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Brain and Behavior > Exam 2 Deck 1 > Flashcards

Exam 2 Deck 1 Flashcards

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1
Q

What is worrysome about a headache that is worse at night/in supine positions?

A

May be a tumor

Further increased ICP

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2
Q

What types of lesions affect the optic chiasm?

A

SATCHMO

Adenoma/Aneurysm, and Meningioma are common

Sarcoid
Adenoma/Aneurysm

Teratoma

Craniopharyngeoma

Hystiocytosis

Meningioma

Optic Glioma

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3
Q

What does the SATCHMO mnemonic stand for?

A

For lesions that can affect the optic chiasm

Sarcoid
Adenoma/Aneurysm

Teratoma

Craniopharyngeoma

Hystiocytosis

Meningioma

Optic Glioma

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4
Q

What is the hormone most commonly elevated in a benign pituitary tumor?

A

Prolactin

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5
Q

What is a drug that reduces prolactin production?

A

Bromocriptine

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6
Q

What is the most common age group for the initial onset of hereditary epilieptic disorders?

A

Teens

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7
Q

What cells in the retina see color?

A

Cones

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8
Q

What cells in the retina see light?

A

Rods

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9
Q

What color light is usually the first one to go in the loss of color vision?

A

Red light

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10
Q

What is a scotoma?

A

A missing patch of your visual field (can be any shape)

e.g.

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11
Q

What can cause pain with eye movements?

A

Optic nerve inflammation

Thyroid disease - extraocular muscle swelling + pain

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12
Q

Which way is nystagmus defined?

A

In the direction of the fast phase

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13
Q

In vestibular neuronitis, towards which side do you tend to fall?

A

Towards affected side

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14
Q

In vestibular neuronitis, towards which side do you see nystagmus?

A

Away from affeted side

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15
Q

What is a mnemonic for the direction of nystagmus in caloric testing?

A

COWS

Cold - opposite

Warm - same

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16
Q

What are exteroreceptors?

A

Sensory receptors receptive to stimuli on or beyond the body surface

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17
Q

What are interoreceptors?

A

Sensory receptors receptive to stimuli arising within the body itself.

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18
Q

What are proprioceptors?

A

Special group of interoceptors which are receptive to the position of the body, head or limbs in space.

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19
Q

What is the nature of the relationship between an axon and a sensory modality?

A

One axon only transmits sensation of one modality

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20
Q

What type of neurons are the sensory neurons?

A

Pseudounipolar DRG neurons

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21
Q

Where are the cell bodies of sensory neurons located?

A

DRG

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22
Q

What are the three main types of peripheral sensory nerve endings?

A

Free nerve endings

Unencapsulated endings associated with accessory structures Encapsulated endings

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23
Q

What are free nerve endings?

A

Majority of the sensory receptors in the skin

They display no obvious structural specialization, but evidence suggests that different fibers respond preferentially to painful stimuli, or warmth or cold, or to mechanical displacement of the skin

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24
Q

What is the difference between a neuropathy, radiculopathy, and myelopathy?

A

Neuropathy - nerve

Radiculopathy - root

myelopathy - spinal cord

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25
Q

What type of nerve fibers give rise to free nerve endings?

A

Unmyelinated (C fibers)

Myelinated (A-delta fibers)

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26
Q

What are unencapsulated nerve endings with accessory structures?

A

Terminal axon branches which end in intimate association with other cell types found in the skin

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27
Q

What is an example of an encapsulated nerve ending with accessory structures?

A

Hair - detects deflection

Merckel’s touch corpuscles - detect pressure

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28
Q

What are encapsulated nerve endings?

A

Nerve endings in which the terminal axon ends inside a distinct connective tissue capsule; these endings are often specialized for determining the direction or type of displacing force that acts on the contained sensory nerve terminals

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29
Q

What are examples of encapsulated nerve endings?

A

Pacinian Corpuscles - Vibratory information

Ruffini Endings - Pressure information

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30
Q

What type of fibers are encapsulated nerve endings innervated by?

A

Largest diameter myelinated fibers - A-beta fibers

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31
Q

How is intensity of a signal encoded by nerves?

A

By the frequency of action potentials and the number of fibers recruited

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32
Q

What is encoded by the frequency of action potentials and the number of fibers recruited?

A

Intensity

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33
Q

How is location of a stimulus encoded?

A

By the position and size of a neuron’s receptive field

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34
Q

What is encoded by the position and size of a neuron’s receptive field?

A

Localization of a stimulus

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35
Q

How is the duration and rate of change of a stimulus encoded?

A

By the discharge characteristics of an axon:

slowly adapting - discharges as long as the stimulus is present

rapidly adapting - discharges at the onset or offset of a stimulus

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36
Q

What are the two main ascending sensory columns in the spinal cord?

A

Dorsal Column-Medial Leminscal (DC-ML) System - Mechanosensation

Spinothalamic (Anterolateral) Tract - Pain and Temperature

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37
Q

How is the dorsal root organized?

A

Medial division contains touch, pressure and vibraton (A-beta fibers) and position and movement (Group I, II fibers); these are larger afferents

Lateral division contains pain and temperature (A-delta and C fibers) and crude touch (Group III, IV fibers); these are smaller afferents

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38
Q

What are the larger muscle sensory afferent fibers?

A

Group Ia - muscle spindle primary fibers

Group Ib - golgi tendon organ (GTO)

Group II - muscle spindle secondary fibers

Group III and IV are smaller, encode pain and temperature

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39
Q

What are the smaller muscle sensory afferent fibers?

A

Group III and Group IV - encode pain and temperature

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40
Q

What are the larger cutaneous sensory afferent fibers?

A

A-beta : encode touch and pressure

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41
Q

What are the smaller cutaneous sensory afferent fibers?

A

A-delta and C fibers : encode pain and temperature and crude touch

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42
Q

What happens to medial fibers entering the dorsal root?

A

They have three fates:

1) can terminate in Lamina III/ IV, VII, IX
2) can ascend a couple of spinal segments and then terminate in the tracts above - these travel through the fasiculus interfasicularis or the fasiculus septomarginalis
3) can ascend via the dorsal columns (fasiculus gracilis or cuneatus) to the medulla

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43
Q

What is the fasiculus interfasiculatus or the fasiculus septomarginalis?

A

Tract that allows for some branches of the medial division of the dorsal root nerve fibers (those that belong to the dorsal column - medial leminscal system) to travel up a few segments in the spinal cord and synapse in the appropriate lamina

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44
Q

What is the fasiculus gracilis?

A

Part of the dorsal columns

The more medial column that is present at ALL cord levels. Carries information from lower levels of the spinal cord (organized so that medial = toes; dorsal and f. cuneatus = arm + above)

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45
Q

What is the fasiculus cuneatus?

A

Dorsal column spinal tract present at T6 and above that carries information from the upper trunk and limbs (recall organization of the dorsal columns)

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46
Q

How is information organized in the dorsal columns?

A

Fibers in the spinal dorsal columns are somatotopically organized: sacral regions are represented by fibers lying most medially, next to the dorsal median septum, then, on moving laterally, foot, thigh, lower trunk (in the gracile fasciculus), upper trunk, upper limbs and neck (in the cuneate fasciculus).

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47
Q

What two tracts make up the dorsal columns?

A

Fasiculus gracilis (medial) and fasiculus cuneatus (lateral)

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48
Q

What side of the body do dorsal column - medial leminscal system fibers in the spinal cord correspond to?

A

Ipsilateral - DC-ML crosses over at the medulla

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49
Q

What happens to the lateral fibers entereing from the dorsal horn?

A

The fibers accumulate on the surface of, and immediately ventral-lateral to, the surface of the dorsal horn, where they form Lissauer’s tract (or dorsolateral tract).

In this tract, the C fibers and A-delta fibers branch over 2-5 segments and enter the ipsilateral dorsal horn, terminating on second-order neurons of laminae I and II mostly (substantia gelatinosa).

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50
Q

What is Lissaurer’s Tract?

A

Tract from the lateral fibers from the dorsal root, where the C fibers and A-delta fibers branch over 2-5 segments and enter the ipsilateral dorsal horn, terminating on second-order neurons of laminae I and II mostly (substantia gelatinosa).

(i.e. spinothalamic tract)

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51
Q

What information does the dorsal column-medial leminscal pathway transmit?

A

It is the principal pathway through which information about position, movement, touch and vibration is conveyed to higher perceptive centers of the brain (e.g. the cerebral cortex)—that is, it is concerned with discriminative aspects of somatic sensation.

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52
Q

Where do neurons of the dorsal column-medial lemiscal pathway synapse?

A

They synapse at the dorsal column nuclei

Either the gracile nucleus or the cuneate nucleus, depending on the fasiculus which it ascended in. These nuclei maintain the somatotopy, place, and modality specificity and send their neurons across the midline via the great sensory decussation to the medial lemniscus and up to the thalamus.

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53
Q

Where do the neurons of the dorsal column nuclei send their axons?

A

Send their axons across the midline via the great sensory decussation and then ascend up the opposite side of the brain to the thalamus via the medial lemniscus

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54
Q

What is the medial lemniscus?

A

Ascending sensory tract after the great sensory decussation that sends dorsal column nuclei axons up to the thalamus

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55
Q

What is the dorsal column-medial lemniscal pathway?

A

The continuation of the fibers which form the medial division of the dorsal roots. Extends up from the spinal cord through the gracile and cuneate faciculi where they end on their respective nuclei (nucleus gracilis and nucleas cuneatus). These dorsal column nuclei then send axons across the great sensory decussation and up the medial lemniscus. These fibers terminate in the thalamus.

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56
Q

What is the great sensory decussation?

A

Crossing over of sensory fibers in the medulla.

Fibers are those of the dorsal column nuclei (gracile nucleus or cuneate nucleus)

These fibers then ascend up the medial lemniscus and into the thalamus

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57
Q

What is the spinothalamic pathway?

