Neurobiology - Somatic Sensation 3 & 4

Front 1

Which two nerves are involved in the corneal or blink reflex?

Back 1

V and VII

CN V sends afferent to nuclei of V in the pons --> 2nd order fibers project on to both VIIth nerve nuclei --> orbicularis oculi

Front 2

What nerve primarily mediates somatic sensation of the head?

Back 2

Trigeminal

Front 3

* In the trigeminal system, where do large diameter axons (pressure, touch, position) synapse? small diameter (pain, temp)?

Back 3

Group I & II: main sensory Nucleus of V (pons)

Group III & IV: spinal nucleus of V (medulla)

Front 4

* After the epicritic and protopathic synapses in the trigeminal system, where do the second order axon go/do in each case?

Back 4

Epicritic: Cross mid line, ascend to VPM (in thalamus), synapse again, up to S1

Protopathic: Cross mid line, ascend to thalamus and synapse on VPM, intralaminar nucleus or post. group., then ascend to S1, S2 or others (remember AL system branches more)

Front 5

Where do both epicritic and protopathic axons of the trigeminal system enter the brainstem?

Back 5

pons

Front 6

at what level is the main sensory nucleus of V?

Back 6

pons

Front 7

if you can see the olivary nucleus in cross section, what level are you at?

Back 7

medulla

Front 8

What would lateral medullary syndrome (Wallenberg's synd., PICA synd.) cause?

Back 8

ipsi/contralateral loss of pain and temp in face (CN V)

contralateral loss of pain and temp in body (AL system)

Front 9

In cutaneous receptors, how do the receptive fields differ from superficial to deep? how does the rate of response differ?

Back 9

superficial = small receptive fields, rapidly adapting (fine touch, vibration, motion across skin)

deep = large receptive fields, slowly adapting (sense pressure and shape)

Front 10

where is two-point resolution greatest? lesser?

Back 10

hand, feet, lips

back, legs, forearm

Front 11

do receptive fields of cutaneous receptors overlap?

Back 11

Yes!

Front 12

How does innervation density relate to spatial resolution?

Back 12

greater density = better resolution

Front 13

* what are the two ways in which two-point resolution can be increased?

Back 13

1. increasing receptor density
2. decreasing receptive field size

Front 14

where does all somatosensory information reaching the somatosensory cortex (behind central sulcus) flow through?

Back 14

Thalamus (receives and interprets)

Front 15

why is somatotopy in the cortex not uniform?

Back 15

more cortex dedicated to areas of greater discrimination (e.g. lips get more space than legs ... relative to actual size)

Front 16

what happens to fine motor control when sensory feedback is lost?

Back 16

impaired

Front 17

what receptors contribute to proprioception?

Back 17

muscle stretch receptors
golgi tendon organs
stretch sensitive skin receptors
free nerve endings in joint

*many"

Front 18

what inputs does the posterior parietal cortex receive?

Back 18

- somatosensory cortex
- visual cortex
- auditory cortex
- hippocampus

Front 19

What is the inability to recognize objects even though simple sensory skills are intact?

denial of injury or deficit;
Associated with posterior parietal lesion
(particularly right-side)

Back 19

Agnosia

Anosognosia

Front 20

* What are 3-D perceptual constructs from skin and position information that require primary somatosensory and posterior parietal cortex? what is the deficit called?

Back 20

Stereognosis

Astereognosis

(gnosis = knowledge)

Front 21

What is acquired inability to
carry out skilled actions without sensory or motor deficits?

Back 21

Apraxia

(praxis = action)

Front 22

* What is it called when visual, auditory and somatosensory information presented contralateral to a lesion is ignored? where is the lesion most common?

Back 22

hemineglect

right posterior parietal lesion (causing neglect of left side) --> recall functions of posterior parietal cortex

Front 23

Do neglect syndromes tend to improve over time or stay the same?

Back 23

usually show great improvement

Front 24

Can pain occur without activity in nociceptors?

Back 24

Yes, but also nociceptor activity does not lead to a perception of pain

Front 25

what is meant by pain is a percept?

Back 25

Pain is a purely psychological experience or concept

Front 26

* What is a purely physiological term for an axon or receptor that fires when tissue is damaged or nearly damaged?

Back 26

Nociceptor

Front 27

* What types of axons do nociceptors use?

Back 27

Ad and C (Group III and IV)

Front 28

Are the majority of nociceptors in capsules or free nerve endings?

Back 28

free

Front 29

What are the three categories of nociceptors and associated axons?

Back 29

Thermal: Ad

Mechanical: Ad

Polymodal: C (C fibers also sense itching)

Front 30

* What type of fiber transmits fast pain? slow pain?

