10/28 - Sensory System- Central Processing Flashcards

1
Q

DRG NEURON:

Proprioception Peripheral process:

A

Large diameter, heavily myelinated axons carry information from muscle spindles/joint receptors

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2
Q

DRG NEURON:

Touch, Vibration Peripheral process:

A

Slightly smaller diameter, myelinated axons, carry information from cutaneous receptors

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3
Q

Enters through dorsal root and courses directly to posterior column where they ascend to the brainstem forming the fasciculus gracilis or fasciculus cuneatus.

A

DRG NEURON’s Central process

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4
Q

TOUCH Modalities

A

Low Threshold Cutaneous,
Joint & Muscle Receptors.

Touch, Pressure, Vibration, Fine Form and Texture Discrimination, Form Recognition of 3-dimensional objects (Stereognosis)

Conscious Awareness of Body Position (Proprioception)

Limb Movement In Space (Kinesthesia)

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5
Q

Proprioception

A

Conscious Awareness of Body Position

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6
Q

Stereognosis

A

Form Recognition of 3-dimensional objects

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7
Q

Input From Lower Limb & Trunk (T6-S5) Forms the ___ .

A

Fasciculus Gracilis

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8
Q

Input From Upper Limb & Trunk (C1-T5) Forms the ____ .

A

Fasciculus Cuneatus

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9
Q

TOUCH PATHWAY

1ST ORDER NEURON:

A

DORSAL ROOT GANGLIA CELLS

Primary afferent axons enter via dorsal root to enter ipsilateral posterior column.

Below T5 only fasciculus gracilis.

Above T5, 2 tracts – fasciculus gracilis (FG) and fasciculus cuneatus (FC).

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10
Q

TOUCH PATHWAY:

2ND ORDER NEURONS

A

2ND ORDER NEURONS ARE IN CAUDAL MEDULLA IN N. GRACILIS AND N. CUNEATUS.

Axons arising from neurons in these nuclei CROSS the midline and form the MEDIAL LEMNISCUS.

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11
Q

TOUCH PATHWAY:

3RD ORDER NEURON

A

3RD ORDER NEURON IN THALAMUS (VENTRAL POSTERIOR LATERAL NUCLEUS, VPL).

Axons arising from these neurons project to primary sensory (parietal) cortex

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12
Q

1st-order sensation neurons will always be in a ganglion.

A

EITHER a DRG or TRIGEMINAL Ganglion (or other cranial nerve ganglion).

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13
Q

Axons from the MAIN SENSORY NUCLEUS, carrying touch information from the ____, cross the midline and join the ______ in the PONS.

A

Axons from the MAIN SENSORY NUCLEUS, carrying touch information from the FACE, cross the midline and join the MEDIAL LEMNISCUS in the PONS.

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14
Q

Axons from the _____, carrying touch information from the FACE, terminate in the _____.

A

Axons from the MAIN SENSORY NUCLEUS, carrying touch information from the FACE, terminate in the VPM of the THALAMUS.

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15
Q

UNCROSSED TRIGEMINAL AXONS

A

Small number of axons remain uncrossed as the dorsal trigeminal tract.

These carry information from the inside of the oral cavity and end in VPM.

Their significance is unknown.

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16
Q

Do the axons from the spinal trigeminal nucleus (pain and

temparature) join the medial leminiscus?

A

NO.

Axons from the MAIN SENSORY NUCLEUS, (touch from the FACE) join the MEDIAL LEMNISCUS.

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17
Q

What tract is conserned with the Location and Intensity of pain & temperature sensory input

A

SPINOTHALAMIC TRACT

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18
Q

1st ORDER NEURON of the

SPINOTHALAMIC TRACT

A

DORSAL ROOT GANGLIA CELLS.

Primary afferent axons enter via dorsal root and SYNAPSE
on neurons in the superficial portion of the dorsal horn

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19
Q

2nd ORDER NEURON of the

SPINOTHALAMIC TRACT

A

NEURONS IN DORSAL HORN OF SPINAL CORD AT ALL LEVELS.

Axon CROSSES MIDLINE and forms spinothalamic
(anterolateral) tract in the anterior half white matter of the spinal cord.

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20
Q

3rd ORDER NEURON of the

SPINOTHALAMIC TRACT

A

NEURONS IN THALAMUS VPL (VENTRAL POSTERIOR LATERAL NUCLEUS).