A

The continuation of fibers which form the lateral division of the dorsal roots.

Transmits information of pain and temperature to the brain via A-delta and C fibers

Via laminae I and lamina V

Crosses in the cord via the ventral white commissure

Ascend via the anterolateral funiculus to the thalamus without interruption

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58
Q

Where does the dorsal column-medial lemiscal pathway cross over?

A

In the medulla at the great somensory decussation

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59
Q

Where does the spinothalamic pathway cross over?

A

In the spinal cord - at the ventral white commisure

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60
Q

What is syringomyelia?

A

A cavitation in the center of the spinal cord

Will cause segmential lesions to the sensory fields represented by the spinothalamic tract (pain and temperature) since they cross over in the spinal cord (bilateral).

Cape-like (suspended) sensory loss

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61
Q

What occurs in Brown-Sequard Syndrome?

A

Hemisection of the spinal cord causes:

IPSILATERAL loss of position and vibration

CONTRALATERAL loss of pain and temperature

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62
Q

What types of fibers are involved in the DC/ML system?

A

Large diameter, myelinated fibers that are topographically organized and convery proprioception and mechanosensation (touch, pressure, vibration)

Group I, Group II, A-beta fibers

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63
Q

What types of fibers are involved in the ST (spinothalamic) system?

A

Small-diameter, thinly/non-myelinated fibers that convey pain and temperature information

A-delta and C fibers

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64
Q

Where do large-diameter sensory fibers from the face terminate?

A

In the principal (or chief) trigeminal nucleus, in the pons on the ipsilateral side

These convey touch, pressure, and vibration

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65
Q

Where do touch, pressure and vibration sensory afferents from the face terminate?

A

In the principal (or chief) trigeminal nucleus, in the pons on the ipsilateral side

These are the large diameter fibers

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66
Q

What is the the analagous structure to the dorsal column nuclei for the trigeminal sensory system?

A

the principal (or chief) trigeminal nucleus

It is in the pons on the ipsilateral side of the sensory afferents

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67
Q

What is the course of touch, pressure, and vibration information (i.e. large diameter fibers) from the face?

A

From face to the trigeminal ganlgion where it synapses at the principal sensory nucleus (principal or chief trigeminal nucleus). Then secondary neurons cross in the pons and join the ascending medial lemiscal fibers, adding the face to the body plan that is conveyed and conserved in the tract. They then go up to the thalamus

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68
Q

What is the spinal tract of V?

A

Analagous to Lissauer’s Tracts but for the trigeminal nerve.

Axons course caudally to terminate in the spinal nucleus of V on the ipsilateral side

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69
Q

What is the analagous structure to Lissauer’s tract for the trigeminal nerve?

A

Spinal tract of V

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70
Q

Where do small diameter and unmyelinated fibers from the face terminate?

A

Course through the ipsilateral spinal tract of V to the caudal 1/3 of the spinal nucleus of V.

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71
Q

Where do the pain and temperature information fibers from the face terminate?

A

Course through the ipsilateral spinal tract of V to the caudal 1/3 of the spinal nucleus of V.

These are the small diameter fibers (A-delta) and the unmyelinated (C fibers)

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72
Q

What is the course of pain and temperature information from the face?

A

A-delta and C fibers from the face enter in the pons, but course caudally to the medulla via the ipsilateral spinal tract of V.

Once at the medulla, they terminate at the caudal 1/3 of the spinal nucleus of V (ipsilateral)

From here, the second and third order neurons cross the midline and join the ascending spinothalamic tract and go up to the thalamus

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73
Q

What do lesions that damage the medullary levels of the trigeminal pathways manifest as?

A

Ipsilateral pain and temperature sensation loss of the face

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74
Q

What do lesions that damage the pontine levels of the trigeminal pathways manifest as?

A

Ipsilateral touch, pressure, and proprioception loss; damage to the motor neurons

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75
Q

What do lesions that damage above the brainstem levels of the trigeminal pathways manifest as?

A

All sensory modalities affeted contralaterally

Motor function not affected - these are innervated bilaterally

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76
Q

How are sensory fibers somatotopically organized in the brainstem?

A
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77
Q

What is the somatotopy of the medial lemiscal tract at the point of entry to the thalamus?

A

More dorsal is legs, more ventral is face

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78
Q

What is the somatotopy of the spinothalamic tract upon entry to the thalamus?

A

None at this point

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79
Q

What is the major somatosensory relay nucleus of the thalamus?

A

The ventral posterior nucleus (contains VPL and VPM)

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80
Q

What is significant about the ventral posterior nucleus?

A

It is the major somatosensory relay nucleus of the thalamus and is the only site of termination of the medial lemiscus and a major site of termination of spinothalmaic fibers

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81
Q

Where do axons of VP neruons project to?

A

The first somatosensory cortex SI in the caudal bank of the central sulcus and the postcentral gyrus

Also to part of the parietal operculum, to an area called the second somatosensory area (SII or S2)

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82
Q

Where do dorsal column nuclei fibers terminate?

A

On the contralateral VPL

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83
Q

Where do principal trigeminal nuclei fibers terminate?

A

On the contralateral VPM

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84
Q

What is the relationship between VPL, VPM and the somatotopic organization of the sensory information from the dorsal column-medial leminiscal system?

A

Legs are lateral, face is medial, etc

Further extremities are ventral

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85
Q

Which areas have disproportionately large representaitons in the ventral posterior thalamus?

A

Foot, hand and lips

they have highest density of innervation

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86
Q

What is the relationship between VPL, VPM, and the sensory information relayed from the spinothalmaic tract?

A

Not much

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87
Q

How is the somatosensory information of the thalamus represented in the primary sensory cortex (S1)?

A
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88
Q

What types of neurons exist in the thalamic nuclei?

A

Relay neurons (relay to the cortex)

Inhibitory interneurons (which use GABA)

They exhibit properties which mirror those of their input (lemniscal or spinothalamic, not both)

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89
Q

What are properties of thalamic relay neurons with lemniscal inputs?

A

Great synaptic security (reproduce faithfully the temporal pattern of APs)

Modality and place specificity

Clustering of place and modality characteristics

Surround inhibition - activaiton of one group inhibits neighbors

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90
Q

What are properties of thalamic relay neurons with spinothalamic inputs?

A

Fewer cells that are hard to drive (require intense stimuli)

Large receptive fields

Respond specifically to noxious stimuli and thermal (cooling) stimuli

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91
Q

What information is projected to areas 3a and 2 of S1?

A

Proprioceptive information (i.e. from muscle spindle primary and secondary afferents and from joints) that comes from VP cell axons

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92
Q

What information is projected to areas 3b and 1 of S1?

A

Cutaneous tactile information (i.e. from A-beta fibers) from VP cell axons

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93
Q

What areas in S1 recieve thalamic innervation from the spinothalamic inputs?

A

all four areas (1, 2, 3a, 3b)

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94
Q

Which areas of S1 recieve proprioceptive information?

A

3a and 2

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95
Q

Which areas of S1 recieve cutaneous tactile information?

A

3b and 1

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96
Q

What cortical layers do spinothalamic thalamic neurons project to?

A

I

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97
Q

What cortical layers do lemniscal thalamic neurons project to?

A

IV

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98
Q

What information is represented in S2?

A

Bilateral neurons from VP thalamus

Somatotopically represented with the face anterior and the legs posterior

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99
Q

What are descriminative features of pain?

A

Ability to perceive and localize

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100
Q

What are affective features of pain?

A

Behaviors and emotions that affect mood and motivation (more nebulous a concept than the discriminative features of pain)

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101
Q

What is the pathway of pain perception from the neck down?

A

Spinothalamic tract from lateral fibers of dorsal root. Up to VPL and to cortex

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102
Q

What is the pathway of pain perception in the face?

A

From trigeminal nerve down the spinal trigeminal tract and across to join the spinothalamic tract and goes up to the VPM. Then to cortex

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103
Q

How is affective pain perception acheived?

A

There are many collateral branches from the ascending basic pathways of discriminative pain perception. These innervate structures along the way to the thalamus:

Periaqueductal Grey (PAG)

Rostroventral medulla (RVM) - parabrachial nucleus, reticular formation, raphe nucleus

VM and MD nuclei in the thalamus

Ventromedial hypothalamus (VMH)

amygdala

Globus pallidus

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104
Q

What structures contribute the emotional content of pain?

A

Amygdala, cingulate gyrus

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105
Q

What structures contribute to the motivational content of pain?

A

Globus pallidus, cingulate S1 gyrus, insula

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106
Q

What structures contribute to the generation of appropriate behaviors to threats?

A

Ventromedial hypothalamus (VMH)

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107
Q

What structures contribute descending control of nocioceptive information in the cord?

A

Amygdala, ventromedial hypothalamus, periacqueductal gray, rostroventral medulla (parabrachial nucleus, medullary reticular formation, locus cerulius (norepinephrine), raphe nucleus (serotonin))

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108
Q

How is pain perception modulated from the top down (descending modulatory systems)?

A

Periaqueductal grey plays a big role in integrating information from the top and from the ascending spinothalamic tracts

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109
Q

What is the end activity of top-down modulation of pain perception?

A

Periacqueductal grey neurons activate raphe nucleus (serotonin) and locus ceruleus (norepinephrine) neurons that act on local inhibitory interneurons that can release enkephalin to reduce the throughput of ascending spinothalamic signals (via lamina I and V neuron inhibition)

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110
Q

What is the effect of endogenous opiates on the transmission of pain signals in the cord?

A

Enkephalin shortens the duration of action potentials (limits calcium entry), which decreases neurotransmitter release. This diminishes the response of the subsequent neuron

Pre-synaptic (A-delta and C fibers): decreases neurotransmitter release

Post-synaptic - decrease afferent evoked EPSP by hyperpolarizing the cells

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111
Q

What are the four types of pain disorders?

