Week 2 - Neuro Big Ideas Flashcards
lacrimation pathway (tearing)
parasympathetic, hypothalamus to superior salivatory nucleus
ptosis pathway (drooping of eyelid)
parasympathetic, hypothalamus to superior salivatory nucleus
pupil constriction pathway
parasympathetic, hypothalamus to superior salivatory nucleus
daiphoresis pathway (sweating)
sympathetic via muscarinic ACh receptors, hypothalamus to spinal trigeminal complex
vasoconstriction pathway
sympathetic via norepinephrine/epinephrine to andrenergic receptors, hypothalamus to spinal trigeminal complex
serotonergic synapse
pre - serotonin vesicle, 5HT1D autoreceptor, reuptake transporter; post - serotonin receptor (5HT1a)
5HT1d autoreceptor
serotonin, presynaptic, if activated - blocks serotonin release
monoamine oxidase and aldehyse dehydrogenase enzymes
break serotonin down into 5-hydroxyindoleacetic acid, leaves the brain in the blood
5HT1a receptor
activation in brainstem (raphe nuclei) inhibits serotonergic neurons
itch
perception, conscious process, brain modulates
touch
sense, has receptor
pressure
sense, has receptor
vibration
sense, has receptor
warmth
sense, has receptor
pain
perception, brain continually modulates
3 fundamental steps of information processing
transduction, transmission, and perception
perception
brain is capable of switching priority, paying attention, conscious process, ex: pain is perception, localized by stimulus modality
sensation
not a conscious process, brain can’t switch attention, ex: nociception is sensation, mapped to key orderly respresentation - hummunculus
transduction
all sensory systems, stimulus energy converted into electrical potential that can be interpreted by nervous system
stimulus energy
electromagnetic, mechanical, chemical
essential step for transduction
confirmational change in transducer protein, ex: stretch receptors
receptor potential
graded response to stimulus, can be depolarizing or hyperpolarizing
transduction
stimulus energy -> receptor -> receptor potential (graded) -> depolarization increase with stimulus increase -> action potential at node of ravier -> intensity of stimulus translates to number of action potentials
adequate stimulus
stimulus that receptor best responds to, hummunculus map in every sensory system, receptor will respond to other stimulus but interepret incorrectly, ex: pressure on eyes makes you see stars
receptors
encode stimulus modality by responding better to one form of energy in a narrow range
coding for stimulus intensity
increase in firing of primary afferent, saturation of response of individual receptor cell, recruitment of overlapping sensory neurons, lack of response to some stimuli (if not adequate)
dynamic range
between threshold and saturation point for a receptor
range of system of receptors
sum of the ranges of all receptors within system
population coding (recruitment)
as the stimulation increases, the number of sensory cells increases with increasing stimulus intensity
receptor potential threshold
stimulus amplitude that must be reached before a response is generated
receptor potential saturation
in response to intense stimulus
frequency coding
firing rate of sensory neurons increases with increasing stimulus intensity
adaptation
response of receptor to constant stimulus declines over time
tonic adaptation
receptor potential decreases slowly with constant stimulus
phasic adaptation
receptor potential decreases rapidly with constant stimulus
acuity
ability to localize stimulus, determined by receptive field size and receptor density
intensity and localizing paradox
as stimulus intensity increases, acuity decreases because more receptors respond making it harder to localize
lateral inhibition
for localizing and encoding intensity, inhibitory CNS interneurons synapse with collaterals from main sensory neuron, by inhibiting signal strength from more distant neurons - helps localize stimulus, ex: retina to help see contrast
can’t see marker on board
stimulus doesn’t reach threshold
allodynia
pain from stimulus that does not normally evoke pain, ex: sharp pain when brushed lightly
hyperalgesia
increased sensitivity to pain, ex: more sensitive to pain after being stabbed by a platypus
