Neuro Exam 3.6

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brau2308
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Neuro Exam 3.6
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2013-04-05 19:52:16
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neurology neuroanatomy neuroscience
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review neuro lecture 6 for exam 3
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  1. Pain:
    subjective perception (people feel pain differently)
  2. Pain perception is sensed from:
    noxious stimulus, anatomy, integration and neurochemistry
  3. What must be stimulated for pain perception?
    neurons
  4. Noxious stimulation:
    chemical, thermal, electromagnetic, and mechanical stimuli which damage or have potential to damage cells [thermal, mechanical, chemical, inflammatory process, pathological process]
  5. innocuous stimulation:
    no potential to damage cells/tissue
  6. What are the potential energy sources of pain?
    • mechanical
    • chemical
    • thermal
  7. nociceptors:
    specialized neurons which respond to noxious stimulaiton
  8. What special anatomical structure do nociceptors have?
    free nerve endings
  9. free nerve endings:
    compared to specialized sensory end organs (i.e., muscle spindles, Meissner's, Corpuscles, etc.)
  10. What are the types of nociceptors?
    • A-delta fibers
    • C-fibers
  11. What type of fibers are A-delta fibers?
    Type III
  12. How are A-delta fibers myelinated?
    thinly
  13. What is the conduction velocity of A-delta fibers?
    b/w 6-30 m/sec (fast)
  14. What do A-delta fibers transmit?
    acute pain, sharp, and prickling pain sensations
  15. Are A-delta fibers well localized?
    yes, well localized as to source of noxious stimulation
  16. Do A-delta fibers have more or less emotional overtone than C-fibers?
    less
  17. What is emotional overtone?
    affective behavior
  18. What type of fibers are C fibers?
    type IV
  19. How are C fibers myelinated?
    they are non-myelinated
  20. What is the conduction velocity of C fibers?
    b/w 0.5-2.0m/sec (slow)
  21. What do C fibers transmit?
    chronic pain, burning, and aching pain
  22. What is pain felt by C fibers like?
    long duration and diffuse
  23. What are C fibers involved in?
    affective behavior (emotional overtone) --Pain can make you grumpy; people can act differently due to chronic pain
  24. How does noxious stimulation transmitted via A-delta and C fibers reach the CNS?
    Nerves of PNS
  25. What makes up the nerves of the PNS?
    • 31 pairs of spinal nn
    • 4 pairs of cranial nn
    • nerves of the ANS
  26. Which cranial nn make up the nerves of the PNS?
    CN V, VII, IX, X
  27. Which nerves share the spinal nucleus of V to transmit general sensation?
    CN V, VII, IX, X
  28. What are the nerves of the ANS?
    • splanchnic and sympathetic nn of sympathetic system
    • pelvic nn of parasympathetic system
  29. How does noxious stimulation reach the brain via the CNS?
    • spinothalamic tract
    • spinotectal tract
    • spinoreticular tract
    • dorsal column system
    • trigeminal tract
  30. What is the spinothalamic tract divided into?
    lateral and medial tracts
  31. What is the lateral spinothalamic tract called?
    neospinothalamic
  32. What type of pain does the lateral spinothalamic tract transmit?
    acute pain
  33. Where is the lateral spinothalamic tract found?
    anterior-lateral white columns of spinal cord
  34. How many neurons make up the lateral spinothalamic pathway?
    3
  35. What does the lateral spinothalamic tract receive input from?
    A-delta (nociceptors--sharp pain/acute) neurons
  36. What type of neurons are A-delta fibers?
    Type III
  37. Where do the 2nd order neurons of the lateral spinothalamic tract synapse with the 3rd order?
    VPL (ventral-posterior-lateral nucleus) of thalamus
  38. Where do the 3rd order neurons of the lateral spinothalamic tract terminate?
    post central gyrus
  39. What does the lateral spinothalamic tract allow?
    specific localization of pain source (sensory discriminative aspect of pain)
  40. What type of pain is perceived by the lateral spinothalamic tract?
    somatic and visceral pain
  41. What is the medial spinothalamic tract called?
    paleospinothalamic
  42. What type of pain does the medial spinothalamic tract convey?
    chronic pain
  43. What does the medial spinothalamic tract receive input from?
    C fiber neurons (dull, diffuse noxious info)