A

Nociceptive (cutaneous adn visceral)

Inflammatory

Dysfunctional

Neuropathic

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112
Q

What is nociceptive pain (in the context of pain disorders)?

A

Physiological pain produced by noxious stimuli that activate high-threshold nociceptor neurons

Concept of first and second pain is involved here

As well as Gate Theory

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113
Q

What is the concept of first and second pain?

A

First pain is experienced because of A-delta fibers (sharp, quick)

Second pain is experiened because of C-fibers (duller, longer)

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114
Q

What is the Gate Theory?

A

Spinothalamic nerves receive convergent input from both Aδ/C (pain and temp) and Aβ fibers (mechanosensation). Aβ fibers can activate an inhibitory interneuron, which dampens the throughput of pain info from Aδ/C fibers to the spinothalamic pathway

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115
Q

What is referred pain?

A

Group III, IV (visceral pain afferents) terminate on spinothalamic tract neurons that are also receiving cutaneous Aδ/C fibers, so pain is perceived to be coming from the cutaneous receptive field

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116
Q

What is inflammatory pain (in the context of pain disorders)?

A

Pain hypersensitivity due to peripheral inflammation. Whole system is amped up.

Can serve a protective role

Can cause allodynia - normally non-painful stimuli become painful

Can cause hyperalgesia - exaggerated response to normally painful stimulus

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117
Q

What is allodynia?

A

Normally non-painful stimuli become painful. Seen in the context of inflammatory pain

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118
Q

What is hyperalgesia?

A

Exaggerated response to a normally painful stimulus

Seen in the context of inflammatory pain

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119
Q

What is the mechanism of inflammatory pain?

A

neurochemical mediators (IL-1β, IL-6, NO, bradykinin, NGF, H+) secreted by immune cells cause pain fibers to discharge APs aberrantly, which causes both peripheral and central amplification of pain pathways

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120
Q

What is dysfunctional pain?

A

Maladaptive pain that neither protects or supports healing and repair

Pain present without stimulus

Has all of the same components as inflammatory pain (hyperalgesia, allogynia) without evidence of inflammation

Examples include primary erythermalgia, fibromyalgia

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121
Q

What is primary erythermalgia?

A

Dysfunctional pain disorder - peripheral amplification (vs central like in fibromyalgia)

Rare

Red, warm, burning sensation in hand and feet

Caused by a sodium channelopathy where there is a gain of function mutation

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122
Q

What is fibromyalgia in the context of pain disorders?

A

Disfunctional pain disorder presenting with body-wide pain in joints and muscles

A process that is due to central amplification of pain (vs peripheral as in primary erythermalgia)

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123
Q

What is neuropathic pain in the context of pain disorders?

A

Maladaptive plasticity caused by a lesion or disease that alters nociceptive processing

Pain is felt in the absence of a stimulus

Can be chronic and debilitating

Hyperalgesia, allodynia, and pain that outlasts the stimulus

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124
Q

What are mechanisms of neuropathic pain?

A

CNS lesion or disease (stroke, spinal cord injury, MS)

PNS lesion or disease (nerve trauma, toxic and metabolic neuropathies, Herpes zoster, AIDS)

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125
Q

What is phantom limb pain?

A

Type of neuropathic pain that refers to pain in a body part that has been amputated or deafferented

Almost all amputees report this, but not all are painful

Can be short-lasting shocks to excruciating, chronic pain

Maladaptive reorganization of connections in CNS centers, mostly S1

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126
Q

What is the mechanism for phantom limb pain?

A

Cortical reorganization of S1: axons from neighboring cortex sprout into denervated regions of the cortex (previously receiving input from the amputated limb) and, for unknown reasons, this causes ectopic discharges (axons fire unpredictably), which is interpreted as pain

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127
Q

What are therapeutic strategies that attempt to manage pain?

A

Monoamine reuptake inhibition - enhance descending inhibitory control (antidepressants)

Block ectopic discharge (anticonvulsants - sodium channel)

Block transmitter release (anticonvulsants - calcium channel)

Enhance endogenous analgesic system (opiod agonists)

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128
Q

What are complications of using exogenous opiods (e.g. morphine)?

A

They drive the brain reward pathways too

Causes physcial, psychological dependence

Can see tolerance

Overdose

Constipation

Cognitive impairment

Cardiac arrhythmias

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129
Q

What occurs in central sensitization that is responsible for the development of chronic pain?

A

Synaptic signaling strength of pain pathways is greatly exageratted by maladaptive neoplastic mechanisms:

  • increased membrane excitability in peripheral axons (Na channel upregulation)
  • Increased synaptic efficacy (upregulation of glutamate receptors at non-primary neurons)
  • Decreased inhibition in local interneuron networks
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130
Q

What structure does the epithalimus primarily connect to?

A

The hypothalamus

Notably not the cortex

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131
Q

What structure does the dorsal thalmus (i.e. the thalamus) primarily send and recieve axons from?

A

The cerebral cortex

Each relay nucleus projects to one (sometimes a few) cortical area in what are called thalmaocortical projections

They each also recieve feedback input from the same areas, called corticothalamic projections

These are notably ipsilateral, and excitatory (use glutamate)

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132
Q

To which side of the brain do thalamic communications with the cerebral cortex occur?

A

Ipsilateral

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133
Q

What type of signals (inhibitory/excitatory) do signals between the thalamus and cerebral cortex use?

A

Excitatory!

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134
Q

What neurotransmitter is used in the thalamocortical and corticothalamic projections?

A

Glutamate - excitatory

They are also ipsilateral

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135
Q

What is significant about the ventral thalamus?

A

It is a sheet of GABAergic inhibitory interneurons that surrounds the thalamus (dorsal thalamus). They send their axons ONLY to the dorsal thalamus and do not project to the cerebral cortex.

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136
Q

What is the thalamic reticular nucelus (TRN)?

A

Ventral thalamus structure that is a sheet of GABAergic inhibitory interneuron.

Sends axons ONLY to the dorsal thalamus and not to the cerebral cortex

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137
Q

What structure do the axons of the ventral thalamus (thalamic reticular nucleus - TRN) project to?

A

The dorsal thalamus only

No projections to the cerebral cortex

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138
Q

What are the three main nuclear groups of the thalamus?

A

Medial

Lateral

Anterior

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139
Q

What divides the three nuclear groups of the thalamus?

A

The internal medullary lamina

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140
Q

Which nucleus receives afferents from the dorsal column nuclei, the spinothalamic tract and the vestibular nuclei?

A

VPL

Sends efferents to S1, S2, and the posterior parietal cortex

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141
Q

Where does the VPL receive afferents and where does it send efferents to?

A

From: dorsal column nuclei, spinothalamic tract, vestibular nuclei

To: S1, S2, posterior parietal cortex

(sensory)

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142
Q

What is the primary function of the VPL relay neurons?

A

Sensory

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143
Q

What is the primary funciton of the VPM?

A

Sensory

From trigeminal nucleus and spinal nucleus of V

To S1, S2

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144
Q

Where does VPM recieve afferents from and send efferents to?

A

From: principal trigeminal nucleus, spinal nucleus of V

To: S1, S2

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145
Q

What thalamic nucleus do afferents from the prinicpal trigeminal nucleus and spinal nucleus of V relay at?

A

VPM

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146
Q

Where do axons of the nuclei of the solitary tract (taste) and of the spinothalamic tract project to in the hypothalamus?

A

VM nucleus

Send efferents to the gustatory cortex and insula

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147
Q

Where do VM nucleus neurons in the hypothalamus receive and send axons to?

A

From: Solitary tract nuclei (taste), spinothalamic tract

To: Gustatory cortex, insula

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148
Q

Where do LGN neurons receive afferents from and send efferents to?

A

From: Retina via optic tract

To: V1

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149
Q

What thalamic nucleus receives afferents from the retina via the optic tract?

A

LGN

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150
Q

To which thalamic nucleus do afferents from the superior colliculus send their axons?

A

LP (lateral posterior)/ pulvinar nucleus

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151
Q

Where does the LP/pulvinar nucleus in the thalamus receive afferents from and send efferents to?

A

From: Superior colliculus

To: Temporal and parietal visual association cortical areas

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152
Q

Which thalamic nucleus do neurons from the inferior colliculus send their axons?

A

Medial Geniculate Nucleus (MGN)

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153
Q

Where does the MGN send and receive its efferents/afferents?

A

From: Inferior colliculus

To: A1

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154
Q

Which thalamic nucleus receives its afferents from the substantia nigra and globus pallidus?

A

VA - motor

Sends to several frontal cortical areas

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155
Q

Where does the VA nucleus in the thalamus send/recieve efferents/afferents from?

A

From: Substantia nigra, globus pallidus

To: Several frontal cortical areas

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156
Q

What thalamic nucleus receives afferents from the globus pallidus?

A

VLa

(VA receives from globus pallidus too, but also receives from substantia nigra)

VLa sends efferents to the premotor cortex

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157
Q

Where does the VLa nucelus in the thalamus send/receive efferents/afferents to/from?

A

From: Globus pallidus

To: Premotor cortex

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158
Q

Which thalamic nucleus receives afferents from the cerebellum?

A

VLp

Sends efferents to M1

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159
Q

Where does the VLp nucleus in the thalamus send/receive efferents/afferents to/from?

A

From: Cerebellum

To: M1

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160
Q

Which thalamic nucleus receives afferents from the hypothalamus?

A

The anterior group

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161
Q

Where does the anterior group of the thalamus send/receive efferents/afferents to/from?

A

From: Hypothalamus

To: Cingulate cortex

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162
Q

Which thalamic nucleus receives afferent signals from the amygdala and subiculum?

A

The MD nucleus (Medial dorsal)

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163
Q

Where does the MD nucleus of the thalamus send/receive efferents/afferents to/from?

A

From: Amygdala, subiculum

To: Prefrontal cortex

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164
Q

Which thalamic nucleus receives afferent signals from the subiculum?