acute nociceptive pain
fast - sharp, pricking, well localized, Adelta fibers; slow - dull, aching, poorly localized, C fibers; thermal, mechanical, chemical; visceral (smooth muscle), deep somatic (tendons, bones), superficial somatic (wounds, small burns)
inflammatory pain
damage or sensitization of peripheral nociceptors by PG, can lead to chronic pain syndromes
neuropathic pain
complex, pain state, peripheral / central neuron damage, can lead to chronic pain syndromes, burning / electrical / stabbing / needles, ex: bumping funny bone
nociceptor activation
heat, protons, and vanillinoids (capsacin) cause TRPV1 to open sending messages up C fibers
nociceptor sensitization
bradykinins, prostaglandins, protein kinases make receptor open more easily - blocking prostaglandins is key to some analgesic drugs
referred pain
two sensory receptors use same pathway, brain assumes that it is the most common sensation coming on the pathway, ex: heart and skin nociceptors share same tract and brain assumes skin pain when there is actually heart pain
key step in nociceptive stimuli transmission
activation of ligand gated channel -> 1st order neuron glutamate to 2nd order metabatropic AMPA receptor (excitatory) -> 1st order collaterals glutamate to mGluR receptor (normally closed) on interneuron, as transmission increases gate will open
Gate Theory of Pain
nociceptors -> ligand gated channel -> C fibers -> glutamate to 2nd order metabatropic AMPA receptor -> collaterals glutamate to mGluR receptors on inhibitory interneuron -> stimulus increase gate on inhibitory interneuron opens and sends message up AB fibers in mechanoreceptor
perception of pain
activation of nociceptors, modulation of nociceptors and inhibitory interneurons, inhibitory interneurons regulate transmission at 2nd order neuron level, explains phantom limb pain and TENS treatment and opioid analgesics
local anaesthetics
block pain at low concentrations
conduction velocity of fibers
diameter (thicker = faster) and degree of myelination (myelinated = faster)
Abeta fibers
fastest, largest diameter, myelinated, mechanoreceptors
Adelta fibers
fast, middle diameter, myelinated, mechanoreceptors, cold, fast pain
C fibers
slowest, narrow, unmyelinated, mechanoreceptors, thermoreception, slow pain
Adelta cold receptors open in response to…
menthol, CMR1
transduction channel
transient receptor potential ion channels
thermoreceptors
cold and warm, adapt rapidly to temp changes and chemical stimuli
mechanoreceptors
respond to deformation of cell membrane
nociceptors
respond to heat, protons, and vanillinoids (capsacin); responses potentiated by prostaglandins - blocking PG is mechanism of some analgesic drugs
dermatomes review
area supplied by one spinal nerve / dorsal root ganlgion; C1 no DRG, C2 top and back of head, C5-8 arm / hand, T4 nipples, T10 umbilicus, L1 inginal, L4-S1 lower lef / foot, S2-5 back of legs / butt / genitals; shingles is varicella-zoster latent on DRG - L6 / 7 most common area
cutting one dorsal root
has little effect on sensory due to overlap of sensory areas
cutting several dorsal roots
has anesthetic effect on sensory where all roots overlap
dorsal column
white matter, lesion here causes reduced (not absent due to overlap) fine touch / vibration / propioception below point
dorsal column - medial lemniscal pathway (somatosensation)
touch / proprioception / vibration, entire spine to thalamus, receptor in skin -> peripheral nerve -> cell body in DRG -> enter spine via dorsal root -> ascend in gracile and cuneate fasiculus on ipsilateral side -> synapse in gracile and cuneate nucleus -> cross to contralateral at medial lemniscus in caudal medulla -> synapse in ventral posterolateral nucleus of thalamus -> postcentral sensory gyrus
first order sensory neuron
receptor in peripheral nervous system, cell body outside CNS
second order sensory neuron
nuclei, 1st synapse, crossing over, cell body inside CNS
third order sensory neuron
nuclei to cortex, 2nd synapse
dorsal columns input
mechanoreceptors - Merkle disc endings (slow afferent type I), meisner corpuscles (indentation), pacinian corpusles (vibration / proprioception)