  44. What type of neurons are the C fibers?
    Type IV
  45. Where do the 2nd order neurons of the medial spinothalamic tract synapse w/ 3rd order?
    medial nucleus of thalamus
  46. Where do the 3rd order neurons of the medial spinothalamic tract project?
    post central gryus
  47. What type of pain is perceived in the medial spinothalamic tract?
    somatic an visceral pain
  48. What happens as the 2nd order neurons of the medial spinothalamic tract ascends?
    project collaterals to reticular formation
  49. What is responsible for the association of the medial spinothalamic tract w/ the limbic system?
    collaterals from the 2nd order neurons to the reticular formation
  50. What is the medial spinothalamic tract related to?
    motivational and affective aspects of pain (emotional overtone)
  51. Where does the spinotectal tract conduct noxious stimuli?
    from SC and terminates in tectum of midbrain
  52. What is contained in the tectum of the midbrain?
    superior and inferior colliculi
  53. What functions are the superior and inferior colliculi involved in?
    auditory and visual reflexes important in avoiding noxious stimuli
  54. What type of pathway is the spinotectal tract?
    reflex pathway (also processed in cerebral cortex)
  55. Where does the spinoreticular tract conduct noxious information?
    from SC to reticular formation of brainstem (ARAS)
  56. What is the spinoreticular tract responsible for?
    • waking you up if being noxiously stimulated
    • arousal and consciousness
  57. What is the main function of the dorsal column system?
    • proprioception
    • fine touch
  58. What is the dorsal column system a backup for?
    spinothalamic tract --parallel redundant system for perceiving noxious stimulation is damage occurs
  59. Which crainial nn are involved in the trigeminal tract?
    CN V, VII, IX, and X
  60. What do CN V, VII, IX, and X share?
    spinal nucleus of V
  61. What is the spinal nucleus of V responsible for?
    general sensation
  62. Where does the trigeminal tract transmit pain from?
    head and neck
  63. What does the trigeminal tract receive input from?
    either A-delta or C fibers
  64. Where do the 1st order neurons of the trigeminal tract synapse with the 2nd order?
    spinal nucleus of medulla
  65. Where do the 2nd order neurons of the trigeminal tract synapse with the 3rd order?
    thalamus
  66. Where do the 3rd order neurons of the trigeminal tract terminate?
    post central gyrus
  67. How does the CNS respond to noxious stimulation?
    • reflexively using a protective avoidance reflex
    • modulatory mechanisms
    • gating mechanism
    • referral of pain
  68. What does it mean that the protective avoidance reflex is automatic?
    goes straight to the cortex
  69. In the protective avoidance reflex, does input from A-delta or C fibers have to go to the brain for perception and action?
    no
  70. Where does input from A-delta or C fibers go if not to the cortex?
    • straight to spinal cord and then to skeletal muscle for reaction (standard reflex arc)
    • brainstem (similar to spinal cord, sends pathway to brain)
  71. Splinting/gaurding:
    protective avoidance reflex dealing with visceral structures (NOT somatic)
  72. Where are some examples of noxious stimulation in visceral organs?
    stomach, intestine, lungs...
  73. Does guarding cause splinting?
    OR
    Does splinting cause guarding?
    splinting causes gaurding
  74. Guarding:
    • skeletal mm that overlie a visceral structure that receives noxious stimulation may contract
    • resultant increase in muscle tone protects underlying visceral structures
  75. modulatory mechanisms:
    intensity of pain sensation is modified (generally decreased) despite continued presence of noxious stimuli
  76. Descending supraspinal inhibitory mechanism:
    modulates how much info ascends spinothalamic tract
  77. Where does the supraspinal influence in the descending supraspinal inhibitory mechanism come from?
    different areas (hypothalamus, thalamus, limbic system, frontal lobe)
  78. What does the supraspinal influence from the descending supraspinal inhibitory mechanism synapse with?
    periaqueductal gray area
  79. Where does the supraspinal influence from the descending supraspinal inhibitory mechanism project after synapsing w/ periaqueductal gray area?
    nuclues raphe magnus (part of reticular formation)
  80. Why does the descending reticulospinal tract synapse w/ 2nd order sensory neurons?
    to release inhibitory neurotransmitter to decrease amount of pain being sent to post-central gyrus
  81. When can mechanism activation happen?
    automatically b/c we don't like to be in pain
  82. What can patients be taught to avoid pain?
    biofeedback mechanisms
  83. What can patients use to decrease pain?
    • placebo effect
    • spiritual beliefs
    • TENS units
    • dorsal column stimulators
  84. Gating mechanism:
    peripheral afferents interact w/ and modulate noxious info to other parts of CNS (to thalamus and post-central gyrus)
  85. What is the theory of gating mechanisms?
    gate control theory of pain
  86. What happens during a gating mechanism?
    • convergence of noxious (type III and IV fibers) and non0noxious (type I and II) info to transmission cell in dorsal horn
    • noscious pathway competes w/ incoming innocuous stimulation (rubbing, shaking, etc.)
