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Neural Control of Human Movement > Topic 4: Sensory Systems > Flashcards

Topic 4: Sensory Systems Flashcards

1
Q

Which 3 sensory systems support movement?

A
  • Vision
  • Vestibular
  • Somatosensory
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2
Q

Visual Pathway

A

Retina, thalamus, primary visual cortex

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3
Q

How do neurons in the visual system create perception of the world?

A
  • based on electromagnetic radiation
  • eyes detect visible light (400-700nm)
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4
Q

Primary visual cortex

A

First area of the cortex to receive visual information
- Brodmann’s area 17 in the occipital lobe
- AKA V1
- begins mapping and processing visual info
- Splits info into two main pathways

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5
Q

Dorsal stream of visual processing

A

Information passed toward parietal lobe which specializes in processing of visual motions
- NAVIGATING: perceiving the direction and speed of objects helps us navigate safely
- DIRECTING EYE MOVEMENTS: sense motion and quickly react to it
- MOTION PERCEPTION: interpretation of moving objects

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6
Q

Ventral stream of visual processing

A

Information passed towards the temporal lobe - specilized processing of vision other than motion
- Object perception and facial recognition

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7
Q

The vestibular system

A
  • Balance, equilibrium and posture
  • Based on the motion of hair cells
  • Made up of otolith organs and semicircular canals
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8
Q

Otolith Organs and components

A

Measures acceleration and tilt
- MACULA: epithelium filled pouch with hair cells
- KINOCILIUM: Tallest, most important cilia
- OTOCONIA (ear stones): Calcium carbonate crystals

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9
Q

How do the otolith organs work?

A
  • Baseline nerve impulse generated in vestibular fiber
  • DEPOLARITATION: when hairs bend toward the kinocilium, the hair cell depolarizes, exciting the nerve fiber, which generates more frequent AP
  • HYPERPOLARIZATION: when hair beds away from the kinocilium, the hair cell hyperpolarizes, inhibiting the nerve fiber, and decreasing AP frequency
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10
Q

Macular orientation

A

Array of orientations within organ
- Saccular macula - vertically oriented
- Utricular macula - horizontally oriented
Allows measure of all possible linear movements

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11
Q

Semicircular Canals

A

Measures head rotation (angular acceleration)
- three canals on each side helping sense all possible head rotation angles
- CRISTA AMPULLARIS: cupula (bubble) full of cilia found within an ampulla (bulge)
- Endolymph reacts slowly to quick rotations which deflects the cupula
- paired on opposite side of head acting in push-pull activation of vestibular axons

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12
Q

Purpose of central vestibular pathways

A

Pathways of vestibular information and reflexes to control head, body, eye movement

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13
Q

Central vestibular pathway

A
  1. Otolith organs + semicircular canals
  2. Vestibulocochlear nerve
    - Bipolar neurons
  3. Vestibular nuclei
    - Dorsolateral regions of medulla
    - integrate with other information (visual/motor)
  4. Send out information above and below
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14
Q

Where does the vestibular pathway send information to

A
  1. Cerebellum
    - Vestibular sensations needed for coordinating movements
  2. Thalamus (VP nucleus)
    - Then projects to postcentral gyrus
    - Info received by the cortex maintains a representation of the body in space
  3. Extraocular Motor Neurons
    - Reflexive eye movements
    - Primary goal is to maintain gaze
  4. Limbs
    - Reflexive limbs movement
    - primary goal is to keep body upright
  5. Neck and Trunk
    - Reflexive neck/trunk movements
    - Primary goal is to keep head upright
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15
Q

Vestibulo-ocular reflex

A
  • Function: to fixate line of sight on visual target during head movement
  • Mechanism: senses rotations of head, commands compensatory movement of eyes in opposite direction
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16
Q

How are horizontal eye movements mediated?

