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Neur3005 > somatosensation > Flashcards

somatosensation Flashcards

1
Q

what modalities do free nerve endings detect?

A

nociception, temperature, crude touch.

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2
Q

name 2 deep and 2 superficial mechanoreceptors?

A

deep-pacinian and ruffini

superficial - meissner and merkel also free nerve ending.

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3
Q

what type of axons carry mechanosensation?

A

A-beta

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4
Q

where do the mechanoreceptor axons from skin synapse?

A

in the spinal cord onto 2nd order neurons in laminae 3-5 of dorsal horn.

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5
Q

what tract do the mechanoreceptor axons constitute? and where are the synapses?

A

dorsal column tract, they synapse in gracile and cuneate nuclei in caudal medulla, then medial lemniscus decussation, ascend and synapse in VPL thalamus. then to cortex.

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6
Q

where do the trigeminal nerve fibres synapse? name all.

A

first at principle sensory nucleus of trigeminal, then decussate in the medial lemniscus with the other fibres from dorsal column, form trigeminal thalamic tract, ascend and synapse again in VPM of thalamus. then to the S1.

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7
Q

what part of thalamus is responsible for projecting to somatosensory, motor, cingulate, parietal and temporal, prefrontal, auditory and visual cortex?

A 
VPL,VPM
VA,VL
ANTERIOR NUCLEUS
PULVINAR
DM 
MGN
LGN
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8
Q

what are the divisions of VP thalamic nuclei?

A

core region-specific for somatosensory

shell region-proprioceptive (VPS)

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9
Q

what are the specific parts of S1 targeted by VP nuclei?

A

tactile/core from VPL-3b

proprioception from VPS-3a

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10
Q

what are the somatosensory association areas?

A

parietal operculum(S2) which is deep to lateral sulcus, posterior parietal cortex (5 and 7)

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11
Q

where do the somatosensory info from face and lower limbs mapped onto S1?

A

medial s1-lower limb and genitals (VPL)

lateral S1-face, tongue (VPM)

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12
Q

In what level do the thalamic projections from somatosensation terminate in the S1?

A

layer IV.

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13
Q

what sensory modality do areas 1 and 2 transmit?

A

1-texture, massive input from 3b

2-hand posture, grip, assessing the shape and size of objects, input from both 3b and 3a.

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14
Q

what is a difference in s1 and s2 in terms of input receiving?

A

s1 is contralateral , s2 is bilateral.

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15
Q

where does S2 also project?

A

to prefrontal cortex, indicative of memory formation for first stimulus.

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16
Q

what is the gene and the ion channel responsible for pain sensation?

A

SCN9A gene, associated specifically with Nav1.7

17
Q

types of nociceptors?

A

mechanical, chemical, thermal.

also silent, polymodal -c fibres, modality specific Adelta,

18
Q

are nociceptors rapid or slow adaptors?

A

slow-never stop responding to noxious stimulus.

19
Q

what are the specific ion channels for hot and cold sensation?

A

heat-TRPV1

Cold-TRPV8

20
Q

how are polymodal nociceptive receptors categorised?

A

based on presence of substance p.

peptidergic like TRPV1, TRPA1. and non peptidergic like TRAAK and TREK.

21
Q

what are the two CNS mediators of hyperalgesia?

A

glutamate and substance p (for polymodal neurons).

substance p causes oedema , glutamate increases sensitivity.

22
Q

what are the peripheral mediators of pain pathway which eventually cause hyperalgesia?

A

chemical: bradykinin, K+, histamine released by mast cells and promotes swelling for itch, substance p.
inflammatory-prostaglandins (can change ion channel property) and cytokines.

23
Q

where is substantia gelatinosa located in the spinal cord?

A

dorsal horn, lamina 1 and 2.

24
Q

where do c fibres and A-delta fibres synapse in spinal cord?

A

c fibres-lamina 1 for peptidergic, lamina 2 for non-peptidergic which is part of substantia gelatinosa.
A-delta: lamina 1 (SG) and lamina 5.

25
Q

in what structure do the c fibres travel up and down the sc?

A

in the zone of Lissauer

26
Q

how does secondary hyperalgesia occur?

A

the primary neuron transmitting noxious stimulus releases glutamate and substance p(if an intense pain), they activate NMDA receptors along with AMPA and NK-1 receptors on 2nd neuron. their collective activation releases the Mg plug of NMDA causing the influx of Ca into the neuron. this is the priming effect to increase sensitivity to future noxious stimuli.

27
Q

what is the Gate theory of pain?

A

basically-pain and touch are interconnected. Abeta fibre activation along with noxious input e.g. rubbing, A beta activates GABAnergic interneuron that inhibits the pain system C fibre neuron and also the secondary neuron that enters spinothalamic tract.- this only for ACUTE PAIN.

28
Q

how is allodynia induced in chronic pain?

A

through Abeta fibres which synapse onto lamina V, which leads to painful signal in chronic pain situation.

29
Q

what does the neo-spinothalamic pathway encode?

A

the sensation of pain i.e. no emotion

30
Q

what part of thalamus is associated with pain?

A

VPL-from contralateral side of body-spinothalamic.

VPM from face and head-contralateral also.

31
Q

what trigeminal nucleus is involved in pain?

A

spinal nucleus of trigeminal-laterally in caudal medulla.

32
Q

how is VP thalamus categorised for pain fibres?

A

A delta-core regions i.e. VPL/VPM.

C fibres, VMpo

33
Q

where do VMpo and VPL thalamic nuclei project to?

A

VMpo to 3a.
VPL to 3b and then 1. 3a proprioceptive specific, 3b is mechanosensitive. so infor from VMpo to 3a have poor pain localisation.

34
Q

What is damaged in Brown-sequard syndrome and what are the modalities lost? which side?

A

dorsal column damage- touch and proprioception loss on ipsilateral side as it is below decussation.
spinothalamic damage- loss of pain, temp and crude touch on contralateral as it is after decussation.

35
Q

where does nucleus proprius exist?

A

dorsal horn of sc in lamina 3-5

Neur3005 (6 decks)

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