A

LD nucleus (Lateral dorsal)

The MD nucleus does too, but it also receives from the amygdala

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165
Q

Where does the LD nucelus of the thalamus send/receive efferents/afferents from/to?

A

From: subiculum

To: Prefrontal, retrosplenial cortices, parahippocampal gyrus

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166
Q

Where do the intralaminar nuclei of the thalamus send/receive efferens/afferents from/to?

A

From: Globus pallidus, spinothalamic tract, cerebellum, substantia nigra, multiple cortical areas

To: Striatum (caudate and putamen), multiple cortical areas - layer I

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167
Q

What is contained in every relay nucleus in the thalamus?

A

Excitatory relay neurons that project through the internal capsule to middle layers (mostly layer 4) of their cortical target fields

GABAergic inhibitory interneurons whose axons remain local - NOT part of the TRN.

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168
Q

How does corticothalamic input modulate the output of relay neurons in thalamic nuclei?

A

Feedback inhibition from the TRN, via thalamic-cortical collaterals

Feedforward inhibition from descending cortical fibers, via cortical-thalamic axon collaterals

And feedforward inhibition from ascending afferent fibers

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169
Q

What are the main roles of the thalamus?

A

Relay functions - synapses that preserve and sharpen topographic information and modality specificity while transferring information from the periphery to the cerebral cortex

States of consciousness - Different behavioral states (awake vs sleep) are associated with firing frequencies of thalamic neurons

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170
Q

How does the thalamus regulate states of consciousness?

A

By the frequency of its neuronal firing

Tonic firing = awake, alert

Burst firing = drowsy, asleep

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171
Q

What is tonic firing?

A

Thalamic state of relative depolarization (caused by neurotransmitters ACh, histamine, norepinephrine) that allows dorsal thalamic relay neurons to fire faithfully in response to depolarization.

This allows information to flow through the cotex and corresponds to wakefullness

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172
Q

Which thalamic firing pattern is associated with wakefullness/alertness/

A

Tonic firing

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173
Q

What is burst firing?

A

Thalamic neuron firing pattern that corresponds with drowsiness and sleep.

the resting membrane potential is hyperpolarized (serotonin can do this) and thalamic relay neurons fire in an oscillatory manner, which blocks the flow of information to the cortex. A functional loop between the TRN and dorsal thalamus maintains this pattern:

  • TRN action potentails cause GABA release, generating IPSPs which hyperpolarize the dorsal thalamus relay neurons
  • IPSPs trigger hyperpolarization-sensitive channels that allow for increased Na conduction and action potential firing
  • This triggers an action potential in the TRN, which starts teh cycle again
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174
Q

Which thalamic firing pattern is associated with deep sleep/drowsiness?

A

Burst firing

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175
Q

What neurotransmitters regulate the thalamic firing pattern?

A

ACh, histamine, norepinephrine depolarize the membranes of dorsal thalamic nuclei, kicking the neurons into tonic firing

Serotonin hyperpolarizes the membranes of dorsal thalamic nuclei and TRNs, which triggers burst firing and prevents information from goign to the cortex

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176
Q

What is the effect of serotonin (5HT) on the thalamus?

A

Promotes burst-firing pattern of activity by hyperpolarizing the membranes of the dorsal thalamicn uclei and TRN

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177
Q

What is the effect of ACh on the thalamus?

A

Depolarizes the membrane of the dorsal thalamic nuclei, kicking neurons into tonic firing mode

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178
Q

What is the effect of histamine on the thalamus?

A

Depolarizes the membrane of the dorsal thalamic nuclei, kicking neurons into tonic firing mode

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179
Q

What is the effect of norepinephrine on the thalamus?

A

Depolarizes the membrane of the dorsal thalamic nuclei, kicking neurons into tonic firing mode

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180
Q

What is typically the cause of thalamic lesions?

A

Vascular issues

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181
Q

What is the reticular activating system?

A

parabrachial, pedunculopontine and other brainstem nuclei (ACh)

Locus ceruleus (norepinephrine)

Raphe nucleus (serotonin)

hypothalamic nuclei (histamine)

Help control the firing pattern of thalamic nuclei

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182
Q

What is thalamic syndrome?

A

Damage to posterior structures o the thalamus, including VPL/VPM

Characterized by contralateral hemianesthesia and excruciating pain

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183
Q

What is the effect of damage to the posterior thalamus (VPL, VPM)?

A

Thalamic syndrome

Contralateral hemianesthesia, excruciating pain

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184
Q

What are tremor states?

A

Rhythmic bursts in VA/VLa due to frequency abnormalities in GP-thalamus circuits (e.g. parkinsons)

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185
Q

What is caused by frequency abnormalities in GP-thalamus circuits?

A

Rhythmic bursts in VA/VLa that result in tremor states

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186
Q

What causes amnesia?

A

Lesions in anterior nuclei, MD nuclei that disrupt amygdala-hippocampal circuitry

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187
Q

What is caused by lesions in the anterior nuclei, MD nuclei that disrupt amygdala-hippocampal circuitry?

A

Amnesia

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188
Q

What are absence seizures?

A

Spike and wave patterns entrained by very long bursts in TRN GABAergic neurons that cause

Marked by sudden onset of consciousness that lasts a brief amount of time.

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189
Q

What is caused by very long bursts in TRN GABAergic neurons?

A

Spike and wave patterns that are characteristic for absence seizures

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190
Q

What are the broad components of the eye?

A

3 Layers (External, Intermediate, Internal)

3 Fluid Compartments (Anterior chamber, posterior chamber, vitreous body)

Crystalline Lens

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191
Q

What components make up the external layer of the eye?

A

Sclera and cornea

192
Q

What is the sclera?

A

Tough, fibrous, opaque white outer covering that covers the entire eye except the anterior area covered by the cornea

Continuous posteriorly with dura (sheath) around optic nerve

Continuous anteriorly with the cornea

193
Q

What is the cornea?

A

The clear, outermost layer of the front of the eye. Provides protection and helps focus the entry of light into the eye

Provides 2/3 of the focusing capcity of the eye

194
Q

What is a corneal disorder where the cornea has an irregular shape?

A

Astigmatism

Can be corrected with glasses, contacts, or refractive eye surgery

195
Q

What is an astigmatism?

A

A corneal disorder in which the cornea has an irregular shape.

Causes refractive effor or poor light focusing capacity. Can be corrected with glasses/contacts/surgery

196
Q

What are the components of the intermediate layer of the eye?

A

Iris, ciliary body, and the choroid

197
Q

What is the iris?

A

The circular, pigmented membrane enclosing the pupil

The source of eye color and houses the muscles that control pupil size.

Located between the cornea and lens

198
Q

What is the ciliary body?

A

Located beneath the sclera and lateral to the lens. It makes aqueous humor and contains the ciliary muscle that allows the lesn to change shape to focus

199
Q

What structure makes aqueous humor?

A

The ciliary body

200
Q

What is the choroid?

A

A layer of connective tissue and blood vessels between the sclera and the retina that supplies nutrients to the eye

201
Q

What supplies nutrients to the eye?

A

The choroid

202
Q

What are the components of the internal layer of the eye?

A

Retina

203
Q

What is the anterior chamber of the eye?

A

One of the three fluid compartments of the eye that is located in between the cornea and the iris

204
Q

What is the posterior chamber of the eye?

A

One of the three fluid compartments of the eye located behind the iris.

Aqueous humor is created by the ciliary body and flows through the posterior chamber into the anterior chamber

205
Q

What is glaucoma?

A

An aqueous humor disorder in which there is excess aqueous humor in the eye from drainage obstruction and other causes

Causes high ocular pressure and can injure the optic nerve, causing vision loss.

206
Q

What is an aqueous humor disorder in the eye that is caused by drainange obstruction or other causes that results in increaed ocular pressure?

A

Glaucoma

Can cause vision loss by impinging the optic nerve

207
Q

What is the vitreous body?

A

One of the three fluid compartments of the eye

Found between the back of the lens and the retina

Contains a transparent, jelly-like substance

208
Q

What is the lens?

A

A transparent, biconvex structure that refracts light to focus it on the retina (the cornea also does this)

209
Q

What is presbyopia?

A

Loss of the ability with age of the lens to change shape, or accomodate

210
Q

What is the term for the loss, with age, of the ability to change the shape of the lens (accomodate)?

A

Presbyopia

211
Q

What are cataracts?

A

Clouding of the lens that develops slowly with advanced age

212
Q

What is the term for the progressive clouding of the lens?

A

Cataract

213
Q

What is myopia?

A

near-sightedness

Caused by a long anterior-posterior eye length

214
Q

What is hyperopia?

A

Far-sightedness

Caused by short anterior-posterior eye length

215
Q

What is caused by a short anterior-posterior eye length?

A

Hyperopia (far-sightedness)

216
Q

What is caused by a large anterior-posterior eye length?

A

Myopia (nearsightedness)

217
Q

What is the embyrologic origin of the retina and retinal pigment?

A

From outpocketing of the neural tube into optic vesicles

218
Q

What is the embryologic origin of the lens?

A

Surface ectoderm

219
Q

What is special about horizontal, bipolar, and amacrine cells of the retina?

A

They do not produce action potentials.

They are interneurons that release neurotransmitters in response to polarization

220
Q

What is special about ganglion cells in the retina?

A

They generate action potentials in response to polarization changes (distinct from horizontal, bipolar, and amacrine cells, whcih do not generate action potentials)

221
Q

What are the 10 layers of the retina?

A

From deep to superficial:

  • retinal pigment epithelium
  • rods and cones
  • external limiitng membrane
  • outer nuclear layer
  • outer plexiform layer
  • inner nuclear layer
  • inner plexiform layer
  • layer of ganglion cells
  • nerve fiber layer
  • internal limiting layer
222
Q

What is the RPE?