A

Mediated by vestibular connections
- When head rotation occurs, fluid in the semicircular canals moves in the opposite direction
- Results in positive stimulation to canal that the head is moving towards and negative stimulation to the canal that the head is moving away from
- causes eye movement to move in the opposite direction to head movement by activating muscles on the side of the eye that the movement goes towards

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16
Q

Vestibular Changes with age

A

Peripheral changes likely to occur first
OTOLITH ORGANS
- Loss of cilia
- alterations in otoconia (shape and size)
SEMICIRCULAR CANALS
- Loss of cilia, to greater extent than otolith organs
- Greater impact in VOR and fall risk
Central changes likely to occur later (after 60 years of age)
VESTIBULAR NUCLEI
- slow loss of neurons
CEREBELLUM
- slow loss or change in connectivity
Together, this leads to a reduction in sensory information necessary to control head, eyes and body and maintain balance
- when combined with changes to other sensory structures (vision, touch, proprioception) and loss of muscle strength it leads to an increased fall risk

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17
Q

What are the 4 common vestibular pathologies?

A
  • Benign Paroxysmal Position vertigo
  • Vestibular Neuronitis
  • Labyrinthitis
  • Meniere’s Disease
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18
Q

Benign Paroxysmal Positional Vertigo (BPPV)

A
  • Benign = harmless in long-term
  • Paroxysmal = sudden onset/recurrence of symptoms
  • vertigo = Sensation of spinning/dizziness
    CAUSED BY:
  • Ear stones (otoconia) migrating into semi-circular canals
  • Disrupting the cupula located in ampulla
    TREATMENT:
  • Often resolves on own
  • specific head maneuvers can reposition debris out
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19
Q

Vestibular Neuronitis

A

CAUSED BY:
- Inflammation of the vestibular nerve
SYMPTOMS:
- sudden vertigo that can last several days
- Does not affect hearing
TREATMENT:
- anti-nausea medication until inflammation reduces
- Steroids to reduce inflammation
- Physical therapy/activity can help the body compensate

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20
Q

Labyrinthitis

A

CAUSED BY:
- inflammation of the entire inner ear due to infection
SYMPTOMS:
- Sudden vertigo that can last for several days
- does affect hearing
TREATMENT:
- Treat infection
- Anti-nausea medication until inflammation reduces
- physical therapy/activity can help the body compensate

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21
Q

Meniere’s Disease

A

CAUSED BY:
- Excessive fluid build up in inner ear
- unknown why this occurs
SYMPTOMS:
- sudden episodes of: tinnitus, hearing loss, and/or vertigo
- Each episode can last minutes to hours
- May occur in clusters, then subside for years
TREATMENT:
- No cure; managing symptoms
- can lead to permanent hearing loss, but rare

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22
Q

Mechanoreceptors in skin

A
  • Most somatosensory receptors are mechanoreceptors which are receptive to physical distortion
  • 4 primary receptors in skin: pacinian corpuscles, meissner’s corpuscles, ruffini endings, merkel’s disks
  • Vary in terms of receptive field and adaptation rate
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23
Q

Pacinian Corpuscles

A
  • Largest and deepest mechanoreceptor in skin
  • Get compressed and detect pressure and vibration
  • large receptive field
  • rapid adapting: react quickly to initial contact, but not sustained contact
  • best at detecting finer textures and high frequency vibrations
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24
Q

Meissner’s Corpuscles

A
  • Small receptors in upper dermis; common in fingers
  • detect fine touch and pressure
  • small receptive field
  • rapid adapting
  • best at detecting heavier textures and lower frequency vibrations
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25
Q

Ruffini Endings

A
  • Large receptors in dermis layer
  • detect stretch and deformation
  • large receptive field
  • slow adapting
  • react to sustained deformations
  • best at detecting grip and position
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26
Q

Merkel’s Disks

A
  • Small receptors in epidermis, common in fingers
  • Detect fine touch and pressure
  • small receptive field
  • slow adapting
  • react to sustained deformations
  • best at static discrimination of shapes/textures
27
Q

Two-point discrimination

A

Sensitivity to discriminate small points varies greatly across the body
- more sensitive in more important places
ACCOMPLISHED BY:
- greater density of mechanoreceptors
- smaller field size (meissner/merkel)
- greater brain tissue devoted to these areas

