somatosensory, pain, plasticity

somatosensation and movement

sensation required for fine movement but not for gross movement or experience of pain (does require consciousness)

sensory receptors

transduce physical stimulus into electrical signal, movement of receptors opens channels
decision making process for AP generated at receptor, cell body has no decision making abilities

receptive field

area of skin innervated by a single afferent fiber
smaller distally with greater density, better discrimination spatially (localization, 2 pt discrimination)
skin areas with smaller receptive fields have larger representations in SI cortex

threshold

PC lowest threshold/highest sensitivity → RA → SAI → SAII

discharge adaptation

rapidly adapting/phasic/dynamic: respond to onset/offset of stimulus only, sensitive to change
slowly adapting/tonic/static: static response to stimulus, absolute value

discriminative touch and vibration

AB fibers, DCML pathway, low threshold mechanoreceptors, test with 2 pt discrimination
underlies capacity for: fine form and texture discrimination, 3D shape discrimination (stereognosis), motion detection on skin

DCML superficial cutaneous receptors

small receptive fields, good localization
meissner’s corpuscles: light touch, vibration, RA
merkel’s disks: pressure, SA
hair follicle receptors: sensitive to displacement of hair, direction of motion, SA and RA

DCML deep cutaneous receptors

large receptive fields, less localization
pacinian corpuscles: touch and vibration, RA, very active
ruffini’s corpuscles: skin stretch, SA

proprioceptive receptors: muscle spindle

absolute muscle length change (SA), change in muscle length (RA), rate of change of muscle length (RA)
most complex of somatosensory receptors, fusiform shaped and attached in parallel with muscle fibers, more numerous in muscle controlling fine movements except face

proprioceptive receptors: muscle spindle structure

intrafusal fibers (~7 per spindle), contractile elements in the ends of the fibers
nuclear bag fibers: dynamic are sensitive to rate of change in muscle length, static signal change in muscle length
nuclear chain fibers

muscle spindle sensory innervation: primary ending

length and rate of change, myelinated Ia fibers, best at RA but also SA
wrap around central region of both intrafusal fibers
responds primarily to phasic but also to tonic stretch
firing frequency proportional to degree of spindle stretch

muscle spindle sensory innervation: secondary ending

length and tension, farther away from center, myelinated II fibers, SA
innervate nuclear chain fibers, respond to tonic stretch

muscle spindle motor innervation

dynamic: gamma MN innervating dynamic bag fibers, related to phasic response, adjusts spindle sensitivity
static: gamma MN innervating static bag fibers and chain fibers, adjusts spindle length so it remains sensitive throughout range

golgi tendon organ

tension info, near musculotendinous junction, Ib afferents, SA
silent in relaxed muscle, sensitive to slight changes in tension

proprioceptive receptors: joint receptors

sufficient but not necessary to perceive joint movement, 2-4 deg joint ROM detectable

proprioceptive receptors: ligament receptors

similar to GTOs, signal tension, Ib fibers

course touch, temp, and nociception

ALS, mediated by free nerve endings throughout skin (density varies), test with pin prick
axons are either Adelta (myelinated) or C fibers (unmyelinated)

ALS symptoms

hypesthesia, numbness, tingling/prickling, anesthesia

Adelta fibers

conduct faster, localized/sharp pain sensations, no affective component to response

C fibers

slower conduction, poorly localized (dull persistent ache), affective component to response

non-nociceptive receptors

high threshold mechanoreceptors: crude touch (poor localization), rubbing, squeezing, skin stretching
thermoreceptors: cold (17-35 C), hot (35-45 C)

nociceptive receptors

higher threshold
mechanonociceptors, thermonociceptors, chemonociceptors, polymodal nociceptors

sensory detection

modality specific, determined by area of cortex to which fiber projects

perception

abstraction and elaboration of sensory input, experience and coincident sensory input can affect perception

single nerve peripheral info coding

AP, binary code, summation determines on/off mode

place coding

relative to internal map

frequency coding

firing rate of APs, signals stimulus intensity or encodes frequency of stimulation (vibration)

population coding

most stimuli set off multiple neurons, info about extent of stimulus/directional info, info about location of stimulus

modulation: external factors

stimulus starts in periphery, chemicals can be released by cells to change sensitivity of receptors
prostaglandins, leukotrienes, substance p

modulation: transduction mechanism

change sensitivity at level of receptors, modulation before info becomes an AP
ex changing auditory membrane stiffness, muscle spindle sensitivity

modulation: dorsal horn

descending tracts, afferent collaterals, interneurons
many connections makes it possible to change info as it comes into CNS