sensory entry into spinal cord
peripheral process -> cell body in DRG -> central process -> medial dorsal root ascends in dorsal column ipsilaterally (some branches terminate in dorsal horn)
organization of dorsal column
at thoracic level - sacral (medial) / lumbar / thoracic (lateral); at cervical level - sacral (medial) / lumbar / thoracic / cervical (lateral)
injury to lateral dorsal column
deficit on same side below point
injury to medial dorsal column
deficit on both sides below that point because ipsilateral tracts travel side by side
gracile fasciculus
medial to dorsal intermediate sulcus, carries T7 and lower (lumbar / sacral)
cuneate fasciculus
lateral to intermediate sulcus, T6 - C2 (thoracic / cervical)
lesion on dorsal column midline at L2
below L2 affected fine touch / proprioception / vibration on both sides
dorsal column nuclei
medulla, 1st synapse with 2nd order neuron, in gracile and cuneate nuclei
physiological class segregation
type of sensory axons end together in dorsal column nuclei, ex: slowly adapting type I, proprioceptors, pacinians, stimulus is dissected
dorsal column nuclei
many 2nd order neurons receive input from hand (cuneate nucleus) or foot (gracile nucleus) because they have many receptors to start with
dorsal column ascending ipsilateral fibers
25% end at dorsal column nuclei in the medulla, the rest make propriospinal connections to help produce complex movements
convergence in dorsal column nuclei
same type of 1st order neurons end together on same nuclei to synapse with 2nd order nuclei, receptive field is 40-100x larger than nuclei synapse in brain stem
population response for dorsal column sensory
overlapping receptive fields allow for finer touch descrimination
medial lemniscus
part of dorsal column sensory, caudal medulla, 2nd order neurons from gracile and cuneate nuclei cross over to contralateral, organized - cervical (dorsal), sacral (ventral), “person on pyramids”
lesion in medial lemniscus
contralateral sensory deficits
ventral posterior lateral nucleus (VPL) of thalamus
2nd synapse with 3rd order neurons, organized - sacral (lateral), cervical (medial), receptor segregation maintained
lesion in ventral posterior lateral nucleus of thalamus (VPL)
contralateral sensory deficits
thalamocortical projections from ventral posterior lateral nucleus in thalamus
3rd order neuron axons of VPL through posterior limb internal capsule to postcentral gyrus (primary somatosensory cortex) on ipsilateral side, homunculus
spinothalamic tract system (somatosensation)
pain and temp, damage reduces pain and temp (not touch), nociceptors and thermoreceptors -> peripheral nerve -> cell body in DRG -> synapse with 2nr order neuron in dorsal horn -> immediately cross over to contralateral in spinal cord -> ascend in spinothalamic tract to ventral posterior lateral nucleus in thalamus -> synapse with 3rd order neurons -> postcentral gyrus and insula
convergence and segregation of sensory type
persists in spinothalamic tract system
spinothalamic tract system receptors
nociceptors, thermoreceptors, and somewhat mechanoreceptors
nociceptors in spinothalamic tract system
enter lateral dorsal tract, pass through Lissauer’s Tract, enter dorsal horn and synapse with 2nd order neurons by releasing glutamate and SP
intense noxious stimuli
cause release of both glutamate and SP neurotransmitters at synapse in dorsal horn, both AMPA and NMDA receptors activated, other peptides released, changes synapse
second messenger changes at nociceptor synapse
changes in 2nd order neuron via second messenger / cascade -> new receptors or modified receptors, causes chronic pain
spinothalamic tract
2nd order neuron axons from marginal zone and lamina V in dorsal horn project to thalalmus after crossing over at anterior white commissure and ascending in spinothalamic tract in ventral lateral funiculus of spinal cord
marginal zone
most dorsal point of dorsal horn, 2nd order neurons of spinothalamic tract system
lamina V
lateral dorsal horn, 2nd order neurons of spinothalamic tract system
anterior white commissure
immediately ventral to central canal, crossing over of 2nd order spinothalamic neurons to contralateral side of spinal cord