28
Q

Primary afferent axon

A
  • Enters spinal cord at dorsal root
  • cell bodies lie in dorsal root ganglion
  • Four types A alpha, A beta, A delta, C
  • A beta mediates touch
29
Q

Various sizes and myelination of primary afferent axons

A
  • All A’s are myelinated (larger + myelination = faster) (alpha, beta, delta then C)
  • C’s are not myelinated (smaller and slower)
30
Q

What are the two branches of the A beta axons

A
  1. Directly ascending the spinal cord to the brain
  2. Synapses with second-order sensory neurons (for reflexes)
31
Q

Dorsal Column- Medial Lemniscal Pathway

A
  1. Ascending branch goes up the dorsal column
  2. Synapse on the dorsal column nuclei in medulla
  3. Dorsal column nuclei axons decussate and ascend the medial lemniscus
  4. Synapse in the VP nucleus of the thalamic
  5. Neurons in the VP nucleus project to somatosensory cortex
32
Q

Dermatomes Diagram

A

The distribution/mapping of spinal nerves

33
Q

Herniated Disc

A
  • Most common in 30-50s
  • Most common in the lower back (L4/5 &L5/S1 - 95% of cases)
  • Pain (back and legs - glutes, thigh, calf, eve foot)
  • Numbness or tingling
  • weakness
  • Diagnosed through physical exam, imaging or even nerve tests
34
Q

Treatment for herniated disc

A
  1. Rest, physical therapy, pain medications (85% RESOLVE IN 8-12 WEEKS)
  2. Surgical - discectomy/ microdiscectomy
    - Conservative failed to resolve
    - progressive/debilitating pain, numbness, and weakness
35
Q

Lateral Inhibition

A
  • Inhibit adjacent inputs to enhance tactile sensitivity
  • Increase contrast to allow for more precise/finer location of sensation
    HOW IT WORKS:
  • greater AP frequency in central afferent neuron
  • interneuron inhibits peripheral neurons
  • peripheral neurons have low initial AP frequency which has minimal lateral inhibition on central and then gets inhibited resulting in decrease in AP frequency leading to greater contrast
36
Q

Sensory Gating

A
  • Corticothalamic feedback influences sensory processing
  • cortex helps to filter irrelevant or repetitive information
  • these complex pathways remain unclear
  • issues in pathway may be related to cognitive disorders (schizophrenia)
37
Q

Primary Sensory Cortex

A

3b (located on the curve down towards central sulcus on postcentral gyrus)
- Receives inputs from VP nucleus
- Highly responsive to somatosensory input
- Damage impairs sensation
- Electrical stimulus creates sensations

38
Q

Somatosensory 3a

A
  • Located deep in central sulcus on postcentral gyrus
  • Dense thalamus input, but more body position (proprioception)
39
Q

Somatosensory 1& 2

A
  • 1 located on hump of postcentral gyrus
  • 2 located towards posterior parietal cortex
  • Receives information from 3b
  • generally related to texture, size, and shape
40
Q

Posterior parietal cortex

A

Allows for processing of basic sensory information and integration with other senses

41
Q

Posterior parietal cortex 5

A
  • located directly posterior to postcentral gyrus
  • Sensory integration for the planning and organization of movement
42
Q

Posterior parietal cortex 7

A
  • Located posterior to PPC5
  • Sensory integration for object recognition and spatial relationships
43
Q

Nociception

A

Receptors of painful stimuli
- Sensory process that provides signals that MAY trigger pain
- Activated by stimulus that may damage tissue ( strong mechanical stimulation, temperature extremes, oxygen deprivation, chemicals; even substances released by damaged cells
- nociception doesn’t = pain

44
Q

Pain

A

Sore, aching throbbing sensations we “feel”; can be influenced by past experiences

45
Q

Nociceptors

A

Free Nerve endings which bring the sensation of pain to CNS

46
Q

Types of Nociceptors

A
  • Mechanical: Respond to damage such as cutting, crushing or pinching
  • Thermal: Respond to temperature extremes
  • Chemical: respond to histamine and other chemicals
  • Polymodal: Respond equally to all kinds of damaging stimuli
47
Q