    • competition causes decrease in frequency of pain activity
    • result of rubbing/shaking affected area: feel less pain
  87. What is referral of pain due to?
    convergence of afferent input
  88. referral of pain:
    pain originating in visceral structure perceived as coming from a somatic structure (referred from true source to false source)
  89. Convergence projection theory of Ruch:
    input from nociceptors of somatic and visceral structures converge upon neurons at some point in the pain pathway
  90. Pain from day one is used to receive pain from what?
    somatic structures
  91. What type of fibers do visceral structures have to transfer pain?
    A-delta and C fibers (aren't used often so brain is conditioned to perceive somatic pain)
  92. Where does the brain assume visceral pain is coming from?
    somatic structure
  93. Some research suggests that somatic and visceral nociceptive info converges where?
    on same dorsal horn
  94. Under normal conditions, pain pathways are usually associated w/:
    somatic nociceptor, rarely a visceral one
  95. When noxious stimuli does originate from visceral structure and activates same neurons (that would otherwise be activated by a somatic nociceptor), the brain perceives the info as:
    somatic based on previous experience
  96. Somatic structure/A-delta and C-fibers/visceral structure project where?
    to dorsal horn cell where they synapse and project to thalamus where they synapse and project to cerebral cortex
  97. What are the potential combinations of convergence?
    • viscerosomatic
    • visceroviscerosomatic
    • somatosomatic
  98. Viscerosomatic:
    • most common
    • ex: angina; pain in upper extremity associated w/ MI or low back pain associated w/ kidney infection
  99. Viceroviscerosomatic:
    clinical correlation results in mimicking of heart pain as originating from upper extremity.  Perception of pain is same from all 3 structures--brain doesn't know where it is really coming from
  100. Somatosomatic:
    little research b/w somatic pain is rarely life threatening (one sore MM v. another sore MM)
  101. Acute pain:
    • short-lived w/ duration being a function of underlying pathology, which is usually known (A-delta fibers)
    • 1st pain --gets attention
  102. chronic pain:
    • any pain that persists for more than 3 months and is unresponsive to appropriate treatment (C fibers)
    • 2nd pain
    • ex: arthritis
  103. recurrent pain:
    pain that may reoccur: HA, LBP, MSK pain
  104. Sometimes must treat pain as:
    disease v. a symptom
  105. What are types of pan due to hypersensitivation?
    • allodynia
    • hyperalgesia
    • causalgia
  106. Allodynia:
    • pain due to a stimulus that doesn't usually provoke pain
    • (ie: touch back of sunburnt hand and it hurts when it doesn't hurt normally)
  107. Hyperalgesia:
    increased response to a stimulus that is normally painful (i.e., more painful than you would expect)
  108. Causalgia:
    syndrome of sustained, burning pain and allodynia after a traumatic nerve lesion; often combined w/ vasomotor dysfunction and later trophic changes to tissue
  109. What are the physiological and anatomical types of pain?
    • neuropathic
    • nociceptive
    • idiopathic
    • neuralgia
  110. Neuropathic:
    any pain syndrome in which predominating mechanism is a site of aberrant (abnormal) somatosensory processing in CNS or PNS
  111. Nociceptive pain:
    reflects degree of activation of peripheral nociceptors in direct response to tissue damage
  112. idiopathic pain:
    occurs in absence of identifiable organic cause
  113. neuralgia:
    pain in distribution of nerve/nerves (i.e., sciatica, shingles)
  114. What are the systems of hypersensitivity?
    • peripherally mediated hypersensitivity
    • centrally mediated hypersensitivity
  115. peripherally mediated hypersensitivity:
    common physiologic substrate that underlies hypersensitivity of PNS neurons
  116. What happens to the resting membrane potential during the peripherally mediated hypersensitivity?
    reset at lower level (less negative--easier to fire)
  117. When the resting membrane potential is reset at a lower level (less negative) what does this mean in relation to the threshold of activation?
    takes cell closer to threshold of activation (hyperpolarized) [-70 gets closer to -60 w/ hypersensitivity]
  118. What are the anatomical sites of peripheral sensitization?
    • receptor organs
    • DRG (which contains cell bodies)
    • distal cellular processes
    • proximal cellular processes
  119. What are the hypersensitivity chemicals?
    • ligands (hyperpolarize PNS threshold)
    • kinins (bradykinin, kallidin)
    • interleukins (produced by WBCs; hypersensitize tissue)
    • Nerve growth factor
    • prostaglandins
    • tumor necrosis factor
    • epinephrine, formalin, capsasin
  120. Which is more important?
    centrally mediated hypersensitivity
    OR
    peripherally mediated hypersensitivity?