spinothalalmic tract system
max activation from noxious stimuli (pain, heat), respond weakly to innocuous tactile stimuli from mechanoreceptors (reason why dorsal column lesions do not completely eliminate sense of touch)
crossing over of 2nd order neurons in spinaothalalmic tract system
axons cross over within two segments up spinal cord, then ascend to thalamus
lesions in ventral lateral funiculus
cut off pain and temp completely two spinal segments below on opposite side, some fibers get past in segments closer to lesion, ex: cut at T6 = loss of pain and temp at T8 and lower
unilateral lesion in ventral lateral funiculus
analgesia and athemia on contralateral side
cordotomy
bilateral surgical cutting of ventral lateral funiculus to relieve pain in terminally ill, pain sensation returns within 6 months because other pathway begin to carry nociceptive information
syringomyelia - central cord syndrome
rostrocaudal hole in central canal, cuts off spinothalamic axons that cross over in that area, ex: L2-L5 hole would cause L4-L5 loss
reticular formation collateral branches of spinothalamic tract
2nd order neuron collateral branches to reticular formation in medulla / pons, controls waking /attention, depolarizes cortical neurons to wake you up
central gray collateral branches of spinothalamic tract
collateral branches of 2nd order neurons in spinothalamic tract at central gray around cerebral aqueduct in midbrain, sends excitatory projections down spinal cord to inhibitory projections that inhibit nociceptive transmission - part of placebo effect
termination of spinothalamic tract at ventral posterior lateral nucleus in thalamus
synapses with 3rd order neurons, organization helps localize pain - sacral / lumbar (lateral), cervical (medial)
termination of spinothalamic tract at central lateral nucleus in thalamus
synapse with 3rd order neurons, no axon organization by location, responds to pain in all areas of body, projects to limbic system -> emotion
spinothalamic tract termination at ventral posterior lateral nuclei in thalamus
somatotopic organization, 3rd order synapse, lesion -> blocks ability to localize pain but still suffer from it, projections to ipsilateral postcentral gyrus
spinothalamic tract termination at central lateral nucleus in thalamus
no somatotopic organization, synapse with 3rd order neurons, lesion -> can localize pain but do not suffer from it, projections to ipsilateral limbic area like cingulate gyrus and insula
pain from trigeminal dermatomes
tooth ache, sinus pain, tension headache, ear ache, TMJ disorder, trigeminal neuralgia
3 trigeminal areas where pain only is sensed
teeth, cornea, tympanic membrane
trigeminal afferent to ipsilateral
face, top of head, anterior 2/3 tongue, ear drums, jaw proprioceptors
trigeminal efferent to ipsilateral
muscle of mastication, tensor tympani (dampens sound - if nerve injured problems with loud sounds)
trigeminal motor portion (in V3 - mandibular)
ipsilateral muscles of mastication, tensor tympani, cell bodies and synapse in motor nucleus of V, axons to nueromuscular junction, releases ACh on nicotinic receptors
trigeminal mechanoreceptors
bilateral, cell body in trigeminal ganglion, mostly to chief sensory nucleus of V in ipsilateral pons and synapse with 2nd order neuron with ipsilateral and contralateral projections to thalamus, few descend in spinal tract of V to spinal nucleus of V which synapses and crosses over to contralateral in trigeminialthalamic tract
trigeminal nociceptors
contralateral, cell body in trigeminal ganglion, descends down spinal tract of V to spinal nucleus of V and synapses with 2nd order neurons, crosses to contralateral side as trigeminalthalamic tract and ascends
trigeminal jaw proprioceptors
ipsilateral, cell body in trigeminal ganglion, ascends to mesencephalic tract of V to synapse in mesencephalic nucleus (midbrain), collateral branches to motor nucleus and synapse with motor fibers of trigeminal nerve - forms jaw jerk reflex loop
brainstem lesions
lesions anywhere on brainstem affect trigeminal nerve in some what because it is so wide spread
trigeminal tractotomy
treats chronic pain in trigeminal dermatomes by cutting spinal tract of V