A

Retinal Pigment Epithelium

Deepest layer of the retina, contains melanin that absorbs extra light so there is not reflective scattering

Crucial in renewal of components of the photoreceptors:

Provides vitamin A for visual pigment synthesis

Phagocytosis of discarded visual pigments

223
Q

What is a disorder that occurs between the RPE and the photoreceptors?

A

Retinal detachment

224
Q

What is the second layer of the retina (from deep to superficial)?

A

The photoreceptor layer (rods and cones)

225
Q

Which retinal layer contains the cell bodies of the photoreceptors?

A

The outer nuclear layer (ONL)

226
Q

Which is the first synaptic layer of the retina?

A

The outer plexiform layer

Here, interactions between photoreceptors, bipolar cells, adn horizontal cells modulate transmission of visual information

227
Q

Which retinal layer contains teh cell bodies of horizontal, bipolar and amacrince cells?

A

Inner nuclear layer

228
Q

In which retinal layer do interactions between bipolar cells, amacrine cells and ganglion cells modulate transmission of visual information?

A

Inner plexiform layer

229
Q

Which retinal layer is the second synaptic layer?

A

Inner plexiform layer

Modulation of transmission of visual information by interactions between bipolar, amacrine, and ganglion cells

230
Q

What occurs in central retinal artery infarcts?

A

The blood supply to the central retinal artery that branches off of the opthalmic artery is occluded, producing retinal disorders

231
Q

What is a retinal disorder caused by vascular issues to the central retinal artery?

A

central retinal artery infarctions

232
Q

What are the photoreceptors?

A

Rods and cones

233
Q

What is the purpose of the stacking of membranous disks in the photoreceptors?

A

Increases surface area to maximize light capture

234
Q

What is the difference between rods and cones with respect to the membranous disks?

A

Rods: disks are separated completely from the plasma membrane

Cones: disks are made of plasma membrane folds

235
Q

What are structural differences between rods and cones?

A

Rods: Disks that house visual pigment are separated completely from membrane; Long, slender outer segments

Cones: Disks that house the visual pigment are made from the plasma membrane; short, conical outer segments

236
Q

What is contained in the outer segment of photorecepors?

A

The membranous disks that contain the visual pigment

237
Q

What is contained in the inner segment of photoreceptors?

A

mitochondria, golgi apparatus, endoplasmic reticulum, and the nucleus of the photoreceptor

238
Q

What neurotransmitter is used by the photoreceptor cells?

A

Glutamate

239
Q

What are functional differences between rods and cones?

A
240
Q

What is caused by a dysfunction of rod cells?

A

Night blindness (defects in night vision)

Recall, rods are great for vision in dim light

241
Q

What is caused by defects in cone cells?

A

Decreased visual acuity and loss of color vision

Recall, cone cells are responsible for high quality vision

242
Q

What is retinitis pigmentosa?

A

A degenerative retinal condition with pigmentary deposits in the retina.

Often familial/genetic

Symptoms include night blindness, tunnel vision

243
Q

Where are rods located in greater numbers?

A

At outer edges of retina

244
Q

Where are cones located in greater numbers?

A

At fovea

245
Q

What is scotopic vision?

A

Vision at lowest light levels

Mediated by rods

Poor resolution and no color vision

246
Q

What is photopic vision?

A

Vision at brighter light levels

Rods are saturated and all channels are closed

Mediated by cones

247
Q

What is Mesopic vision?

A

Vision where both rods and cones contribute

248
Q

What is the fovea?

A

Area of the retina richest in cones

Responsible for our high-acuitiy vision

Used whenever we look at an object directly

249
Q

What are the three different types of cones?

A

Short, middle, and long wavelength cones

Help in seeing color

250
Q

What is special about the retina at the fovea?

A

Enriched in cones

Retinal layers fold away, which decreases tha mount of tissue that light has to pass through before transmission of visual information begins

251
Q

What is macular degeneration?

A

Foveal and macular (retinal area surrounding fovea) disorder that is the leading cause of blindness over age 65

Degnerative disease of macula

(Age related macular degenration)

252
Q

What is the macula?

A

The retina that surrounds the fovea

253
Q

What is phototransduction?

A

Process by which light energy is tranformed into chemical signals via neurotransmitter release from photoreceptors

Occurs via a process of gradual polarization changes, rather than photoreceptor action potentials

Graded membrane potential

G-protein signaling pathway

254
Q

Describe the process of photransducton in the photoreceptors?

A

In the dark, there is steady glutamate release by photoreceptors due to the high levels of cGMP in the cell that keeps the membrane depolarized

With light, Rhodopsin is activated, which activates Transducin, which activates cGMP phosphodiesterase (PDE), which hydrolyzes cGMP to GMP. As a result, the membrane hyperpolarizes and the release of glutamate ceases

Transducin inactivates itself and rhodopsin interacts with arrestin, which halts its activity

255
Q

What steps occur downstream of the photoreceptors in the process of transmitting visual information from the retina to the optic nerve?

A

Bipolar cells variably hyperpolarize or depolarize in response to decreased glutamate transmission

They transmit their information to ganglion cells which transmit standard action potentials to optic nerve and brain. Interactions with horizontal and amacrine cells modulate information transmission

256
Q

What is significant about the convergence of rods and cones to ganglion cells?

A

Rods converge highly which inreases their sensitivity but diminishes thier acuity

Cones do not converge that much, which increases their acuity, and spatial resoution

vs

257
Q

What is significant about retinal ganglion cells in the visual information pathway?

A

They translate chemical information to electrical information.

Their axons become the optic nerve, which takes visual information from the eye to the brain

258
Q

What are magnocellular cells?

A

Ganglion cells that:

primarily carry rod-generated signals

dominate the peripheral retina

have large receptive fields

are motion and direction sensitive

are color and detail insensitive

259
Q

Which ganglion cells primarily carry rod-generated signals, dominate the peripheral retina, have large receptive fields, are motion and direction sensitive, and are color and detail insensitive?

A

Magnocellular cells

260
Q

Which ganglion cells primarily carry cone-generated signals, dominate the central retina, have small receptive fields, and are acuity and color sensitive?

A

Parvocellular

261
Q

What are parvocellular cells?

A

Ganglion cells that:

Primarily carry cone-generated signals

Dominate the central retina

Have small receptive fields

Are acuity and color sensitive

262
Q

What is the receptive field of a retinal neuron?

A

The region of the retina within which a stimulus will result in a response from that neuron.

263
Q

Describe ganglion cell receptive fields

A

Have a senter and an antagonistic surround

There are two types: ON-center and OFF-center

ON-center increase firing rate when stimulated and center, adn decrease when stimulated at surround

OFF-center decrease firing when light hits center, and increase rate when light hits surround

264
Q

What are ON-center receptive fields?

A

Receptive fields for ganglion cells that increase firing rate when light hits the center of the receptive field and derease firing rate when light hits the surround

265
Q

What are OFF-center receptive fields?

A

Ganglion cell receptive fields which decrease their firing rate when light hits their center and increases their firing rate when light hits their surround

266
Q

What is the biological basis behind the ON-center and OFF-center receptive fields?

A

ON-center ganglion cells express the metabotropic glutamate receptor which is inhibitory. When light hits, less glutamate is released, which results in less inhibition, causing depolarization and signal transduction

OFF-center ganglion cells express the ionotropic glutamate receptor which is excitatory. When light hits, less glutamate is released which results in less signal, causing hyperpolarization and no signal tranduction.

267
Q

What glutamate receptor is expressed in ON-center bipolar cells?

A

Metabotropic - inhibitory

268
Q

What glutamate receptor is expressed in OFF-center bipolar cells?

A

Ionotropic receptor (excitatory)

269
Q

What generates the surround of a bipolar cell’s receptive field?

A

Horizontal cells (release GABA) - attenuates glutamate release at adjacent photoreceptors

Glutamate released from a photoreceptor cell depolarizes horizontal cells

270
Q

Where does the optic nerve exit the posterior eye?

A

Through the lamina cribrosa - scleral fenestrations

271
Q

What is the physiologic blind spot?

A

Area where there is no photoreceptors (where the optic nerve is) so there is no corresponding visual stimuli

The brain fills this space with information from the other eye

272
Q

What is the optic chiasm?

A

Area of the visual system that allows for over half of the nerve fibers from the optic nerves to cross sides. The rest of the fibers remain uncorssed

273
Q

Which thalamic nucleus do the optic tracts project to?

A

The lateral geniculate nucleus

274
Q

Where do the fibers of the optic nerve first synapse?

A

The lateral geniculate nucleus

275
Q

What is the outflow tract of the lateral geniculate nucleus called?

A

Optic radiations - in temporal and parietal lobes

276
Q

What is the temporal optic radiation called?

A

Meyer’s loop

277
Q

What is Meyer’s loop?

A

The temporal optic radiation from the lateral geniculate nucleus

278
Q

Where do the nerve fibers that make up the optic radiations synapse?

A

In the occipital cortex (striate cortex, V1, Broadmans area 17)

279
Q

Which fibers travel through the temporal radiation?

A

Lower retinal fibers (upper visual field)

280
Q

Which fibers travel through the parietal radiation?

A

Upper retinal fibers (lower visual field)

281
Q

Which radiation do the lower retinal fibers travel through?

A

(upper visual field)

Temporal radiation

282
Q

Which radiation do the upper retinal fibers travel through?

A

(lower visual field)

Parietal radiation

283
Q

What is the striate cortex?

A

Primary visual cortex

284
Q

What processes motion vision?

A

The dorsal extrastriate pathway

Information goes to the parietal lobe

Interprets spatial information

285
Q

What processes color and detail vision?

A

The ventral extrastriate pathway

Information goes to the temporal lobe

Important for object recognition

286
Q

What are the temporal fields?

A

Outer fields, by ear

287
Q

What are the nasal fields?

A

Inner visual fields, by the nose

288
Q

What ist he convention of how visual fields are drawn?

A

The way a person sees the world.

Left eye on left, right on right

289
Q

How do visual fields represent the information that is received by the retina?