Axons arising from these neurons project to primary
sensory (parietal) cortex and insular cortex.

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21
Q

SPINOTHALAMIC TRACT

A

Carries Discriminative Aspects of Pain/Temperature:

Location & Intensity of sensory input.

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22
Q

PAIN PATHWAYS FROM THE FACE:

1st ORDER NEURONS

A

Axons enter in the pons and descend via the Spinal Trigeminal Tract to the medulla where they synapse on 2nd order neurons in the Spinal Trigeminal Nucleus.

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23
Q

PAIN PATHWAYS FROM THE FACE:

2nd ORDER NEURONS

A

Axons of 2nd order neurons, located in Spinal Nucleus of V,
CROSS the midline and join the Contralateral Spinothalamic Tract as it courses rostrally through the pons and midbrain

Axons from trigeminal nucleus terminate in ventral posterior
medial (VPM) nucleus of the thalamus.

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24
Q

Postcentral-Gyrus

A

= Primary Sensory Cortex

= S1 of the Parietal Lobe

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25
Q

More posterior gyri of the Parietal Lobe are involved in what?

A

sensory association

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26
Q

More posterior gyri involved in sensory association areas specialize in what?

A

spatial orientation and directing attention.

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27
Q

On the somatotopic map, sensory input from what body parts are centralized in the deep fissure that separates the 2 hemispheres?

A

lower extremeties: feet, toes, legs, genitals

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28
Q

Moleunculus

A

The mole sensory cortex maps the area of the appendages very precisely and in such a way that a cross section of that part of the brain looks almost like a 2-dimensional image of the appendages.

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29
Q

Information Flow in the Somatosensory Cortex

A

> > > Brainstem via Ascending pathways (Trigeminal, Medial Lemniscus, Spinothalamic tract, etc.)

> > > to VPM/VPL
to S1 (primary sensory cortex) or SA (association areas).

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30
Q

Area 3:

Basics

A

Obligatory first step in cortical processing of somatosensory information.

The primary part of the primary cortex.

Intensity, localization….

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31
Q

Area 3:

4 Specifics

A
  1. Almost entirely buried in the central sulcus – forms posterior wall of the sulcus.
  2. Receives majority of thalamocortical input
  3. LOCALIZES sensory input (i.e., area of skin being touched) and INTENSITY of stimulus.
  4. Lesions of Area 3 result in profound deficits in all forms of tactile sensations mediated by
    cutaneous mechanoreceptors
32
Q

Primary Somatosensory Cortex includes what Brodman’s Areas?

A

Areas 1, 2, and 3

33
Q

Area 1

A

the exposed part of S1

Lesions in Areas 1 result in partial deficits and an inability to use tactile information to
discriminate texture.

34
Q

Area 2

A

buried in postcentral sulcus

Lesions in Areas 2 result in partial deficits and an inability to use tactile information to
discriminate size & shape of an object.

35
Q

Areas 1 & 2:

A
  1. Receives less input from thalamus and more from Area 3
  2. More complex receptive field – responds to Limb Position, or Shape of object touching skin rather than localizing area of skin being touched or intensity of pressure (role of Area 3).
36
Q

SECONDARY SOMATOSENSORY CORTEX

A

Adjacent to insula in the upper bank of the lateral sulcus.

  1. Input from all areas of S1. Little from VPL/VPM of the Thalaumus.
  2. Lesions in S1 eliminate responses of neurons in S2.
  3. Have bilateral receptive fields
  4. Contains pain sensitive neurons.
  5. Projects to limbic structures (amygdalya, hippocampus).
  6. Plays a role in tactile learning and memory
37
Q

Brodmann’s areas 5 and 7

A

Brodmann’s areas 5 and 7 are posterior to S1.

They make up the bulk of the parietal lobe.

5 & 7 are Somatosensory Association Areas

38
Q

ASSOCIATION AREA OF CORTEX

AREAS 5 AND 7

A

Higher level integration – combine input from different sensory receptors

39
Q

Lesions of Areas 5,7

A

produce complex sensory deficits

TACTILE AGNOSIA – Cannot identify object based on touch. May sense you are touching it but cannot determine what it is.

40
Q

TACTILE AGNOSIA

A

Cannot identify object based on touch. May sense you are touching it but cannot
determine what it is.

41
Q

PARIETAL NEGLECT SYNDROME

A

• Failure to recognize side of body contralateral to injury.

