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91 Cards in this Set

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define pain
an "unpleasant sensory and emotional experience associated with actual or potential physical damage."
pain is not just another sensory modality, it is a ___________.
perception
Acute pain has two stages. What are they and what fibers mediate them?
1. Sharp Pain: Fast, first
mediated by A-delta fibers
2. Dull Pain: Slow, Second
mediated by C fibers
There are three phases of pain: acute, ___________ and ___________.
1. Prolonged, Persistent (ie. during injury repair/healing - sensitive thumb that was wacked by a hammer earlier)
2. Chronic - >6 months
there are several different classes of nociceptors. How do they differ? What are the 4 classes?
Free endings contain specialized ionotropic receptors.
mechanical, thermochemical, polymodal, silent
Which classes of nociceptors use A-delta fibers? What is the receptor type and neurotransmitter used?
1. Mechanical
2. Thermomechanical (>45 and <5 deg. C)
Ionotropic receptors; Use Glutamate
Which classes of nociceptors use C fibers? What is the receptor type and the neurotransmitter used?
1. Polymodal (mechanical, thermal, chemical)
2. Silent (only active after inflammation)
metabotropic (slower) receptors: use glutamate and peptides as NTs.
Fast nociceptors utilize ____________ transmission, whereas Slow nociceptors use __________ transmission.
FAST - very localized transmission
SLOW - paracrine transmission
1. Where in the body are pain receptors found?
2. More specifically, where are A-delta fibers found?
3. How about C fibers?
1. everywhere
2. restricted to cutaneus
3. everywhere else
Describe nociceptor innervation of the viscera.
What does this have to do with referred pain?
viscera has diffuse central innervation with lots of convergence (yields a very diffuse signal). When the pain fibers leave the viscera they converge, so cutaneous and visceral P/T now travels on a common neuron. The difference is hard for the cortex to differentiate. This is the basis for referred pain
Which pathway mediates pain for the anterior head?
Spinal Trigeminal Tract (V)
Describe the path taken by the spinal trigeminal tract
1. sensory neurons enter at pons via CN-V root
2. descend ipsilaterally to medulla via S.T. tract.
3. Synapse in pars caudalis (in spinal trigeminal nucleus)
4. crosses midline and ascends via trigeminal lemniscus
5. terminates in conralat VPM
The LST and spinal V tract can alternatively synapse at the __________, which is responsible for arousal and affective response.
reticular formation of the midbrain
LST and spinal V tract can alternatively synapse on the___________, this mediates descending pain control.
periaqueductal gray of the midbrain
LST and spinal V tract can alternaltively synapse on the___________, this is responsible for the autonomic responses associated with pain.
Hypothalamus
What is the triple response?
What must be intact for this response to work?
reddening
edema (wheal)
flare
* peripheral nerves must be intact (mediates CNS input & output)
insult to tissue causes release of pain causing substances. Name 3 of them. What is the MOA of these substances?
COX
Histamine
Substance P
* stimulate free nerve endings and activate nociceptors
Reflexes can be beneficial or harmful. Give an example of each.
beneficial - withdraw from painful stimulus via axon reflex
harmful - reflex sympathetic dystrophy
What is the MOA of reflex sympathetic dystrophy (RSD)
Nociceptors become sensitive to NE: viscious cycle (+ feedback loop) because sympathetics increase pain and pain increases sympathetics.
What can occur at the dorsal horn (that is related to pain stimuli)
pain signal can be modified here (increased or decreased)
The portion of the pain pathway that is responsible for emotion/affect is associated with what areas?
1. medial nucleus of posterior complex of thalamus
2. cingulate gyrus
Which part of the cortex is responsible for the "unpleasant" aspect of pain?
The insular cortex (if it is lesioned pain can still be identified but it is no longer unpleasant)
The portion of the pain pathway that is responsible for the autonomic response is _____________.
the reticular formation of the midbrain. (along with arousal)
What is pain sensitization? There are two types - name them.
enhanced responsiveness of the pain pathway (usually after an injury)
hyperalgesia
allodynia
define hyperalgesia
differentiate between primary and secondary.
increase in magnitude or duration of pain response.
primary - at site of injury (ie. triple response)
secondary - increased excitability of CNS neurons
A classic example of secondary hyperalgesia is Wind-up. Explain this example.
wind-up: Cells increase their firing; results in greater response to the same input. This is a permanent change.
define allodynia
pain from a nonpainful stimuli (CNS origin) (ie. rub hair on forearm - percieved as painful)
What are 3 useful roles for sensitization?