A

It is inverted right/left and up/down

290
Q

Whech retinal fibers do not cross in the optic chiasm?

A

temporal retinal fibers (corresponding to nasal visual fields)

291
Q

Which retinal fibers cross in the optic chiasm?

A

nasal retinal fibers (corresponding to termporal visual fields)

292
Q

What visual field defects will be seen in the event of optic nerve disease?

A

Monocular blindness

Can be caused by Optic Neuritis (MS) or Temporal Arteritis

293
Q

What visual pathway lesion will result in monocular blindness?

A

Optic nerve damage

e.g. optic neuritis or ischemic optic neuropathy

294
Q

What is temporal arteritis?

A

Ischemic optic neuropathy

Typically seen in elderly patients with sudden severe vision loss, jaw claudication and scalp tenderness

Can lose all vision if left untreated

295
Q

What will a lesion in the optic chiasm present as (visual fields)?

A

Vision loss in temporal visual field of each eye, because it affects crossing nasal retinal fibers

Bitemporal hemianopia

E.g. compression of chiasm from a pituitary adenoma (benign pituitary gland tumor) - reversible

296
Q

What is bitemporal hemianopia?

A

Vision loss in both temporal visual fields

Caused by optic chiasm lesions

297
Q

What lesion of the visual system will cause bitemporal hemianopia?

A

Optic chiasm lesions

298
Q

What visual defects can you see in the case of a pituitary adenoma?

A

Bipolar hemianopia (midline chiasm lesion)

299
Q

What visual field patterns do you see when a lesion affects one optic nerve and the optic chiasm?

A

Visual field loss of central visual field in optic nerve damage side, and temporal field loss in the other eye

300
Q

What is the relationship between the visual fields and the side of the brain of their projections?

A

Contralateral:

Left visual fields (on left side = temporal, on right side = nasal) correspond to right brain (right tracts, right radiations)

Right visual fields (on left side = nasal, on right side = temporal) correspond to left brain (left tracts, left radiations)

Note, these are NOT retinal fields

301
Q

What visual field defect will you see in lesions to the optic tracts?

A

Contralateral, homonymous, binocular defects

Left optic tract = right visual field defecits (right homonymous hemianopia)

Right optic tract = left visual field defecits (left homonymous hemianopia)

(#4)

302
Q

What lesion will produce a left homonymous hemianopia?

A

Right optic tract lesions

303
Q

What visual field defecits wil you see in damage to an optic radiation?

A

Temporal radiation: contralateral superior homonymous quadrantopia

Parietal radiation: contralateral inferior homonymous quadrantanopia

Lower visual field = Parietal

Upper visual field = Temporal

(# 5, 6)

304
Q

What lesions can cause quadrant anopias?

A

Optic radiation lesions

Upper losses = temporal

Lower losses = parietal

305
Q

What lesion produces a “pie in the sky” lesion?

A

Temporal optic radiation lesions (upper quadrantanopsia)

(#6)

306
Q

What visual field defecits will you see in occipital cortex damage?

A

Contralateral homonymous hemianopia with macular sparing

Lose contralateral visual field except for fovea

(foveal regions have collateral circulation from MCA in addition to PCA)

307
Q

What separates superior and inferior visual field representations in the primary visual cortex?

A

The calcarine fissure

Above the fissure = inferior visual field

Below the fissure = superior visual field

308
Q

What is the lateral geniculate nucleus?

A

The thalamic relay for the visual system.

Receives input from the magnocellular and parvocellular ganglion cells and maintains segregation of information from rods vs cones, right vs left eye.

Circular center-surround is maintained

309
Q

Which LGN layers do magnocellular ganglion cells project to?

A

1 and 2

Motion vision

310
Q

Which LGN layers do parvocellular ganglion cells project to?

A

3-6

Acuity, color

311
Q

Which LGN layers receive contralateral eye inputs?

A

1, 4, 6

312
Q

Which LGN layers receive ipsilateral eye inputs?

A

2, 3, 5

313
Q

How are the layers of the LGN organized?

A


314
Q

Which layer of the striate cortex receives direct input from the optic radiations?

A

Layer 4C

315
Q

What is layer 4C?

A

The only layer of the striate cortex (visual cortex) that receives direct input from the optic radiations

316
Q

How is the striate cortex organized?

A

Laminar, into 6 layers

Input from the LGN is maintained in its segregated form into layer 4C. From there, information is distributed to the rest of the cortical layers, extrastriate cortices, and higher order pathways

317
Q

What are ocular dominance columns?

A

Column of neurons in the 4C layer of the striate cortex thar preferentially receives input from one eye.

These require visual experience for their development.

Developmental issues where one eye is misaligned or malfunctional will result in vision not developing well in the unused eye - amblyopia

318
Q

What is strabismus?

A

Cross eyed-ness

Can result in ablyopia - poor development of vision in one eye (poor development of ocular dominance columns)

319
Q

What is amblyopia?

A

Poor development of ocular dominance columns, casued by strabismus or asymmetric refractive error such that visual experience is not symmetric in both eyes

320
Q

What are cortical receptive fields?

A

Cortical neurons that resond to lines, bars, and edges in certain orientations (give orientation selectivity), and to tthem moving in certain directions (give directional selectivity)

Still in layer 4 of visual (striate) cortex

321
Q

What provides orientation and directonal selectivity?

A

Cortical receptive fields

322
Q

What are simple cell receptive fields?

A

Cortical receptive fields with on and off regions that respond to information of light in bars

323
Q

What are complex cell receptive fields?

A

Generated by the summation of simple cells and respond to lines of a specific orientation that occur at any locations within their receptive fields

Do not have ON and OFF regions

324
Q

What function does the sphincter pupillae have?

A

Constricts pupil upon exposure to light

Parasympathetic innervation

325
Q

Which muscle constricts the pupil?

A

Sphicnter pupillae

326
Q

What type of innervation controls pupil constriction?

A

Parasympathetic

327
Q

What type of innervation controls pupil dilation?

A

Sympathetic

328
Q

What muscle dilates the pupil?

A

Dilator pupillae

329
Q

What is mydriasis?

A

Pupil dilation

330
Q

What is miosis?

A

Pupil constriction

331
Q

What is the medical term for pupil dilation?

A

Mydriasis

332
Q

What is the medical term for pupil constriction?

A

Miosis

333
Q

What is the dilator pupillae?

A

Muscle that dilates the pupil

Under sympathetic control

334
Q

How does the pupillary light reflex differ from retinal vision?

A

Similar up to optic tracts, but then does not course through the LGN, optic radiations or striate cortex

Fibers go to the midbrain, where they decussate and go to both Edinger-Westphal nuclei of CN III (oculomotor). Output from here proceeds bilaterally and synapes in the ciliary ganglion, which innervates the sphincter pupillae

335
Q

What is the course of the pupillary light reflex?

A

Sensory input proceeds from the optic nerve to the chiasm and optic tract. The fibers proceed to the midbrain, where they decussate and go to both Edinger Westphal nuclei (parasympathetic) of CN III

Efferent outputs exit with CN III bilaterally and synapse at the ciliary ganglion. From ehre they innervate the sphincter pupillae

Pupillary light reflex is consensual (both eyes constrict)

336
Q

What is the near triad?

A

Pupillary near reflex - constriction of the pupil

Convergence - inward movement of the eyes toward the nose

Accomodation - change in the shape of the lens

337
Q

What is convergence?

A

inward movement of the eyes toward the nose - seen as part of the pupillary near reflex

338
Q

What is accomodation?

A

Change in the shape of the lens of the eye

339
Q

What is pupillary near reflex?

A

Pupillary constriciton when we shift our gaze from distant to near target

340
Q

How do sympathetics reach the dilator pupilllae?

A

3 neuron pathway

Nerves originate in hypothalamus descend in brainstem and synapse in the intermediolateral spinal column

Preganglionic sympathetics from T1-T2 ascend with carotid and synapse in the superior cervical ganglion

Postganglionic sympathetics innervate the pupil dilator muscle via long or short ciliary nerves

341
Q

What is a tonic pupil?

A

Dilated pupil that does not constrict to light but does constrict (slowly) to near, followed by slow re-dilation

light-near dissociation

Lesions in ciliary ganglion

Unopposed sympathetics

342
Q

What is Argyll-Robertson pupils?

A

Small, irregular pupils commonly caused by neurosyphilis or diabetes

Dissociation of light-near reflexes

Pupils that accomodate but dont react to light

Similar to tonic pupil

343
Q

What is light-near dissociation?

A

Pupillary reflexes of light and accomodation are not both functional

Seen in tonic pupil and Argyll-Robertson pupil

Can accomodate, but cannot react to light

344
Q

What is Horner’s Syndrome?

A

Sympathetic dysfunction that causes ptosis (mild) and miosis (small pupil)

May also see anhidrosis

Sympathetic disorder that could indicate dissection of carotid

345
Q

What is Marcus Gunn pupil?

A

Afferent pupillary defect caused by optic neuropathy, optic neuritis

Tested by swinging flashlight - paradoxical pupil dilation (pupils will enlarge when light shifts from good eye to bad eye)

346
Q

What pupil abnormalities can be seen in CN III palsy?

A

Efferent pupillary defect which could indicate pCom aneurysm

Mydriasis due to unopposed sympathetics

Ptosis due to deficit in levator palpebrae

347
Q

Which nerve carries afferents of pupillary light reflex?

A

CN II

348
Q

Which nerve carries efferents of pupillary light reflex?

A

CN III

349
Q

Where do parasympathetics to the pupils travel?

A

On the outer edge of CN III

350
Q

What is a saccade?

A

Rapid eye movement for focusing fovea on salient stimuli

351
Q

What is vergence?

A

disconjugate eye movements that allow eyes to focus on near vs far objects

352
Q

What are dolls eyes (VOR)?

A

Eyes move in opposite direction of head rotation to maintain focus on target

353
Q

What is optokinetic nystagmus?