modulation: higher centers

thalamus, cortex (primary and secondary sensory areas, association areas)

plasticity

change in nervous system, non-periodic, last longer than few seconds
time scale, habituation, functional reorganization, synaptic changes

time scales

short term: changes occur over sec-min, changes often reversible, no permanent structural changes
long-term: changes take longer (up to years), structural changes (synthesis of protein, new synaptic connections)

habituation

repeated stimuli so decreased response because there is less NT released

pain connections

primary afferents (Adelta and C fibers) synapse with projection neurons (ALS), local excitatory and inhibitory interneurons
descending modulation: somatosensory cortex
periventricular nucleus hypothalamus, pontine reticular formation, raphe nuclei, medullary nuclei

modulation of nociception: peripheral level

activation: potassium, serotonin, bradykinin, histamine
sensitization: may cause nonpainful stimuli to become painful, prostaglandins, leukotrienes, substance P
non-narcotic analgesics: decrease synthesis of prostaglandins

modulation of nociception: dorsal horn

inhibitory interneurons: enkephalin, dynorphin
gate control theory: stimulate nearby non-nociceptive fibers (DCML), collaterals activate interneurons that cause presynaptic inhibition of nociceptive neurons, local response
enkephalin depresses release of substance P so secondary nerve has less drive

modulation of nociception: neuronal descending system

descending tracts synapse with inhibitory interneurons, braking system
raphespinal fibers
may be problem in people prone to chronic pain

modulation of nociception: hormonal system

endorphin release from periventricular gray
stress induced analgesia, low frequency high amp TENS

modulation of nociception: central level

expectations, distractions, placebos, excitement
longest lasting modulation

nociceptive pain

nociceptor activation leads to pain perception, acute and chronic

non-nociceptive pain

nociceptors not activated but there is still perception of pain
neuropathic pain, central sensitization, pain syndromes
structural reorganization

chronic primary pain

central sensitization: gain of function of central nociceptive pathways
absence of tissue damage, change in CNS with no peripheral nerve drive

chronic secondary pain

nociceptive: from stimulation of nociceptors, physiological response to tissue damage
neuropathic: arising from lesion or disease, peripheral (sciatic or carpal tunnel) or central (SCI, stroke, phantom limb)

neuropathic pain due to ectopic foci

no stimulus from receptor but middle of nerve spontaneously fires off

neuropathic pain due to ephaptic transmission

lack of myelin allows nerve to induce activity in another, wire cross talk

peripheral sensitization

same stimulus but nociceptive afferent more sensitized so the response is bigger
physiologic correlate of central sensitization

central sensitization

secondary nerve is more sensitized so fires off more to same amount of NT binding
physiologic correlate of central sensitization

structural reorganization in cortex

cortical neurons create new connections with more neurons
physiologic correlate of central sensitization

reduced descending inhibition

reduce brake so connection below is amplified
physiologic correlate of central sensitization

increased descending facilitation

neurons from brainstem facilitate, completely internally driven, negative plastic change
physiologic correlate of central sensitization

synaptic changes: recovery of synaptic effectiveness

swelling compresses presynaptic neuron, decreases synaptic efficacy

synaptic changes: denervation hypersensitivity

presynaptic neuron death results in formation of more postsynaptic receptors

synaptic changes: synaptic hypereffectiveness

degeneration of some axonal branches leads to increase in NT released by remaining branches

synaptic changes: unmasking of silent synapse

synapses that already exist but are unused start to become stronger

central sensitivity

disruption of pain matrix, decrease in anti-nociception or increase in pro-nociception pathways
fibromyalgia: pain inhibition areas impaired, disruption of multiple NT actions
also myofascial pain, migraines, chronic whiplash

chronic pain

changes in pain system and another system
chronic LBP syndrome and CRPS

chronic LBP syndrome

pain system and motor dysfunction
deconditioning, central sensitization, central reorganization

CRPS

central sensitization, structural reorganization of pain matrix, possible sympathetic and autoimmune dysfunction
from trauma and genetic predisposition

CRPS mechanism theory

multifactorial
fewer peripheral receptors become hypersensitive to circulating adrenergic NT, neurogenic inflammation, blood flow changes, central sensitization, cortical reorganization

CRPS s/s

more frequent females
continuous and disproportionate pain, abnormal sweating/edema, vasodilation in skin, temp changes, paresis, spasms, difficulty initiating movement
late stages: osteoporosis, arthritis, muscle atrophy

CRPS treatment

injection: sympathetic block for early stages only in stellate ganglion for UE or lumbar sympathetic chain for LE
PT: AROM and AAROM most beneficial, tactile stimulation, TENS, movement therapy