1. protect injured area (hyperalgesia and allodynia)
2. promote healing by increasing blood flow (triple response)
3. local inflammation guards against infection. (triple response)
Chronic pain is also called __________ pain because of its origin in the nervous system itself. What normally causes chronic pain?
neuropathic
Chronic pain is a result of plasticity of the nervous system or affective factors
Give an example of chronic pain of peripheral origin (due to the PNS).
How about central origin (due to the CNS)?
PNS - neuroma, RSD
CNS - phantom limb pain
Where are 3 places the pain signal can be regulated?
1. Cerebral Cortex
2. Reticular Formation
3. Dorsal Horn of spinal cord
stress, hypnosis, and the placebo effect are all examples of pain response regulated by the _________.
Will naloxone have an effect on any of these?
CNS
naloxone has NO effect on hypnosis
naloxone decreases the placebo effect
What is the projection pathway for pain response beginning at the reticular formation?
PAG in RF -> locus ceruleus -> raphe -> dorsal horn
What does the reticular formation control?
controls primitive functions (CV, respiratory, sensory/motor reflexes, posture, organization of eye mvmnt., sleep and wakefulness, emesis, analgesia)
Why are the raphe, locus ceruleus and PAG so important in analgesia?
they have lots of opiod receptors and peptides
The raphe nucleus has _________ output to the spinal cord. The locus ceruleus has _________ neurons.
serotonergic output
noradrenergic (NA) neurons
1. Where is the Raphe nucleus located?
2. What about the locus ceruleus?
3. and the PAG?
1. Medulla
2. Pons and Midbrain
3. midbrain
What are the ultimate functions of the seratonergic and noradrinergic fibers?
Both fiber types:
activate opiod interneurons which decreases pain transmission
enkephalin, endorphin and dynorphin are all ____________. What drug class works just like these?
endogenous opioids that naturally occur in the CNS.
Narcotics
What is the opioid receptor that is the target of morphine? Where else in the body are these receptors also found?
Mu opioid receptor.
* bowel, EAS (constipation major side effect)
* solitary tract nucleus (explains respiratory depression and CV changes)
What is the gate theory of pain?
when a nonpainful stimulus can decrease the painful stimulus in the dorsal root. (ie. rub leg or shake hand when pain is felt - will decrease pain)
What is the science behind the gate theory?
activation of mechanoreceptors (by additional stimulus) can decrease the pain sensation. Non-nociceptive input will inhibit LST via an IN.
What is diffuse noxious inhibitory control (DNIC)?
inhibition of a painful stimuli in a specific location via initiating a painful stimulus elsewhere on the body. (press hand, decrease headache)
What is the mechanism of DNIC?
1. outstanding pain signal is lost in noise of other pain
2. may activate descending inhibition
What does DEENO stand for in regards to causes of neuronal injury?
D-Drugs
E-Electrolytes
E-Endocrine
N-Nutrition (vits. B12, E)
O-Organ failure
Define primary neuronopathy
Damage to the soma and processes of a neuron
What is the mechanism behind neuronal tissue death in the case of a stroke?
Loss of blood flow to a neuron makes it stop producing ATP. The ATPases are no longer working, causing ion level disruption. Cells swell due to osmosis; this results in brain swelling, which compresses vasculature (further decrease in blood flow to brain)
Where are the only two regions in the CNS where new neurons are made? What is the source of these neurons?
1. Granule Cell Layer of Olfactory Bulb
2. Dentate Gyrus of the Hippocampus
Source = neuronal stem cells
Somatic injuries lead to the death of ___________________.
the entire neuron
What are the two types of neuropathies?
1. mononeuropathy - one nerve
2. polyneuropathy - nerves throughout body effected
What is neurapraxia? What is the mechanism behind this?
a conduction block in an axon. There is no structural damage. Nerve is slightly compressed, temp. loss of blood flow, nv. can't fire completely.
Transection of an axon while the connective tissue sheath is intact is called______?
axontmesis
Transection of an entire nerve is called ____________?
neuruotmesis
Transection of an entire nerve is called ____________?
neurotmesis
What are some signs of axonal damage to the PNS?
paresthesia (pins&needles), Tinel's sign, weakness, paralysis, decreased tendon reflexes, impaired sensations
Guillain-Barre and Varicella Zoster (shingles) are both _____________(acute/chronic) injuries to the _____(CNS/PNS).
acute injuries to the PNS
When axonal transection occurs the distal axon & myelin is broken up and phagocytosed. What is this called?