spinal nuclei of V (spinal trigeminal nuclei)
nociceptors and some mechanoreceptors descend to nuclei in spinal tract of V, synapse with 2nd order neuron, cross to contralateral side in trigeminalthalamic tract and ascend to ventral posterior medial nucleus of thalamus
organization of spinal nuclei of V
caudal medulla - ophthlamic (ventral), jaw (dorsal)
chief sensory nucleus of V
lateral ventral pons, mostly mechanoreceptor input, synapse with 2nd order neuron, project to contralateral ventral posterior medial nucleus of thalamus via ventral trigeminothalamic tract, projects to ipsilateral ventral posterior medial nucleus of thalamus via dorsal trigeminothalamic tract
intraoral trigeminal sensation
bilateral representation in both VPL and VPM, can still chew and swallow after a stroke
trigeminothalamic axons to ventral posterior medial nucleus of thalamus
synapse with 3rd order neurons that project to cortex near lateral fissure, intraoral mechanoreception bilateral from chief sensory nucleus to VPM, contralateral from spinal nucleus of V and contralateral from chief sensory nucleus of V face region (lateral) VPM
organization of ventral posterior medial nucleus of thalamus
face (lateral), intraoral cavity (middle), taste (medial)
mesencephalic trigeminal nucleus
midbrain, stretch (proprioception) receptors in muscles of mastication and peridontium, cell bodies in pons/midbrain at edge of central gray (not in V ganglion), collateral axons to motor nucleus of V -> jaw jerk reflex
trigeminal representation on homunculus
postcentral gyrus, lateral parietal lobe with face
brain size and intelligence
not correlated
2SQ - viral meningitis
<30, death uncommon, symptoms more mild than bacterial meningitis, HIV patients at time of seroconversion, caused by enteroviruses (ss + RNA), arboviruses (ss + / - RNA), HSV2 (ds DNA)
2SQ - meningococcal meningitis
headache, photophobia, PMN (neutrophils) in CSF, low CSF glucose, high CSF protein, rash on legs, crowded spaces - dorms
2SQ - neonatal meningitis
caused by Strep B agalactine (gram + cocci chain), E. coli (gram - rod), listeria monocytogenes (gram + rod), in vaginal tract during birth, go to upper respiratory tract -> pneumonia -> septicimia -> meningitis
2SQ - crytococcal meningitis
encapsulated dimorphic yeast, worldwide, India ink
NILMO - tension headache
dysfunction of serotonergic neural pathway
NILMO - oral sumatriptan
does not work as well, takes longer to reach peak plasma concentration
NILMO - migraine medication
causes dry mouth, constipation, sedation, blurred vision - result of action of drug at serotonin reuptake transport protein
NILMO - headache onset while running
need to be evaluated for secondary causes of headache
NILMO - patient with Hx of heart attack and migraines
can’t take DHE that antagonizes serotonin receptors, may cause vasospasm and heart attack
2SQ - false myocardial infarction
normal ECG, referred pain from acute coronary syndrome, afferent pain fibers from heart enter posterior horn at brachial plexus level, pain perceived as neck and shoulder pain
2SQ - brain size
sperm whale - largest brain, humans have largest brain to body weight ratio 1:50 (most mammals are 1:180)
2SQ - damage to left accessory nerve (CN XI)
supplies trapezius (tested with shoulder shrug) and sternocleidomastoid (turns head opposite from side muscle is on)
2SQ - C fiber pain conduction
slow pain conduction, burning / aching / throbbing, poorly localized, small unmyelinated fibers
movie - CNI / II
tracts at superior brain stem
movie - brainstem
midbrain, pons, medulla
movie - midbrain nerves
CN III / IV
movie - pons nerves
CN V / VI / VII / VIII
movie - medulla nerves
CN IX / X / XI / XII
movie - cranial nerves clinical findings
typically on same side as involved cranial nerve and nucleus
movie - CN I olfactory
olfaction, sensory, direct to cortex - does not pass through thalamus, tract to uncus in temporal lobe
movie - CN II optic
good localizing in x axis, lesion testing areas - view optic disc, acuity, fields, pattern of vision deficit - tells location (pre/post chiasmal, optic tract, optic radation, calcarine cortex)
movie - CN III oculomotor