Fast pain Nociceptors

A
  • Mechanical and thermal
  • myelinated alpha delta fibers
  • Sharp, prickling sensation
  • Easily localized
  • Fast, occurs first
48
Q

Slow pain nociceptors

A
  • Polymodal
  • Unmyelinated C fibers
  • Dull, aching burning sensation
  • Poorly localized
  • Slow, occurs second and for longer time
49
Q

Spinothalamic Tract

A
  1. Enter zone of Lissauer (ascend or descend slightly)
  2. Synapse in the substantia gelatinosa (in dorsal horn)
  3. Second order neurons in the spinal cord immediately decussate
  4. Ascend to the brain in the ventrolateral lateral surface of the spinal cord
  5. Synapse with VP nucleus (and other areas) in the thalamus
  6. Information then projected the somatosensory cortex
50
Q

Compare dorsal column-medial lemniscal pathway and spinothalamic pathway

A
  • Both have 3 neurons and 3 synapses
  • Decussation at dorsal column nuclei vs spinal column before ascending
  • A beta vs A delta and C
51
Q

Organization of DCML pathway

A

Upper body lateral, lower body medial
lateral to medial:
- Neck
- Arm
- Upper trunk
- Lower trunk
- Legs

52
Q

Organization of spinothalamic pathway

A

Upper body deep, lower body superficial
Superficial to deep:
- leg
- trunk
- Arm
- Neck

53
Q

Gate Control theory of pain

A
  • Neurons in the spinothalamic tract may be inhibited by A alpha or A beta nerves (touch) in the dorsal horn of the spinal cord
  • Pain can be reduced by the activity of mechanoreceptors through interneuron
54
Q

Descending Pain regulation

A
  • Strong emotions, stress, etc. can suppress pain
    PERIAQUEDUCTAL GREY MATTER (PAG)
    1. Receives input from many areas in cortex (often emotions)
    2. Neurons descend to medulla (Raphe nuclei)
    3. Neurons descend to spinal cord to depress activity
55
Q

Hyperalgesia

A
  • Reduction in the pain threshold, increased sensitivity, or spontaneous pain
    PRIMARY CHANGES OCCUR PERIPHERALLY:
  • Inflammation = bodies attempt to eliminate injury and stimulate healing
  • A variety of neurotransmitters, peptides, lipids etc. are released which can attach to receptors in/around injury to lower their threshold for activation
56
Q

Primary Hyperalgesia

A

Super-sensitivity within the damaged area

57
Q

Secondary Hyperalgesia

A

Super-sensitivity in the surrounding area

58
Q

Allodynia

A

pain response from stimuli that would normally not cause pain

59
Q

Central Sensitization

A

Amplification of neural signaling within the CNS that elicits pain hypersensitivity or normal stimuli
- Changes in the synapse and potentially the organization of interconnecting neurons may increase excitability/ reducing inhibition of pain pathways
- Contributions are difficult to identify and treatments difficult to target

60
Q

What factors relate to central sensitivity

A
  • Osteoarthritis and various MSK disorders
  • Fibromyalgia
  • Other chronic pain conditions
61
Q

Referred pain

A
  • Cross-talk between sensory neurons
  • convergence of visceral and somatic afferent neurons
62
Q

Thermoreceptors

A
  • Varying sensitivities to hot and cold temperatures
  • Cold (A delta and C) and hot (C fibers)
  • Adapt to long durations of stimuli
  • Follow the same pathway as pain
63
Q

Proprioception

A
  • Our perception of the location and movement of our body
  • Allows us to control limb and joint position for optimal movement
  • Group one neurons
64
Q

What are the two primary proprioception receptors?

A
  • Muscle Spindle: amount of stretch in a muscle
  • Golgi tendon organ: amount of force
65
Q

Proprioception information pathways

A

CONSCIOUS PROPRIOCEPTIVE INFO
- Dorsal column medial lemniscus pathway
UNCONSCIOUS PROPRIOCEPTIVE INFO
- Spinocerebellar tract (to cerebellum)
- Spinal interneurons (Spinal reflexes)

Neural Control of Human Movement (6 decks)

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