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Neuroscience BB Exam 2 > Somatosensory System > Flashcards

Somatosensory System Flashcards

1
Q

These cells respond to transient, phasic, or vibratory stimuli; no maintained stimulation; rapidly-adapting

A
  • Meissner corpuscles
  • Pacinian corpuscles
  • Some hair follicle receptors
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2
Q

These cells respond to tonic events; encode intensity and duration; related to displacement and velocity of stimulus; slowly-adapting

A
  • Merkel cells
  • Ruffini corpuscles
  • Some hair follicle receptors
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3
Q

Deep tactile mechanoreceptors are:

A

Pacinian and Ruffini corpuscles

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4
Q

Large diameter fiber types are:

A

A-beta and A-alpha

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5
Q

Small diameter fiber types are:

A

A-delta and C

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6
Q

Lesion of the thalamogeniculate arteries of the PCA can cause what?

A

Loss of blood to VPL and VPM, and therefore loss of all tactile sensation over the contralateral body and head

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7
Q

What is kinesthesia?

A

Positional awareness information, conveyed via proprioceptive sensory receptors within mm. and joints; serves balance, posture, and limb movement

  • Dynamic and static nuclear bag fibers
  • Golgi tendon organs via A-alpha fibers
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8
Q

What is stereognosis?

A

Ability to recognize a 3D object form texture, size, and spatial sensory modalities

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9
Q

What is agnosia?

A

Loss of ability to recognize objects, sounds, smells, or other sense modalities

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10
Q

Describe the Jaw Jerk Reflex.

A
  • Ruffini endings in jaw, periodontal ligaments send signals to mesencephalic nucleus
  • Send input to trigeminal motor nucleus to contract temporalis/masseter
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11
Q

What is complex regional pain syndrome?

A

Increased sensitization to pain within the body manifesting as chronic pain, often resulting from peripheral nerve damage. Most commonly manifests as back pain.

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12
Q

What is allodynia?

A

Lowered stimulus threshold for the A-delta fibers, leading to painful sensation to non-painful stimuli

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13
Q

What is hyperesthesia?

A

Lowered stimulus threshold for the C fibers

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14
Q

How do NSAIDS act?

A

Inhibit production of prostaglandin from neutrophils and macrophages by inhibiting COX2; PG normally binds nociceptor terminal to elicit a painful sensation

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15
Q

How does a capsaicin receptor inhibitor work?

A

Inhibition of voltage-gated sodium channel (typically elicits painful sensation during inflammation and in response to heat)

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16
Q

How does a bradykinin receptor inhibitor work?

A

Inhibition of response to bradykinin released from leukocytes, which binds nociceptor terminal membrane

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17
Q

How does gabapentin (neurontin) work?

A

Blocks calcium channels on the nociceptor, prohibiting neurotransmitter release in the SC

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18
Q

What is Brown-Sequard Syndrome? What can cause it?

A

Ipsilateral loss/reduction of discriminative, positional, vibratory sensation at/below level of lesion AND contralateral loss of pain/temp/crude touch two levels down and below AND ipsilateral motor loss

  • Occlusion of posterior spinal artery (just for dorsal columns probably)
  • Spinal cord hemisection
  • Tabes dorsalis (progressive locomotor ataxia, degeneration of posterior columns)
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19
Q

Tabes dorsalis patients often walk in what specific way?

A

Wide-based stance (lack of proprioceptive sense), placing feet down hard

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20
Q

Lesion of area 1 in primary somatosensory cortex causes:

A

Deficit in TEXTURE discrimination (functions with 3b for discrimination of moving stimuli)

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21
Q

Lesion of area 2 in primary somatosensory cortex causes:

A

Loss of size and shape discrimination (astereogenesis); receptive for palpation of shape and curvature of objects

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22
Q

Lesion of area 3b in primary somatosensory cortex causes:

A

Deficits in both texture and size/shape discrimination - more profound deficits in 3b, indicating that is performs initial processing (which is carried on by 1 and 2)

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23
Q

Lesions is parietal association cortex (5 and 7) will cause:

A

Agnosia, from loss of contralateral body map –> limb not recognized by the body

24
Q

What is plasticity, in terms of loss of limb?

A

Reassignment of brain functions within synaptic regions (after amputation, stroke) –> proximal areas overgrow into lost region

Leads to phantom limb / chronic pain

25
Q

What is Friedreich ataxia?

A

Degeneration of spinocerebellar tracts –> lack of coordination during walking or other movements due to lack of cerebellar sensory feedback to regulate the movements (mossy fibers to vermis and paravermal regions)

26
Q

List a few symptoms of ALS lesions.

A

Hypesthesia (reduced sensibility), numbness, paresthesia, anesthesia

27
Q

What is peripheral sensitization?