Wallerian degeneration
What are Bugner Bands?
Schwann cells and endoneurium that guide axonal regrowth.
What are the four reactions that occur in the soma when an axon is transected?
1. Chromatolysis (Nissl substance disperses)
2. Eccentric Nucleus
3. Soma Swells
4. Regrowth
What is synaptic stripping?
When the injured cell loses synapses
T/F: The same genes are expressed for axonal regrowth as are expressed in embryological development.
True
The regenerating axon tip is called a _____________.
Growth cone
What guides the growth cone into the Bugner Bands and therefore is required for neuronal regeneration?
the Epineurium.
What happens when the growth cones miss the bands?
a NEUROMA forms (basically a big ball of axon tips that fires spontaneously=painful)
What is the average neuronal growth rate after injury?
~ 1.5 mm/day
What is Tinel's sign?
if you percuss at the site of the growth cone tingling occurs. (Can be used to follow neuronal regrowth)
Functional recovery in the PNS is often restored before regrowth is complete. Explain
happens via:
1. collateral sprouting (from nondamaged neurons)
2. reactive synaptogenesis (synapses form in response to a stimulus)
What is the role of astrocytes following a CNS lesion?
Their processes sprout around the lesion and form a tangled mass
There are 2 sources of microglia that are involved in CNS damage. What are they? Function?
1. blood
2. CNS
Function - phagocytose damaged axon and myelin
In the CNS, the proximal axon begins to regrow but stops after how long?
2 weeks (big difference from PNS = 300 days+)
Why does axon regrowth stop so soon in the CNS?
Astrocytes and protiens from oligodendrocytes block the growth cone.
How is most functional recovery in CNS regained?
Through plasticity of neuronal connections (axonal sprouting)
trans-synaptic plasticity is _________.
indirect changes (occuring in a neighboring neuron) in response to removal of neuronal input
Define:
1. trans-synaptic deafferentation
2. trans-synaptic degeneration
1. loss of synaptic input changes the receptor and ion channel distribution
2. neuron or muscle starts to degenerate
What is gliosis?
when astrocytes increase in number and sprout many processes near the site of the CNS lesion
gliosis eventually forms a ___________. Consequence?
glial scar
stays for years; blocks neuronal growth in that area
When myelin is wrapped around an axon, ________ is squeezed out and __________ fuse together.
cytoplasm of (Schwann or Oligodendrocyte)
2 inner lipid bilayers
What are Schmidt-Lanterman clefts?
Areas where not all the cytoplasm was squeezed out - looks like a little node inbetween the fused lipid bilayers.
Hypomyelination is a lack of myelin due to ___1___, demyelination is due to ___2____.
1. developmental insufficiency (never formed)
2. loss of normal myelin after it is formed
Name an example of a demyelination disease of the PNS.
Guillain-Barre
How is it possible that a demyelinating disease can be specific to either the CNS or the PNS?
myelin has a different protein composition in the CNS vs. the PNS
In the PNS, myelin debris is cleaned up by ___1_____? In the CNS, myelin debris is cleaned up by ____2_____?
1. Schwann cells
2. reactive gliosis (astrocytes and microglia)
1. What is primary progressive MS?
2. What is secondary progressive MS?
1. No remittance
2. Remittance
What is the life expectancy of an MS patient?
80% of the non-MS population
1. How do you diagnose MS?
2. Other diagnostic hint?
1. must see 2 separate areas of CNS lesions at 2 separate times. Must confirm at autopsy.
2. increase in IgG in CSF
Treatments of the symptoms of MS include:
muscle relaxants, corticosteroids, baclofen, PT
Drug class prescribed to slow the advancement of MS?
Immunosuppressants, cyclosporins
Describe Guillain-Barre disease
the axon is usually spared, think it is an immune rxn, demyelination follows 1-2 wks after mild infection. Characterized by progressive weakness, paresthesia - usually resolves itself
1. When, developmentally, does myelination of the CNS occur?
2. What nutritional deficits during this period could lead to hypomyelination?
1. during final prenatal months and first years of life.
2. decreased protein, fatty acids, B vitamins, copper
T/F: the Schwann cell that just phagocytosed the myelin is the same one that begins remyelination.
FALSE - new Schwann cells arise by cell division: these remyelinate
remyelination begins at the lesion and progresses ___________.
distally