• Primarily occurs when RIGHT parietal association area is
involved.
Right Parietal Lesion&raquo_space;> Deficit is on Left side of the body

• May not bathe contralateral side of body or shave
contralateral side of face

  • Deny own limbs
  • Objects in contralateral visual field ignored
42
Q

APRAXIA

A

Unable to use sensory information needed to plan movements.

Usually occurs with lesions to the right parietal association area.

Apparent paralysis although muscles are functional and connections from motor cortex are intact.

May not be able to touch their nose when directed, but will scratch their nose if it itches

43
Q

BUCCOFACIAL OR OROFACIAL APRAXIA

A

Cannot carry out movements of the face on demand, such as licking the lips, sticking out the tongue, or whistling.

44
Q

IDEATIONAL APRAXIA

A

Cannot carry out learned complex tasks in the proper order, such as putting on socks before putting on shoes.

45
Q

IDEOMOTOR APRAXIA:

A

Cannot voluntarily perform a learned task when given the necessary objects.

For instance, if given a screwdriver, the person may try to write with it as if it were a pen.

46
Q

APRAXIA

A

The inability to execute a voluntary motor movement despite being able to
demonstrate normal muscle function.

47
Q

PATIENT GL

A

Claimed “loss of tactile sensation but could still sense temperature & pain”

Objective testing revealed….
• Could NOT detect vibration on palm or arm
• Could NOT detect stroking on palm BUT
• COULD detect stroking on arm

Stroking arm felt WEAKER than for control subjects and 
NO discriminations (e.g., direction) could be made

BUT the sensation was described as PLEASANT

Thus, the DISCRIMINATIVE content of the stroking sensation on arm was DIMINISHED but the emotional impact of the stroking was NOT DIFFERENT compared to control subjects

48
Q

Sensory localization illuminated by patient with specific loss of myelinated Aβ fibers…

PATIENT GL

A

Autoimmune syndrome resulting in loss of large diameter sensory fibers in spinal nerves.

Cranial nerves remained intact.

49
Q

There ARE some C fibers with low-threshold touch sensitivity: exclusively in hairy skin

A

Exclusively located in hairy skin.

Slow stroking most effective in activating these cells.

This is why Patient GL could feel a little on her arm, nut not in her hand.

50
Q

Brain area activated by low threshold C Fibers…..

A

(for pain and pleasant sensation of stroking) in Patient GL is
Insular cortex but NOT S1 or S2

(Area activated by gentle stroking of forearm)

51
Q

VPM

A

Face, Trigeminal

52
Q

VPL

A

Body, Spinothalamic, Touch

53
Q

Anterolateral system:

A

Discriminative

multiple tracts that convey different aspects of pain including location
and intensity of painful stimulus, emotional response to pain, autonomic response to pain, increased attention to painful input.

54
Q

Spinothalamic tract:

A

Discriminative Tract that conveys conscious awareness of nature of a painful stimulus (burning, stinging, aching) and where it is located.

Also conveys temperature information.

As in the periphery, this information is conducted by small diameter, lightly myelinated axons.

55
Q

Reticular formation throughout brainstem

A

attention

56
Q

Periaqueductal grey

A

intrinsic pain control mechanisms

57
Q

Hypothalamus

A

autonomic response

58
Q

Limbic system

A

emotion, memory

59
Q

Two distinct aspects of the experience of pain:

A

Affective

Discriminative

60
Q

Most of these do not reach the level of the cerebral cortex with the exception of one pathway that involves the limbic system and the midline thalamic nuclei.

A

This pathway is more involved in interpreting “pleasantness”
or “unpleasantness” of a painful stimulus rather than recording it’s physiological intensity.

61
Q

Other aspects of pain are mediated by other pathways. These end in:

A
  1. Reticular formation throughout brainstem (attention)
  2. Periaqueductal grey (intrinsic pain control mechanisms)
  3. Hypothalamus (autonomic response)
  4. Limbic system (emotion, memory)
62
Q

INSULAR CORTEX

A

BURIED DEEP IN THE LATERAL SULCUS.

COVERED BY GYRI FROM THE TEMPORAL, PARIETAL AND FRONTAL LOBES.

CONTAINS GUSTATORY, AUTONOMIC, PAIN, VESTIBULAR AREAS.