A

Pain receptors exhibit sensitization following an insult; receptor becomes MORE sensitive (hyperalgesia)

Due to: irritating chemical (capsaicin), inflammatory mediators (bradykinin, prostaglandins), NTs (serotonin, histamine, norepinephrine)

28
Q

What is primary hyperalgesia?

A

Occurs in region of damaged skin (receptor sensitization)

29
Q

What is secondary hyperalgesia?

A

In the skin bordering the damaged tissue (central sensitization)

30
Q

Describe central sensitization.

A

Ongoing input from C and A-delta fibers –> increased receptive field size of posterior horn neurons –> increased response to suprathreshold stimuli, decreased threshold, activation in response to novel inputs (allodynia)

31
Q

What are pain receptors in muscles?

A

Receptors of Groups III and IV afferents (excessive m. stretch/contraction)

IV can be stimulated from algesic compound release following muscle injury or ischemia

32
Q

What are pain receptors for arthritis?

A

Groups III and IV

33
Q

What activates visceral pain?

A

Mechanical distention, ischemia, endogenous compounds (bradykinin, H+, K+)

34
Q

Anoxia affects ______ fibers first

A

Larger diameter (DCML deficity)

35
Q

Local anesthetics preferentially affect _______ fibers first

A

Smaller diameter fibers; act via blocking sodium channels (analgesia)

36
Q

Posterior rhizotomy for pain may not be completely effective…why?

A

Select few C fibers that enter the anterior horn, so some nociceptive fibers may remain after those entering the dorsal horn were sectioned.

37
Q 
Some dermatomes to know - 
C7: 
T4,5: 
T10: 
L1: 
L5: 
S4,5:
A 
C7: index finger
T4,5: border of nipple
T10: navel
L1: pelvic rim
L5: big toe
S4,5: genitalia and anus
38
Q

What is shingles?

A

Viral DRG or trigeminal ganglion latent residence of varicella zoster, periodically exhibiting painful dermatomal skin rash

39
Q

What is postherpetic neuralgia?

A

Debilitating recurrent pain following a Herpes Zoster infection (neuropathic pain)

40
Q

What is the test for ALS function?

A

Pinpoint application to skin evokes perception of pain (compare distal, proximal)

Diabetes mellitus patients experience distal loss first (stocking-glove sensory loss)

41
Q

What is the test for DCML function?

A

1: 2-point discrimination (large to small intervals)
2: 128-Hz tuning fork for testing vibration on bone/tip of finger/toe

42
Q

What is ALS ischemia?

A

Blood supply from arterial vasocorona and sulcal branches and anterior spinal a. occlusion –> PATCHY loss of pain/temp/crude touch over contralateral side beginning two levels down

43
Q

What is a syringomyelia?

A

Cystic cavitation of central regions of spinal gray matter; impinge on anterior white commissure: ALS loss several segments below lesion

When in C4-5, cape distribution of bilateral ALS

44
Q

Dull, aching pain from pulp inflammation is conveyed by:

A

C fibers

45
Q

Dental hypersensitivity characterized as “sharp” is conveyed by:

A

A-delta fibers

46
Q

Inflamed meninges cause many headaches and are supplied by:

A

CN V

47
Q

Know the vascular lesions from Exam 1.

A

Probably all of them. Sorry.

48
Q

Occlusion of MCA or ACA can cause what?

A

Loss of sensibility of contralateral region of body, head, face (depending on which artery)

Pain is first to return, then crude touch/thermal, then DCML input (might actually fail to return)

49
Q

Pain perception and suffering arise from DIFFERENT brain regions!

A

It’s true.

50
Q

Neospinothalamic tract is responsible for:

A

Primary somatosensory = localization

51
Q

Paleospinothalamic tract is responsible for:

A

Hypothalamus, limbic system (via RF and PAG) = pain experience/suffering :(

Valium users lack suffering, but can localize pain

52
Q

Deep Brain Stimulation is used for what?

A

Treatment of chronic/deafferentation pain; stimulation to somatosensory thalamus, PAG, etc. to activate pain modulation neurons (stimulation-induced analgesia)

53
Q

Treatment for central pain syndrome?

A

TENS (Transcutaneous electrical nerve stimulation) - electrical stimulation of DC for retrograde input to spinal cord lamina III for pain suppression

Or, neuroablative procedures (rhizotomy, anterolateral cordotomy, commissural myelotomy, thalamic lesioning)

54
Q

What is dysrhythmia?

A

Lack of correct movement timing

55
Q

What is dysmetria?

A

Lack of coordinated movements

56
Q

What is truncal ataxia?

A

Wide-based gait

57
Q

What is central pain syndrome?

A

Often from CNS vascular lesions –> spontaneous paresthesia, dysesthesia, alldoynia, or hyperalgesia (burning, aching, prickling, lacerating, paroxysms, maybe exacerbated by unusual stimuli)

Neuroscience BB Exam 2 (7 decks)

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