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163 Cards in this Set
- Front
- Back
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area of injury (destructive or irritative)
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lesion
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abnormalities you observe
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signs
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abnormalities or complaints that the pt is experiencing
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symptoms
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same side
opposite side |
ipsilateral
contralateral |
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loss of sensation
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anesthesia
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loss of pain sensation
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analgesia
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abnormal sensation (pins and needles)
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paraesthesia
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pain from non-painful stimuli
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allodynia
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unpleasant abnormal sensation (never had it before - not pain)
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dysthesia
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uncoordinated voluntary movement
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ataxia
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how are somatosensory pathways organized?
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somatotopic localization pattern
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somatosensory pathways convey general sensations from entire body to?
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higher centers
consciousness |
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minimum of 3 neurons involved what are they?
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3 sensory neuron = thalamic cell = projects to cortex
2 sensory neuron = projection cell = axon decussates 1 sensory neuron = ganglion cell = with receptor |
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3 major pathways
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VTTT (head)
DCML (body) STT (body) |
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VTTT contains?
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phylogenetically mixed pathway
epicritic and protopathic |
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DCML contains?
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phylogenetically NEW pathway
epicritic sensations |
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what are 4 epicritic sensations
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discriminative 2 point touch
pressure proprioception vibration |
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STT contains?
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phylogenetically OLD pathway
protopathic sensations |
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what are 4 protopathic sensations
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crude/light touch
pain (fast and slow) temperature tickle - itch - sexual sensations |
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DCML
what kind of components? axons? receptive fields? |
GSA
large, myelinated, rapidly-conducting (types I and II) small |
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principal sensory input to somatosensory cortex?
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DCML
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STT
kind of components? |
GSA and GVA
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medial division of dorsal root
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heavily myelinated type I and II fibers
DCML |
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lateral division of dorsal root
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finely myelinated type III and unmyelinated type IV fibers
STT |
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Posterolateral Fasciculus AKA
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Lissauer's Fasciculus
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DCML synapses and crosses over?
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medulla
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STT synapses and crosses over?
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2 segments above where it came in (in spinal cord)
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specialized sensory ending at the terminal end of the peripheral process of a primary sensory neuron's axon
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receptor
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what occurs at these receptors?
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unique stimulus causes receptor membrane to depolarize
mechanical, thermal, or noxious stimuli is converted (TRANSDUCTION) into an ELECTRICAL SIGNAL |
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free nerve endings respond to?
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pain, heat, cold
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Merkel discs, Krause end bulbs, root hair plexus, Meissner corpuscles respond to?
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touch
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Pacinian corpuscles respond to?
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vibration and pressure
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Ruffini endings respond to?
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pressure
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what is receptor adaptation?
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decrease in receptor potential with continued stimulation
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only respond when stimulus starts or ends
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rapidly adapting - info related to changing stimuli
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continue to discharge during stimulus
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slowly adapting - info about ongoing stimulation
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Slow adapting (x3)
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pain - nocioceptor
thermoreceptors muscle spindles |
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rapidly adapting (x2)
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pacinian corpuscles
peritrichial hair follicle ending |
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Mechanoreceptors
receptors? type? myelin? conduction velocity? pathway? |
discriminative 2 point touch
pressure proprioception vibration ENCAPSULATED with CT I and II FAST DCML |
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Crude light touch
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encapsulated
II and III Medium STT |
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thermoreceptors
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hot/cold
free nerve endings III slow STT |
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Nociceptors
Mechano and Thermo |
FAST PAIN
Free nerve endings III slow STT |
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Nociceptors
Polymodal (mechano/thermo/chemo) |
SLOW PAIN
free nerve endings IV very slow STT |
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area of skin which when stimulated changes the AP frequency of sensory neurons with receptors in the field
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receptive field
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areas of skin with small receptive fields have?