midbrain, controls eye adduction (MR) / elevation (SR) / depression (IR) / and elevation of eyelid (levator papillae superius), parasympathetics to pupil, lesion = eye turned out and down, with ptosis (drooping eye lids) and mydratic pupils (dilated)
movie - CN VI trochlear
SO, turns eye downward and medially, lesion = eye up and out with head tilt to opposite should to minimize dyplopia (double vision)
midline cranial nerves
III, IV (dorsally), VI, and XII
movie - CN VI abducens
LR, adducts the eye, lesion = eye abduction lost and eye turns in
dyplopia
double vision if CN III, IV, and VI do not work together to produce conjugate movement
medial longitudinal fascicule
from CN III nucleus to CN VI nucleus on ventral, medial pons, aids conjugate eye movement
oculomotor gaze systems
saccadic eye movement, smooth pursuit, vestibulo-ocular movement, vergence
saccidic eye movement
rapid eye movement that brings new objects into view, frontal center to pyramidal pontine reticular formation
smooth pursuit
eye movement to keep moving image on fovea, parietal-occipital gaze center via cerebellar and vestibular pathways
vestibulo-ocular movement
vestibular system to motor movement nuclei, keeps image on fovea during head movement
vergence
optic pathway to oculomotor nuclei, keeps image on fovea when object moves closer –> near triad with convergence accomidation and pupillary constriction
movie - CN V facial
mid lateral pons, descending axons for pain / temp to spinal nucleus of V, synapse, cross over, ascend to VPM in thalamus; motor test - masseter and ptyergoids, sensory test - light touch + pin at V1 / V2 / V3
movie - CN VII facial
motor to facial expression, parasympathetic to tear and salivary glands, sensory to taste, lesions = bell palsy, PNS lesion = ipsilateral, CNS lesion = contralateral lower face (bilateral innervation in upper)
movie - CN VIII vestibulocochlear
sensory, auditory - acquity, Weber, Rinne, unilateral neurological hearing loss is lesion in sensory organ to cochlear nucleus, lesions above cochlear nucleus = no hearing loss; vestibular tests - balance, occulocephalic reflex, occulovestibular reflex
movie - CN IX glossopharyngeal
clinically locked to CN X, superior lateral medulla, motor to pharynx and larynx, sensory to pharynx and post tongue (taste), voluntary “Ahhhh” reflex, involuntary gag reflex, lower motor neuron lesion = absent voluntary / unilateral palatine weakness with ulvula deviation to normal side and reflexes, upper motor neuron lesion = no voluntary/bilateral palatine and hyperreflexive gag
movie - CN XI accessory
motor to SCM and trap, ipsilateral control, SCM turns head opposite from side of body it is on
movie - CN XII hypoglossal
motor to tongue, LMN lesion = tongue deviated to side of lesion, UMN lesion = bilateral psuedobulbar palsy and slow movement side to side
movie CN VI abducens
has longest intracranial route, most susceptible to ICP
diplopia
double vision, max in direction of parelytic muscle, the most peripherally seen image is the false one and comes from eye with paralytic muscle, is horizontal if medial/lateral recti, verticle if superior/inferior recti
intramuscular ophthamoplagia (INO)
lesion on medial longitudinal fasiculus, unilateral lesion = nystagmus in abducting eye and no adduction in other eye and lesion is on side that should be adducting, bilateral = neither eye adducting horizontally
2SQ - cluster headache
due to hypothalamic activation of trigeminal autonomic nervous system
2SQ - migraines
20-25% lifetime prevalence, common
2SQ - acute disseminated encephalomyelitis (ADEM)
CNS, diffuse, monophasic demyelination following viral infection, looks like MS, rapid onset headache, lethargy, coma, higher mortality
2SQ - Guillain Barr syndrome
PNS, demyelination following infection, ascending peripheral neuopathy, lower mortality
2SQ - recurrent laryngeal nerve
loops under aortic arch and right subclavian, supplies muscles of larynx, damage causes hoarseness, branch of vagus nerve
2SQ - Perinaud Syndrome
dorsal midbrain syndrome, MRI, tumor in pineal region, lateral ventricular dilation, paralyzed in upward gaze, lost pupil to light reflex, tumor in superior colliculus / pretectal area