A

Combination of saccades + smooth pursuit that llows to follow a moving object

354
Q

Where are the oculomotor nuclei located?

A

Midbrain at the level of the superior colliculus

355
Q

What is the pathway of CN III?

A

The nuclei and Edinger-Westphal are in the midbrain, where the fascicles exit ventrally. They pass between the posterior cerebral artery and the superior cerebellar arteries and through the dural sinus wall of the cavernous sinus. It then exits via the superior orbital fissure

356
Q

What eye movements is CN III responsible for?

A

Elevation, Depression, Adduction and Parasympathetics

357
Q

What would a lesion to CN III look like?

A

Down and out

Ptosis

Mydriasis

Absent light reflex

358
Q

What lesion can cause a CN III defect?

A

pCom aneurysm - compresses nerve

Herniation of temporal lobe uncus

359
Q

Describe the path of CN IV.

A

Nuclei are in the midbrain (level of the inferior colliculus)

Exits dorsally, decussates

Courses through the cavernous sinus and exits through the superior orbital fissure

(contralateral!)

360
Q

What eye movements is CN IV responsible for?

A

Moving the eye down and in

361
Q

What would a lesion to CN IV look like?

A

Vertical diploplia, hypertropia (elevation of affected eye) which worsen with downward gaze

Head tilt that attempts to compensate and minimize the diploplia

362
Q

What can cause a CN IV defect?

A

Head trauma

Congenital abnormalities

363
Q

Where is the nucleus of CN IV located?

A

Midbrain

364
Q

Where is the nucleus of CN VI located?

A

Pons at the facial genu/colliculus

365
Q

What is the pathway of CN VI?

A

Nucleus in the pons, exits and passes under Gruber’s ligament and to the cavernous sinus and exits through the superior orbital fissure

366
Q

What eye movements is CN VI responsible fore?

A

Abduction of the eyes

367
Q

What woudl a lesion to CN VI look like?

A

Horizontal diploplia

Esotropia (eyes deviated towards each other)

368
Q

What can cause CN VI defects?

A

High ICP - nerve is anchored to the skull by Gruber’s ligament; high pressure can cause it to stretch

369
Q

What CN palsy can occur as a direct result of high ICP?

A

CN VI palsy

370
Q

What is in each CN VI nucleus?

A

Abducens motor neurons which form the abducens and interneurons which decussate at the nuclear level and ascend in teh medial longitudinal fasciculus (MLF) to the contralateral oculomotor medial rectus subnucleus to help conjugate horizontal gaze

371
Q

Where is the lesion if the oculomotor, trochlear, and abducens nerves are all affected?

A

Likely to be in the orbital apex or the cavernous sinus

Orbital apex - optic nerve likely affected, as well as V1 nerve division

Cavernous sinus lesion will affect both V1 and V2 nerve divisions

372
Q

What is the internuclear pathway for eye movements?

A

Medial Longitudinal Fasciculus, a periventricular fiber tract used by interneurons of the abducens nucleus to syapse on teh contralateral medial rectus subnucleus of CN III

This coordinates simultaneous contraction of the appropriate eye muscles to conjugate horizontal eye movements

373
Q

What is the Medial Longitudinal Fasciculus?

A

Periventricular fiber tract along the cerebral aqueduct and IV ventricle that is used by abducens interneurons to synapse on contralateral medial recuts subnucleus of CN III to coordinate contralateral eye movements to maintain steady horizontal eye movements.

374
Q

What is internuclear opthalmoplegia?

A

Lesion of the MLF (medial longitudinal fasciculus) in either the midbrain or the pons

Usually occur after immediate decussation of fibers, so the predominant clinical feature is impaired adduction ipsilateral to MLF lesion and dissociated nystagmus of the contralateral abducting eye

Vergence is preserved

375
Q

What do lesions in the MLF present as?

A

Interocular opthalmoplegia (INO)

Ipsilateral impaired adduction, dissociated nystagmus of abducting eye

376
Q

What is the paramedian pontien reticular formation (PPRF)?

A

Neurons in the pons that provide initiating discharges for the control of eye movements that are planned and executed by cortical, cerebellar, and brainstem inputs

Synapse on motor neurons and interneurons in the abducens, and direct Abducens + MLF

Control saccades, smooth pursuit, vestibulo-ocular reflex (Doll’s eyes), optokinetic nystagmus, vergence

377
Q

What do lesions of the PPRF result in?

A

PPRF = Paramedian Pontine Reticular Formation

Result in impaired supranuclear burst neurons that are required for horizontal gaze

Complete ipsilateral horizontal gaze palsy for all types of eye movements. More common is slowing or absence of horizontal eye movements

378
Q

What is a horizontal gaze palsy?

A

Impaired conjugate gaze in both eyes to the side of the PPRF lesion (slowed saccade)

Caused by unilateral lesion of the PPRF which casues you to lose the supranuclear burst neurons

379
Q

What is one-and-a-half syndrome?

A

Lesion to ipsilateral PPRF and ipsilateral MLF (e.g. dorsal caudal pons stroke)

Patients present with:

ipsilateral horizontal gaze palsy (lateral rectus and medial rectus)

Ipsilateral internuclear opthalmoplegia (impaired ipsilateral adduction (medial rectus)

Preserved abduction in contralateral eye

380
Q

What is a gaze preference?

A

Eye movement deficit that comes from a lesion to frontal lobe fields that project to the contralateral PPRFs

Primary roles are in saccades (so patients may have no saccades)

You may have an ipsilateral gaze deviation (look at the lesion)

Vestibulo-ocular reflex can get the eyes to cross the midline

381
Q

What can cause gaze preference?

A

Frontal lobe strokes

382
Q

What is the audible range of humans?

A

20-20,000 Hz

1-120 dB

383
Q

What frequencies of sound are humans most sensitive to?

A

1-3 kHz

384
Q

What are conversational sound frequencies?

A

500-3000 Hz

385
Q

What are the three parts of the ear?

A

Outer, middle and inner

386
Q

What are the components of the outer ear?

A

Pinna - vertical localizaiton of sounds

External auditory meatus - magnifies sound by resonance (20-100 fold)

387
Q

What is the function of the outer ear?

A

Gathers, focuses sound

388
Q

What is the function of the pinna?

A

Vertical localization of sound

389
Q

What is the function of the external auditory meatus?

A

Magnifies sound by passive resonance

390
Q

What is the function of the function of the middle ear?

A

Amplifies sound pressures conducted through the air

391
Q

What are the components of the middle ear?

A

Malleus - attached to tympanic membrane and incus - attachment for tensor tympani

Incus - connected in series with other two ossicles

Stapes - inserts into the oval window, provides attachment for stapedius muscle

Tensor tympani - CN V stretches tympanic membrane, facilitates high frequency vibrations

Stapedius - CN VII, dampens movement of stapes into oval window, attenuating impact of loud sounds (acoustic reflex)

Eustachian tube - conduit b/w nasal passages and middle ear

392
Q

What is the function of the malleus?

A

Attaches to the tympanic membrane and incus

Serves as attachment of the tensor tympani

393
Q

What is the function of the incus?

A

Connects the malleus and stapes in series

394
Q

What is the function of the stapes?

A

Inserts into the oval window

Provides attachment for the stapedius muscles

395
Q

What is the function of the tensor tympani?

A

Stretches the tympanic membrane

Facilitates high frequency vibrations

396
Q

What is the CN that innervates the tensor tympani?

A

CN V

397
Q

What is the function of the stapedius?

A

Muscle that dampens the movement of the stapes into the oval window

Attenuates the impact of loud sounds (low frequency)

This is known as the acoustic reflex

CN VII

398
Q

Which CN innervates the stapedius?

A

CN VII

399
Q

What is the function of the Eustachian tube?

A

Provides conduit b/w the nasal passages and the middle ear

Opens up to equilibrate air pressure of the middle ear with that of the environment

400
Q

What is is bone conduction?

A

Mechanism by which sound can bypass the middle ear through the bones of the middle ear

401
Q

What are the components of the inner ear?

A

Vestibule - contains otolith organs (utricle, saccule) which detect linear acceleration

Cochlea - converts sound pressure into electrochemical impulses that it passes to the brain

Semicircular canals (3) - detect rotational motion

Perilymphatic duct - connects vestibule to the subarachnoid, useful for perilymph drainage

402
Q

What is the function of the inner ear?

A

Transduction of auditory and vestibular information

403
Q

What is perilymph?

A

A fluid, similar to CSF, that fills the bony cochlea (scala vestibuli and tympani)

Low K, high Na

404
Q

What is the cochlea?

A

Bony cavity that coils around itself 2 3/4 times in humans

Central bony core is called the modiolus.

Spiral lamina is a ridge of bone protruding from modiolus

405
Q

What are the compartments of the cochlea?

A

Scala vestibuli (inflow)

Scala media (membranus inner part)

Scala tympani (outflow)

Vestibuli and tympani are filled with perilympjh

Media is filled with endolymph

406
Q

What is endolymph?

A

Viscous fluid that fills the membranous cochlea (scala media)

Contains higher K and lower Na than perilymph

Produced by the stria vascularis lining the outer wall of the scala media

407
Q

What is the stria vascularis?

A

Lines the outer wall of the scala media and produces endolymph

408
Q

What is the endocochlear potential?

A

~80 mV

Endolymph is more positive than perilymph due to differences in K and Na concentrations

(Endo has higher K, lower Na)

Maintains acoustic thresholds

409
Q

What is the effect of loop diuretics that block the Na/K/2Cl transporter on the ear?

A

Decrease the endocochlear potential and raise acoustic thresholds

410
Q

What is the significance of the base of the scala media?

A

Where the scala media is separated from teh scala tympani

Formed by the basilar membrane, Organ of Corti rests on the basilar membrane

411
Q

What is the basilar membrane of the cochlea?

A

Separates the scala media from scala tympani

412
Q

What separates the scala media from the scala tympani?