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greater #s of receptive fields
MORE discriminating refined sensory experience |
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each receptive field has?
leads to what? |
excitatory center
inhibitory surround LATERAL INHIBITION |
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increases the signal to background noise ratio - enhances contrast b/w stimulated and unstimulated areas and improving spacial resolution
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lateral inhibition
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area of skin supplied by a single pair of spinal nerves or spinal cord segment
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dermatome
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since there is overlap of innervation b/w adjacent dermatomes, lesion of T4 results in?
lesion of T3, T4, T5 results in? |
diminished sensation of T4
diminished sensation of T3 and T5 and complete loss of sensation in T4 |
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what disease follows dermatome pattern?
may cause nerve damage? |
shingles
nerve damage beyond the dermatome with postherpetic Neuralgia |
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DCML
1 sensory axons enter the _ of dorsal root and _, giving rise to _ and _ which give off several _ to the spinal gray matter for _ |
MEDIAL division
bifurcate long ascending and short descending collateral both give off collaterals reflexes |
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DCML for lower 1/2 body - T7 down
upper 1/2 body - above T7 |
fasciculus gracilis
fasciculus cuneatus |
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DCML crosses over at what level?
forming what? |
medullary level - tegmentum - pyramidal decussation
medial lemniscus |
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arrangement of DCML in medulla
mid pons? |
vertical (CTLS)
horizontal (CTLS) |
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DCML 2 synapse on 3 neuron in?
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dorsal thalamus
VPL |
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3 neurons go where?
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posterior limb of internal capsule
postcentral gyrus paracentral lobule medial surface S1 cortex |
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somatosensory cortex S1 is organized into what?
what are kept separated? |
6 vertical layers
cutaneous and muscle receptor areas |
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ability to localize touch; discriminate b/w 2 point
tested? |
discriminative touch
2 point touch threshold |
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recognition of objects by touch
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stereognosis
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touch recognition of letters/# drawn on skin
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graphesthesia
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mediated by pacinian corpuscles
SEVERELY compromised in what lesion? tested? |
vibratory sense
DCML tuning fork vibrating at 130-200 cps |
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sense of body and movement
mediated by muscle spindles, golgi tendon organs, joint receptors tested? |
proprioception
PASSIVE movement of a joint |
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one can visually compensate for a?
but not for a? |
sensory DCML or Vestibular deficit
motor/Cerebellar deficit |
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lesion of the gracilis fasciculi results in?
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ataxic wide-base gait and ROMBERG SIGN (postural instability worsens with eyes closed and feet together)
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which way will they fall if lesion is unilateral?
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fall without visual cues TOWARDS side of deficit
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peripheral neuropathies
infection x3 autoimmune x1 metabolic x3 endocrine x1 genetic x1 |
leprosy, exotoxin if diphtheria, viral infection
Guillain-Barre syndrome B Vit deficient, heavy metal poison, drugs DM hereditary motor sensory neuropathy (axonal/myelin gene mutations) |
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axonopathies exhibit?
seen in? |
dying-back phenomenon
most distal portion of nerve dies first DM, renal failure, EtOH, toxins, chemotherapy |
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sensory deficits exhibit?
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glove and stocking distribution EARLY in disease process
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peripheral neuropathy vs multiple entrapment neuropathies?
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dying-back/ glove and stocking
falls along a dermatome/cutaneous - strip or patches |
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ability to look at proprioceptive input
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kinesthesia
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DCML lesions
level of spinal cord? level of caudal medulla? level of medial lemniscus? |
IPSILATERAL loss of epicritic below level of lesion
IPSILATERAL loss of epicritic from neck down CONTRALATERAL loss of epicritic from neck down (akinesthesia + stereoanesthesia) |
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STT
Neospinothalamic Paleospinothalamic |
Neo = crude/light touch, FAST pain, temp, GSA
Paleo = SLOW pain, GSA, GVA |
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touch mediated by low threshold (sensitive) receptors and characterized by very large receptive fields which allow poor ability to localize touch
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crude/light touch
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sex and pelvic pressure are usually?
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bilateral projection - highly protected
midline structure |
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which sense travels in more than one pathway in STT
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itch
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STT - 1 sensory neuron axon enters the _ of dorsal root and bifurcate, give rise to long ascending and short descending collateral which give off collaterals to spinal gray matter
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LATERAL division
reflexes |
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axons ascend how many segments before synapsing on 2 projection neuron?
what kind of fibers? |
2 segments
type III and IV |
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lesion of S1 STT?