2SQ - default network
network that is active in brain even though cognition is not happening
2SQ - Neisseria meningitidis bacterial meningitis
gram -, diplococcus, dorms, fever, headache, coma, CSF - high PMNs (neutrophils), low glucose, high proteins
2SQ - myelination
asynchronous, peaks in frontal / temporal at 50, peaks overall at 60
2SQ - dorsal column / medial lemniscal system
touch/vibration/pressure sensory, synapses in dorsal column nuclei in caudal medulla, crosses over to thalamus in medial lemniscus
2SQ - tumor inferior to left jugular foramen
compressed CN IX / X / XI, vagus motor fibers to palate / pharynx / larynx affect –> weakened gag reflex
2SQ - hypoglossal nerve
motor to tongue, nerve damage -> denervation atrophy on affected side and deviation to side of injury
2SQ - Horner’s syndrome
ptosis (drooping eyelids), anhidrosis (lack of sweating), miosis (constricted pupils), apical bronchogenic carcinoma causes interrupted sympathetic nerve fibers in cervical ganglion
PBL - pain from GI
visceral pain, ulcer due to less mucus and more acid, sensory via vagus nerve, 1st order triggered by increased H+, 2nd order triggered by glutamate via NDMA and ADMN receptors
PBL - pain from knees and spinal column
osteoclast activity –> increased H+ –> nociceptors triggered in periosteum -> 2nd order neuron in substantia gelatinosum –> cross over and ascend to VML, deep somatic pain
PBL - acute nociceptive pain
fast (sharp/pricking) via Adelta fibers, slow (dull/aching) via C fibers, immediate stimulation of nociceptor
PBL - inflammatory pain
damaged of sensitized (by prostaglandins) peripheral receptors, sensitization mean that stimulation threshold is lowered for nociceptor
PBL - neuropathic pain
complex, CNS / PNS damage, burning / electrical, ex: funny bone
PBL - chronic pain syndrome
increased stimulation of 2nd order neurons by glutamate via NMDA, AMDA receptors increased the number of receptors in the 2nd order cell membrane
PBL - opioid constipation
act on receptors on GI tract in enteric NS, Tx with laxative (magnesium hydroxide)
PBL - pain scales
not accurate, reliable, different for each person, good to track one person over time, Px look at palor / rigidity / guarding / high BP / high HR
PBL - social support
better social support -> better health care outcomes, risk - single, elderly, poor, minorities
PBL - sclerosis
white areas on x-ray showing calcification with osteoarthritis
PBL - compression fracture
wedge shaped vertebra on x-ray
PBL - disc space narrowing
bone on bone between vertebra in x-ray
PBL - metastatic cancer
popcorn appearance inside bone on x-ray
PBL - aged bones
bones look less calcified (blacker) with age
PBL - osteoblastic lesions
bone deposition by osteoblasts stimulated to activity by metastatic cancer
PBL - bone pain
disruption of periosteum
PBL - pain management with metastatic cancer
addiction not an issue, morphine drip tappered to fentanyl patch for long term pain reduction, give laxative with it for constipation side effect
PBL - aspirin (NSAIDs)
for inflammation, COX inhibitor -> less prostaglandins -> decreased inflammation
PBL - nociceptor GATE THEORY
1st order nociceptor, 2nd order neuron, interneuron, shut gate by stimulating inhibitory interneuron (opioids can act at presynpatic 1st order, inhibitory interneuron itself; descending PAG inhibitory pathway acts at presynaptic 1st order)
PBL - opioids
all pain, antagonizes Mu / Kappa / Delta opioid receptors in PAG which sends an descending inhibitory message to synapse in substantia gelatinosum, inhibits neuron by decreased Ca, increased K, decreased adenylcycline
PBL - opioid receptors
Mu / Kappa / Delta, found in PAG and peripherally, normally acted on by endogenous enkephalons
PBL - opioid addiction
opioid receptors stimulated by exogenous opioid, when taken away body does not have enough endogenous opioids and withdrawal happens, addiction also happend via ascending pathway to pleasure center, know addicted patient by constipation and small pupils in dark room
PBL - prostate cancer metastasis
often to bone because venous drainage passes by prostate and then by spine on way back to heart, carries epithelial cells