A

Basilar membrane

413
Q

What separates the scala media from the scala vestibuli?

A

Vestibular membrane

414
Q

What is the vestibular membrane of the ear?

A

Separates the scala vestibuli from the scala media

415
Q

What is the helicotrema?

A

The top of the cochlea, where the scala tympani is confluent with the scala vestibuli

416
Q

Where are sensory receptors for audition located?

A

Hair cells

Located within the Organ of Corti on the basilar membrane

417
Q

What are the sensory receptors for audition?

A

Hair cells

In the organ of Corti

Rest on the basilar membrane

418
Q

What are the two types of hair cells?

A

There are 3 rows of “outer hair cells” and one row of “inner hair cells”

419
Q

Which hair cells are most responsible for audition?

A

Inner hair cells

95% of auditory nerve

420
Q

What is the function of inner hair cells?

A

Most audition

421
Q

What is the function of outer hair cells?

A

Receive input from the superior olive

Sharpen sound frequency resolution (cochlear amplifier)

Protect hair cells from harmfully loud noise

Structural, functional, and metabolic support for inner hair cells

422
Q

What is the tectorial membrane?

A

Thick, dense gel matrix that overlies the hair cells

Helps create shear forces that bend the inner hair cell stereociliary bundles (relative motion of basilar membrane and tectorial membrane)

423
Q

What is the kinocilium?

A

The tallest cilium on the hair cell

Motion of the cilium towards or away from it determines whether or not the cell will depolarize (towards) or hyperpolarize (away)

424
Q

What produces excitatory nerve impulses from a hair cell?

A

Motion of the ciliary bundle towards the kinocilium

425
Q

What causes produces inhibitory nerve impulses from a hair cell?

A

Movement of the ciliary bundle away from the kinocilium

426
Q

What is the basis for sensorineural transduction in the auditory system?

A

Sound pressure waves move the basilar membrane that causes the hair cells to move against the tectorial membrane and cause a deflection of the ciliary bundles towards (excitatory) or away (inhibitory) from the kinocilium

427
Q

What is the effect of aminoglycoside antibiotics (kanamycin, streptomycin) on hearing?

A

They selectively damage outer hair cells, which is the basis for their ototoxicity

428
Q

What are otoacoustic emissions?

A

Sound produced by the vibration of outer hair cells themselves. (sound comes from within the ear)

Can be used to test hearing in newborns

429
Q

How is sound transduced into neural signals?

A

Within the cochlear region of the inner ear. The hair cells are presynaptic to the sensory neurons of the spiral ganglia, which join proximally to form the cochlear division of the vestibulocochlear nerve (CN VIII)

430
Q

How is frequency information maintained in audition?

A

Cochlear hair cells are distributed along the length of the spiral. Higher frequencies activate basal cells, lower frequencies activate apical cells.

Each of these corresponds to nerve activity in the auditory nerve. Each ganglion cell has a ‘characteristic frequency’

Ganglion cells only fire when their hair cells activated

Also, the basilar membrane is wider and stiffer at apex

431
Q

Where does the auditory nerve enter the brainstem?

A

Cerebello-pontine angle

432
Q

Describe the auditory neural pathway.

A

Primary sensory neurons fire APs in response to hair cell NT release

Axons form cochlear division, and enters brainstem at cerebellopontine angle.

These axons bifurcate and terminate at the ipsilateral dorsal and ventral cochlear nuclei (dorsal = temporal processing; ventral = localization)

Secondary neurons project to bilateral superior olivary complexes (SOC)

Ascend in lateral lemniscus and terminate in inferior colliculus

These project to medial geniculate nucleus

Auditory radiations from MGN course under the inferior colliculus and terminate in Heschl’s gyri (temporal lobe)

433
Q

What are the four cardinal signs of Parkinsonism?

A

Tremor

Bradykinesia

Rigidity

Postural instability

434
Q

What are the three categories of tremor?

A

Resting - as in Parkinson’s

Essential - postural, can get worse with age, better with alcohol

Intention - cerebellar

435
Q

What is masked faces?

A

Bradykinesia of face - blank expression

436
Q

When do you see asymmetric parkinsonism?

A

Idiopathic Parkinson’s (i.e. Parkinson’s Disease)

437
Q

When do you see symmetric parkinsonism?

A

Drug-induced, mostly - antidepressants

438
Q

What is the difference between rigidity and spaticity?

A

Rigidity = lead pipe (difficult throughout)

Spasticity = clasp-knife (difficult at first, easier later)

439
Q

What is spasticity?

A

Hallmark of damage to UMN, motor cortex, or cortical tracts.

Can result in hyperactive mytatic reflexes, hyertonia of anti-gravity muscles

Rate dependent

Changes throughout the range of motion (clasp knife)

440
Q

What is rigidity usually implicate?

A

Basal ganglia issue

Not rate-dependent

Constant throughout full range of motion

441
Q

Which metastases go to the brain?

A

Lung

Breast

Colon

442
Q

At what point are auditory symptoms unilateral, and where are they bilateral?

A

Unilateral - up until the cochlear nuclei

Bilateral - from cochlear nuclei up to cerebral cortex

443
Q

What is Wernicke’s area?

A

higher order auditory cortical area important for speech recognition and comprehension

Caudal to primary auditory cortex on language-dominant hemisphere

444
Q

Which thalamic nucleus is associated with audition?

A

Medial geniculate nucleus

445
Q

How is sound localized in the horizontal plane?

A

Bilateral input to the superior olivary complex

SOC cells compute the difference in intensity from the signals from both ears

Dependent on bilateral input from the ventral cochlear nuclei.

Intensity and timing differences

446
Q

What is used to localize sound at high frequencies?

A

Inter-aural intensity differences (IID) - difference in loudness of both ears

447
Q

What is used to localize sounds at low frequenceis?

A

Inter-aural timing differences (ITD) - differences of time of arrival of sound at both ears

448
Q

How is localization of sound in the vertical plane acheived?

A

ITDs (inter-aural timing differences) generated by sound reflection at the pinna

449
Q

How is the primary auditory cortex localized?

A

Tonotopically - Highest sound frequencies are located more posteriorly

450
Q

What is the function of the vestibular system?

A

Senses head motion and position in 3D space

Tells you where you’re going and which way is up

451
Q

Which part of the vestibular system helps us identify where we’re going (angular acceleration)?

A

Semicircular canals

452
Q

Which part of the vestibular system helps us identify which way is up (linear accelerations)?

A

Otolith organs

453
Q

Where does information from the vestibular system generally go?

A

To autonomic functions and motor pathways - not consciously perceived most of the time

454
Q

Which functional pathway mediates the conscious perception of equilibrium?

A

Vestibulo-thalamo-cortical projections

455
Q

What is the role of Vestibulo-thalamo-cortical projections?

A

Mediate conscious perception of equilibrium

456
Q

What is the purpose of the vestibulo-ocular reflex, or the otolith-ocular reflex?

A

Maintains stable gaze during head movements

457
Q

What functional pathway maintains stable gaze during head movements?

A

Vestibulo-ocular reflex (otolith-ocular reflex)

458
Q

What is the purpose of the vestibulo-spinal pathway?

A

Maintins postural equilibrium

459
Q

What vestibular pathway maintains postural equilibrium?

A

Vestibulo-spinal

460
Q

What vestibular pathway maintains head stability during body movements?

A

Vestibulo-colic reflex

461
Q

What is the function of the vestibulo-colic reflex?

A

Maintains head stability during body movements

462
Q

What is the function of the vestibulo-autonomic reflex?

A

Effects compensatory changes in blood flow, respiration, and digestion with changes in posture

463
Q

Which vestibular pathway effects compensatory changes in blood flow, respiration, and digestion with changes in posture?

A

Vestibulo-autonomic reflex

464
Q

What are some symptoms that can be caused by damage to the vestibular system?

A

Poor balance, dizziness, vertigo, motion sickness, fainting.

465
Q

What are the names of the three semicircular canals?

A

Horizontal (lateral)

Anterior (superior)

Posterior (inferior)

466
Q

Describe the structure of the semicircular canals?

A

Bony structure filled with perilymph with a swelling at one end (ampulla).

Has a membranous semicircular canal within it filled with endolymph that also has an ampulla

467
Q

What is the crista ampullaris?

A

The sensory sheet within the ampulla that contains hair cells and supporting cells

Sensory part of vestibular canals

468
Q

What is the cupula?

A

Gelatinous mass that surrounds hair cells at the crista ampularis that helps exert shear forces on hair cells in the vestibular system

469
Q

How are vestibular signals initiated?

A

Shear force by cupula within endolymph causes movement of the stereocilia of the hair cells towards (depolarizes) or away from (hyperpolarization) the kinocilium

470
Q

What are the otolith organs?

A

Saccule and utricle

Transduce linear head accelerations

Filled with endolymph, surrounded by perilymph

Each have macula to detect motion

471
Q

How are the semicircular canals coupled?

A

Horizontal together

Right Anterior/Left Posterior

Left Anterior/Right Posterior

472
Q

What detects movements in the horizontal plane?

A

Utricle

473
Q

What detects movement in the vertical plane?

A

Saccule

474
Q

What is the otolithic membrane?

A

Membrane analagous to tectorial membrane and cupula that is a gelatinous membrane that covers hair cells in the macula of the saccule and utricle (otolith organs)

Has otoconia embedded in the membrane (calcium carbonate crystals) that make the membrane heavier

475
Q

What are otoconia?

A

Calcium carbonate crystals embedded in the otolithic membrane in the saccule and utricle (otolith organs) that make the membrane heavier

476
Q

Where are the cell bodies located for the nerves that innervate the semicircular canals and otolith organs?

A

Scarpa’s Ganglion

477
Q

What is Scarpa’s Ganglion?

A

Cell bodies of the vestibular nerves that innervate the semicircular canals and otolith organs

Brain and Behavior (9 decks)

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