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analgesia, thermal anesthesia beginning at S3 CONTRALATERAL
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primary neuron in STT enters?
crosses over in? area is stays in through tegmentum? |
Lissauer's fasciculus
anterior white commissure LATERAL fasciculus (peripheral portion) |
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paleospinothalamic gives off connections?
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RF
PAG tectum intralaminar nu hypothalamus limbic cortex insular cortex |
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neospinothalamic fibers have 3 synapse where?
then goes where? |
VPL
everything but SLOW PAIN posterior limb of internal capsule |
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projects to where?
smaller or larger than DCML? |
S1 cortex
smaller distribution |
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fast pain goes where?
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S1 and S2 cortex
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slow pain goes?
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insular cortex and limbic lobe
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S1 cortex gets?
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DCML epicritic + STT crude touch, temp, and fast pain (protopathic)
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neospinothalamic has what kind of fibers?
synapse on 3 where? go where? |
GSA fibers
VPL S1 = GSA temp, crude touch, fast pain S2 = GSA fast pain |
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test for crude/light touch?
fast pain? |
whisp of cotton
pin prick |
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which 2 STT are not completely lost in unilateral lesions?
is completely lost? |
ITCH and sexual sensations
tickle |
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lesions of STT at spinal cord level?
at brainstem level? |
CONTRALATERAL analgesia + thermal anesthesia + crude touch anesthesia
about 2 segments below level of lesion loss of protopathic affecting neck down |
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GSA to head via CN?
what path? |
5,6,7,10
mostly 5 VTTT |
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what types of sensation in VTTT?
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epicritic and protopathic
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epicritic go?
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main/chief sensory nu of V
mesencephalic nu of V |
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protopathic go?
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spinal nu of V
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pathway for VTTT?
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1 in semilunar ganglion from head region (GSA) -> 2 neuron located at level of trigeminal nerve (protopathic go down to spinal nu which is continuation of lissauer's fasciculus; epicritic go to chief nu) -> CROSS OVER -> 3 at VPM
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mesencephalic nu primary unipolar neuron?
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NOT semilunar ganglion - it is its own ganglion
proprioceptive reflexes for muscles and periodontal membranes tooth socket |
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VTTT sits where in mid pons?
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on top of medial lemniscus and next to STT
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after VPM they project to cortex via
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posterior limb of internal capsule
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DTTT originates?
carries? |
from trigeminal nuclei (smaller and more dorsal)
CONTRALATERAL and some IPSILATERAL sensations from the oral region |
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in a unilateral lesion of the TTT tracts?
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soem sensation in the oral region is spared bilaterally due to the DTTT
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Fast pain characteristics?
fibers? projections to? |
sharp, well localized
Type III afferents mechano/thermo nociceptors VPL/VPM and S1, S2 cortical areas |
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Slow pain
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aching, burning
Type IV afferents are POLYMODAL nociceptors brainstem RF, PAG, intralaminar thalmic nu, hypothalamus, amygdala, anterior cingulate gyrus, insular cortex |
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Fast pain stimulus, nerve fiber, distribution, reflex, effect of opioids
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pin prick
Type III/A delta skin and mucous membranes - GSA withdrawal NONE |
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Slow pain
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tissue damage, muscle contraction, distension, ischemia
Type IV/C unmyelinated everywhere except CNS (GSA & GVA) muscle tension and spasm suppression of pain and muscle spasm |
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1 sensory neuron axon of fast pain synapse?
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2 projection neuron in FIRST LAYER OF GRAY MATTER
LAMINA I OR POSTEROMARGINAL LAYER |
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Slow pain 1 sensory neuron utilize?
synapse on 2 projection neuron where? |
Substance P, CGRP, somatostatin NT
DEEP DORSAL GRAY - LAMINA V or Nu Proprius |
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interneurons in _ of dorsal horn play complex role in modulation of pain
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substantia gelatinosa - LAMINA 2
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modality of slow pain perceived?
suffering? |
intralaminar thalmic nu, RF
limbic cortex, subcortical limbic area |
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chronic slow pain can lead to?
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clinical depression
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slow pain be eliminated?