PBL - opioid administration to specific spot
prevents opioid action in the brain
chronic pain barriers
Pt - fear / acceptance / concerns, Provider - training / biases / legal fear, System - time / tools / fragemented / insurance / EMR / reimbursement, Cultural - language / racial bias / access, Legal - controlled sub act, DEA, REMS, medical boards
overcoming chronic pain barriers
acknowledge bias, evidence based care, team, comprehensive pt. eval, educate, share goals
chronic pain managment
integrated care, addiction support, conditional Rx, tox screening, pill counts, quantity / frequency of prescribing, longer acting meds, contract, records sharing
chronic pain (hyperallgesia, allodynia)
glutamate released by 1st order to AMPA receptors on 2nd order, enough glutamate kicks Mg+ off NMDA and Ca+ enters NMDA receptor, Ca+ second messengers cause more AMPA receptors in the cell membrane = less glutamate needed to stimulate pathway
hyperallgesia
excessive pain
allodynia
pain from a stimulus that should not be painful
sympathetic control of eye
dilator pupillae muscle (pupil dilation), superior tarsal muscle in upper eye lid
parasympathetic control of eye
sphincter pupillar muscle (pupil constriction), ciliary muscle
facial / ophthalmic vein anastomoses
how infections spread to dural venous sinuses
superior tarsal muscle
in upper eyelid, innervated by postganlionic sympathetic fibers from superior cervical ganglion, elevates eyelid
optic disc appears choked
ICP
olfactory stimuli : gustatory stimuli
10,000 (1,000 receptors) : 5
olfaction
chemical stimuli, 1,000 receptor proteins, separated in multiple dimensions to give 10,000 orderants, sense receptor is on 1st order neuron (unlike all other senses), 1st order neurons replaced regularly, few receptor types on an olfactory neuron
gustation
chemical stimuli, 5 tastants - sweet, sour, salty, bitter, umami
steps of olfactory transduction
oderant -> diffuses through mucus layer by olfactory binding protein -> receptor on 1st order neuron membrane -> activated g protein (Golf) messanger -> adenylate cyclase (effector protein) -> increases cAMP -> opens ligand gated cation channels -> Na+ entry -> area depolarizes (graded potential) -> neuron depolarizes (action potential)
labelled line coding (homunculus) in olfaction
receptor 1st order neurons segregated by type at 2nd order synapse in olfactory bulb - creates an odourtypic map
olfactory inhibition
response to one odor decreased by another similar odor
olfactory redundancy
different odorants can activate same receptors
olfactory receptor patterns
patterns of stimulation allow 1,000 receptors to code of 10,000 ordorants
lateral inhibition in olfaction
occurs in olfactory bulb to sharp response and definition of olfactory map
gustation receptors
taste cell receptors are scattered equally throughout the tongue, the old taste map is wrong, different papillae can be seen in different places on the tongue
bitter
transduced by gustducin activation
salty
transduced by Na+ through ion channel
sour
transduced by H+ through ion channel
sweet
transduced by gustducin activation
umami
transduced by gustducin activation
steps of gustation transduction
no chaperoning protein - through mucus membrane -> gustducin g protein receptor (effector protein) -> ligand gated nonspecific cation channel -> depolarized area (graded potential) -> voltage gated Ca2+ channels open -> NT release -> primary neuron action potential
bitter / sweet / umami
no chaperoning protein, diffuses through mucus membrane on its own
flavour
combination of smell, taste, and texture; patients with anosmia often complain of agustia too
peripheral hypogustia
rhinitis (cold), cystic fibrosis (saliva)
neuroepithelial anosmia
chemical burn of receptors, head trauma to cribriform plate
central anosmia / agustia
stroke, schizophrenia (hallucinations)
Parkinsons
loss of chemosensation due to loss of dopamine in CNS
increased sensory stimulation
causes increased amplitude of receptor potentials
efferent means
going away from neuron
afferent means
coming into neuron
corneal reflex
sensory of cornea via V1 triggers motor to close eye via CN VII