    centrally mediated hypersensitivity
  121. What occurs in the Centrally mediated hypersensitivity?
    • CNS no longer gets afferent input (deafferations) from PNS
    • there are adjustments in amount of receptors on postsynaptic cell membrane (up and down regulation of genes)
    • genes are upregulated at dorsal horn (generate more receptors); more receptors will get more input
  122. Are the neurons in pain pathway and integrative areas harder or easier to fire?
    easier (hypersensitization-allodynia-hyperalgesia)
  123. What produces increased quantities of neuromodulators?
    nociceptors A-delta and C-fibers
  124. What are examples of NMs produced in centrally mediated hypersensitivity?
    • substance P
    • C-Fos
    • CGRP
    • others
  125. NMs produced in the centrally mediated hypersensitivity influence what?
    characteristics of post synaptic membranes of CNS (first order sensory neurons are releasing more NM)
  126. Due to convergence, the result is that the neurons in the pain pathway respond to what?
    different types of innocuous input (mechanoreceptors) which is interpreted as noxious (painful)
  127. Where are anatomical sites of central sensitization?
    • dorsal horn
    • brain stem (reticular formation)
    • thalamus
    • somatosensation and association cortices
  128. If pt has experienced a major inflammatory or pathological event and still complains of pain following negative hematologic, blood chemistry, histological, radiographic and physical examinations, the pain may be due to:
    hypersensitization of the CNS (may be basis of psychogenic pain)
  129. Treatment of pain due to hypersensitization of the CNS falls into what 3 categories?
    • Pharmacological
    • physical
    • pschological (situational)
  130. Phanntom Limb:
    perception of a missing body part, which is no longer present. Most amputees experience a phantom limb
  131. Phantom pain:
    perception of chronic pain in an absent body part; usually manifests itself after surgical amputation
  132. Where is phantom pain most common?
    lower extremitiy
  133. Where are common places of phantom pain beside the lower extremity?
    nose, tongue, teeth, breasts, testes, penis, bladder, and anus
  134. What are the theories of phantom pain?
    • there is no one well made theory
    • Neuroplasticity: some abnormalities may occur in set up
    • Hypersentization: due to loss of afferent input
  135. How often does phantom pain occur?
    may be continuous, intermittent, or random
  136. What are attacks of phantom pain like?
    often very severe
  137. How do 25% of pts describe phantom pain?
    burning, cramping, aching, crushing, stabbing, or shooting pain
  138. What other disorders are the symptoms of phantom pain similar to?
    • causalgia
    • peripheral nerve damage
  139. Does everyone that experiences phantom limb experience phantom pain?
    no, most people experience phantom limb, but not always phantom pain
  140. What are some treatment strategies for phantom pain?
    • mirror reflection (decreases pain)
    • pharm: meds/analgesia
    • Physical: TENS, DCS
    • Physiological: biofeedback
  141. How does the CNS internally modulate pain?
    under influence of pain or stress, certain neurons can release chemicals called opioid peptides which activate an opioid endogenous analgesic mechanism (system)
  142. Where are opioids released?
    • Brain (amygdala, hypothalamus, medulla, periaqueductal gray region (PAG))
    • Spinal cord (dorsal horn)
  143. What must occur in order to release opioid mediated analgesia system?
    • pain must be prolonged
    • could be due to psychological stress
  144. How does the opioid mediated analgesia system work?
    • cell membranes of 2nd order spinothalamic tract contain opioid receptors
    • opiod binds to receptor on 2nd order neurons
    • binding causes 2nd order neurons to become hyperpolarized (harder to fire AP), so less noxious stimuli is transmitted
  145. What happens when opioids are released?
    causes hyperpolarization of neurons (inhibitory)
  146. What type of analgesias are opioids?
    centrally mediated analgesias
  147. What does it mean that opioids are centrally mediated analgesias?
    decrease noxious info going from neuron to neuron
  148. What are opioids?
    neuropeptides (protein molecules that affect the NS)
  149. What are the 3 major chemical families of endogenous opioids?
    • endorphins
    • dynorphins
    • enkephalins
  150. endorphins:
    concentrated in brainstem (raphe nucleus) (CNS)
  151. Dynorphins:
    concentrated in hypothalamus and limbic system
  152. enkephalins:
    concentrated in dorsal horns

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