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NO
it is a fundamental part of the survival mechanism of all animal species |
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characteristics of slow pain
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diffuse, resilient, pervasive, plastic relentless
multiple aberrant 2 pathways that can convey pain when main pathway is disabled |
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provides temporary fix resulting in analgesia of contralateral side, but pain will return
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spinothalamic tractotomy
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what can develop as result of the loss of main pain pathways
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central pain syndromes
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slow pain - visceral pain
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GVA
1 sensory GVA pain fibers from viscera are SLOW PAIN fibers |
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these GVAs follow what back to CNS?
and project? |
SYMPATHETICS
bilaterally |
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conveys slow pain fiber from post tongue, ear, oral/nasal pharynx
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glossopharyngeal
follow sympathetics |
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none of them follow?
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Vagus nerve
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GVA do not respond to same types of stimuli as?
run in what kind of fashion? |
GSA
retrograde fashion - up the white ramus into the spinal cord (sympathetics go down the white rams) |
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nociceptors for slow pain are?
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polymodal
slowly-adapting free nerve endings |
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tissue damage and inflammation results in release of?
which cause what? |
algogenic substances
decrease in pain threshold and increase sensitivity |
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cause hyperalgesia
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serotonin, PG, histamine, bradykinin, substance P, CGRP, K and H ions, neurotrophins, cytokines
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produce analgesia at the receptor site
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capsaicin from hot peppers
DEPLETES SUBSTANCE P FROM NEURON |
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produce analgesia/anesthesia by preventing axonal transmission of action potentials
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novacaine
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drugs can target what which would avoid narcotic side effects of opioids
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sodium channels
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visceral pain is not precisely localized and referred to a?
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somatic dermatome area
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are there any PURE visceral pain fibers in the CNS pain pathways
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NO
transmitted via subset of interneurons which receive both somatic and visceral pain inputs |
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pancreatic disease referred pain?
liver and gall bladder? |
central = upper and and back
lateralized = RUQ and back also in liver there is referred pain to shoulder via phrenic nerve |
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pain caused by pain receptor response or tissue damage?
responds to? |
physiologic nociceptive pain
opiate analgesics (morphine, codeine) |
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pain caused by direct injury to nervous system?
responds to? |
neuropathic pain
antidepressants and antiseizure meds |
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physiological/nociceptive pain
fibers? 2 types of sensitization |
type IV C
peripheral sensitization = release of algogenic substances by tissue injury and changes in nociceptors central sensitization = chronic stimulation leads to hypersensitive projection neurons |
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pain syndrome related to pain and fatigue and associated with increase in substance P (pain neural transmitter)
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fibromyalgia
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pain caused by peripheral nerve damage (tumor, trauma, entrapment, neuralgia peripheral neuropathies)
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peripheral PNS pain syndromes
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pain caused b CNS damage resulting in altered thresholds and spontaneous discharge of neurons in slow pain pathway
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central CNS pain syndromes
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pain felt NOT at the point of injury but projected to area of nerve terminal/receptor distribution
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projected pain
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causes of this
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herniated disc
causalgia (sustained burning pain following trauma to nerve injury combined with faso/pseudomotor dysfunction) = REFLEX SYMPATHETIC DYSTROPHY (brachial plexus injury) phantom limb |
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peripheral neuropathies in addition to epicritic sensory loss can have?
early signs? |
neuropathy = entrapment
polyneuropathy = dying-back pain and hyperalgesia |
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lesions anywhere along the pain pathway within the CNS
initial analgesia is replaced by? causes? |
central pain syndomes
severe burning, aching pain loss of GABAnergic activity, synaptic reorganization, pro inflammatory cytokines released from glial cells |
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best documented central pain syndrome
caused by vascular accident in dorsal thalamus, results in persistent, often severe, pain on contralateral side |
thalamic syndrome
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neuropathic pain in the distribution of a peripheral nerve
pain is often paroxysmal and extremely painful CN susceptible? |
neuralgia
short and frequent attacks CN V and IX |
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one of the most common neuralgia
affects ppl > 50 suicide disease classic symptom? |
trigeminal neuralgia
tic douluoreux (painful tick and contraction of muscle) |
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cause of trigeminal neuralgia?
