within T1 dermatome, so cardiac pain fibres enter SC at same segmental level as somatic afferents from T1 dermatome on left side. In SC grey matter, cardiac pain fibres and somatic afferents from T1 converge on same 2nd order afferent neurone in spinothalamic tracts so pain originating from heart perceived in somatosensory cortex as being from T1 dermatome, hence left shoulder, as pain normally conveyed from here, whereas heart isn’t normally painful.
what is nocicpetion?
this refers to all the transmission carried by pain fibres up to pain actually being detected, so processing of info. up to perception and hence is the non-conscious neural traffic orginating with trauma or potential tissue damage.
difference between pain threshold and tolerance?
threshold= same for all individuals, the point at which nociceptors are activated when tissue damage occurs is the same in all of us
BUT our variable reaction to pain stimulus= tolerance- depends on many factors e.g. psycho./emotional, what you were doing at the time, increases with age, ongoing pain
which pathways in the anterolateral system are examples of indirect (slow) tracts?
spinohypothalamic tract
spinotectal tract
spinomesencephalic tract
spinoreticular tract
functions of indirect (slow) tracts in anterolateral system?
spinoreticular= arousal, wakefulness spinomesencephalic= contribute to activation of descending pain inhibition, and emotion spinotectal= reflex eye, upper body and head movements spinohypothalamic= ANS and reflex responses
stages of nociception (process of transmission up to pain being detected)?
transduction
transmission
modulation
perception
describe transduction in nociception
stimulus evokes action potential by activating nociceptor
tissue damage causes K+, PG, bradykinin, histamine and 5-HT release onto nociceptor terminal, causing depolarisation, threshold reached, and AP fired. Nociceptor then releases more chemical e.g. substance P and CGRP- causes vasodilation, hence redness, and leaky capillaries- so oedema, and swelling. Can also cause mast cell degranulation, so histamine release, which further activates nociceptor, so increased sensitisation of nociceptor, so ensuring protection as the local area becomes sensitised. Like +ve feedback mechanism.
stimulus modality which Adelta fibres respond to?
mechanical
stimulus modality which C fibres respond to?
mechanical, thermal and chemical
BUT most A delta and C fibres actually polymodal if stimulus of a great enough intensity
How do NSAIDs target nociceptive pathway?
inhibit chemical production at site site of tissue damage and hence stop nociceptor activation, thereby stopping the transduction process.
steroids also act at site of tissue damage to inhibit chemical production and stop nociceptor from being activated.
What type of pain is felt initially with a painful stimulus and what fibres are responsible for this pain transmission?
A delta fibres sharp, stabbing intense pain well localised very fast, phase 1= first part of pain we feel lower threshold initiates withdrawl reflex OW
What type of pain is felt after the initial sharp stabbing intense pain felt with a painful stimulus and which fibres are responsible for this type of nociceptive transmission?
C fibres dull, throbbing slow, phase 2 pain poorly localised higher threshold tissue damage occurring OH felt in chronic pain*