63
Q

Pain information terminates in 2 areas:

A

Primary somatosensory cortex (SI) and anterior cingulate cortex (ACC).

The latter is emotional response (level of “unpleasantness”).

Also input to insular cortex (not shown).

64
Q

MODULATION OF PAIN

A

GATE- CONTROL THEORY:
Initial site of modulation is at the level of the spinal cord where there are interactions between nociceptive
and non-nociceptive afferents. This controls transmission at site of origin.

PREMISE:
Dorsal horn neurons in laminas 1 and 5 receive convergent input from both nocicpetive and non-nociceptive
afferents (i.e., large myelinated axons from touch receptors).
A- beta afferents inhibit dorsal horn neurons by activating inhibitory interneurons.
A-delta and C fibers excite dorsal horn neurons and inhibit an inhibitory interneuron through a circuitous
pathway involving several other interneurons.

65
Q

MODULATION OF PAIN:

GATE-CONTROL THEORY:

A

Initial site of modulation is at the level of the spinal cord where there are interactions between nociceptive
and non-nociceptive afferents.

This controls transmission at site of origin.

66
Q

MODULATION OF PAIN

PREMISE:

A

Dorsal horn neurons in laminas 1 and 5 receive convergent input from both nocicpetive and non-nociceptive
afferents (i.e., large myelinated axons from touch receptors).

A- beta afferents inhibit dorsal horn neurons by activating inhibitory interneurons.

A-delta and C fibers excite dorsal horn neurons and inhibit an inhibitory interneuron through a circuitous
pathway involving several other interneurons.

67
Q

Gate Theory of Pain Modulation

A

A-beta fiber and C fiber terminate on the same dorsal
horn neuron.

C fiber inhibits the interneuron (not directly) and the
dorsal horn neuron is activated.

A-beta activates an inhibitory interneuron that
suppresses the dorsal horn neuron and pain is not
transmitted.

Think about rubbing a painful site to relieve pain.

Basis for use of transcutaneous electrical stimulation (TENS) to relieve pain. Stimulation is in range to activate large diameter processes within painful area.

68
Q

Pain transmission may be modulated by descending afferents including those arising in the:

A

Periaqueductal Gray

Midline reticular formation

69
Q

Input to ___ from ascending axons in spinothalamic tract.

A

Input to Periaqueductal Gray from ascending axons in spinothalamic tract.

70
Q

Modulate the Transmission of Information in Pain Pathways.

A

a. Regulates our ability to focus attention on particular sensory
modality such as pain.

b. Pathway involves input to PAG from ascending pain pathways.
From PAG output is to reticular formation and then to dorsal
horn of spinal cord to inhibit pain pathways.

c. Opiate receptors are found throughout PAG and raphe nuclei.
Activated by drugs such as morphine or endogenous opiates such as enkephalin and dynorphin released from local
inhibitory interneurons.

71
Q

Morphine

A

– opioid derivative

– has been known to have analgesic effects

72
Q

Areas that control pain are excited by exogenous application of opioids.

A

Neurons in PAG and dorsal horn express opioid receptors.

73
Q

All 3 of the major classes or endogenous opioid peptides are present in the PAG including:

A

Endorphins
Enkephalins
Dynorphins

74
Q

CINGULATE AND INSULAR CORTEX

A
  • Cingulate & insular cortex more important for “motivational & emotional” aspects of pain…
  • Pain has most obvious motivational/emotional impact
  • BUT so do other somatosensory submodalities, e.g. touch
  • Touch signals also activate insular cortex
75
Q

Descending systems modulate the transmission of ascending pain signals

A

Axons from neurons in the PAG synapse on neurons in the lower part of the brainstem, e.g., raphe nuclei which release serotonin.

These excite an inhibitory interneuron that contains enkephalin which contacts the terminal of the C-fiber.

ENK inhibits release of excitatory transmitter onto dorsal horn projection neuron, blocking further transmission of the pain signal.

76
Q

insular cortex

A

In each hemisphere of the mammalian brain the insular cortex (also called insula, insulary cortex, or insular lobe) is a portion of the cerebral cortex folded deep within the lateral sulcus (the fissure separating the temporal lobe from the parietal and frontal lobes).

The insula is another region of the brain that remained little understood for a long time because of its position deep in the folds of the cortex. Also, because it was not associated with the “higher” brain functions, it was of less interest to scientists who were investigating consciousness.