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loop or aberrant arterial branch of SUPERIOR CEREBELLAR ARTERY
compress and pulsates on surface of nerve causing erratic axonal hyperactivity |
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fix pulsatile vascular compression
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surgical microvascular decomrpession
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paroxysmal pain in the distribution of nerve - oral, nasal pharynx, post tongue, ear?
cause? |
glossopharyngeal neuralgia
compressing loop of the PICA |
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trigeminal and glossopharyngeal neuralgia are examples of?
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projected pain
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endogenous slow pain inhibition
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limbic system can inhibit slow pain
limbic = pro survival |
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limbic system ->
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PAG
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the brain under control of the _ has ability to inhibit slow pain transmission during life-threatening survival situations where affect of pain must be overridden to survive. The _ contains neurons which can activate neurons in the _ and _ of the brainstem. Both of these give rise to descending pathways which excite _ as well as neurons in the _ which suppress activity in the slow pain pathway.
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limbic system
Periaqueductal Gray (PAG) Locus Ceruleus and Raphe Nuclei enkephalinergic Substantia Gelatinosa |
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have major effect on PAG and centers on the "pain-pleasure" axis which extends from where?
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Opioid drugs - morphine
from limbic areas in forebrain to substantial gelatinosa in spinal cord |
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slow pain inhibition is transmitted from PAG to substantial gelatinosa via?
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ceruleospinal - noradrenergic
Raphespinal - Serotonergic |
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collaterals of large diameter touch fibers (DCML) have complex synaptic interactions with pain fibers in dorsal horn. They can inhibit transmission of pain and close or open a "gate" for pain transmission
may explain? |
gate control theory
transcutaneous electrical stimulation and acupuncture |
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Acupuncture analgesic effect is due to increase in?
at the same time is triggers? and may also stimulate? |
endorphins and endorphin receptors
endogenous pain inhibiting pathway originating in the midbrain PAG DCML system thereby jam pain transmission via the "gate control" system |
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lesion of R post spinal artery
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involves the fascicles gracilis
Ipsilateral (below level of lesion) loss of epicritic ataxic gait romberg sign (falls to R) |
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occlusion of sulcal branch of anterior spinal artery
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involves R side ventral horn
CONTRALATERAL and 2 segments below level of lesion protopathic sensation |
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radiculopathy dorsal root lesion
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lose fibers going to fascicles gracilis and lissauer's tract
on R side IPSILATERAL diminished sensation in the S1 dermatome and diminished reflexes and muscle tone (lose 1a fiber to gamma-motor neuron) |
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segmental lesion of anterior white commissure
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BILATERAL (midline lesions) loss of protopathic sensation beginning 2 segments below
disease = Syringomyelia |
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spinal cord hemisection
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Brown-Sequard syndrome
R side means IPSILATERAL loss of epicritic sense, ataxic gait, romberg (falls to R) CONTRALATERAL loss of protopathic beginning 2 segments below losing primary DCML and secondary STT |
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most common brainstem stroked occluded artery
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PICA (branches to posterior lateral area of medulla)
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occlusions of PICA/lesions of lateral quadrant of medulla
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PICA syndrome
if lesions on L side ALTERNATING ANALGESIA IPSILATERAL head sensation lost from VTTT CONTRALATERAL protopathic sensation lost includes the spinal nu of V and STT but not the DCML pathway |
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occlusions of pontine arteries in caudal pons region on left side
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complete anesthesia (loss of all sensation) on CONTRALATERAL side of body and head
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lesions on Left mid pons level from long circumferential branch coming into the tegmentum or lacunar infarct
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CONTRALATERAL complete anesthesia/loss of all sensations on right side of body and head
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lesion at dorsal thalamus from occlusion of a perforating central artery (left side)
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CONTRALATERAL complete anesthesia on R side of body and head
can cause thalamic pain syndrome with spontaneous burning pain on RIGHT side |
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lesion of Left internal capsule post limb from occlusion of anterior choroidal artery
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CONTRALATERAL complete anesthesia on R side of body and head
no pain |
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occlusions of MCA or lesions in S1 post central gyrus on L side
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CONTRALATERAL complete anesthesia of head, upper extremity, and trunk on R side
no lower extremity STILL have pain |
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occlusions of ACA or lesion in S1 medial on L side
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CONTRALATERAL complete anesthesia on right lower extremity
STILL have pain |