Back 30

Fast = Ad

Slow = C

Front 31

How is pain a unique sensory system relative to repeated stimuli?

Back 31

Sensitization can occur ... when stimuli are gradually increased, the effect is lesser than sudden, abrupt increases, this is unique to the pain sensory system

Front 32

What is the difference between Allodynia and Hyperalgesia? what is Hyperalgesia?

Back 32

Allodynia = painful response to something that is usually non-noxious (central mechanism)

Hyperalgesia = excessive painful response to noxious stimuli (peripheral and central mechanism)

Front 33

what is a major mediator of secondary hyperalgesia via central mechanisms?

what is an "axon reflex", and what is essentially happening here?

Back 33

substance P (released by nociceptors, causes plasma extravasation)

sensory input gets cycled back out to other receptors (positive feedback loop --> more pain perception)

Front 34

what is the difference between neuropathic pain and nociceptive pain?

Back 34

neuropathic pain results from direct injury TO NERVES in the CNS or PNS

nociceptive pain is from activation of nociceptors in RESPONSE TO TISSUE damage

Front 35

What is meant by 'referred pain' and what causes it?

Back 35

the sensed area of pain and the actual damaged area are different

*convergence of nociceptive and visceral fibers onto the same dorsal horn neurons --> improper message sent up to brain

Front 36

How many pathways are there of Ascending pain? Descending?

Back 36

Ascending: multiple (Discriminative features and Affective features)

Descending: also multiple

Front 37

How do the pathways for the Discriminative and Affective features of pain differ?

Back 37

Discriminative: synapse in VPL (thalamus) --> SI, SII

Affective: synapse at Reticular Formation (brain stem) --> synapse Intralaminar nuclei --> on to cortex

Front 38

Where does the "mechanism" of the Gate Control Theory take place?

Back 38

in the substantia gelatinosa of the dorsal horn.

Front 39

** Explain what is happening in the Gate Control Theory:

Back 39

Rubbing your skin (Touch, Ab, DC/ML) sends signal to a "Gate Keeper Cell", a sort of interneuron that then has an inhibitory effect on the signal of the pain pathway (Pain, Ad & C, AL) coming in via nociceptive afferents (all this occurs in the dorsal horn)

Front 40

** KEY CONCEPT: Both Ascending and Descending pain pathways are Polysynaptic, diffuse; project to brainstem as well as cerebrum

Back 40

FYI

Front 41

* What is the pathway of Descending Pain (modified by brain)?

(one example given, there are others)

Back 41

PAG (periaqueductal gray) (in midbrain) stimulated --> Raphe nuclei (in medulla, crossing over here, synapse --> 2nd order neuron) --> Dorsal horn : impact on nociceptive input

Front 42

Can nociception be "modified" or blocked by the Ascending and/or Descending pathways?

and if so, how?

Back 42

BOTH.

Ascending: Gate Control (DC/ML stimulation)

Descending: multiple (originate from PAG, cross at raphe nuclei near seam of midline in medulla)

Front 43

Somatopic vs. limbic & frontal, which is fast or slow pain associated with?

Back 43

fast = somatopic

slow = limbic, frontal

(Cosgrove lecture)

Front 44

What is a common endogenous opioid (pain suppressor)?

Back 44

Endorphins

Front 45

What are the different forms of opiods?

Back 45

Natural: morphine, codeine
Semisynthetic: heroin, oxycodone (percosett), vicodin
Synthetic
Long acting: Oxycontin


(Cosgrove lecture)

Front 46

What are Adjuvant Therapies?

Back 46

Anticonvulsants, Corticosteroids, Muscle relaxants (valium), Antidepressants


(Cosgrove lecture)

Front 47

What are the surgical treatments of pain?

Back 47

Ablative, Neuromodulation (stimulation -- Gate Control Theory), Pharmacologic augmentation (morphine pump)


(Cosgrove lecture)

Front 48

What is the most common treatment of pain?

Back 48

NSAIDs

(Cosgrove lecture)

Front 49

What are the common themes in pain treatment?

Back 49

- treat the underlying cause
- pharmacologic treatment should be appropriate for level of pain
- avoid narcotics in chronic pain
- surgical intervention is appropriate in carefully selected pts

(Cosgrove lecture)

Front 50

What are the three nuclei of the anterolateral system found in the Thalamus?

Back 50

VPL
Intralaminar nucleus
Posterior group

Front 51

What is it called when a pt with sensory ataxia uses their vision to walk, then when blindfolded, wobble back and forth?

Back 51

Romberg's sign